FORENSIC NEUROPSYCHOLOGY

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 SECOND EDITION

FORENSIC
NEUROPSYCHOLOGY

A Scientific Approach

EDITED BY

G L E N N J. L A R R A B E E

1
1
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Library of Congress Cataloging-in-Publication Data

Forensic neuropsychology : a scientific approach / edited by Glenn J. Larrabee. — 2nd ed.

p. cm.
Includes bibliographical references and index.
ISBN 978-0-19-538352-2 (hardback : alk. paper)
1. Forensic neuropsychology. I. Larrabee, Glenn J.
RA1147.5.F668 2011
614'.15—dc23 2011036769
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This material is not intended to be, and should not be considered, a substitute for medical or other professional advice. Treatment for
the conditions described in this material is highly dependent on the individual circumstances. And, while this material is designed to
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 To Sebastian LaSpina and Andy Vince.

As my son Zack said, “A teacher passes on knowledge about their subject.

A mentor passes on knowledge about life. It is only a great coach
who does both.”

I could not have asked for better coaches for my son. It is with
sincere gratitude that I dedicate this book to you.
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 P R E FAC E
The first edition of this book was published in
2005, at which time the preface identified the
rapid growth of the field of forensic neuropsy-
chology. In the ensuing six years this growth has
accelerated, as reviewed in Chapter 18 in the cur-
rent volume by Sweet and Meyer. These authors
show in their Figure 18-1 a more than tripling of
the mention of “neuropsychology,” “neuropsy-
chologist,” or “neuropsychological,” in the legal
search engine LexisNexis® Academic for the
decade of 2000 to 2010, in comparison to 1990 to
1999. Complimentary data presented in Figure
2-1 in Chapter 2 by Kaufmann shows a near dou-
bling of legal citations from 2004 to 2009, with a
projected accelerated growth in coming years.
Many important developments have occurred
since the first edition, including the decision of the
New Hampshire Supreme Court upholding the
use of a flexible test battery (Baxter v. Temple,
2008) and the consensus statement of the American
Academy of Clinical Neuropsychology on the use
of measures of symptom validity and response bias
(Heilbronner, Sweet, Morgan, Larrabee, Millis, &
conference participants, 2009). The continuing
rapid growth and significant developments in
forensic neuropsychology have resulted in the
need for a revision of the first edition.
I was extremely fortunate to have all of the
senior authors agree to contribute revisions of the
work they contributed to the first edition.
Additionally, there are five new chapters, includ-
ing a chapter on admissibility of evidence by
Kaufmann, a chapter on perinatal injury by Taylor,
a chapter by Greve, Bianchini, and Ord on foren-
sic assessment of chronic pain, a chapter by
Andrikopoulos and Greiffenstein on posttrau-
matic stress disorder, and a concluding chapter by
Sweet and Meyer on trends in forensic practice
and research. As before, all of the contributors are
recognized scientists and clinicians who have
contributed to the peer-reviewed literature in
neuropsychology and forensic neuropsychology.
I gratefully acknowledge the assistance of
Patricia Reynolds, M. L. S. of the Bishopric
Medical Library at Sarasota Memorial Hospital
in Florida, who was most helpful in providing
articles for the three chapters I prepared for the
current volume. I am also grateful to Matthew
Miliano, B. A., who helped read and proof the
contents of the entire volume. I further appreciate
the encouragement and assistance of my editors
at Oxford University Press, Joan Bossert, Vice
President/Editorial Director, Medical Division,
and Tracy K. O’Hara, Development Editor,
Medicine. Finally and most important, I appreci-
ate the love, support, and understanding of my
wife, Jan, and our son, Zack, who tolerated the
additional demands on my time during the
completion of this revision.
G.J.L.
May 2011
REFERENCES
Baxter v. Temple, 949 A. 2d 167, (N.H., 2008).
Heilbronner, R. L., Sweet, J. J., Morgan, J. E., Larrabee,
G. J., Millis, S. R., & Conference Participants.
(2009). American Academy of Clinical Neuro-
psychology consensus conference statement on the
neuropsychological assessment of effort, response
bias, and malingering. The Clinical Neuro-
psychologist, 23, 1093–129.
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 CONTENTS

Contributors xi 11 Neurotoxic Injury 281

karen i. bolla
1 A Scientific Approach to
12 The Psychological Assessment
Forensic Neuropsychology 3
of Persons with Chronic Pain 302
glenn j. larrabee
kevin w. greve, kevin j. bianchini,
2 Neuropsychology and the Law: and jonathan s. ord
Principles of Productive Attorney-
13 Forensic Assessment of Medically
Neuropsychologist Relations 23
Unexplained Symptoms 336
manfred f. greiffenstein and
laurence m. binder
paul m. kaufmann
14 Something to Talk About? The Status
3 Admissibility of Expert Opinions based
of Post-traumatic Stress Disorder in
on Neuropsychological Evidence 70
Clinical Neuropsychology 365
paul m. kaufmann
jim andrikopoulos and
4 Ethical Practice of Forensic manfred f. greiffenstein
Neuropsychology 101
15 Assessing Civil Competencies in Older
christopher l. grote and Adults with Dementia: Consent
benjamin a. pyykkonen Capacity, Financial Capacity, and
5 Assessment of Malingering 116 Testamentary Capacity 401
glenn j. larrabee daniel c. marson, katina hebert,
and andrea c. solomon
6 Functional Neuroimaging in Forensic
Neuropsychology 160 16 Criminal Forensic Neuropsychology
and Assessment of Competency 438
joseph ricker
robert l. denney
7 Perinatal Brain Injury 179
17 Criminal Responsibility and
h. gerry taylor
Other Criminal Forensic Issues 473
8 Forensic Aspects of Pediatric robert l. denney
Traumatic Brain Injury 211
18 Trends in Forensic Practice
jacobus donders
and Research 501
9 Mild Traumatic Brain Injury 231 jerry j. sweet and
glenn j. larrabee dawn giuffre meyer
10 Moderate and Severe Traumatic Index 517
Brain Injury 260
tresa roebuck-spencer and
mark sherer
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 C O N T R I BU TO R S
Jim Andrikopoulos, PhD, ABPP
Board Certified in Clinical Neuropsychology
Ruan Neurology Clinic
Des Moines, IA
Kevin J. Bianchini, PhD, ABN
Board Certified in Professional Neuropsychology
Jefferson Neurobehavioral Group
Metairie, LA
Department of Psychology
University of New Orleans
New Orleans, LA
Laurence M. Binder, PhD, ABPP
Board Certified in Clinical Neuropsychology
Independent practice, Beaverton, OR
Departments of Neurology and Psychiatry
Oregon Health and Science University
Portland, OR
Karen I. Bolla, PhD
Departments of Neurology, Psychiatry and
Behavioral Sciences, and Environmental
Health Sciences
Johns Hopkins University, Bayview
Medical Center
Baltimore, MD
Robert L. Denney, PsyD, ABPP
Board Certified in Clinical Neuropsychology
and Forensic Psychology
U.S. Medical Center for Federal Prisoners
School of Professional Psychology at
Forest Institute
Springfield, MO
Jacobus Donders, PhD, ABPP
Board Certified in Clinical Neuropsychology
and Rehabilitation Psychology
Psychology Service
Mary Free Bed Rehabilitation Hospital
Grand Rapids, MI
Manfred F. Greiffenstein, PhD, ABPP
Board Certified in Clinical Neuropsychology and
Forensic Psychology
Psychological Systems, Inc.
Royal Oak, MI
Dawn Giuffre Meyer, PhD
National Rehabilitation Hospital
Washington, D.C.
Kevin W. Greve, PhD, ABPP
Board Certified in Clinical Neuropsychology
Department of Psychology
University of New Orleans
New Orleans, LA
Jefferson Neurobehavioral Group
Metairie, LA
Christopher L. Grote, PhD, ABPP
Board Certified in Clinical Neuropsychology
Department of Behavioral Sciences
Rush University Medical Center
Chicago, IL
Katina Hebert, PhD
Department of Veterans Affairs
Medical Center
Tuscaloosa, AL
xii contibutors
Paul M. Kaufmann, JD, PhD, ABPP
Board Certified in Clinical Neuropsychology
Nebraska Department of Health and
Human Services
University of Nebraska
Lincoln, NE
Glenn J. Larrabee, PhD, ABPP
Board Certified in Clinical Neuropsychology
Independent practice, Sarasota, FL
Daniel C. Marson, JD, PhD
Department of Neurology and Alzheimer’s
Disease Center
University of Alabama at Birmingham
Birmingham, AL
Jonathan S. Ord, MS
Department of Psychology
University of New Orleans
New Orleans, LA
Jefferson Neurobehavioral Group
Metairie, LA
Benjamin A. Pyykkonen, PhD
Department of Behavioral Sciences
Rush University Medical Center
Chicago, IL
Joseph Ricker, PhD, ABPP
Board Certified in Clinical Neuropsychology
and Rehabilitation Psychology
University of Pittsburgh School of Medicine
Pittsburgh, PA
Tresa Roebuck-Spencer, PhD, ABPP
Board Certified in Clinical Neuropsychology
Department of Psychology
University of Oklahoma
Norman, OK
Mark Sherer, PhD, ABPP
Board Certified in Clinical Neuropsychology
TIRR Memorial Hermann
Baylor College of Medicine
Houston, TX
Andrea C. Solomon, PhD
Solomon Neuropsychology, LLC
Montgomery, AL
Jerry J. Sweet, PhD, ABPP
Board Certified in Clinical Neuropsychology and
Clinical Psychology
NorthShore University HealthSystem
Evanston, IL
University of Chicago Pritzker School of
Medicine
Chicago, IL
H. Gerry Taylor, PhD., ABPP
Board Certified in Clinical Neuropsychology
Department of Pediatrics
Case Western Reserve University, and
Rainbow Babies & Children’s Hospital
University Hospitals Case Medical Center
Cleveland, OH
FORENSIC NEUROPSYCHOLOGY
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 1
A Scientific Approach to Forensic Neuropsychology
G L E N N J. L A R R A B E E
This book emphasizes a scientific approach to the
practice of forensic neuropsychology: the applica-
tion of neuropsychology to legal issues that arise
in both civil and criminal legal proceedings. In
certain circumstances, neuropsychological defi-
cits have a direct bearing on legal issues; for exam-
ple, in establishment of damages in a personal
injury case (see chapters 5 and 7–14, this volume).
In other settings, a person may have impaired
neuropsychological test scores, but the impair-
ment alone does not provide the answer to the
legal issue; for example, an older person may have
dementia, but still possess competency to execute
a valid will (chapter 15, this volume); a person
facing criminal charges may have neuropsycho-
logical impairment, but still be found competent
to stand trial and be responsible for the criminal
act (chapters 16 and 17, this volume).
Greiffenstein and Kaufmann (chapter 2), and
Kaufmann (chapter 3) discuss issues related to the
admissibility of expert neuropsychological testi-
mony related to Frye v. United States (1923) and to
Daubert v. Merrell Dow (1993), legal standards
that emphasize acceptability of a particular scien-
tific methodology by one’s peers and standards
that mandate a particular methodology meet sci-
entific principles, such as possessing a known
error rate, and the potential to be falsified or dis-
credited (cf. Popper, 1959).
W H AT I S S C I E N C E ?
The goals of the empirical natural sciences include
exploration, description, explanation, and predic-
tion of worldly occurrences or phenomena (Badia
& Runyon, 1982; Hempel, 1966; Kerlinger, 1973).
Science is concerned with things that can be
publicly observed and tested as opposed to meta-
physical explanations (Kerlinger, 1973).
Science differs from pseudoscience in a
number of ways (Lilienfeld, Lynn, & Lohr, 2003).
Some of the features of pseudoscience include
overuse of ad hoc hypotheses to immunize claims
from falsification; evasion of peer review; absence
of self-correction; and emphasis on confirmation
rather than refutation. Regarding this last point,
Lilienfeld et al. (2003) cited the physicist Feynman
(1985), who maintained that the essence of
science is a bending over backward to prove one-
self wrong. Referencing Popper (1959) and Meehl
(1978), Lilienfeld et al. noted that scientists ideally
subject their claims to grave risk of refutation,
contrasted with pseudoscientists, who tend to
seek only confirming evidence for their claims.
Because a determined advocate for a particular
pseudoscientific position can find at least some
supportive evidence for essentially any claim,
Lilienfeld et al. described this confirmatory
hypothesis testing strategy as “an inefficient means
of rooting out error in one’s web of beliefs” (p. 7).
Subsequently, Lilienfeld (in press) provided a
basic definition of science as a set of systematic
safeguards against confirmation bias.
The basic aim of science is explanation, and
the explanations offered by science are theories
(Kerlinger, 1973). More formally specified, theo-
ries are sets of concepts, definitions, and proposi-
tions that present a systematic view of phenomena
by specifying relations among variables, with the
purpose of explaining and predicting the phe-
nomena (Kerlinger, 1973). Kerlinger further
defined research as “systematic, controlled, empir-
ical, and critical investigation of hypothetical
propositions about the presumed relations among
rational phenomena” (p. 11).
Science is hypotheticodeductive (Badia &
Runyon, 1982; Hempel, 1966; Kerlinger, 1973).
A hypothesis represents a conjectural statement
or tentative proposition about the relation between
two or more variables, for example, between
duration of coma and memory test performance
1-year status post–traumatic brain injury (TBI).
The scientist then deduces the consequences of
4 forensic neuropsychology
the hypothesis he or she has formulated (e.g.,
those brain-injured subjects with shorter dura-
tions of coma will perform better on memory
testing than will those with longer durations of
coma).
A long tradition in psychology is the Fisherian
tradition of specifying a hypothesis for a given
relationship (e.g., between coma and memory test
performance), which is then contrasted with a
hypothesis of no effect, otherwise known as the
null hypothesis (Kerlinger, 1973; Meehl, 1978).
Meehl criticized the null hypothesis testing
approach as responsible for the slow progress of
“soft psychology,” resulting in “a disturbing
absence of that cumulative character that is so
impressive in disciplines like astronomy, molecu-
lar biology, and genetics” (p. 807). As Meehl noted,
the null hypothesis, taken literally, is always false.
He recommended the Popperian approach
(Popper, 1959) of subjecting hypotheses to grave
danger of refutation with modus tollens: “If p, then
q; not q, therefore not p.” In this manner, theories
or hypotheses that survive the most attempts at
refutation are the best-supported theories.
In his 1978 article, Meehl did specify “five
noble traditions in clinical psychology,” two of
which are directly relevant to the practice of
clinical and forensic neuropsychology: (a) descrip-
tive clinical psychiatry (for the discipline of
neuropsychology, descriptive behavioral neurol-
ogy can also be included) and (b) psychometric
assessment. Arguably, both of these “noble tradi-
tions” have led to an accumulation of information
in clinical psychology in general, and neuropsy-
chology in particular, contributing to the cumula-
tive nature of knowledge in these disciplines that
Meehl found lacking in comparisons of the “soft”
science of psychology with the “hard” sciences
such as astronomy.
A S C I E N T I F I C A P P ROAC H
TO N E U RO P S Y C H O L O G I C A L
E VA L UAT I O N
Conducting a neuropsychological evaluation and
making a neuropsychological diagnosis regarding
the presence of brain damage can be conce-
ptualized as a scientific endeavor. The scientific
endeavor includes formulation of hypotheses
that are then checked for support or, better yet,
subjected to attempts at refutation. The formula-
tion of various different hypotheses corresponds
to formulation of differential diagnoses. More
specifically, in a particular civil forensic case
seeking compensation for damages from an
alleged TBI, alternative hypotheses could include
(a) neuropsychological deficits secondary to TBI;
(b) no evidence for any neuropsychological
deficits; (c) neuropsychological deficits secondary
to a preexisting condition such as learning dis-
ability, hypertension, or dementia; (d) neuropsy-
chological deficits secondary to a psychiatric
condition that is related or unrelated to the
accident in question; or (e) neuropsychological
deficits secondary to malingering.
The appropriate use of logical and scientific
reasoning in performing a forensic evaluation is
critical to avoid committing diagnostic errors.
At present, there is a growing problem of overdiag-
nosis of neuropsychological deficits in legal set-
tings because of failure to analyze cases critically
and scientifically (Faust, Ziskin, & Hiers, 1991;
Larrabee, 1990, 2000b; Russell, 1990; Wedding &
Faust, 1989). This failure frequently results in inad-
equate differential diagnosis (Binder, 1997).
Faulty logic commonly leads to diagnostic
error. Miller (1983) noted the argument “if
damage to structure X is known to produce a
decline on Test T, it is tempting to argue that any
new subject or group of subjects having a rela-
tively poor performance on T must have a lesion
at X” is the same as the argument “because a horse
meets the test of being a large animal with four
legs, then any newly encountered large animal
with four legs is a horse” (p. 131). Larrabee (1990,
2000b) extended Miller’s (1983) example to
the diagnostic decision of “brain damage” versus
“no brain damage”: If brain-damaged subjects
perform poorly on neuropsychological tests, then
any new person who performs poorly on neurop-
sychological tests must be brain damaged.
As Russell (1990) and Russell and Kolitz-
Russell (2003) observed, neuropsychological tests
are measures of cognitive abilities rather than tests
of brain damage. Consequently, neuropsychologi-
cal test performance can be poor for many reasons
other than brain damage, including limited coop-
eration or inattentiveness caused by fatigue, pain,
discomfort, medication effects, substance abuse,
learning disability, psychiatric diagnosis, or poor
motivation (Binder, 1997; Larrabee, 1990).
Faust and colleagues have written extensively
about sources of error and bias in clinical decision
making (Faust, 1989; Faust & Nurcombe, 1989;
Faust et al., 1991; Wedding & Faust, 1989). Failure
to consider base rate information can be a major
factor in misdiagnosis. The term base rate refers to
the frequency with which something occurs; for
example, if 5 in 100 persons with mild traumatic
 A Scientific Approach to Forensic Neuropsychology
brain injury (MTBI) suffer persisting neuropsy-
chological deficits, the base rate is 5%. Lack of
awareness of base rates and biases such as confir-
mation bias or hindsight bias can lead to the forma-
tion of illusory correlations or “seeing” relationships
that do not exist (Wedding & Faust, 1989).
The original work on illusory correlations
was conducted by the Chapmans (Chapman &
Chapman, 1967), who presented psychology
undergraduates with human figure drawings
accompanied by randomly paired symptom
statements (e.g., “suspiciousness” would appear in
association with accented eyes as frequently as it
appeared in association with nonaccented eyes).
Despite the absence of systematic relationships in
the data, the psychology students attributed
diagnostic “signs” to the relationships they had
assumed existed in the first place (e.g., associating
accented eyes in human figure drawings with
“suspiciousness”). Chapman and Chapman com-
mented that the erroneously reported correlations
corresponded to associative connections between
symptoms and drawing characteristics (formed
by their research subjects), as well as to what their
subjects expect to see before they actually observed.
Essentially, the Chapman and Chapman research
subjects demonstrated both a failure to consider
base rates as well as a confirmation bias (i.e.,
seeing what they expected to see).
Chapman and Chapman (1969) further dem-
onstrated the presence of illusory correlations
based on the judgments of practicing clinicians.
As shown by Kurtz and Garfield (1978), the bias
toward forming illusory correlation could not be
overcome, even when subjects were provided with
special training against illusory correlations.
The diagnostic significance of base rate data
is further underscored by the investigation by
Lees-Haley and Brown (1993), who tabulated the
frequency of so-called neuropsychological com-
plaints in two groups of subjects: (a) 50 outpa-
tients from a group family practice clinic and
(b) 170 litigants filing personal injury claims for
emotional distress or industrial stress, with no
known history of head injury, toxic exposure,
seizure disorder, or neuropsychological impair-
ment and without any claim for central nervous
system (CNS) injury (non-CNS litigants).
Symptoms commonly thought of as indicative or
“diagnostic” of TBI and neurotoxic exposure
occurred frequently in the medical controls (MCs)
and non-CNS litigants. For example, “difficulty
concentrating” was reported by 26% of MCs and
78% of non-CNS litigants; “headache” was
5
reported by 62% of MCs and 88% of non-CNS
litigants; and “irritability” was reported by 38% of
MCs and 77% of non-CNS litigants.
The data presented by Lees-Haley and Brown
(1993) highlighted significant problems with the
sensitivity and specificity of common neuropsy-
chological symptom checklists. Sensitivity refers
to the frequency or rate of occurrence of a finding
among patients with the condition in question,
whereas specificity refers to the frequency of nega-
tive test results among patients who do not have
the illness or condition in question (Baldessarini,
Finklestein, & Arana, 1983). If the base rate of a
symptom used to diagnose concussion such as
headache in non-CNS samples is ignored, this
would lead to misdiagnosis of brain damage or
dysfunction in 62% of MCs and 88% of non-CNS
litigants based on the data compiled by Lees-
Haley and Brown.
Faust et al. (1991) and Wedding and Faust
(1989) discussed two major types of bias in clini-
cal judgment and decision making: hindsight bias
and confirmation bias. Hindsight bias is the ten-
dency to believe, once the outcome of an event is
known, that the outcome could have been more
easily predicted than is actually the case. Thus,
knowing about an event through clinical history
(e.g., a blow to the head in an automobile acci-
dent) leads clinicians to believe they can predict
the outcome of the event and diagnose neuropsy-
chological deficits consistent with TBI.
Hindsight bias can be closely associated with
confirmation bias, which has been discussed as the
tendency to seek confirming evidence at the
expense of ignoring disconfirming evidence for a
set of diagnostic hypotheses. In confirmation bias,
initial hypotheses are subjected to preferential
analysis, so that the clinician is much more lenient
or accepting of information supporting the initial
hypothesis and more critical and less accepting of
information contradicting the initial hypothesis,
demonstrating a propensity toward asymmetric
error costs (Trope, Gervey, & Liberman, 1997).
Moreover, Trope et al. observed that persons are
more likely to terminate hypothesis testing pre-
maturely once they receive information support-
ing their described hypothesis. Although it is
tempting to attribute confirmation bias to the
emphasis on null hypothesis testing in psycholog-
ical research (cf. Meehl, 1978), confirmation bias
may simply represent a common judgment error
in human decision making (cf. Trope et al., 1997).
I previously described an example of confir-
mation bias in a litigant alleging TBI (Larrabee,
6 forensic neuropsychology
2000b). In this case, it was questionable that
the litigant ever struck her head (she claimed
she did; records did not substantiate this claim).
Nonetheless, the litigant had no loss of conscious-
ness, post-traumatic amnesia, history of acute
focal neurological signs, or abnormal neurological
findings, yet she was diagnosed as suffering brain
damage on the basis of a Wechsler Memory Scale–
Revised (WMS-R; Wechsler, 1987) Attention
Concentration Index (AC) of 75. The psychologist
in this case selectively ignored the WMS-R
General Memory Index (GM) of 129, which not
only contradicted the presence of brain damage,
but also was highly inconsistent with the patient’s
AC of 75. It is logically and clinically inconsistent
that a person with impaired attention at the 5th
percentile could have memory function at the
97th percentile. Actually, the 54-point GM minus
AC difference score had a probability of malinger-
ing greater than 0.99 based on Mittenberg, Azrin,
Millsaps, and Heilbronner’s (1993) research on
detection of malingered head trauma using atypi-
cal patterns of performance on the WMS-R.
Wedding and Faust (1989) provided a number
of strategies that can be employed to reduce biases
in clinical judgment, beginning with the recom-
mendation that the clinician know the literature
on human judgment. Trope et al. (1997) provided
a concise review of human judgment and decision
making. The Wedding and Faust article also
reviewed relevant literature on judgment, decision
making, and clinical versus actuarial prediction.
Wedding and Faust cautioned against prematurely
abandoning useful decision-making rules by start-
ing with the most valid information, listing alter-
native diagnostic options and seeking evidence for
each, and systematically listing disconfirmatory
information. Consideration of disconfirmatory
information is particularly important for reducing
confirmation bias. Wedding and Faust noted that
neuropsychologists frequently make up lists of
test findings that support particular hypotheses,
but recommended also listing all data that argue
against these hypotheses.
Along these lines, I (Larrabee, 2000b) found it
useful to frame hypothetical questions such as,
“What kind of brain damage causes poor perfor-
mance on the Category Test (Reitan & Wolfson,
1993), California Verbal Learning Test-Second
Edition (CVLT-II; Delis, Kramer, Kaplan, & Ober,
2000), and Finger Tapping (Reitan & Wolfson,
1993), with above-average performance on the
Wisconsin Card Sorting Test (Heaton, Chelune,
Talley, Kay, & Curtiss, 1993), Verbal Selective
Reminding Test (Buschke, 1973; Hannay & Levin,
1985; Larrabee, Trahan, & Levin, 2000), Trail
Making B (Army Individual Test Battery, 1944),
and the Grooved Pegboard (Lafayette Instrument,
P.O. Box 5729, Lafayette, IN)?” Indeed, to counter
the diagnostic bias to find brain impairment when
there is none (cf. Russell, 1990; Wedding & Faust,
1989), the neuropsychologist should first list all
evidence suggesting no evidence for brain impair-
ment (e.g., clinical history of no loss of conscious-
ness or post-traumatic amnesia, normal magnetic
resonance imaging scan, normal performance on
sensitive tests such as Trail Making B and Verbal
Selective Reminding).
I suggested a four-component consistency
analysis in neuropsychological decision making
(Larrabee, 1990, 1992, 1997, 2000b):
1. Are the data consistent within and
between neuropsychological domains?
2. Is the neuropsychological profile
consistent with the suspected etiologic
condition?
3. Are the neuropsychological data
consistent with the documented severity
of injury?
4. Are the neuropsychological data
consistent with the subject’s behavioral
presentation?
The data to be considered in this consistency
analysis include a detailed and extensive inter-
view, detailed record review, and extensive and
redundant neuropsychological test measures
within each of several functional domains, includ-
ing language, perception, sensorimotor function,
attention/information processing, psychomotor
speed, verbal and visual learning and memory,
intelligence and problem solving, and motivation
and personality.
The clinical interview is conducted prior to
testing and yields information about the subject’s
recollection of the original injury or trauma (e.g.,
head injury, toxic exposure, hypoxic event); sub-
sequent symptoms and change in symptoms over
time; other health care providers the subject has
seen; and the procedures, diagnoses, and treat-
ments the subject has received. This information,
when cross-checked against the medical records
for accuracy, provides an informal clinical assess-
ment of the subject’s memory function. In the
specific case of closed head injury, detailed ques-
tioning about the events leading up to and follow-
ing the accident (e.g., where the person was
 A Scientific Approach to Forensic Neuropsychology
headed prior to the accident, the time the accident
occurred, recall of events from the scene of the
accident, diagnostic procedures in the hospital)
can be compared to the medical records and
allows a retrospective determination of the pres-
ence and duration of posttraumatic amnesia.
Detailed interviewing about the events of the
accident also allows the opportunity to evaluate
for the presence/absence of the arousal or distress
that could indicate potential for post-traumatic
stress disorder. A background interview covering
early development, nuclear family, school experi-
ences, occupational history, marital history, prior
personal and family medical history, substance
abuse, and prior litigation and criminal history
must also be conducted. The data from this inter-
view are then checked and validated against med-
ical, school, work, and criminal records.
Following completion of the interview, record
review, and collection of the neuropsychological
test data, the consistency analysis is conducted.
First, analysis of the consistency within and
between domains should be conducted. Within
domains, a person who performs poorly on the
Working Memory Index of the Wechsler Adult
Intelligence Scale, Fourth Edition (WAIS-IV;
Wechsler, 2008) should not perform above aver-
age on the Paced Auditory Serial Addition Test
(Gronwall, 1977); a person who performs poorly
on Trail Making A should not perform normally
on Trail Making B; a person with very poor per-
formance on Finger Tapping should not have
normal Grooved Pegboard Performance. Between
domains, a subject with very poor attention
should not perform normally on memory tests; a
person with borderline scores on intelligence and
problem solving should not have superior memory
function.
Second, the neuropsychological test score pro-
file should be consistent with established patterns
for known disorders such as amnesia or dementia.
In my experience, litigants with neuropsychologi-
cal deficits typically do not present with test pat-
terns that suggest focal neurobehavioral disorders
such as aphasia or neglect; rather, litigants either
present with a pattern of test results suggestive of
amnesia (i.e., specific impairment in memory
functions, with other neuropsychological func-
tions essentially preserved) or dementia (i.e.,
impairment in memory as well as in other neu-
ropsychological functions, typically intelligence
and problem-solving skills). Patients with true
amnestic disturbance do not perform poorly on
the WAIS-IV (Wechsler, 2008) Digit Span,
7
Arithmetic, or Digit Symbol; although patients
with dementia may perform poorly on Digit Span,
Arithmetic, or Digit Symbol, they do not perform
at above-average levels on complex problem-
solving tasks such as WAIS-IV Block Design or
the Category Test.
This general principle also applies to awareness
of test profile patterns that could indicate the pres-
ence of a preexisting condition. I (Larrabee, 1990)
previously described a case of misdiagnosis in
which a psychologist diagnosed left hemisphere
brain damage in a patient with an alleged MTBI
(no loss of consciousness or post-traumatic amne-
sia, normal neuroradiological findings) who had
reduced right-hand motor functions, lower Verbal
IQ relative to Performance IQ, and poor verbal
memory. The psychologist did not consider evi-
dence of learning disability verified through school
records and the effects of peripheral injury to the
right upper extremity (with evidence suggesting
functional overlay). These neglected factors pro-
vided a much more compelling interpretation of
the subject’s performance than the original diag-
nosis of left hemisphere brain damage.
The third consistency requirement is that level
of neuropsychological test performance should be
consistent with the severity of injury. This can be
considered as biological severity “indexing” or
“referencing” (Larrabee, 1990, 1997, 2000b).
Dikmen, Machamer, Winn, and Temkin (1995)
provided 1-year outcome data for varying degrees
of head trauma severity, ranging from subjects
who could follow a doctor’s commands within
one hour to persons who took longer than one
month to follow a doctor’s commands following a
TBI. Consequently, a litigant who was briefly
unconscious at the scene of the accident, who
recalls transportation to the hospital, and who
has a Glasgow Coma Scale (GCS) of 15 (i.e., is
oriented, follows commands, eyes open spontane-
ously), no focal neurological signs, and normal
magnetic resonance imaging scan of the brain,
should not perform on neuropsychological tests
at a level equivalent to that produced by subjects
who have suffered two weeks of coma following
their TBI.
Rohling, Meyers, and Millis (2003) provided a
statistical methodology, based on the Rohling
interpretive method of deriving an overall test
battery mean (OTBM; L. S. Miller & Rohling,
2001), that allows for an analysis of neuropsycho-
logical data as a function of head injury severity.
The methodology proposed by Rohling et al.
(2003) yields essentially identical results when
8 forensic neuropsychology
based on an expanded Halstead-Reitan Battery
(HRB; Reitan & Wolfson, 1993) such as that used
by Dikmen et al. (1995), as well as when based on
a battery employing standard measures of motor
function, attention, processing speed, verbal and
visual memory, and intellectual and problem-
solving skills (the Meyers Neuropsychological
Battery; Volbrecht, Meyers, & Kaster-Bundgaard,
2000).
Finally, test performance should be compared
to other aspects of a subject’s behavior. A person
who has good memory in the clinical interview,
demonstrated by accurate recall of doctors seen,
evaluations, and treatments and validated by
cross-checking the actual medical records, should
not perform in a significantly impaired fashion on
formal memory testing. I previously described
two examples of this type of inconsistency
(Larrabee, 2000b). One case of alleged MTBI
accurately analyzed his current Wechsler Adult
Intelligence Scale–Revised (WAIS-R; Wechsler,
1981) Digit Symbol performance as superior to
testing conducted two years earlier, showing evi-
dence of excellent memory, yet the subject per-
formed very poorly on all memory tests
administered by the author. Another subject with
alleged MTBI performed on memory tests at a
level similar to that associated with Alzheimer’s
disease (AD), yet on the second day of examina-
tion noticed that the clock had been removed
from the wall of the examining suite.
Hill (1965) presented nine factors that should
be considered before moving from the observa-
tion of an association between a particular envi-
ronmental condition and a particular disease, to
inferring that the environmental condition is
related to causation of that disease. Although the
factors posited by Hill are particularly relevant to
inferring causation in neurotoxicology, certain of
those factors are also related to other traumatic
CNS events.
The first of Hill’s (1965) factors is the strength
of the association, which he illustrated by describ-
ing the association between lung cancer and
smoking. In particular, the strength of association
was demonstrated by the dose–response relation-
ship between number of cigarettes smoked
per day and increased incidence of lung cancer.
The paper by Rohling et al. (2003) provides an
example of a dose-response relationship between
severity of TBI and neuropsychological outcome.
Hill’s (1965) second factor is the consistency of
the association; that is, if the association has
been repeatedly observed by different persons, in
different places, circumstances, and times. The
example used by Hill was the increased incidence
of cancer of the lung and nasal sinuses among
nickel refiners in South Wales, found by Hill as
well as by other investigators. When a change was
instituted in the refining process, not a single
person working after the change was made devel-
oped cancer of the nose. An example relevant to
neuropsychology is the repeated observation that
memory impairment and slowed information-
processing speed are common long-term residual
effects of severe closed head trauma.
Third is Hill’s (1965) factor of specificity; that
is, the association between disease and environ-
ment is only seen in specific subjects exposed to a
specific environment. If the association between
the environment and disease is limited to specific
workers and to particular sites and types of dis-
ease and there is no association between the work
and other fatal illnesses, there clearly is a strong
argument supporting causation. Hill’s principle of
specificity is perhaps the most difficult to satisfy
in neuropsychology, given the nonspecific nature
of symptomatic complaints (cf. Lees-Haley &
Brown, 1993) and the fact that deficits in atten-
tion, memory, and executive functions can be
seen in a variety of neurobehavioral disorders.
The process of careful differential diagnosis
advocated in this chapter is particularly important
because of the low specificity of these complaints
and performance patterns.
Hill’s (1965) fourth causal factor, temporality,
refers to the temporal contingency between the
environmental factor and development of disease.
In one recent case of mine, memory complaints
were present before the accident in question;
indeed, there was a closer temporal relationship
between the pre-accident memory complaints
and the accident than there was for onset of
memory complaints following the accident.
Fifth is Hill’s (1965) biological gradient or
dose–response curve. Of course, this is related to
Hill’s first principle of strength, as well as to my
recommendation to analyze data, particularly for
cases of closed head injury, in relation to the
severity of initial trauma, referred to as biological
indexing or referencing (Larrabee, 1990; also see
Rohling et al., 2003). Bolla discusses the impor-
tance of analyzing dose–response when evaluat-
ing neurotoxic injury in chapter 11, this volume.
Hill’s (1965) sixth factor, plausibility, refers to
the biological plausibility of the purported causal
relationship. Bolla provides additional discussion
of biological plausibility in chapter 11. As she
 A Scientific Approach to Forensic Neuropsychology
argues, if several animal studies show that
a particularly high level of exposure to a specific
chemical does not produce any health effects in
animals, then there is little reason to suspect that
health effects would be produced in humans at a
lower level.
The seventh causal factor posited by Hill
(1965) is that of coherence. Hill stated that the
cause-and-effect interpretation of data should not
seriously conflict with the natural history and
biology of a particular disease or disorder. An
example of a failure to consider this principle is
the interpretation of severe memory impairment
as indicative of sequelae of uncomplicated
MTBI when this is not characteristic of the natu-
ral history of MTBI (see chapter 9, this volume).
Hill’s (1965) eighth factor, experiment, allows
for demonstration of a causal relationship
between environment and disease by manipulat-
ing an environmental factor and then evaluating
the results. For example, taking some preventive
action that consequently lowers the incidence
of the disease, such as reducing dust in the work-
place and finding a reduction in a particular dis-
ease. Experiment or quasi-experiment can provide
the strongest evidence for the causation hypo-
thesis. Chapters 9 and 11 in this volume discuss
the importance of careful control of competing
variables in research on the outcome of MTBI and
neurotoxic injury, respectively.
Analogy is Hill’s (1965) ninth factor for dem-
onstrating a causal association. As an example,
Hill noted that, given the known effects of thali-
domide and rubella on fetal development, doctors
would be prepared to accept slighter but similar
evidence regarding effects of another drug or
another viral disease on pregnancy.
Hill (1965) pointed out that none of his nine
factors can bring indisputable evidence for or
against a cause–effect hypothesis, and none can be
required as a sine qua non. Moreover, formal tests
of significance cannot provide the answers to the
nine factors, although these statistical tests can
remind the investigator of the effects that chance
can create; beyond that, statistics contribute noth-
ing to the proof of the cause–effect hypothesis.
In summarizing Hill’s points as they relate to
neuropsychological decision making as well as
the consistency analysis I advocate, everything
must make “neuropsychological sense” (Larrabee,
1990; Stuss, 1995). When significant departures
from Hill’s principles are observed or inconsisten-
cies appear in the neuropsychological data, diag-
noses other than the injury or illness alleged by
9
the litigant must be considered, including the
possibility of invalid test performance.
C L A S S I F I C AT I O N S TAT I S T I C S
IN NEUROPSYCHOLOGICAL
DIAGNO SIS
Similar to clinical psychology research in general,
neuropsychological research has relied primarily
on null hypothesis significance testing. Such
testing can yield statistically significant mean
differences between reference groups on a given
dependent variable that do not necessarily either
reflect a clinically meaningful finding or provide
clinically useful information (Woods, Weinborn,
& Lovejoy, 2003). In contrast, classification
accuracy statistics do provide information diag-
nostically important in individual clinical use
(Baldessarini et al., 1983; Glaros & Kline, 1988;
Meehl & Rosen, 1955; Millis, 2009).
Traditional classification accuracy statistics
include sensitivity, specificity, hit rates, predictive
values, likelihood ratios, and odds ratios
(Baldessarini et al., 1983; Glaros & Kline, 1988;
Ivnik et al., 2001; Woods et al., 2003). As defined
in this chapter, sensitivity refers to the proportion
of patients with a given disorder who show a char-
acteristic of interest (i.e., an impaired neuropsy-
chological test score), defined as true positives/
(true positives + false negatives). Specificity refers
to the proportion of control subjects or some
other reference sample without the characteristic
of interest (i.e., who have nonimpaired neuropsy-
chological test scores), defined as true negatives/
(true negatives + false positives). Sensitivity and
specificity serve different diagnostic purposes
(Millis, 2009; Straus, Richardson, Glasziou, &
Haynes, 2005); that is, when a test cutoff score has
a very high sensitivity, a negative test result rules
out the diagnosis, whereas conversely, when a test
cutoff has a very high specificity, a positive test
result rules in the diagnosis. Straus et al. (2005)
provide a useful mnemonic for the different
impacts of sensitivity and specificity: With high
sensitivity (Sn) a (N)egative test rules (out) the
diagnosis, or SnNout; with high specificity (Sp), a
(P)ositive test result rules (IN) the diagnosis, or
SpPin. Last, the hit rate index describes the total
proportion of accurately classified cases, (true
positives + true negatives)/N.
It is not uncommon that when cutoff scores
are derived to define sensitivity, specificity, and hit
rate, these cutoff scores are based on equal sample
sizes of persons (a) with a given disorder, such as
TBI, and (b) those without the given disorder,
10 forensic neuropsychology
such as normal or nonneurological medical
orthopedic patient control subjects (cf. Dikmen
et al., 1995). This essentially sets the base rate or
frequency of occurrence of the disorder at 50%,
which may not be the actual base rate in the total
population (also see Baldessarini et al., 1983).
Predictive value statistics do take into account the
population base rate of the disorder in question.
Theoretically, sensitivity and specificity are inde-
pendent of the base rate or prevalence of illness in
the population tested (Baldessarini et al., 1983).
Positive predictive power (PPP; also referred to as
positive predictive value, PPV) is the ratio of
true positive scores to total positive scores: true
positive/(true positive + false positive). PPP
reflects the probability of the presence of a disease
or disorder given a positive test finding. Negative
predictive power (NPP; also referred to as nega-
tive predictive value, NPV) is the ratio of true
negatives to total negative scores, true negatives/
(true negatives + false negatives), and reflects the
probability of the absence of a disease or disorder
given a negative test finding.
Ivnik et al. (2001) observe that clinicians need
to quantify the probability that a patient does or
does not have a condition of interest (COI), so
that the “risk” of having the COI specific to the
obtained test results can be determined. Ivnik
et al. (2001, citing Fletcher, Fletcher & Wagner,
1996) note that risk is expressed as “odds,” and
odds are the ratio of two probabilities. Odds that
are associated with a single event are defined as
the probability of the event occurring divided
by the probability of the event not occurring. One
of the risk statistics discussed by Ivnik et al. (2001)
is the likelihood ratio (LR), defined as the proba-
bility of the obtained test result in the presence of
the condition of interest (COI) divided by the
probability of the obtained test result in the
absence of the condition; in other words, the sen-
sitivity divided by 1 minus specificity [i.e., (true
positive)/(false positive)]. Another way to quan-
tify risk is the odds ratio (OR), which really is the
ratio of two risks: the risk of having a COI for all
people who earn a test score that indicates they
should have the COI (risk 1) in comparison to the
risk of having the COI for all people who earn a
test score that indicates they should not have the
COI (risk 2; Ivnik et al., 2001). Per Woods et al.
(2003) and Ivnik et al. (2001), the odds ratio is
computed as [(true positive)(true negative)]/
[(false positive)(false negative)]. Ivnik et al. (2001)
note that since the reference group for LRs is
patients who have the same score as the patient,
the LR is the more meaningful statistic for quanti-
fying the risk of having a COI after a patient’s test
score has been obtained (italics theirs). By contrast,
Ivnik et al. (2001) highlight that ORs are better for
comparing the overall diagnostic usefulness of a
test’s selected cut-score for group analysis.
Otherwise stated, LR is preferred for diagnosis of
the individual patient, with ORs preferred for
group comparisons.
Obviously, sensitivity, specificity, LRs and ORs
are dependent on the setting of a particular cutoff
score for the determination of abnormality. PPP
and NPP are dependent on sensitivity, specificity,
and prevalence of the condition of interest. The
LR has a unique relationship to the prevalence
(base rate) of the COI in that premultiplying the
LR for a particular test cutting score by the base
rate odds yields the posttest odds of the COI,
which can be converted back to the posttest
probability of the disorder by the formula odds/
odds + 1 (Grimes & Schulz, 2005). For example, if
the base rate of malingering is 0.40, and a particu-
lar cutoff score for a symptom validity test (SVT)
has a sensitivity of 0.50 and specificity of 0.90, the
base rate odds are 0.40/1–.40 or 0.67, which is
then used to multiply the LR, 0.50/.10 or 5.0, to
yield posttest odds of 3.35, which can then be con-
verted to a posttest probability of 0.77 (3.35/4.35).
If there is more than one diagnostic test for a COI,
and the diagnostic tests are independent of one
another, LRs can be chained such that the posttest
odds following application of one test become the
pretest odds by which the LR for the next test is
multiplied. Continuing with the example above, if
a second SVT independent of the first SVT but
with the same sensitivity of 0.50 and specificity of
0.90 for the test score achieved by the examinee is
obtained, the LR again is 5.0 (0.50/.10) which is
multiplied by the posttest odds of 3.35 from appli-
cation of the first SVT, to now yield new posttest
odds of 16.75, for a posttest probability following
failure of two independent SVTs of 16.75/17.75 or
0.94 (see Larrabee, 2008 for additional examples
of the power of chaining of LRs).
Caution is urged when diagnostic indicators
are not independent, which can lead to inflated
posttest probabilities for chained likelihood ratios
(Grimes & Schulz, 2005). Logistic regression
employing multivariable models is preferred to
chaining of likelihood ratios for correlated indica-
tors, since logistic regression accounts for variable
intercorrelation, as well as allows for differential
weighting of the more salient diagnostic indica-
tors (Millis, 2009). Of course, logistic regression

may not always be available for a unique combi-
nation of multiple SVTs. Research of mine
(Larrabee, 2003a) and Victor, Boone, Serpa,
Buehler, and Ziegler (2009), using cutoff scores
above/below which SVT failure is determined,
has shown that combinations of any two of five
failed SVTs (Larrabee, 2003a) or any two of four
failed SVTs (Victor et al., 2009) yields essentially
the same diagnostic discrimination as when the
individual SVTs are considered altogether as
continuous variables in a logistic regression.
By plotting true-positive rates and false-
positive rates for all possible cutoff scores on a
particular test, the receiver operating characteris-
tic (ROC; also known as the relative operating
characteristic) of the test can be determined
(Hsiao, Bartko, & Potter, 1989; Swets, 1973). The
area under the ROC generated by the different
cutoff scores and their associated true-positive
and false-positive rates gives the overall diagnos-
tic efficiency of the test, with an upper limit of 1.0
(perfect diagnostic accuracy) and a lower limit of
0.50 (chance). Hosmer and Lemeshow (2000)
present guidelines for interpreting the magnitude
of ROC area under curve (AUC): values of 0.90 or
more reflect outstanding discrimination, 0.80 to
<0.90 show excellent discrimination, 0.70 to <0.80
show acceptable discrimination, and 0.50 shows
no discrimination. Figure 1.1, from Larrabee and
1.0
0.8
Sensitivity
0.6
0.4
0.2
0.0
0.0 0.2 0.4 0.6
1-Specificity
Diagonal segments are produced by ties.
FIGURE 1.1: Receiver operating characteristic for
discrimination of definite and probable malingerers
from patients with moderate to severe traumatic
brain injury using the FBS of the MMPI-2. From
Larrabee and Berry (2007) with permission.
A Scientific Approach to Forensic Neuropsychology 11
Berry (2007), displays a ROC for discrimination
of a group of definite/probable malingerers from a
group of patients with moderate/severe traumatic
brain injury with the MMPI-2 Symptom Validity
Scale (FBS), using combined data from Larrabee
(2003b) and Ross, Millis, Krukowski, Putnam,
and Adams (2004). The AUC of 0.96 for the ROC
in Figure 1.1 shows outstanding discrimination of
the definite/probable malingerers and the moder-
ate/severe TBI cases.
Baldessarini et al. (1983) provided the formula
for computing PPP and NPP. Sensitivity is repre-
sented as x; specificity is represented as y; preva-
lence (base rate) is represented as p.
PPP = [(p)(x)]/[(p)(x) + (1−p)(1−y)]
NPP = [(1−p)(y)]/[(1−p)(y) + (p)(1−x)]
Baldessarini et al. (1983) provided an example
demonstrating the effect of prevalence/base rate
on PPP and NPP from a study employing the dex-
amethasone suppression test as an indicator of the
presence of major depression. In the original
study sample, 100 depressed patients were com-
pared to 100 neurotic patients, creating a preva-
lence/base rate of depression of 50%. Of the 100
depressed patients, 70 were identified as depressed
(true positives), and 30 were misidentified (false
negatives), giving a sensitivity of 70. Of the 100
neurotic patients, 5 tested positive for depression
(false positives), whereas 95 tested negative for
depression, yielding a specificity of 95%. In the
original derivation sample, the PPP was 70 (true
positive)/(70 true positive + 5 false positive),
which equals 70/75 or 93.3%. Similarly, derived
via the formula, [(0.5)(0.7)]/[(0.5)(0.7) + (1 − 0.5)
(1 − 0.95)], PPP is 93.3%. NPP is (95 true nega-
tive)/(95 true negative + 30 false negative), which
equals 95/125 or 76.0%. Also, derived via the for-
mula, NPP is [(1 − 0.5)(0.95)]/[(1 − 0.5)(0.95) +
(0.5)(1 − 0.7)] = 0.76 or 76%.
Baldessarini et al. (1983) demonstrated the
effect of change in prevalence/base rate of depres-
sion on PPP and NPP for the test of depression.
0.8 1.0
Moving from the derivation study in which the
base rate of major depressive disorder was 50% to a
general psychiatric practice in which the base rate
of major depressive disorder was 10%, but keeping
sensitivity at 70% and specificity at 95%, reduces
PPP to 12.3%, but increases NPP to 99.7%.
Baldessarini et al. (1983) described a recipro-
cal relationship between PPP and NPP as a func-
tion of prevalence/base rate, with sensitivity and
12 forensic neuropsychology
specificity held constant. At low prevalence/base
rates, a negative test result is more likely to be true
than a positive result. This results in a loss of PPP
moving from an artificial setting in test popula-
tions with a high prevalence of an illness or condi-
tion of interest into more realistic clinical settings.
The converse is true of NPP as a function of prev-
alence/base rate, with sensitivity and specificity
held constant. Thus, at high prevalence/base rates,
a positive test result is more likely to be true than
a negative test result.
When prevalence/base rate is held constant,
PPP is affected more by changes in specificity;
that is, when the rate of false positives is low.
Conversely, NPP is highest when sensitivity is
high; that is, when the rate of false negatives is low
(Baldessarini et al., 1983). When multiple, inde-
pendent tests sensitive to a COI are positive, the
posttest probabilities increase significantly, so that
even with low base-rate conditions, diagnostic
probability for the COI can be high. For example,
I (Larrabee, 2008) showed, using the assumption
of independent SVTs, each with a sensitivity of
0.50 and specificity of 0.90, that failure of one SVT
at a base rate of 0.10 yielded a posttest probability
of 0.56, which increased to 0.74 with failure of two
SVTs, and to 0.93 with failure of three SVTs.
The overall accuracy of a test cutting score is a
function of the positive and negative base rates in
the population as well as the positive and false-
positive rates associated with the cutting score
(Meehl & Rosen, 1955). The ratio of the positive
base rate P to the negative base rate Q must be
greater than the ratio of the false-positive rate p2
to the true-positive rate p1, or P/Q > p2/p1. Stated
otherwise (Gouvier, 1999), the combined error
rate of a test must be smaller than the base rate of
the condition that the test is designed to detect.
As reviewed by Woods et al. (2003), classifica-
tion statistics, particularly those related to PPP,
NPP, and odds ratios, are underused in neuropsy-
chological research. Indeed, in their review of five
prominent neuropsychology journals published
during the years 2000 and 2001, only 31% of neu-
ropsychology articles published indices of sensi-
tivity, with fewer than 3% reporting predictive
values or risk ratios.
Two studies in which I have been involved
provide a further perspective on PPP and NPP. In
the first, Binder, Rohling, and Larrabee (1997)
determined 5% prevalence of chronic persisting
neuropsychological deficit following MTBI.
Assuming sensitivity of 80% and specificity of
88% for neuropsychological tests (using the
Heaton, Grant, & Matthews, 1991, data, and an
Average Impairment Rating cut score of T score =
39), PPP for neuropsychological detection of per-
sisting impairment following MTBI was 0.26,
with NPP at 0.99, at the base rate of 5%. Thus, a
clinician is more likely to be correct when diag-
nosing no persisting impairment in MTBI.
I (Larrabee, 2003a) developed a five-variable
algorithm for detection of malingering based on
atypical (for moderate or severe TBI) performance
on any two (or three) variables, including Benton
Visual Form Discrimination (Benton, Sivan,
Hamsher, Varney, & Spreen, 1994), Finger
Tapping, Reliable Digit Span (Greiffenstein, Baker,
& Gola, 1994), Wisconsin Card Sorting Failure to
Maintain Set, and the Lees-Haley Fake Bad Scale
(Lees-Haley, English, & Glenn, 1991; now known
as the Symptom Validity Scale; Ben Porath,
Graham & Tellegen, 2009). Based on a positive
score (i.e., in the malingering range) on any two of
the five indicators, sensitivity for detection of def-
inite or probable malingered neurocognitive dys-
function (Slick, Sherman, & Iverson, 1999) was
0.878 and specificity (for correct detection of
moderate/severe TBI, neurological or psychiatric
patients) was 0.944. Using a base rate of mali-
ngering of 40% in litigated minor head injury
(Larrabee, 2003a; Mittenberg, Patton, Canyock, &
Condit, 2002), PPP for this formula was 0.913,
with NPP of 0.921. When a positive score was
obtained on any three of the five indicators, sensi-
tivity dropped to 0.542; however, specificity was a
perfect 1.00. Consequently, PPP for failure of any
three indicators was 1.00, since the simplified for-
mula for PPP (true positive/true positive + false
positive) results in 0.542/.542 (with zero false
positives), yielding 100% probability of malinger-
ing. This latter finding underscores the important
relationship of specificity to PPP.
S C I E N T I F I C S TAT U S O F
NEUROPSYCHOLOGICAL
TESTING
This section provides a brief overview of general
issues related to the scientific status of neuropsy-
chological test procedures. This is by no means an
exhaustive review, and the reader is directed to
more comprehensive reviews, including the
widely referenced texts by Lezak, Howieson, and
Loring (2004) and Strauss, Sherman, and Spreen
(2006).
The discipline of neuropsychology in America
dates to the 1940s and 1950s with the establish-
ment of laboratories by Arthur Benton, Ward
 A Scientific Approach to Forensic Neuropsychology
Halstead, and Ralph Reitan (Reitan & Wolfson,
2009; Tranel, 2009). During this same time period,
laboratories were formed by Zangwill in England
and Hécaen in France, and Luria had initiated
his investigations in Russia (Soviet Union)
(Hécaen & Albert, 1978; Luria, 1966; McFie,
1975). As currently practiced, neuropsychology
has benefited from psychometric influences (e.g.,
principles of test construction, methodology for
determining reliability and validity), develop-
ments in experimental psychology (e.g., signal
detection methodology; information-processing
models), and behavioral neurology (e.g. neuro-
behavioral analysis of syndromes of aphasia,
apraxia, agnosia and amnesia; Larrabee & Crook,
1988; Lezak et al., 2004; Milberg, Hebben, &
Kaplan, 2009).
Psychological and neuropsychological testing
has established validity, comparable to the validity
of tests used in clinical medicine (Meyer et al.,
2001). A meta-analytic review by Zakzanis, Leach,
and Kaplan (1999) demonstrated varying patterns
of effect sizes for measures of verbal and perfor-
mance skill, attention, memory, cognitive flexibil-
ity/abstraction, and manual dexterity as a function
of different neurobehavioral disorders such as
AD, frontotemporal dementia, Parkinson’s dis-
ease, multiple sclerosis, Huntington’s disease, and
as a function of psychiatric disorders such as
schizophrenia and major depressive disorder.
Neuropsychological testing of adults is accepted
by neurologists as “established,” with Class II
evidence and Type A recommendation, and was
found by the Therapeutics and Technology
Assessment Subcommittee of the American
Academy of Neurology (AAN) to be appropriate
for a wide range of neurological disorders,
including TBI, cerebrovascular disease, Parkinson’s
disease, HIV encephalopathy, multiple sclerosis,
epilepsy, and neurotoxic exposure (“Assessment:
Neuropsychological Testing of Adults,” 1996). In
particular, the AAN views neuropsychological
documentation as critical in cases where litigation
concerns the presence of cognitive impairment
(“Assessment: Neuropsychological Testing,”
1996). Although some have questioned certain
conclusions reached by the Technology and
Therapeutics Subcommittee (Reynolds, 2001),
“These criticisms aside, the AAN report does
make a positive contribution to the field of neu-
ropsychology and concludes by recommending
that neuropsychological assessment of adults has
value to neurologists in particular circumstances”
(p. 200).
13
Some have stated that certain fixed battery
neuropsychological test procedures such as the
HRB or Luria Nebraska Neuropsychological
Battery (LNNB; Golden, Purisch, & Hammeke,
1985) are the only acceptably validated proce-
dures for use in forensic neuropsychology (Hom,
2003; Hom, 2008; McKinzey, 2000; Russell, 2007).
In contrast, a survey by Lees-Haley, Smith,
Williams, and Dunn (1996) found, in a review of
100 forensic neuropsychological evaluations con-
ducted in 20 states and in the province of Ontario,
Canada, that the HRB and LNNB were rarely
used. Lees-Haley et al. found that only 10% used
the LNNB, and approximately 21% used the HRB,
contrasted with 75% that used the WAIS-R, 68%
that used the Minnesota Multiphasic Personality
Inventory (MMPI; Hathaway & McKinley, 1983)/
MMPI-2 (Butcher, Dahlstrom, Graham, Tellegen,
& Kaemmer, 1989), and 51% that used the WMS
(Wechsler, 1945) and WMS-R. These percentages
make it difficult to argue that fixed batteries are
the standard of practice in forensic settings.
Subsequent surveys further established the
primacy of approaches other than fixed batteries
such as the HRB or LNNB. Sweet, Nelson and
Moberg (2006) surveyed practicing neuropsy-
chologists regarding their basic assessment
approaches and found that 76% used a flexible
battery, defined as variable but routine groups of
tests for different types of patients (e.g., head
injury, alcoholism, elderly patients), whereas 18%
used a purely flexible approach dependant upon
the needs of an individual case but not uniform
across patients, and only 7% used a standardized
battery such as the HRB. A contemporaneous but
independent survey by Rabin et al. (2005) found
that most neuropsychologists frequently assessed
attention, verbal memory, executive functions,
visuospatial skills, nonverbal memory, intelli-
gence, language, and construction. The most
widely used procedures included the Wechsler
intelligence scales (WAIS-R/WAIS-III; 63.1%),
and Wechsler Memory Scales (WMS-R/Wechsler
Memory Scale-Third Edition or WMS-III;
Wechsler, 1997; 42.7%), with the Trail Making
Test used by 17.6%, and California Verbal
Learning Test (CVLT; Delis, Kramer, Kaplan,
Ober, & Fridlund, 1987; CVLT-2; Delis et al.,
2000) used by 17.3%. Consistent with the Sweet
et al. (2006) survey, only 15.5% used the HRB.
Recommendations for the use of the HRB or
LNNB over other neuropsychological procedures
are not supported by empirical studies that have
compared both batteries to the WAIS (Wechsler,
14 forensic neuropsychology
1955), WAIS-R, or Auditory Verbal Learning Test
(Rey, 1964). Based on WAIS IQ scores and global
impairment scores for the HRB and LNNB, Kane,
Parsons, and Goldstein (1985) found essentially
equivalent classification of brain damage versus
control subjects. Reanalysis of the Kane et al.
(1985) published data, computing effect sizes
(Cohen’s d) showed d values of 1.63 for an HRB
average T score and 1.88 for the HRB Average
Impairment Rating, comparable to a d of 1.71 for
WAIS PIQ (Loring &Larrabee, 2006). These HRB
and PIQ effect sizes were all inferior to the effect
size of 2.40 for WAIS VIQ (Loring & Larrabee,
2008). Sherer, Scott, Parsons, and Adams (1994)
also found that the WAIS-R and HRB were both
sensitive to the presence of brain damage. When
Cohen’s d was computed for the Sherer et al.
(1994) data, d was 0.92 for WAIS-R FIQ, a value
over double the d of 0.43 computed for the HRB
(Loring & Larrabee, 2006).
Chelune (1982) attributed the equivalent
sensitivity to brain damage of the HRB and
LNNB to the variance these procedures share
with WAIS IQ. The equivalent sensitivity of the
WAIS/WAIS-R and HRB for brain damage is
further understood as a function of shared
underlying (neuro)psychological constructs of
(a) visuospatial reasoning and problem solving,
(b) attention/concentration, and (c) psychomotor
speed, as demonstrated in a factor analysis of
the HRB, WAIS-R, and WMS-R (Larrabee,
2000a; Leonberger, Nicks, Larrabee, & Goldfader,
1992).
Memory is only weakly assessed on the origi-
nal LNNB (Larrabee, Kane, Schuck, & Francis,
1985) and is not assessed at all on the HRB
(Leonberger et al., 1992). This explains why
Powell, Cripe, and Dodrill (1991) found that the
Auditory Verbal Learning Test, particularly Trial
5, was more sensitive than any other single test on
the HRB, as well as more sensitive than the HRB
Impairment Index, in discriminating normal
subjects from a group of subjects with a variety of
neurological disorders.
Dikmen et al. (1995), in their study of long-
term sequence of TBI, found that the two most
sensitive tests (i.e., the first tests to pick up differ-
ences in performance 1-year status post-injury, as
a function of trauma severity) were the Verbal
Selective Reminding Test and Trail Making B for
the head-injured subjects who took between 1
and 24 hours to follow commands. The HRB
Impairment Index did not show differences in
1-year outcome until TBI severity reached 25
hours to 6 days of coma (with coma defined by
time to follow commands).
Rohling et al. (2003) found that a flexible
battery, employing a core set of tests of language,
spatial judgment, motor and tactile function,
verbal and visual learning and memory, and
intelligence and problem solving, showed the
same dose–response association with head injury
severity found by Dikmen et al. (1995), who used
an HRB augmented by the WAIS and memory
procedures such as the Verbal Selective Reminding
test. What was particularly impressive is that the
Overall Test Battery Mean (OTBM) average
T score for the Meyers Neuropsychological Battery
(a core for a flexible battery) was 39.2, essentially
identical to the expanded HRB OTBM of 38.9;
additionally, the MNB correlated 0.99 with five
levels of TBI severity (<1 hour time to follow
commands [TFC], 1–23 hours TFC, 1–6 days
TFC, 7–13 days TFC, and 14–28 days TFC),
whereas the HRB OTBM correlated 0.96 with
these same levels of severity, with no difference in
slope or intercept from the MNB data. Last, the
two OTBMs correlated 0.97 with one another
across the five levels of trauma severity. These
essentially identical values support not only the
equivalent validity of a core flexible battery to an
expanded HRB, but equally as important, estab-
lish the comparability of a collection of individu-
ally normed tests (the tests comprising the MNB)
to a co-normed battery of tests comprising the
Dikmen et al. (1995) expanded HRB.
My colleagues and I (Larrabee, Millis, &
Meyers, 2008) compared the performance of a
mixed group of patients with neurological dys-
function to that of a group of pseudoneurologic
controls on the seven core measures of the HRB
(Category Test; TPT Total Time, Memory and
Location; Finger Tapping; Seashore Rhythm Test;
Speech Sounds Perception Test) and the core of a
flexible battery, which we named an Ability
Focused Battery (AFB). The AFB was designed to
capture several core neuropsychological con-
structs/domains/abilities including language/
verbal skills, perceptual/spatial skills, sensorimo-
tor ability, working memory, processing speed,
verbal and visual memory, and intellectual and
problem-solving skills, and included eight tests
(H-Words, a written word fluency test; Grooved
Pegboard; WMS Delayed Logical Memory and
Delayed Visual Reproduction; WAIS-R
Arithmetic, Digit Symbol, Similarities, and Block
Design). Discrimination of the neurologic and
control groups with the AFB yielded a receiver
 A Scientific Approach to Forensic Neuropsychology
operating characteristic area under curve (AUC)
of 0.86, compared to the HRB AUC of 0.83. While
this difference was not statistically significant, the
Bayes Information Criterion (BIC) favored the
AFB over the HRB. We noted that the AFB would
have yielded even more impressive discrimina-
tion if more sensitive measures of verbal and
visual learning and memory, and more sensitive
measures of working memory, had been employed.
Bayesian Model Averaging selected four measures
from the combined set of AFB and HRB subtests,
plus Trail Making B: H-Words, Trail Making B,
Grooved Pegboard, and Finger Tapping (note:
The effect size for Finger Tapping was quite small,
and it appeared Finger Tapping was working as a
measure of symptom validity, in that the brain-
impaired subjects outperformed the controls,
despite performing significantly less well than
the controls on the Grooved Pegboard Test).
The largest effect size for the individual subtests
was d = 1.08 for the Grooved Pegboard Test.
A subsequent investigation by Miller,
Fichtenberg, and Millis (2010) found that an AFB
measuring five domains: attention, processing
speed, visual-spatial reasoning, language/verbal
reasoning, and memory discriminated a mixed
neurological group from a pseudoneurologic
control group, with a receiver operating charac-
teristic AUC of 0.89. Moreover, a more parsimo-
nious model based solely on processing speed and
memory yielded an AUC of 0.90. These values
show excellent diagnostic discrimination and
also demonstrate the superior sensitivity to brain
dysfunction of measures of memory and proce-
ssing speed. These data support the results of
Larrabee et al. (2008) who also found that mea-
sures of processing speed were very sensitive to
brain dysfunction, and confirm our prediction
that more sensitive measures of memory, such as
the CVLT-II used by Miller et al. show better
sensitivity to neurologic dysfunction than the
Logical Memory and Visual Reproduction tests
used in our earlier study.
The investigations by Rohling et al. (2003),
Larrabee, et al. (2008), and Miller et al. (2010)
show that what is important in conducting
neuropsychological evaluation is that the exami-
nation, using standardized and validated tests,
should cover the key areas of neuropsychological
function. These core neuropsychological func-
tions include language/verbal abilities, percep-
tual/spatial ability, sensorimotor function
(particularly manual motor function), attention,
working memory and information processing,
15
psychomotor speed, verbal and visual learning
and memory, intellectual and problem-
solving skills, academic functions, personality,
and motivation (American Academy of Clinical
Neuropsychology, 2007; “Assessment: Neuro-
psychological Testing of Adults,” 1996; Larrabee,
2000a; Lezak et al., 2004; Strauss et al., 2006;
Zakzanis et al., 1999). A battery lacking assess-
ment of certain functions such as memory and
verbal abilities should be augmented by tests
covering the missing areas, as many who use the
HRB have done (Dikmen et al., 1995; Heaton
et al., 1991; Powell et al., 1991).
Multiple measures are recommended for
each of the above areas of function; for example,
Finger Tapping, Grip Strength (Reitan & Wolfson,
1993), and the Grooved Pegboard can be used to
assess manual motor function. This recommenda-
tion goes counter to Wedding and Faust’s (1989)
recommendation to avoid reliance on highly
intercorrelated measures. Wedding and Faust
argued that, to the extent tests are redundant,
using a second test merely remeasures what the
first test does, and diagnostic or predictive
accuracy is minimally increased. This observation
is certainly true if and only if the clinician’s sole
concern was the reliability and validity of test
scores. However, this is not the case in clinical and
forensic neuropsychology, for which the reliabil-
ity and validity of the individual participant’s
performance is also at issue (see chapter 5 on
malingering). Thus, inclusion of multiple mea-
sures of each domain, some easier, some more
difficult, allows analysis of within-domain consis-
tency of performance.
As an example employing multiple measures
of motor function, Greiffenstein, Baker, and
Gola (1996) studied patients with severe TBI who
also had unambiguous motor abnormalities on
standard neurological examination and found
these subjects had different patterns of motor
performance on Finger Tapping, Grip Strength,
and the Grooved Pegboard test, in comparison to
the motor performance patterns of litigants
with persistent post-concussion syndrome. The
patients with severe TBI performed less well on
the Grooved Pegboard relative to Finger Tapping
and Grip Strength, whereas the litigants with
persistent post-concussion syndrome showed
the opposite pattern, performing better on the
Grooved Pegboard in comparison to Finger
Tapping and Grip Strength.
Some have argued for predicting expected
levels of neuropsychological test performance
16 forensic neuropsychology
based on estimated premorbid IQ (Tremont,
Hoffman, Scott, & Adams, 1998). This approach
is only applicable if there is a correlation of
a particular neuropsychological test with IQ;
even then, there can be considerable regression to
the mean, particularly if there is no preexisting
IQ test, and IQ itself must be estimated (Larrabee,
2000a). For example, Tremont et al. (1998) found
that the Category Test correlated 0.5 with Full
Scale IQ (FIQ). In someone for whom preinjury
testing was unavailable but who actually had a
“true” premorbid IQ of 130, the estimated pre-
morbid IQ based on a multiple R of 0.60 (Barona,
Reynolds, & Chastain, 1984) would be 118 (1.2
SD above the mean). If the expected Category Test
score was then estimated on the basis of this esti-
mated IQ, the predicted Category Test score would
be 0.5 × 1.2 or 0.6 SD above the mean, for a T-score
equivalent of 56 (standard error of estimate of
8.66) or an IQ-equivalent score of 109 (standard
error of estimate of 12.99). Estimated premorbid
IQ scores themselves have large standard errors of
estimate (SEEs) when based on demographic fac-
tors (Barona et al., 1984; range of SEE is 12 to 13
IQ points). The size of the SEE can be reduced
using current function measures such as the
Advanced Clinical Solutions Test of Premorbid
Functioning (TOPF; Pearson, 2009), in combina-
tion with demographic factors, but the TOPF
itself must be estimated based on demographic
factors to ensure the score has not been affected
by brain dysfunction (Pearson, 2009). Although
the TOPF can be useful for estimating premorbid
IQ, it is not as useful for predicting premorbid
memory function (Pearson, 2009).
Some have advocated using performance on
current IQ subtests that are resistant to effects of
cerebral dysfunction (i.e., “hold” tests) or picking
the highest subtest scores on current IQ testing
(the “best performance method”; see Lezak et al.,
2004) to estimate premorbid IQ. Krull, Scott, and
Sherer (1995) and Scott, Krull, Williamson,
Adams, and Iverson (1997) have developed a pro-
cedure for predicting premorbid IQ that combines
demographic information with current perfor-
mance on the Vocabulary and Picture Completion
subtests of the WAIS-R, the Oklahoma Premorbid
Intelligence Estimate (OPIE). Powell, Brossart,
and Reynolds (2003) compared the OPIE proce-
dure to Barona et al.’s (1984) demographic estima-
tion of premorbid IQ in both normal and clinical
patients and found that the OPIE was less sensi-
tive (i.e., predicted lower premorbid IQ) in the
clinical sample. This is not unexpected because
the OPIE ignores regression to the mean effects
and contaminates the predictor (Vocabulary and
Picture Completion subtests) with the criterion
(IQ; i.e., the Vocabulary and Picture Completion
subtests are used to predict IQ, which is also based
partly on the Vocabulary and Picture Completion
subtests).
Finally, performance on WAIS-R subtests such
as Vocabulary or Picture Completion that are
thought to be less sensitive to the effects of brain
damage can still be affected by brain dysfunction.
Specifically, Larrabee, Largen, and Levin (1984)
found that using performance on hold or best-
performance WAIS subtests to estimate premor-
bid IQ underestimated premorbid level of function
by a full standard deviation or more for subjects
who had mild-to-moderate AD compared to
WAIS IQ scores produced by normal controls
matched on age, education, and gender. Although
coworkers and I (Larrabee et al., 1984) did not
employ Vocabulary in our investigation, the
Information subtest mean for the AD patients was
3.0 age-scaled score points lower than that of the
age-, education-, and gender-matched controls,
with the Picture Completion subtest mean falling
5.44 age-scaled score points lower for the AD
patients.
The point of the discussion is that estimation
of premorbid neuropsychological ability is a risky
enterprise. In my opinion, the clinician is better
off using neuropsychological test procedures that
have been carefully standardized on the basis of
relevant demographic factors such as age, educa-
tion, and gender (cf. Heaton et al., 1991, but note
the concerns of Fastenau, 1998). By evaluating
and adjusting for demographic factors related
to test performance during test norming and
development, essentially the test procedures are
precorrected for premorbid level of function.
The recently published Advanced Clinical
Solutions also provide demographically corrected
norms for both the WAIS-IV and Wechsler
Memory Scale, Fourth Edition (WMS-IV;
Wechsler, 2009). To date, these demographically
corrected norms for WAIS-IV and WMS-IV have
not been compared directly to premorbid predic-
tions of ability using the TOPF, in relation to diag-
nostic sensitivity to acquired neurological deficits
(e.g. AD; TBI). Thus, the addition of a current
function estimator to demographic factors may
provide a superior benchmark for detection of
impairment, for the particular case of the WAIS-IV
Index Scores, although this remains to be demon-
strated. Last, review of preinjury standardized
 A Scientific Approach to Forensic Neuropsychology
test scores is also helpful for establishing the level
of preinjury function, but provides information
typically related to academic achievement and less
often to intellectual level of function, although the
two are definitely correlated.
As discussed in this chapter, the actual
neuropsychological data must be interpreted in
the context of other data using appropriate
scientific judgment and reasoning. Use of a large
number of tests can result in abnormal scores in
entirely normal individuals. Ingraham and Aiken
(1996) presented an empirical approach to deter-
mine abnormality in test batteries with multiple
measures; for example, in a battery with 30 scores
in which the criterion is three tests falling at 1 SD
below the mean, the probability is nearly 0.90 that
this will occur by chance. Note that Ingraham and
Aiken based their computations on independent
scores, using the binomial theorem, which is
likely not the case in an actual test battery.
Ingraham and Aiken note that since correlated
scores reduce the likelihood of abnormal findings,
the probabilities generated by the binomial theo-
rem are likely somewhat overestimated. Indeed,
Crawford, Garthwaite and Gault (2007) found
that using the binomial theorem with uncorre-
lated data yielded the same percentage of abnor-
mal scores as did a procedure based on a Monte
Carlo method utilizing the standard deviation of
the difference between individuals’ mean scores
on the battery and each of the subtests or indexes
contributing to the mean. When the size of the
subtest intercorrelations increased, the binomial
procedure overestimated the number of abnormal
scores; for example, if a battery consisted of six
tests that are uncorrelated, the percentage of
tests that are abnormally low (<5th percentile) is
26.49%, but when the average subtest inter-
correlation is 0.7, only 14.87% demonstrate
abnormally low scores.
Determination of abnormalities in perfor-
mance based on test score variability depends on
the range of variability in normal subjects, which
can be quite large. Schretlen, Munro, Anthony,
and Pearlson (2003) studied the maximum range
between a normal subject’s highest and lowest
scores on 32 z-transformed scores derived from
15 neuropsychological tests. The smallest maxi-
mum difference was 1.6 SD, with the largest max-
imum difference 6.1 SD. Again, knowledge of the
literature pertaining to patterns of performance in
different neurobehavioral disorders and use of the
judgment strategies recommended in this chapter
can reduce the risk of making an erroneous
17
conclusion of deficit, when the pattern of perfor-
mance is actually the result of nonpathological
normal variability or random factors.
Binder, Iverson, and Brooks (2009) have
comprehensively reviewed the subject of fre-
quency of “abnormal” scores in healthy adults.
They concluded that abnormal performance on
some proportion of tests in a neuropsychological
battery is psychometrically normal (italics theirs).
Binder et al. reviewed several normative data-
bases, reporting on the frequency of abnormal
scores using various definitions of abnormality
(bottom 16%, bottom 5%). For example, using a
cutoff of >1 standard deviation below the mean,
a battery of 40 scores from an expanded HRB
(Heaton et al., 1991) showed that 90% of the
normative sample had at least one score that
exceeded this cutoff, with a median of 4 scores out
of 40 that exceeded the cutoff. Lowering the cutoff
to >1.5 standard deviations, 64% still had at least
one score exceeding the cutoff. On the Neuro-
psychological Assessment Battery (NAB; Stern &
White, 2003), at a cutoff of more than 1 standard
deviation below the mean, 36.9% of the normative
sample had an abnormality on at least one of the
five index scores, and 19.3% had an abnormality
on at least two index scores.
Binder et al. (2009) comment on several
clinical implications of their review. One is the
limitation placed on estimation of premorbid
mental abilities based on current cognitive
performance (also see earlier comments in this
section). Specifically, a few scores much higher
than other scores do not mean that premorbid
mental abilities were at the same level as the
highest scores. Also, Binder et al. (2009) noted
that published data demonstrated large discrep-
ancies occur fairly commonly between IQ, index,
and subtest scores of the WAIS-R, WMS-R, WAIS-
III, and WMS-III, but that no researcher or test
publisher has provided information regarding the
base rates of large discrepancy scores when all
discrepancies are considered simultaneously, as is
typical of the practitioner evaluating data on an
individual case (italics theirs). Regarding the
forensic implications of their review, they observe
that a full appreciation of the extent of the base
rates of low scores and large discrepancies in
normal persons should decrease the frequency of
misdiagnosis of cognitive impairment in forensic
evaluations. Consequently, the forensic practitio-
ner should guard against over-interpreting
isolated low scores, adopting a more scientific
approach to evaluation of test results. Binder and
18 forensic neuropsychology
colleagues close their review by quoting Schretlen
et al. (2003): “the findings reported here under-
score the importance of basing clinical neuropsy-
chological inferences about cerebral dysfunction
on clinically recognizable patterns of performance
in the context of other historical, behavioral,
and diagnostic information, rather than on psy-
chometric variability alone.” (p. 869, italics added
by Binder et al.).
S U M M A RY
This chapter reviewed scientific factors relevant
to the practice of forensic neuropsychology. The
scientific method was reviewed, including the
hypothetico-deductive approach, with particular
emphasis on the importance of seeking discon-
firming evidence to strengthen both scientific and
diagnostic hypotheses. Factors related to diagnos-
tic error were reviewed, including faulty use of
logic, illusory correlation, hindsight bias, and con-
firmation bias. Recommendations for effective
diagnostic formulations aimed at reducing judg-
mental bias were made, and statistics relevant to
diagnostic decision making were reviewed, includ-
ing discussion of base rates, sensitivity, specificity,
and positive and negative predictive power. Finally,
general issues relevant to neuropsychological
testing in forensic settings were considered.
The remainder of this book expands on the
science of forensic neuropsychology. All of the
contributors are actively involved in empirical
research in neuropsychology and are respected
and well-known scientist/clinicians. The cumula-
tive aspect of science is represented by chapters
that present up-to-date reviews of major areas of
concern, including assessment of malingering
(chapter 5), functional neuroimaging (chapter 6),
acquired brain damage in children (chapters
7, 8), MTBI (chapter 9), moderate-to-severe TBI
(chapter 10), neurotoxic injury (chapter 11),
chronic pain (chapter 12), and post-traumatic
stress disorder (chapter 14).
The special circumstances in which the scien-
tist/clinician must effectively communicate results
to attorneys and the court are covered in chapter
2, with admissibility of neuropsychological evi-
dence covered in chapter 3. Issues pertinent to
civil and criminal competencies and criminal
responsibilities are addressed in chapters 15–17.
In particular, chapter 15 demonstrates a cutting-
edge scientific approach to the assessment of com-
petencies in the elderly. Chapter 13 provides a
perspective on somatoform stress disorders that is
important in performing differential diagnosis of
litigants/defendants, and the ethics of appropriate
forensic practice are addressed in chapter 4.
Chapter 18 provides a perspective on past and
future trends in forensic neuropsychology.
AC K N OW L E D G M E N T
I acknowledge the assistance of Matthew Miliano
in the preparation of this chapter.
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 2
Neuropsychology and the Law
Principles of Productive Attorney-Neuropsychologist Relations
M A N F R E D F. G R E I F F E N S T E I N A N D PAU L M . K AU F M A N N
INTRODUCTION
Forensic neuropsychology is defined as the
application of neuropsychological evidence to
inform legal questions. There is empirical evi-
dence that forensic neuropsychology has grown
from the occasional private practice referral, to a
major component of assessment and research.
In a comprehensive survey, Sweet, Moberg, and
Suchy (2000) reported that legal referrals had
become a major source of private practitioner
income. Published research addressing empirical
questions raised by forensic involvement has also
grown steadily. Sweet, King, Malina, Bergman,
and Simmons (2002) compiled a decade of
abstracts from three major neuropsychology jour-
nals and reported the number of articles address-
ing forensic issues more than tripled between
1990 and 2000. And the courts have taken
notice: Kaufmann (2008) reported an average 6%
increase/year in published legal cases referencing
neuropsychology during the past five years.
Given the proven growth of legal applications
for neuropsychology, it logically follows that neu-
ropsychologists have increased personal interac-
tions with agents of the legal system. These agents
include attorneys, judges, hearing officers, and
police, but attorney contacts account for most of
these interactions. For this reason, the nature of the
attorney-neuropsychologist interaction merits
considerable discussion. These interactions can
have many positive consequences, including
enhanced income, inter-professional understand-
ing, and research opportunities. There can also be
negative consequences, including close public scru-
tiny of a neuropsychologist’s cherished methods
and fundamental beliefs. Attorney coaching to sab-
otage assessments is also a risk, as this documented
practice violates a psychologist’s crucial assump-
tion of a naïve test taker (Youngjohn, 1995).
The purpose of this chapter is to outline,
understand, and manage the important compo-
nents of the attorney-neuropsychologist interac-
tion. The reader should be mindful of the
terminology used repeatedly in this chapter. The
term “forensic neuropsychologist” (FN) simply
means any neuropsychologist who provides
opinions in a legal setting, irrespective of the
frequency of this work. The term does not denote
a practitioner who restricts their practice to foren-
sic work. To achieve practice content neutrality,
the authors strive to extract general principles by
focusing on elements of professional conduct
common to both civil plaintiff and defense, and
government and criminal defense experts. The
terms “retaining” and “opposing,” “examining” and
“cross-examining” attorneys are used descriptively,
and avoid a value judgment. There are some issues
unique to plaintiffs or defense experts. In these
matters, the terms “plaintiff ” and “defense” will be
used for accuracy’s sake, but they are still applied
without prejudice.
We further strive for neutrality on assessment
orientation (process/flexible approach, fixed
battery, flexible battery), legal context (civil, crim-
inal, probate, administrative, informal dispute
resolution), or practice pattern (mostly plaintiff or
defense, fulltime versus occasional forensics).
Wherever possible, we stress universal aspects
binding all approaches to neuropsychological
testing. The terms “neuropsychological tests,”
“neurocognitive methods,” and similar wording
are used to denote any procedure relying on
quantitative or qualitative analysis to arrive at
conclusions about cognitive and perceptual-motor
capacities.
However, our test content neutrality is tem-
pered by the existence of generally accepted,
mainstream neuropsychology practices. The test
24 forensic neuropsychology
selection examples offered are of the flexible
battery approach, as opposed to uniform admin-
istration of the same tests to all patients (fixed
battery) and the pure flexible approach (individu-
alized test selection for every patient). The flexible
battery is defined as a core set of tests given to the
same class of patients (e.g., dementia or closed
head injury battery), augmented by additional
measures to inform additional questions raised
by a case (Barr, 2007; Bauer, 1994). The flexible
battery approach is a sound one because it is
modeled on the medical practice of a core exami-
nation (e.g., history and neurological examina-
tion) with additional tests ordered to discriminate
between competing hypotheses (e.g., ordering
EEG, CT/MRI). There is no such thing as a “fixed
medical battery.” Even proponents of the so-called
fixed battery approach often add measures not
considered or recommended by the battery’s
creator, for example, adding memory tests to
overcome the deficiencies of the Halstead-Reitan
Battery (Russell & Starkey, 1993), and replacing
the Wechsler-Bellevue with updated intelligence
tests (Russell, 1994, 2004). Hence, even fixed bat-
tery proponents are actually practicing flexible
battery administration.
Practice pattern surveys show the flexible
battery approach is not only a recurrent majority
preference (Lees-Haley, Smith, Williams & Dunn,
1996), it is gaining an increasingly greater number
of adherents (Sweet, Moberg & Westergaard,
1996; Sweet & Moberg, 2000). As shown by the
most recent 2005 The Clinical Neuropsychologist
survey, (Sweet, Nelson, & Moberg, 2006), the
flexible battery enjoys broad sponsorship in the
neuropsychology community, as 76% of clinicians
reported reliance on that approach. In contrast,
only 7% relied on a fixed battery, a striking 61%
decline in sponsorship since 1989. A preliminary
result from the most recent survey notes that only
5% of the 1,600 respondents use a fixed battery
(Sweet, 2010). Additionally, the flexible battery
approach has withstood challenges brought in
litigation (Bigler, 2007), a point conceded by some
critics of flexible approaches (McKinzey &
Ziegler, 1999). Because neuropsychology’s diag-
nostic reasoning mirrors that of clinical medicine,
and because fixed medical batteries do not exist,
there is no good clinical reason for a fixed cogni-
tive battery.1 M. Greiffenstein made this argument
as co-author of an amicus brief submitted to the
New Hampshire Supreme Court, a case in which
that court reversed a trial court and reinstituted
an expert’s flexible battery evidence (Baxter v.
Temple, 2008). Indeed, every published legal case
addressing the validity of a flexible battery has
determined that fixed batteries offer no advantage
for forensic consulting in civil (Minner v. American
Mortg. & Guar., 2000; Chapple v. Granger, 1994)
and criminal proceedings (People v. Sebastianelli,
1998).
Irrespective of what test grouping the reader
uses, we recognize that even the soundest neurop-
sychological tests should never be interpreted
blindly in isolation from a context or important
extratest data. This is not a new idea. Matarazzo
and Herman (1985) discussed approaches to
interpreting Verbal—Performance differences on
Wechsler IQ tests, and provided a principle that
serves as a useful generalization to any clinical or
forensic endeavor. They note:
A [VIQ versus PIQ)] difference score is
merely the initial datum that should stimulate
the clinician to search for corroborating,
extra-test evidence from the clinical or social
history that such a difference is associated
with a potentially significant diagnostic finding
(p. 928).
Replacing “VIQ-PIQ difference scores” with
the term “an abnormal neurocognitive score”
provides the important maxim of reliance on a
multi-method approach to interpretation. The FN
relies on converging lines of evidence to support
conclusions proffered in court, not on test scores
in isolation (see Larrabee’s introductory chapter
on scientific approaches, this volume). In sum-
mary, your work is not done after you have scored
and profiled the tests.
BASIC PRINCIPLES OF
N E U R O P S Y C H O L O G I S T-
AT T O R N E Y I N T E R A C T I O N S
We promote five basic principles of productive
neuropsychologist-attorney interactions. These
principles are interwoven with each phase of the
attorney-neuropsychologist interaction and for
the remainder of this chapter; we will apply them
to these phases although some principles have
more weight than others do in a particular phase.
These principles are:
• Understand legal bases
• Practice competent neuropsychology
• Support board certification
• Adhere to ethical principles
• Be courtroom familiar.

Understanding legal bases means the FN
develops a working knowledge of key law and
legal practices. This is not just a competence issue;
it is a legal and ethical issue. Being reasonably
familiar with the law is a legal requirement
imposed by states before granting permission
and license to practice psychology, and recent
publications have emphasized the importance of
knowledge and competence in law relevant to
neuropsychological practice (Howe, Sweet, &
Bauer, 2010; Kaufmann, 2008, 2009). Even the
ethics code advises “when assuming forensic roles,
psychologists are or become reasonably familiar
with the judicial or administrative rules govern-
ing their roles” (Standard 2.01f) and all states
require psychologists to pass a test on laws regu-
lating the profession. But preparation for forensic
neuropsychology does not necessarily require a
deep or broad understanding of legal principles.
It does require knowing the most applicable
evidentiary law, landmark legal cases relevant to
psychology, and the basic civil rights of plaintiffs
and defendants. Even the most elementary foren-
sic psychology texts provide a sufficient under-
standing of the law and courtroom procedures to
engage in forensic consulting (Greiffenstein, 2008;
Melton, Petrila, Poythress, Slobogin, & Otto, 2007;
Andrew, Benjamin, & Kazniak, 1991; Glass, 1991).
However, understanding legal bases overlaps with
appreciating legal culture. The upcoming section
on conflicting agendas is devoted exclusively to
legal culture.
One author (P. Kaufmann) frequently uses the
phrase practicing competent neuropsychology in
his legal orientation workshops for neuropsychol-
ogists. The principle simply means the FN
embraces the scientist-practitioner role by com-
bining the body of scientific knowledge with
sound clinical judgment while conducting legal
work involving predictions about individuals. The
scientific component of the FN’s work requires
placing the legal question and assessment meth-
ods in the context of peer-reviewed scientific lit-
erature. This principle is very general, as it must
recognize there are a number of approaches to
neuropsychological testing. Most important is the
FN’s ability to defend the chosen method on
empirical and logical grounds. For example, con-
sideration of the well-established dose-response
relationship between head injury severity
and neuropsychological outcome (Dikmen,
Machamer, Winn, & Temkin, 1995; Rohling,
Meyers, & Millis, 2003; Volbrecht, Meyers, &
Kaster-Bundgaard, 2000) is relied upon to justify
Neuropsychology and the Law 25
conclusions about causation of current neurocog-
nitive performance. Although empiricism is
important in justifying methodology and conclu-
sions, there will not be a published study for every
question that arises in legal disputes. Each legal
case will have unique aspects that can only be
addressed by clinical judgment, that is, extrapola-
tion and logic. When confronted with a 58-year-
old school teacher and asked whether she can
return to work one year after a mild concussion,
do not bother to look for studies entitled
“Prediction of work status in mildly head injured
teachers.” FN must always exercise sound judg-
ment in generalizing from the data and literature
to a specific claimant’s (or defendant’s) behavior.
Even that champion of actuarial approaches, Paul
Meehl, recognized the need to use case-specific
data to modify conclusions in the absence of the
perfect on-point study (Meehl, 1954). The logical
path through the data must be made transparent.
The U.S. Supreme Court decision in Joiner requires
trial courts to separately evaluate the expert’s rea-
soning process that links observation and litera-
ture to conclusions.
The principle of supporting board certification
in neuropsychology should not be a controversial
principle to readers. Our intention is not to pro-
voke or diminish noncertified specialists. We
mean only that peer review of one’s work product
is an important means of proving competence in
neuropsychology, and certification through a rec-
ognized certifying body is acceptable proof of
competence. Professional standards matter. We
do not mean that only psychologists certified by
the American Board of Clinical Neuropsychology
(a specialty board under the umbrella of ABPP)
should be allowed to step into court, or that such
psychologist’s opinions be given more weight.
However, board certification does help to prove
competence in a legal vacuum and courts rou-
tinely accept it as some evidence of competence;
for example, footnoting the 13 member boards of
the American Board of Professional Psychology
(Tarver v. State, 2005). Many state licensing laws
only protect the title of psychologist, so there are
few safeguards against psychologists who adver-
tise neuropsychology services without the requi-
site training or coursework. Certification allows
consumers to better distinguish between choices
in states that allow liberal self-definition of
specialty services.2 As neuropsychologists are ever
more frequently called upon to render expert
opinions, lawyers are increasingly examining the
background, training, and experience of experts.
26 forensic neuropsychology
Ethical questions are more likely to be raised
by forensic work than in any other setting. First,
more ethical principles are invoked because of the
larger number of parties involved and the
protracted nature of litigation. Second, opposing
parties may attempt to intimidate witnesses or
influence opinions by prematurely filing ethical
complaints for the purpose of undermining the
credibility of an opposing expert.3 Third, ethical
issues are embedded in every phase of the forensic
assessment process (Bush, 2007; Bush, Grote,
Johnson-Greene, & Macartney-Filgate, 2008). The
FN should be aware of the unique ethical issues
associated with each phase of attorney-neuropsy-
chology interactions. Courtroom experience offers
constant and subtle pressures to deviate from
sound practices, for example, the pull of advocacy.
The very nature of the adversarial system poses the
following unique challenge to the neuropsycholo-
gist: Legitimate courtroom practices and ethical
attorney behavior would be considered unethical
if practiced by a neuropsychologist.
The difficulty lies in recognizing ethical
dilemmas and the appropriate coping response.
Even the most ethically scrupulous neuropsy-
chologist must be prepared to cope with unfair
ethical charges raised by either advocates pretend-
ing to be neuropsychology experts, or unsavory
attorneys. Recognizing the burden of behaving
ethically is made more difficult by ambiguity in
published ethical guidelines. In cases of ambigu-
ity, the FN must make an honest attempt to distill
the gist or “spirit” of the code in ways that are not
self-serving (Shapiro, 2000). The reader may
cross-reference Christopher Grote’s chapter in the
current volume for a broader and in-depth
exploration of ethical issues.
The principle of being courtroom familiar
means the FN is able to recognize courtroom
dynamics, trial procedures, interpersonal transac-
tions, and personalities (Brodsky, 1991). There are
many indicia of “courtroom familiarity” (a term
credited to Brodsky & Robey, 1973). These may
include knowledge about the presiding judge,
knowing the opposing attorney, suppressing the
“star witness” mentality, minimal emotional reac-
tions to aggressive subpoenas, and easy conces-
sion of minor points during cross-examination.
This principle is similar to the understanding of
legal bases principle, but we kept it separate
because developing courtroom familiarity requires
“insider” knowledge, some of it arcane and spe-
cific to a locale or jurisdiction. Courtroom famil-
iarity also differs because it represents an outcome
of forensic experience, while understanding legal
bases is a precondition for starting forensic work.
After the section on clashing worldviews, the
remainder of the chapter describes the four main
phases of attorney-neuropsychologist interac-
tions: The pre-assessment, assessment, trial, and
post-trial phases. The five basic principles of
productive interactions are then applied to each
phase where appropriate.
CONFLICTS BETWEEN
S C I E N T I S T- P R A C T I T I O N E R
AND LEGAL MODELS
The most difficult adjustment is to the inevitable
conflict between neuropsychological and legal
methods. The law and science are two clashing
epistemologies (Greiffenstein, 2008). The FN must
recognize and manage these basic conflicts in
order to develop a productive relationship with
the attorney and the trier of fact. The three
fundamental conflicts encountered by the FN are
(a) conflicting agendas, (b) conflicting methods,
and (c) conflicting relationships.
Conflicting Agendas
The most basic and pervasive conflict is objectivity
versus zealous advocacy. In a typical clinical
setting, neuropsychologists pursue a goal of
describing a person’s perceptual-motor, cognitive,
and personality characteristics in an objective and
reasonably certain way. All final conclusions are at
least partially grounded in scientific findings and
logical inferences tightly linked to facts. In con-
trast, criminal and civil proceedings in America
take place in an adversarial setting. Attorneys are
advocates. Zealous advocacy is required and tem-
pered only by the ambiguous “candor before the
tribunal” principle. Consequently, winning and
losing cases are more important than accuracy
and objectivity, and justice is more important
than truth. Justice provides the opportunity for
truth to be heard, but it does not guarantee that
the truth shall prevail. The attorney’s goal is to
present a strong case for their client while simul-
taneously minimizing and directly challenging
the opposing attorney’s arguments. Attorneys are
not allowed to lie, even as they strike a balance
between competing ethical imperatives in the
ABA Model Rules of Professional Conduct in
Table 2.1. Balancing rules of professional conduct
is both the obligation and the prerogative of an
attorney. That is, lawyers exercise professional
discretion in how they balance the competing
requirements found in these two rules. Attorneys
 Neuropsychology and the Law 27

TABLE 2.1 ABA MODEL RULES OF PROFESSIONAL CONDUCT

Relevant Excerpts

Rule 1.3 Diligence – A lawyer shall act with reasonable diligence and promptness in representing a client.
Comment [1] A lawyer must also act with commitment and dedication to the interests of the client and with zeal
in advocacy upon the client’s behalf. A lawyer is not bound, however, to press for every advantage that might be
realized for a client. For example, a lawyer may have authority to exercise professional discretion in determining
the means by which a matter should be pursued. [emphasis added]

Rule 3.3 Candor Toward The Tribunal (a) A lawyer shall not knowingly:

(1) make a false statement of fact or law to a tribunal or fail to correct a false statement of material fact or law
previously made to the tribunal by the lawyer;
(2) fail to disclose to the tribunal legal authority in the controlling jurisdiction known to the lawyer to be directly
adverse to the position of the client and not disclosed by opposing counsel; or

(3) offer evidence that the lawyer knows to be false. If a lawyer, the lawyer’s client, or a witness called by the lawyer,
has offered material evidence and the lawyer comes to know of its falsity, the lawyer shall take reasonable
remedial measures, including, if necessary, disclosure to the tribunal. A lawyer may refuse to offer evidence,
other than the testimony of a defendant in a criminal matter, that the lawyer reasonably believes is false.
Comment [2] This Rule sets forth the special duties of lawyers as officers of the court to avoid conduct that
undermines the integrity of the adjudicative process. A lawyer acting as an advocate in an adjudicative proceeding
has an obligation to present the client’s case with persuasive force. Performance of that duty while maintaining
confidences of the client, however, is qualified by the advocate’s duty of candor to the tribunal. Consequently,
although a lawyer in an adversary proceeding is not required to present an impartial exposition of the law or
to vouch for the evidence submitted in a cause, the lawyer must not allow the tribunal to be misled by false
statements of law or fact or evidence that the lawyer knows to be false. [emphasis added].

exercise professional discretion in how they
engage in zealous advocacy for their clients.
However, zealous advocacy must be tempered
with candor before the tribunal. A failure to
exercise candor during legal proceedings is
a violation of professional responsibility.
Failure to acknowledge this basic law-psychol-
ogy conflict will ensure a poor working relation-
ship and quickly sour an interest in forensic work.
For example, the novice FN becomes dismayed
when the retaining attorney invokes the “work
product rule” and insists she not even write a
report. She concludes that the retaining attorney
is dishonest or unappreciative of her well-
developed diagnostic skills. If she is asked to write
a report and makes an appearance at court, she
becomes annoyed that the cross-examining attor-
ney spends time repeatedly asking about a minor
scoring error, but does not affirm her 99%
accuracy in all other scoring. She concludes this
attorney is unfair. These perceptions, while often
true, betray her misunderstanding of legal culture.
An accurate, comprehensive, and balanced report
may be harmful to an attorney’s case. Because
most FNs would be alarmed at any colleague
writing a one-sided report that minimizes incon-
venient findings and highlights only minor
ones, she should realize that it is considered
ethical and fair for an attorney to present his
case in just such a partisan form. An attorney’s
acceptance or rejection of his FN’s report may
make sense in the context of this adversarial
system.
In rare circumstances, the court may retain
the FN as an expert. Federal Rule of Evidence
(FRE; 1975, 2003) 706 allows a court to authorize
its own expert at the expense of both parties.
Having the court for your client mitigates the
conflicts to some degree, as judges are much more
interested in everything an FN has to say and
there is less pressure to tailor findings to an advo-
cate’s needs. However, court appointed expertise
is uncommon in civil proceedings and perhaps
found only in juvenile law. Even in this more
28 forensic neuropsychology
desirable circumstance, the FN is still subject to
aggressive cross-examination by an advocate.
Conflicting Methods
Another pervasive conflict is differing standards of
proof (Blau, 1998). FNs are trained in the scientist-
practitioner model, which relies on two prongs: (1)
Conservative evidentiary standards and (2) repli-
cation. Two common standards of proof used by
FNs to justify selection of measures are (a) the
zero-order validity study (Grove & Barden, 1999)
and (b) the proven classificatory accuracy of a test
(Larrabee & Berry, 2007). A zero-order validity
study is the demonstration of a statistically signifi-
cant correlation between a neurocognitive measure
and a neurological criterion. The statistical thresh-
old for a significant zero-order correlation is
conventionally (but not universally) considered to
be >95% confidence (p < .05) and ideally 99%
(p < .01. A classificatory accuracy study examines
the sensitivity and specificity of a test in predicting
a criterion, that is, how many hits and errors (false
positives and negatives). With either method, how-
ever, many factors can produce artifacts in a single
study: small sample size (insufficient power),
number of variables studied (family-wise error),
plain serendipity (type I error), and uncontrolled
between-group differences (internal validity threat,
the covariate problem). Thus, replication, prefera-
bly in another laboratory, is added as a second
requirement. Scientific standards of proof are uni-
form across settings and are not altered as a func-
tion of socially desired versus potentially unpopular
outcomes. In summary, neuropsychological con-
sensus requires conservative statistical evidence
and consistent results across different settings.
In contrast, the courts require less conservative
evidentiary standards, shaped by a desire to resolve
cases over shorter time frames (Hess, 1999a). The
uniqueness of each case and requirement for
speedy justice makes replication of deficit over
time a practical impossibility. In addition, legal
evidentiary standards themselves float; that is, they
depend on the gravity of the legal outcome, and
whether damages (cash) or fundamental rights
(life/liberty) are at stake. Per Kagehiro (1990),
these evidentiary thresholds (with proposed confi-
dence levels in parentheses) are preponderance of
the evidence (51%), clear and convincing evidence
(75%), and reasonable doubt (90%). Although
these proposed confidence levels make sense to
scientist–practitioners, judges, jurors, and layper-
sons do not apply them systematically (Wright,
2008). The “preponderance of the evidence”
standard means the trier of fact favors parties
having at least 51% of the evidence in their favor.
This is the evidentiary standard in personal injury
cases and worker’s compensation. Criminal courts
rely on a “beyond a reasonable doubt” standard,
but as observed by Hess (1999a), even this level of
legal evidence barely approaches the lower limit
of the p < .05 standard common in scientific
psychology. When asked to assign probabilities to
specific burdens of proof, many judges refuse
to do so (McCauliff, 1982), stating such things as
“percentage or probabilities simply cannot encom-
pass all the factors, tangible and intangible, in
determining guilt—evidence cannot be evaluated
in such terms” (Simon & Mahan, 1971). To this
day, trial consultants continue to advise that jurors
will never agree to decide cases on the basis of
probabilities (Ball, 2008).
Another methods conflict is responsivity to
social and political forces. Scientific neuropsychol-
ogy, in principle at least, is supposed to be resistant
to changing fads, laws, popular beliefs, and politi-
cal forces. However, court rulings and jury verdicts
are not only influenced by popular beliefs and
political trends, lawyers and judges expect out-
comes to be influenced by changing community
standards. Courts may set aside verdicts that are
clearly inconsistent with the law under non obstante
veredicto, judgment as a matter of law, or through
remittitur.4 But this self-correcting mechanism is
rarely invoked in courts; modern science has a
better track record of self-correction. The assertion
that the Constitution is a “living document” is an
example of social forces influencing legal interpre-
tation. This leads to the anomalous situation of
different evidentiary requirements for the same
neuropsychological methodology dependent on
the legal question (Tenopyr, 1999). For example,
the use of IQ tests in employment and school
settings is held to very rigorous standards follow-
ing the Griggs et al. v. Duke Power (1971) and Larry
P. v Riles (1984) rulings. In contrast, despite the
proven insensitivity of IQ tests to remote
mild head injuries (Binder, 1997; Binder, Rohling,
& Larrabee, 1997; Dikmen, Machamer, Winn, &
Temkin, 1995; Dikmen, Temkin, Machamer,
& Holubkov, 1994) neuropsychologists are not
enjoined from using “subtle” intelligence subtest
differences as evidence for “brain damage.”
Conflicting Roles
Conflicts in the forensic arena are not necessarily
between the law and neuropsychology. Role
conflicts arise within the FN as they move from a

clinical to a legal setting, and this is termed “dual
roles.” A dual role means a psychologist has more
than one relationship with a patient or client. Dual
roles are not blanketly unethical—it is the nature
of the dual role that requires reflection; it is only a
problem when the goals associated with the dual
roles conflict. One definite conflict is treater versus
expert. In clinical settings, even the most objective
neuropsychologist treats the patient with empathy
and the goal is primary gain: reducing symptoms
and improving function. In contrast, the expert is
supposed to be objective at all times, assert truths
the plaintiff does not want to hear, and evaluates
the influence of secondary gain: maintenance of
symptoms for reward. The conflict is clear: One
cannot reduce and maintain symptoms at the
same time; one cannot be empathic but increase
emotional costs by making statements damaging
to a patient’s legal pursuits. The conflict between
“treater” and attorney’s agent is the most common
form dual role conflict takes, but views differ on
whether this specific conflict is inherently unethi-
cal. Greenberg and Shuman (1997, 2008a, 2008b)
provide an exhaustive analysis of all the problems
inherent in therapists being asked to be expert
witnesses and trial consultants. As one example,
Greenberg and Shuman point out that if the treater
accepts the role of consultant, then the patient is
no longer the client but the plaintiff attorney is.
There may also be circumstances where the civil
defense attorney or prosecutor asks a treater to
testify. In such cases, the treater should insist on
being a reporting (fact) witness only and answer
questions based on information contained within
the “four corners” of their reports. Shuman,
Greenberg, Heilbrun, and Foote (1998) go even
further—they make the provocative argument
that therapists should not be allowed to testify at
all, and attorneys from both sides should be forced
to retain independent examiners.
We believe these proposals are too restrictive
because they deviate from FRE 702. Kaufmann
(this volume) describes recent practical alterna-
tive positions detailed by Dvoskin (2002), Heltzel
(2007), and Woody (2009). The criterion should
be “probable assistance” to the trier of fact, and a
therapist (or cognitive rehabilitation specialist)
may provide evidence regarding daily function
that an independent examiner could not.
Greenberg and Shuman are correct that inherent
conflicts may contaminate the evidence, but any
strong biases (such as financial interest in trial
outcome) or zealous advocacy can be addressed
during cross-examination.
Neuropsychology and the Law 29
The treater versus expert conflict may be man-
ageable, but with difficulty. The manageability
depends on the treatment model. Those therapists
whose large unpaid bills are part of the legal dis-
pute may be especially vulnerable to this dual role
conflict. In some cases, the provider may have been
hired only to create a traumatic brain injury narra-
tive and perform unneeded treatment to inflate
injury severity. Other providers more appropriately
advocate for the patient’s best interests, which
sometimes includes support for disability pay-
ments, to remove secondary gain as an obstacle to
treatment. This situation often applies when a psy-
chologist has treated a plaintiff before their neuro-
logical injury. Supporting a patient’s demands for
compensation has a long tradition in clinical psy-
chology and medicine, as secondary gain (the legal
requirement of proving damages) may interfere
with primary gain (the therapeutic goal of reducing
symptoms). Fenichel (1945) discussed how sec-
ondary gain prolonged the psychoanalytic treat-
ment of traumatic neuroses and he advised:
“Perhaps the idea of giving a single compensation
at the right time may be the best way out” (p. 126).
Collegiality versus opposition is another con-
flict requiring some adjustment. In pure clinical
settings, neuropsychologists operate in a collegial
fashion with their community. They share data
with each other, strive for points of agreement in
conceptualization of a patient’s cognitive prob-
lems, and collaborate on research. In a forensic
setting, FNs are often asked to forcefully critique
the work of another neuropsychologist who has
been hired by the other side.
MANAGEABLE
C O N T E M P O R A RY
CONFLICTS
The core conflicts discussed to this point are
structural and endemic to every case FNs accept.
They can only be adjusted to, not changed in any
substantial manner. FNs cannot rewrite law, or
dictate lawyer conduct. However, there are con-
flicts that the FNs encounter episodically, where
the law and neuropsychology clash, but the FN
may exercise some control or have considerable
input as to how these conflicts are resolved. The
response to each of these conflicts is a matter of
controversy, and various solutions are available.
Access to Raw Data
Legal decisions, like scientific ones, are based on
evidence. The rules of evidence in every jurisdic-
tion allow attorneys to obtain the data on which
30 forensic neuropsychology
the opposing expert bases their opinions. This pro-
cess is termed discovery. In civil and criminal set-
tings, all relevant information is discoverable,
unless privileged. Cardiologists must provide EKG
tracings, crime scene scientists must provide
bloody clothes, and psychologists must provide
test data to the opposing expert. However,
attorneys are not required to disclose conversa-
tions with a client or work product on a case,
because of the important social need to protect
the attorney-client relationship, and to encourage
clients to be forthcoming within that relationship.
In some states, psychologists are not allowed to
disclose their test results to nonpsychologists. The
evidentiary base upon which neuropsychologists
rely typically includes test scores, records, inter-
view notes, and mental status observations. It is
inevitable that most FNs are eventually asked to
provide a copy of their case file to either retaining
or opposing counsel, hereinafter referred to as
“raw data.”
Legal arguments and strategies of managing
the “raw data” problem are described extensively
elsewhere (Kaufmann, 2005, 2009). In developing
responses to requests for data disclosure, it is
important to define terms. What exactly is meant
by raw data? Matarazzo (1990) defines the several
different types of raw data subject to discovery
demands. Such data includes (1) written reports,
(2) handwritten interview notes, (3) numerical
scores, for example, raw counts of number correct
or standardized scores, (4) test stimuli, (5) the
participant’s actual responses to test stimuli, and
(6) test manuals. As a practical matter, most foren-
sic case files will not contain stand-alone test
stimuli and actual manuals.5 The clash between
the law and neuropsychology usually results from
demands to discover raw data in categories 3 and
5: test forms containing verbatim responses, and
scoring sheets/formulas.
First, we state the law-psychology conflict.
Essentially, many psychologists (wrongly) view a
raw data request as a negotiation between two
equal parties. Perhaps as a reflection of sound
ethical training or alternatively an evasion of
public scrutiny, many psychologists approach the
raw data problem as an ethical dilemma that they
should resolve, rather than a legal question that
courts alone will decide. In addition to this legal
analysis, further conflict may also arise because
the law generally allows discovery of raw data
used to formulate expert opinions, but the ethics
code under which most neuropsychologists
operate has been interpreted by some as placing
strong prohibitions against data sharing. The term
interpreted is chosen because of the inevitable
ambiguous nature of ethical guidelines. Ethics
codes, like American law, are not Napoleonic,
meaning not every possibility or decision is laid
out in detail, to eliminate interpretation. Instead,
principles are broadly abstract and applied by
human judges, not administrators.
Psychologists commonly cite the 2002 edition
of the Ethical Principles for Psychologists
(American Psychological Association, 2002;
hereinafter the 2002 Code) as their authority
controlling the treatment of raw data requests.
A number of the 2002 Code’s principles bear
directly on either forensic activities or the disclo-
sure of raw test data to nonpsychologists.
Unfortunately, there has been no consensus on
Code interpretation in responding to subpoenas,
and there is a wide range of views on handling raw
data requests. Essig, Mittenberg, Peterson,
Strauman, and Cooper (2001) surveyed FNs about
their raw data practices. They reported 61% of
FNs did not share data in half or more of their
forensic cases, while 39% reported honoring the
request in the majority of cases. Looking at the
extremes only, 12% of FNs refused to forward raw
test data at any time and 18% reported sharing
data with the opposition regularly. One reason-
able interpretation of this data is that 30% take the
polarized views reflected in the commentary
literature (discussed elsewhere in this chapter)
and the middle 70% disclose data on an irregular
basis, depending on particulars. Essig et al. (2001)
did not explore the contingencies of this middle
group’s practices. Pieniadz and Kelland (2001) did
explore these contingencies but restricted their
survey to the issue of including test scores in the
report body. They found 35.5% regularly included
scores (the “Yes” group) and 64.5% (the “No”
group) did not. The main reasons for including
scores were “integrity/thoroughness” and “future
comparison” (both 100% of Yes group). The main
reasons for excluding specific scores were “data
protection” (90% of No group) and to “maintain
the [Boston] process focus” (50%). Adherents of
the process approach were more likely to refuse
test score inclusion than flexible battery adher-
ents. Kaufmann (2009) noted that marked
variance in data release practices persists in his
workshop participants, in part, due to widely
varying jurisdictional laws governing the practice.
Although survey data is limited, it appears
neuropsychologists lack uniformity and offer
many different reasons for including, excluding,

or variably supplying the data that serves as the
basis for their opinions.
Other reasons for this lack of practice stan-
dard may originate in the ambiguities and frank
contradictions of the preceding 1992 Code
(American Psychological Association, 1992). One
1992 Code paradox allowed psychologists to give
their raw test data to their own patients, but also
encouraged withholding data from other nonpsy-
chologists (e.g., courts). The 1992 Code also dis-
tinguished between forensic and clinical settings,
further encouraging different approaches to han-
dling data. Review of commentary articles from
the 1992–2002 eras reveals a wide array of
opinions, which may be broadly classified into
two camps based on the public policy debate: test
security and absolute discovery camps.6 The test
security position treats raw test data as distinct
from other forms of legal evidence, and urged
special treatment by the courts. Tranel (1994)
viewed the 1992 Code as “clear” on barring dis-
closure of data by relying solely on 1992 Standard
2.02(b) as his authority. He suggested barring
the reporting of test scores in the report to avoid
(a) “potential misuse” and (b) dissemination of
test items into the public domain; for example,
stopping cross-examining attorneys from asking
questions about individual items rather than
aggregate scores. Kaufmann (2005) drew atten-
tion to an important U.S. Supreme Court decision
and its progeny that favor test security: Detroit
Edison Co. v. National Labor Relations Board
(NLRB) (1979) (hereinafter Edison). In Edison,
the High Court ruled against the utility union that
demanded test scores, materials, and manuals for
psychological tests administered by the utility.
The USSC spoke to the “strong public policy” of
test security for standardized psychological
instruments. Kaufmann (2005) argued the Edison
decision creates a narrow, implied nondisclosure
privilege for psychologists that imposes a duty to
safeguard psychological tests from wrongful dis-
closure. In reaction to Edison, a number of states
enacted legislation designed to protect psycho-
logical test materials. Subsequently, a federal court
(Chiperas v. Rubin, 1998) linked the Edison privi-
lege to a clinical case and state courts have recog-
nized “the psychological profession’s legitimate
interest in preserving the security of tests” (p. 776,
Fla. DOT v. Piccolo, 2007). Kaufmann (2009)
identifies a series of additional federal court and
NLRB administrative decisions that uniformly
recognize that discovery of psychological tests are
restricted under Edison.
Neuropsychology and the Law 31
However, the Edison nondisclosure privilege
is narrow and only implied. Stated alternatively,
test security interests were presumed by all parties
and the Court, such that the Edison decision did
not confront directly the “raw data” controversy.
Consequently, Edison does not contain any test
security holdings because appellate courts gener-
ally do not render opinions on matters not
certified for determination. The duty of psycholo-
gists to safeguard test materials from disclosure to
nonpsychologists (e.g., the Illinois statute) does
not exist in most jurisdictions. Following publi-
cation of Kaufmann (2009), two federal cases
confronted the Edison privilege and commented
on his legal theory (Taylor v. Erna, 2009; Lumsden
v. United States, 2010). In Taylor, the district court
agreed Edison’s holding was that test security
trumped the union’s interests, given the particular
facts (page 7).7 The absence of a universal test
security privilege is also shown in the recent
Lumsden decision. The North Carolina trial court
declined to recognize the Edison privilege because
it was not properly presented, stating that the
psychologist “does not even appear to be asserting
any legal privilege of his own against disclosing
the materials” (page 8).8
In light of these rulings, Kaufmann (2010)
subsequently advised: 1) Parties (plaintiff, defense)
cannot assert the psychologist nondisclosure
privilege/duty to protect psychological test mate-
rials, because the psychologist (nonparty) is the
holder of that privilege; 2) If psychologists do
not independently assert the psychologist non-
disclosure privilege/duty to protect psychological
test materials, then they may be ordered to
produce raw data and test protocols to nonpsy-
chologists. Essentially, there is a fundamental dif-
ference between asserting a privilege not to release
materials and pointing out legal prohibitions
against release. Absent a claim of privilege the
court will not rule on whether it applies in the
case at bar.
The absolute discovery position is best exem-
plified by Lees-Haley and Courtney’s (2000) com-
mentary in a special issue of Neuropsychology
Review. This position asserts civil rights and legal
due process as the only guide that dictates treat-
ment of psychological test data, making no men-
tion of privilege law. Raw test data should not be
afforded special protections, and psychologists
must be subject to the same evidentiary rules as
other experts. According to this argument, broad
nondisclosure rights create a special class of
experts who are not subject to legally mandated
32 forensic neuropsychology
courtroom practices, a potential violation of
due process. Lees-Haley and Courtney (2000) cite
1992 Standard 1.23(b) (Documentation of
Professional Work) as their main authority. How
can one document work performed, yet refuse to
share the documentation for legal scrutiny? The
Specialty Guidelines for Forensic Psychology
(SGFFP) also require complete transparency of
psychological evidence for scrutiny by a court.
Greiffenstein and Cohen (2005) observed that if
in-text test scores were disallowed as proposed by
Tranel (1994), every school psychologist in this
country was subject to ethical sanctions for
reporting WISC-3/4 profiles. The authors do not
find that Tranel’s position is supported under the
current Ethics Code, nor can Kaufmann find any
legal support for such a broad prohibition of test
score disclosure.
The new 2002 Code attempts to address the
ambiguities in the earlier Code to better reflect
the evolving relationship between psychology and
law (Fisher, 2003). The major shift from 1992 to
2002 is from a presumption of withholding raw
data to one of providing it under specified condi-
tions (Behnke, 2003). To meet conflicting goals of
test security versus discovery, the 2002 Code
definition of raw data is subdivided into two
classes in the spirit of Matarazzo (1990), making a
clear distinction between scored test forms from a
case file versus test manuals. Each is given sepa-
rate treatment: Standard 9.04(a) deals with scored
protocols in the individual case and Standard 9.11
deals with test manuals and stimuli. Standard 9.04
allows release of scored protocols in response to a
valid subpoena without the ambiguous “reason-
able steps” contingency of the earlier Code, takes
local law into consideration, and allows for more
uniform treatment of individual raw data than
the old parallel standard: Raw test data can still be
disclosed to a patient/participant, but without the
language that some have used to justify withhold-
ing evidence from attorneys. Code 2002 Standard
9.11 protects test security by maintaining restric-
tions on disclosure of manuals and stimuli. This
separate treatment of manuals may allay some
fears of public dissemination, the main reason
usually given to withhold any data (Tranel, 1994;
Naugle & McSweeny, 1995).
In the first edition of this chapter, Greiffenstein
and Cohen (2005) argued that to maintain fidelity
with the 2002 Code, test data should not be
afforded special protections, but that test manuals
should be. This opinion is also in accord with
Edison, in which the legal issue was whether test
manuals and items were discoverable by a party to
the suit. Until higher courts and/or legislatures
adopt a universal test security privilege, FNs have
an array of choices for dealing with requests
(or subpoenas) for raw data and test manuals.
In states that have no unique protections for test
materials that contain raw data (see Lumsford
2010 described, supra), one can begin with a pre-
sumption against disclosing test manuals (and
perhaps raw data), much like the initial presump-
tion against third-party observation (discussed
later). The presumption can be backed by assert-
ing a privilege for the court to consider, or request-
ing the court issue a protective order (see Table
2.2). Otherwise, Standard 9.04(b) requires psy-
chologists to provide test data as required by law
or court order. Currently, about twenty states pro-
tect psychological tests as a unique methodology,
with some states enacting a psychologist nondis-
closure privilege/duty to safeguard test materials
from wrongful disclosure. Nevertheless, a valid
subpoena is sufficient for disclosing a test partici-
pant’s scored protocols and history notes.9 The
2002 code is imperfect, and it has been criticized
(Behnke, 2003; Rapp, Ferber, & Bush, 2008). For
example, it does not deal with the situation of
neuropsychological measures that contain the test
stimuli on the scoring forms, for example, the
Rey-Osterrieth Complex Figure. Kaufmann
(2009) calls for a code revision that recognizes a
uniform psychologist nondisclosure privilege
consistent with Edison. Nevertheless, the 2002
Code remains a reasonable advance towards
resolving perceived conflicts between ethics and
the law. We will not belabor the strained ethical
analyses in what so many others have attempted
to explain, except to say: Professional psychology
still has not set forth a workable standard to the
wider audience of practitioners outside of the
forensic specialists who require regular raw data
access to address legal questions.10 In summary,
the present authors favor the legal primacy of test
security with respect to manuals and test stimuli
because it is most consistent with the law and best
record policy for psychology practice.
Third-Party Observation (TPO)
The presence of a third-party observer remains a
contentious issue that continues to occupy courts,
attorneys, and FNs. There is a legal foundation for
TPO requests, as almost all jurisdictions, federal
and state, allow consideration of attorneys observ-
ing independent medical examinations (IMEs)
or government-ordered evaluations. The specific
 Neuropsychology and the Law 33

TABLE 2.2 CONDITIONS FOR VIDEOTAPING A NEUROPSYCHOLOGICAL

EVALUATION
Model Court Order
1. A single stationary wireless video camera with microphone will be located in the examination room, focused
on Plaintiff but outside his/her direct line of vision, to minimize distraction. The video monitor and video
operator will be located in a separate room. The video operator will receive the video and audio feeds from the
two output jacks at the back of the video monitor.
2. The video operator and/or plaintiff attorney will not interfere, interrupt or disrupt the examination at any time,
even if the videotape needs to be changed. The operator and any plaintiff ’s representatives are silent observers
in the separate room. The Court recognizes that any distraction introduced by the video monitoring procedure
may impact scores on attention tests.
3. This Court recognizes that psychological and neuropsychological measures are of no use if the test forms,
administration procedures and test responses are broadly disseminated to the public. Videotapes of
neuropsychological procedures may be used to coach clients to improve performance on tasks designed
to detect exaggerated deficit, or to intentionally underperform on standard neuropsychological measures.
For these reasons, reasonable restrictions must be placed on the use of any videotape. These restrictions are
described in section #4.
4. Any and all videotapes and test materials that are produced pursuant to the examination will be returned to
Dr. Ima Legend at the conclusion of the litigation, including any and all appeals, if necessary. Exhibits and
courtroom records containing test materials will be protected or sealed until destroyed or returned to Dr.
Legend at the conclusion of litigation. Information about the videotape and test materials shall not be disclosed
to any person other than to Plaintiff, Plaintiff ’s attorney, Defendant’s attorney and Plaintiff ’s and Defendants
designated experts. In no event shall any information about the videotape or tests materials be reviewed by
nor disclosed to any person not specifically recited herein. Presentations of test materials or videotape in the
courtroom will he minimized to the extent possible.

wording of these statutes may grant the right
for plaintiff ’s personal “physician” or attorney to
be present during a “physical examination” in a
contested matter. It is a matter of judicial discre-
tion whether these statutes broadly cover any
third-party examination requested by the civil
defendant (or government) or whether the statute
should be narrowly construed to the plain lan-
guage that names purely medical investigations.
Trial judges have great latitude in defining the
scope of these terms and in most cases in local
(but not federal) courts. It is inevitable that every
FN will be confronted with this demand at
some time.
Major neuropsychology organizations pub-
lished strongly worded policies discouraging TPO
practice, except in very limited circumstances
(AACN, 2001; Axelrod et al., 2000). But an APA
position paper (Assessment, 2008) avoided
blanket resistance, instead offering a variety of
approaches that included minimizations of
intrusion or using assessment procedures less
affected by an audience, as well as requesting TPO
withdrawal or refusing it. Most recently, Howe
and McCaffrey (2010) encouraged advocacy and
legislation to exclude TPO during civil neuro-
psychological evaluations.
Case law to date shows a wide range of rulings,
from narrow construction to unlimited TPO.
Case law can be grouped into various approaches,
such as a “presumptive right” or “no presumptive
right” to TPO, but most rulings allow for trial
court discretion based on case particulars. Much
depends on the legal context (criminal vs. civil),
the nature of the evaluation (invasive vs. noninva-
sive), and the claims made (legal insanity vs.
traumatic brain injury). Many appellate decisions
contain language proving that courts recognize
the validity of neuropsychological test responses
can be affected by third-party involvement, when
compared to physical responses in medical exam-
inations. For example, in Cline v. Firestone Tire
(1988) the plaintiff moved for a protective order
barring a neuropsychology IME unless strict
conditions were met, but the federal district court
held that plaintiff was not entitled to have an
attorney present. In Tomlin v. Holecek (1993), a
Minnesota district court denied plaintiff ’s motion
to record or observe the examination, reasoning
TPO would influence the plaintiff to “guard, alter
34 forensic neuropsychology
or disguise” test responses during both the history
taking and testing phases. In Ragge v. MCA/
Universal Studios (1995), a USDC denied plain-
tiff ’s request for a third-party observer during a
neuropsychological IME. In a criminal matter
(United States v. Byers, 1984), the DC Circuit
Court ruled that a defendant was not allowed an
attorney TPO during a competency evaluation.11
But in child abuse allegations and death penalty
cases, where much is a stake and there is a greater
demand for reliability of psychologist report, TPO
may be more strongly enforced. Some states, such
as Texas, require audiotaping or videotaping of
interviews and psychological testing whenever
there is child abuse/neglect prosecution. One
factor tying these cases together is that the burden
rests on the movant (the one who petitions for an
observer) to show good cause for potentially
affecting an evaluation’s validity. This is an easier
hurdle to jump if a lot is at stake.
The scientific evidence regarding TPO or
recording empirically supports making distinc-
tions between the interview and testing phases of
the assessment. The counseling psychology and
child abuse literature raises concern about the
accuracy of interviewers when asked to recall
questions and answers (Covner, 1944; Gelso, 1974;
Ceci, Bruck, & Battin 2000).
On the testing side, there is no reasonable dis-
pute that the presence of an audience influences
performance (McCaffrey, Lynch, & Yantz, 2005).
There is a rich, 100+ year-old literature showing
TPO affects performance tests differently. Termed
the “social facilitation” literature, social psycholo-
gists showed that perceptual-motor performance
is affected by observation. A typical finding is that
simple perceptual-motor tests are facilitated by an
audience, but more complex tasks are negatively
affected (Bond & Titus, 1983; Constantinou &
McCaffrey, 2003; McCaffrey et al., 2005). There
are many key studies relevant to neuropsychology.
Kehrer, Sanchez, Habif, Rosenbaum, and Townes
(2000) reported performance decrements on tests
of attention, speed of information processing, and
verbal fluency, but no effect on simple manual
speed. Constantinou, Ashendorf, and McCaffrey
(2002) examined the effects of an audio-recorder
and found a decrement in memory scores, but not
on motor measures. A similar result was found
with a video-recorder (Constantinou & McCaffrey,
2003). Gavett, Lynch, and McCaffrey (2005)
concluded “the presence of an observer during
a neuropsychological evaluation should be
expected to have a clinically meaningful impact
on an examinee’s test performance.” Although the
AACN position statement on TPO asserts that
“involved and uninvolved” are crucial distinctions
in predicting performance, some studies have not
shown any evidence that forensic role or social
connection makes any difference. Yantz and
McCaffrey (2005) demonstrated that a neuro-
psychology supervisor’s presence had just as
impairing an influence as any other observer, and
Greiffenstein, Baker, Fox, Boone, and Tsushima
(2010) showed forensic role (plaintiff or defense)
had no influence on MMPI-2 validity scales.
There is also no support for the idea promoted
by plaintiff attorneys that “supportive” observers
are necessary to facilitate cooperation during an
adversarial examination. Using a single case
ABAB experimental design, Binder and Johnson-
Greene (1995) described a patient performed
worse on malingering measures when her mother
was present then when she was absent. More on
point, Butler and Baumeister (1998) reported
that even warm, supportive observers caused
decrements on skilled tasks relative to unmoni-
tored performance. These studies disprove the
legal assertion that having an “agent” or “support-
ive family member” facilitates the neuropsycho-
logical examination. Regarding the interview
phase, research suggests the recording or observa-
tion may improve the reliability of history, insofar
as mistakes are correctable.
Unlike the raw data issue, practitioner surveys
show stronger attitudes against TPOs, although
actual compliance with observer requests differs
along the civil-criminal divide. In mostly civil
cases, Essig et al. (2001) found that 88% of FNs
never allow third-party observation, 11% allow it
on rare occasion, and none allow on a regular
basis. But in a criminal context, Shealy, Cramer,
and Pirelli (2008) reported 75% of forensic psy-
chologists had conducted examinations with TPO
presence (11% on the civil side, see Essig et al.
supra), but 59% expressed worry that observer
presence influenced their results in a negative
direction. The different practices and attitudes
of forensic neuropsychologists versus forensic
psychologists are also reflected in commentary
papers and official policy statements.
Otto and Krauss (2009) proposed a detailed
decision-making framework for coping with TPO
demands. Their approach is shaped by a forensic
psychology viewpoint, which places greater
emphasis on civil rights and Constitutional
issues, and less emphasis on test standardization
and scientific issues. Although we do not agree

with their legalistic emphasis, they provide
thoughtful guidelines that allow the FN to con-
sider many variables, which includes the costs of
potentially unreliable reporting of the interview
data. McCaffrey, Fisher, Gold, and Lynch (1996)
also offer practical guidelines for decision-making
when responding to attorney requests for obser-
vation. Practical responses to common TPO chal-
lenges and attorney tactics are reviewed in detail
elsewhere (Howe & McCaffrey, 2010).
In the present authors’ view, we recommend
that FNs start with a presumption against TPO
presence during the testing phase. TPO is often a
legal tactic designed to intimidate neuropsy-
chologists, not to protect the rights of the plaintiff
(or criminal defendant). We have no objections to
attorneys sitting in during the interview portion,
as there is a more compelling interest to protect
legal rights. For example, discussion of liability
issues (who caused the accident) is outside the
purview of neuropsychologists, and discussion of
elements of the crime is inappropriate in a trial
competency matter (although not in a legal insan-
ity matter). We agree with Otto and Krauss (2009)
that the literature on child abuse allegations
shows ample proof that retroactive recollection of
interview content is sufficiently inaccurate to
warrant concerns.
But, because test administration is standard-
ized, the answers immediately recorded, and no
case-specific legal issues raised by cognitive test
items, the costs of TPO (negative impact on test
scores) outweighs the minimal benefits (detecting
minor scoring inaccuracies). As judges like to
say to parties attempting to suppress damaging
evidence, “That’s why cross-examination was
invented.” We disagree with APA’s surprisingly
poor advice that selecting tests less-affected by
observation is a viable solution, precisely because
those tests would be less sensitive to brain injury,
and may have the unintended result of false nega-
tive error; that is, not finding cognitive impair-
ment when it is present. If this option were chosen,
it would give the de facto right of any party to liti-
gation to dictate test battery content. For example,
a vocabulary test is unlikely to be affected by third
party observation, but it is also unaffected by most
brain injury. Should we replace a time-sensitive
test like Controlled Oral Word Association with
an untimed vocabulary measure?
Resistance to TPO should be greatest in civil
cases, but in criminal cases where liberty interests
are at stake, the FN should consider allowing
TPO. If the decision is to allow TPO, we
Neuropsychology and the Law 35
recommend two approaches. First, the FN should
include a paragraph in the report, addressing the
influence of the TPO on that particular cognitive
profile. Second, the FN should take reasonable
steps to limit access to any videotape or audiotape
of the test administration. This includes offering a
model court order. Table 2.2 gives an example of a
proposed order.
P H A S E S O F T H E AT T O R N E Y-
NEUROPSYCHOLOGIST
INTERACTION
The FN can expect his interactions with attorneys
to go through a series of typical steps. Each step
requires different preparatory, cognitive, and
ethics-related activities. The typical phases of
attorney-neuropsychologist interaction include
the pre-assessment, assessment, report writing,
discovery, testimony (deposition or trial), and
post-trial phases.
Pre-Assessment: Initial Meeting
First contact with an attorney contains a number
of crucial elements. The first decisions the FN
makes are (a) competence to answer the legal
question, and (b) the specific role that will be
played. Preliminary data collection to support
decision making at bare minimum requires four
pieces of information: (a) a brief case synopsis, (b)
a short list of hypothetical questions to be asked of
the FN, (c) potential dual role conflicts, and (d)
availability of the plaintiff (or criminal defendant).
Other requested information may include antici-
pated court dates, discovery deadlines, and
amount and type of records to be reviewed. This
conversation need not last more than 10 minutes.
The brief case summary is critical for a number
of reasons. The fact set will help determine good-
ness of fit between your expertise and the case, the
elements of the assessment approach, and amount
of time you will spend. More importantly, the case
summary represents the first challenge to your
objectivity. The attorney’s synopsis is from the
viewpoint of an advocate, so be alert to one-sided
portrayals of the case. First contact is when the
FN starts the process of resisting the “pull of affili-
ation” (Brodsky, 1991). Attorneys may contact
FNs on the belief that neuropsychological analysis
will support their medical-legal theory. Thus, they
may try to prejudice you right from the outset by
providing a biased summary that omits or distorts
key facts. A plaintiff attorney may state “I don’t
believe in accepting mild concussion cases, but
I have a client who got a severe closed head injury
36 forensic neuropsychology
two years ago, and he hasn’t worked since.”
You later find out the injury was only minor
orthopedic strain (a/k/a ‘whiplash’). A civil
defense attorney may say, “The plaintiff has a long
history of drug and alcohol abuse, he hasn’t
worked in two years, and I’m sure his brain was
fried before the accident.” You later receive records
showing a trauma neurosurgeon had to debride
5 cc of destroyed prefrontal lobe tissue. We advise
giving attorneys broad latitude by accepting there
will be some attempt to prejudice you; acceptance
or rejection of the case depends on the magnitude
of the partisanship and fact distortion. Refuse
involvement only if the attorney grossly misrepre-
sents the facts, limits your access to key records or
collaterals, or insists on your prejudging the case.
The hypothetical questions of the retaining
attorney determine the activities and roles that the
FN assumes. The hypothetical question is designed
to elicit an opinion that summarizes all the psycho-
logical and neuropsychological issues in a brief
conclusion that is understandable to the typical
juror (Blau, 1998). The attorney may not yet know
the specific questions that she will ask during trial,
but she can gave you a general question that sum-
marizes the issues relevant to a neuropsychologist;
for example, “Did the accident (or failed medical
treatment) cause brain damage?” Feel free to pro-
pose specific preliminary hypothetical questions
raised by the fact set, so that there is a shared under-
standing of your assessment goals, and how they fit
the legal goals. The shared framework also assists
the FN in determining whether he can answer
questions in a reasonably probable way, or whether
the question even falls within his expertise.
This early conversation provides an opportu-
nity to candidly discuss your own views and foren-
sic history. If a plaintiff attorney contacts you and
you do not believe that common adult whiplash
causes diffuse axonal injury or that minor concus-
sion causes disproportionately severe long-term
disability, say so. The plaintiff attorney will appre-
ciate your candor and will look for a neuropsy-
chologist with different views, or maybe drop the
case because of financial risks to his practice.
Alternatively, if contacted by a defense attorney,
and you tell her that you believe that five years of
cannabis smoking is unlikely to cause major brain
damage, also say so at the outset. Even if the attor-
ney decides not to use you, you have established
credibility, and diminished your chances of being
called a hired gun who will testify to support any
outlandish medical-legal theory that the retaining
attorney wants to advance.
Access to the plaintiff (or criminal defendant)
is the third key issue to clarify. Neuropsychological
and psychological testing requires conditions
similar to the standardization groups described in
the test’s instruction manual. If the case demands
a comprehensive neuropsychological assessment,
the FN should insist the plaintiff be examined at
the FN’s offices. Some modern prisons do contain
secure, quiet interview rooms. Otherwise, the
guiding principle is: If the case comes with severe
restrictions imposed by a judge or the retaining
attorney, or lacks an appropriate testing room,
the FN should refuse, but only if the restriction
potentially influences test score validity.
In summary, acceptance of the case depends
on (1) relevance to one’s expertise, (2) sufficient
access to data on which to base an opinion, and
(3) absence of potential conflicts. If the FN has a
prior relationship with any party to the suit, this
relationship needs to be considered. “Treating”
neuropsychologists should precede especially gin-
gerly, as both the plaintiff and the plaintiff attor-
ney become clients. But such a dual relationship
does not automatically disqualify participation if
the FN can give probable assistance to the trier of
fact, but we’ll develop that idea later when dis-
cussing ethics. The remainder of this section will
assume the FN’s acceptance of involvement.
Pre-Assessment: Role Selection
The next crucial element during initial contact is
role selection. The FN must determine which of
the potential roles they will choose. The basic
choices are (a) fact witness, (b) expert witness,
and (c) litigation consulting. The fact (a/k/a
“reporting”) and expert witness roles both involve
live testimony either in court or by deposition. As
a fact witness, the FN can only report facts about
the patient. The testifying expert is a FN who
reports opinions at trial or during a deposition.
Two crucial features distinguish the expert
witness from the fact witness: The expert is
allowed to report hearsay (“The plaintiff said….”)
and is allowed to offer an opinion (“Smith’s
memory problems were caused by a penetrating
missile wound to the brain”). In contrast, the fact
witness reports information gleaned through the
senses only, with little interpretation (“I saw Jones
shoot the gun at Smith’s head” or “I saw the plain-
tiff for an examination on July 5, 1999”). Myths to
the contrary, fact witnesses are allowed to draw
some conclusions, as long as the conclusion is not
based on any specialized knowledge that defines
an expert witness (“Jones looked like he wanted to

kill Smith”). If an original examiner saw the patient
on referral from a physician prior to involvement
(assuming an attorney did not start the referral
chain), that neuropsychologist is technically a fact
witness. As a practical matter, however, the line
between a fact witness who is a doctor and a testify-
ing expert is blurred and state rules vary regarding
these witness designations. A treating doctor, read-
ing from a report, states, “I gave a diagnosis of
closed head injury.” That’s an expert opinion dis-
guised as a factual report. But it is rare for judges to
impose any testimonial limitation on a treating
doctor, so in practice, a “treating” doctor is viewed
no differently than a testifying expert.
The role of litigation consultant means the FN
works “behind the scenes” to educate the attorney
about basic neuropsychological terms and princi-
ples, examine test data supplied by another
neuropsychologist, offer alternative theories of
the facts from a neuropsychological perspective,
and design cross-examination questions for the
opposing neuropsychologist (Derby, 2001;
Greiffenstein, 2008). Any documents developed
in this role are subject to the attorney “work prod-
uct” rule, meaning the FN remains anonymous
and his contributions are not discoverable.
However, if a treating or testifying neuro-
psychologist is also hired as a litigation consultant
(examine the other side’s raw test data), the work
product rule does not apply and all conversations
or documents related to these activities are
discoverable. Also, consulting experts should be
forewarned that the retaining attorney may decide
to convert the consulting “behind the scenes”
expert into a testifying expert as the litigation
strategy changes; for example, if the consulting
expert expresses an opinion that is favorable and
the retaining attorney has nobody else who can
render that opinion (see Federal Rules of Civil
Procedure, #26, “Disclosures”).
The last facet of role selection is determination
of the pertinent issues on which the FN will offer
opinions. Neuropsychological evidence is deemed
helpful in assisting the trier of fact in a broad
range of civil and criminal cases. Table 2.3 sum-
marizes the kinds of legal settings in which FNs
find themselves and the specific issues they are
asked to address. The experienced FN should
have learned how to map legal terminology into
neuropsychological terminology. Communication
between attorney and FN is facilitated when there
is a good understanding of what neuropsycho-
logical issues are associated with which jurisdic-
tional requirement, and vice versa (Grisso, 1988).
Neuropsychology and the Law 37
The retaining attorney may ask the testifying
expert to examine the claimant for evidence of
impaired brain functions and disturbed personal-
ity. Generally, there is no doctor-patient relatio-
nship and such an evaluation is termed an
independent medical examination (IME). However,
at least one duty of the doctor-patient relationship
exists in some jurisdictions during an IME (Harris
v. Kreutzer, 2006). In Harris, the Virginia Supreme
Court ruled that a prima facie malpractice allega-
tion against a clinical psychologist during an IME
may get to a jury. Although the case was ultimately
settled, the Virginia Supreme Court reaffirmed a
“circumscribed duty” to do no harm in the limited
doctor-patient relationship during an IME. In
Dyer v. Trachtman (2004), a Michigan appellate
panel ruled that physical injury during an IME
sounded in medical malpractice law, not ordinary
negligence. IMEs are typically requested by defense
attorneys in civil suits or by claims adjustors in
nonlitigated claims, although plaintiff attorneys
ask for them as well in cases where treating doctors
are unwilling to be involved.
Testimony can also be based on records review
only, although this places limitations on the scope
of opinions. Both of the Codes state a preference
for a direct examination in legal cases, but both
Codes also make clear that opinions based on
records review only are permissible if (a) the doc-
uments are clearly catalogued, (b) the legal ques-
tion does not require an evaluation in order to be
answered, and (c) one testifies to the limitations of
relying solely on records. The SGFFP (Committee,
1991) further adds that if records are sufficient to
answer the question posed, direct examination
becomes unnecessary. The Iowa Supreme Court
upheld neuropsychologists’ qualifications to
testify on basis of records alone (Hutchison v.
American Family Mutual Ins. Co, 1994).
The pre-assessment phase is crucial with
respect to ethical adherence. It is here that the FN
may be offered dual or even triple roles. A good
example of a dual role conflict is a treater testify-
ing for plaintiff, but also being asked to prepare
the plaintiff attorney for cross-examination of
defense expert. To avoid this, the FN should strive
to maintain a single role: testifying expert, treater,
or trial consultant. Some legal journals (e.g.,
Lawyer’s Weekly) publish commentary advising
the use of the “objective treater to also analyze the
defense neuropsychologist’s raw test data and
advice on proper cross-examination questions.”12
Acting as a treater but also testifying and provid-
ing background consulting may turn the treater
38 forensic neuropsychology
TABLE 2.3 PARTIAL SUMMARY OF LEGAL SET TINGS AND ISSUES RELEVANT
TO FORENSIC NEUROPSYCHOLOGY
Court Setting Specific Legal Issue
Probate Testamentary Competence
Capacity for Contracts, Trusts
Competency to Testify
Guardianship
Administrative Worker’s Compensation Social
Security Disability
School district due process
Civil Causation & Damages
Disability under ADA
Mental health and commitment
Criminal Mens rea or Not guilty by
reason of insanity
Competent Waiver Miranda
Rights
Competence to stand trial
into an agent of the attorney. To combat this, the
FN needs to keep in mind the pervasive principle
running throughout this chapter: What many attor-
neys consider good practice is questionable practice
for a neuropsychologist. The FN does not have to
do everything an attorney expects them to do.
Neuropsychological Issues
• Post-mortem analyses of cognitive state on critical
legal dates
• Recent and remote memory
• Social perception and delusional status
• Vulnerability to persuasion
• Recent memory and intelligence
• Delusional status
• Usually an issue with children; determine
cognitive developmental stage
• IQ and memory
• Functional abilities
• Judgment
• Distinguishing old vs. acquired cognitive
deficits
• Prediction of Functional Deficits
• Symptom validity
• IQ and academic achievement
• Intellectual and learning disabilities
• Qualification for special education services
• Neurogenic vs. psychosocial factors
• Closed Head Injury
• Low-dose exposure organic solvents
• Black mold causing occult CNS damage
• Acquired versus old cognitive weaknesses
• Post-traumatic versus premorbid psychological
attributes
• Primary and secondary gain, symptom validity
• Formal diagnosis of cognition-based disability
• Prediction of reasonable accommodations to
remediated deficit
• Danger to self or others
• Inability to care for self
• Transient amnesic disorder
• Dysexecutive Syndrome
• IQ and mental retardation
• Auditory Comprehension
• Reading Comprehension
• Attention
• Comprehension
• Memory
As pointed out by Brodsky (1991), bias and ethi-
cal conflict occur when a psychologist allows the
“pull of affiliation” to subtly enmesh the treater or
expert into dual advocacy roles.
Trial consulting work has special ethical ramifi-
cations that get limited attention. McSweeny (1997)

interpreted the 1992 Code Standard 1.16(a)
(Misuses of Psychologists Work) to support a
conclusion that trial-consulting work by its very
nature may be unethical. He reasons that because
FN trial consultants are typically anonymous,
there is no “corrective mechanism” present as
required by 1.16(a). Although the present authors
believe that trial consulting is not an inherently
unethical activity, we agree with McSweeny (1997)
that such “behind the scenes” work places a spe-
cial burden on FN found nowhere else in legal
work. Anonymity creates a psychological state
with reduced likelihood of negative consequences
for behavior. This absence of “moral hazard” may
uninhibit aggressive tendencies. Examples of
aggressive behavior include designing cross-
examination questions that misuse neuropsycho-
logical test data, providing irrelevant personal
anecdotes attacking the opposing neuropsycholo-
gist, or biasing neuropsychological interpretation
away from the best fitting but inconvenient diag-
nosis. A good example of questionable ethical
behavior is for the FN consultant to tell the retain-
ing attorney that “fixed batteries such as the
Halstead-Reitan are the only measures accepted
in the neuropsychology community,” “process
neuropsychology is the only method for detecting
deficits,” or “age and education corrections do
not need to be used.” In other words, anytime a
consulting FN replaces accepted practice param-
eters with a polarizing polemic, a potential ethical
violation may be taking place. A FN who regularly
performs such work should note that anonymity
is not guaranteed. In federal law, there are
exceptions to the anonymous trial consultant rule
and under certain circumstances an attorney
must provide the name of the previously secret
consultant (FRCP Rule 26).
The trial consultant’s work product should be
shaped by two parameters: (1) Offer advice based
on honestly debatable issues of fact, and (2) provide
consultation as if your identity will eventually be
revealed. For example, reliance on age-based cor-
rections is a well-established and sound practice
parameter. It would be ludicrous for an FN to argue
that age corrections are not needed for neuropsy-
chological tests while simultaneously relying on
instruments with age-specific deviation metrics,
for example, Wechsler Intelligence scales. What is
honestly debatable, however, is the particular
choice of age-based normative tables to use with
any given neuropsychological measure, as there
are competing normative databases for the same
measure (Mitrushina, Boone, & D’Elia, 1999).
Neuropsychology and the Law 39
Pre-Assessment: Compensation
for Services
The last step is determining compensation for
services. This is usually dealt with in the initial
meeting. The fees should be reasonable; that is,
no different from the fees charged for clinical
examinations, assuming similarities in battery
composition and testing duration. There is no
clinical equivalent to deposition or trial testimony,
so it is customary for experts to charge a higher
hourly rate and/or charge a minimum fee
irrespective of the deposition’s length. This is
justifiable because the higher fee is to reserve a
block of time; many depositions are cancelled at
the last minute, literally on the courthouse
steps. The FN has no way of predicting how long a
deposition will take or how long they will sit in a
court corridor, so steps are taken to compensate
for loss of a day’s income from regular activity.
Avoid the temptation to charge more for a foren-
sic assessment than a clinical test battery of the
same size and content.
The FN should maintain a detailed, annually
updated fee schedule that describes the hourly,
bundled, and/or per diem charges. This list can
easily be faxed or electronically mailed. List
elements usually include: The basic hourly rate
for records review or conferences; “bundled”
fee for each type of test battery (e.g., neuropsy-
chological or chronic pain); deposition or trial
testimony; and expense policies regarding travel.
Some FN use paralegal or graduate student staff
to perform literature searches, review records,
author case synopses, or conduct statistical ana-
lyses. Supporting staff ’s time for nontesting activ-
ity should be billed at a lower rate. Do not pretend
you did the work yourself. The fee schedule should
include an explicit policy for live testimony. Some
experts bill “portal to portal” (the time you leave
home until the time you arrive back home after
testifying) at the hourly testimony rate, others
charge less for commuting time. A popular alter-
native is a per diem charge if assessment or
testimony involves traveling to a different city, or
sitting in court for the day. A per diem charge
is easily defensible for the same reasons as a
minimum deposition charge: You have to reserve
a large time block during hours you would
normally perform other billable work.
Practices vary, as do the formality of retention
agreements. Some FNs ask the attorney to initial
and date the fee schedule, or sign a brief agreement
to pay for services rendered. Payment plans can be
flexible to respond to the role or reputation of the
40 forensic neuropsychology
retaining attorney. Per the advice of Blau (1998),
do not fall for vague promises such as “Don’t worry,
you’ll get paid” or “I’ll protect your fee.” In one
author’s experience (M. Greiffenstein), some attor-
neys insist the neuropsychologist bill their clients,
on the grounds that paying the FN directly “is
unethical for a lawyer to pay you because it is like
loaning money to client.” But that same attorney
will pay investigators directly. To circumvent this,
consider demanding retainer fees before initiating
any work from an unfamiliar attorney. This prac-
tice dissolves the issue of having a personal finan-
cial interest in the outcome. Some plaintiff attorneys
will insist you accept a lien on any settlement or
jury verdict. Avoid this arrangement at all costs.
Accepting this arrangement introduces bias and
is considered unethical under the Specialty
Guidelines for Forensic Psychologists (SGFFP;
Committee on Ethical Guidelines for Forensic
Psychology, 1991). These ethical guidelines are only
binding on members of the American Academy of
Forensic Psychology (those who earned the ABPP
in Forensic Psychology), but we accept this docu-
ment as a best practice guideline for all FNs.13
Accepting a lien creates a financial interest in the
outcome of a trial, increasing the “pull of affilia-
tion” to the retaining side and creating a dual role
conflict (e.g., moneylender vs. treater). Otherwise,
the 2002 Code is silent on this practice.
Assessment Phase
This section describes the data collection process
to gather the evidence on which future opinions
are based. The general contour of the forensic
neuropsychological assessment is made up of
these important steps:
• Considering what neuropsychological
evidence will inform the legal question
• Reliance on convergent evidentiary method
wherever possible
• Recognizing limitations of isolated (single)
methods
• Evaluating social influences on
presentation, not just organic factors
• Supplementing forensic instruments most
suited to legal judgment to be made
• Using normative and scientific bases
sufficient to support test use
• Reliance on tests in common use
• Using valid tests, with known sensitivity
and specificity
• Including measures of response style
and effort
• Managing diagnostic error
• Incorporating debiasing procedures
Assessment Phase: General Contours
What evidence best informs the legal question
posed? Deciding what neuropsychological
evidence is necessary to answer the question
posed is not an automatic step. This is the point at
which the principle of “practicing competent
neuropsychology” first applies. Some FNs insist
that an examination is inadequate without an
extensive battery of tests (particularly “fixed
‘ones), regardless of forensic question. In reality,
some questions are easily answered by simple
records review. The question ‘did the plaintiff sus-
tain a closed head injury on January 1, 2010’ can
be answered just with a review of ambulance run
sheet and ER records. Records are sufficient to
answer questions regarding the existence of
a condition, and later neuropsychological testing
cannot retrospectively detect brain injury some-
how overlooked by ER trauma specialists. The
question ‘Are there long-term effects of a closed
head injury’ evokes a need for extensive testing,
however. Competency to stand trial (CST) gener-
ally requires a good interview, formal mental
status, and a specific forensic test. Extensive
testing is not required to answer CST questions.
Do not succumb to the temptation to lend an ‘air
of science and objectivity’ to your work by a large
battery (Melton et al., 2007, p. 47).
The competent FN relies on a multi-method,
convergent means of data gathering, if the legal
questions are multifaceted (e.g., damages in
a personal injury case). Three recommended
overlapping methods of the assessment phase are:
Review of outside records (e.g., brain scans, first
responder records); direct and collateral inter-
view, with mental status observations; and
neurocognitive, forensic, and psychological test
scores. Lally (2003) refers to these three eviden-
tiary sources as the “tripod” on which psycholo-
gical testimony rests, and further argues this
approach places psychologists at an advantage
over other mental health professionals. Kaufmann
(2009) writes:
Psychologists evaluate clinical impressions
from interviews, behavioral observations, and
informal assessment, with the added benefit of
comparing the individual’s test performance to
norms. Unlike other mental health profession-
als, psychologists use objective psychological
tests to refine clinical impressions when

formulating working diagnoses, initial treat-
ment plans, and expert opinions. Neuro-
psychology adds the brain–behavior knowledge
base and incorporates neuroimaging, neuro-
diagnostic, and other neurologic findings to
the aforementioned evaluation techniques,
thereby creating the unique practice of forensic
neuropsychology consulting (p. 1149).
A convergent evidentiary model allows greater
confidence in one’s opinions and makes rejection
of alternative hypotheses more credible. An opin-
ion that a litigated head injury caused cognitive
impairment is defensible with a convergent
pattern of: poor scores on memory tests but
“passing” scores on effort test (test scores), behav-
ior observation of memory retrieval difficulty
during interview (mental status), and acute brain
changes and low Glasgow Coma Scale on hospital
admission (outside records). Also, the reader is
referred to the Larrabee chapter on scientific
approaches in this volume.
Records review is important because third-
party data helps inform diagnostic accuracy in a
setting known for strong validity threats. We rec-
ommend the FN create a standing list of recom-
mended records for the retaining attorney to
obtain, records most likely to contain relatively
objective data. This includes school records con-
taining standardized testing, date-of-incident
records that contain neurological and mental
status testing (or arrest reports), neuroimaging
studies, routine and 24-hour electroencephalog-
raphy, and pharmacy records. Litigants may give
inaccurate histories during the interview, in some
cases biasing information to the point of frank
deceit (Faust, 1995; Lees-Haley & Brown, 1992;
Mittenberg, DiGuilio, Perrin, & Bass, (1992);
Nelson, Drebing, Satz, & Uchiyama, 1998; Schrag,
Brown, & Trimble, 2004). One form of reporting
bias takes is positive inflation of preinjury cogni-
tive and mental health status (Greiffenstein, Baker,
& Johnson-Greene, 2002; Johnson-Greene et al.,
1997), more recently referred to as the “good old
days” bias (Iverson, Lange, Brooks, & Rennison,
2009). Keep in mind that biased reporting is not
always conscious. Factors such as normal forget-
ting and misremembering also influence present
recall (Barsky, 2002; Schachter, 2001).
The value of third-party data is shown in
Table 2.4. The table is from an author’s (MFG)
case file, and shows the value of third-party data
in detecting compelling historical discrepancies
in a worker’s compensation claimant suspected of
Neuropsychology and the Law 41
psychopathy. This 59-year-old male claimed
irreversible brain damage from a 2008 slip-and-
fall while selling “pork-belly futures” in a working
class Indiana neighborhood. He remained alert
and lucid, but later required surgical drainage of a
left subdural hematoma, followed by transient
mild aphasia. He recovered fully and neuro-
psychological testing showed unimpaired scores
in every cognitive and perceptual-motor domain.
He pursued three forms of secondary gain:
permanent workers compensation disability, a
premises liability suit against a city, and day-long
attendant care services from his wife. His wife
dropped a domestic abuse charge against him
shortly after filing suit.
Mental status and interview are fundamental
features of psychological evaluation separate from
formal tests, and provide a context. It bears
emphasizing that they are sufficient to render
diagnoses per the DSM-IV-TR (APA, 2000). The
context for interpretation is developed by distill-
ing historical information into a few areas such as
(a) the severity of the initial neurological injury,
(b) background variables that help establish
preinjury aptitude and achievement levels, and
(c) establishing the symptom time line. Symptom
evolution also informs accurate diagnosis.
Cognitive symptoms that suddenly erupt or evolve
long after a head injury are not consistent with the
disease of traumatic brain injury (TBI); rather,
true TBI symptoms appear in maximum intensity
immediately following head trauma. Paniak,
MacDonald, Toller-Lobe, Durand, and Nagy
(1998) provide a normative profile for acute injury
characteristics of a mild TBI (e.g., anterograde
and retrograde amnesia, loss of consciousness,
time to first memory) that can be used as
a template. For this reason, it is important to
inquire when the symptoms started, and self-
report must be correlated with the records.
A typical approach to interviewing is to develop a
structured interview form. This confers standard-
ization on the interview process (see test adminis-
tration section). The mental status examination
(MSE) component is a systematic monitoring of
behavioral cues during the interview, cues that
will be integrated into the total impression and
final opinions (Cronbach, 1984; Melton, Petrila,
Poythress, & Slobogin, 2007; Strub & Black, 1988).
The MSE includes a description of the claimant’s
speech and language, verbal content and discourse
organization, logic and reasoning, affect, mental
trends, nonverbal behavior, and social related-
ness. These observations are necessary for clinical
42 forensic neuropsychology

TABLE 2.4 THIRDPART Y RECORD ANALYSIS IN PLAINTIFF SUSPECTED OF

PREMORBID PSYCHOPATHY

Mr. Jones’s Present Assertion Third-Party Data Implication

1969 car accident, “no injuries”
Fabulously wealthy because of
work success
Retired young, in 1994
Intercourse 4-5 times a week up
to accident
Gave up drinking 10 years ago
Unsteady gait is a problem only
since work injury
Avoided contact with daughter
through voluntary choice
No prior contact with police
VA records show MVA at age 18 with
head trauma, LOC, and neurological
residuals of ataxia; but told other
doctors diffuse pain ever since
SSA records showed most years earned
below payroll tax cap
IRS records show continuous work in
1990s and 2000s, drifted from job to job
VAMC records show frequent impotence
complaint, requests for Viagra, dating
back to early 2000’s
VAMC records show ongoing alcohol
abuse and dependence, up to and after
the work incident; abstinent periods
brief and rely on plaintiff ’s self-report
only
Palo Alto records show diagnosis of
cerebellar ataxia, blamed on presumed
closed head injury at age 18, although
plaintiff gave different accounts of that
injury.
VAMC social worker documented a
court PPO barring any contact with
daughter
Federal indictment for bank fraud in
2000, but charges dropped; arrested for
domestic violence while intoxicated
in Indianapolis; California and Ohio
records not yet available
Inconsistent with current
report; probable premorbid
neurological problems,
because no incentive to
embellish head injury history
Inconsistent with plaintiff claim
of business success; implies
grandiose sense of self-
importance
Inconsistent with plaintiff claim;
actually unable to sustain
employment
Inconsistent with plaintiff claim
of posttraumatic impotence
Inconsistent with plaintiff claim
of abstinence or reduced
drinking; currently a heavy
drinker
Inconsistent with plaintiff ’s
causal attribution to the
recent accident
Inconsistent with plaintiff
report; proves judicial notice
of past behavior problems
Inconsistent with self-report;
aggression while drinking a
known feature of psychopathy

correlation, that is, converging lines of evidence
towards a conclusion.
The limitations of each method should inform
the reasoning process. A blind interpretation of
test scores should be avoided when relevant extrat-
est data are available. There can be many reasons
for a low test score, including genuine brain injury,
demographics, effort, mood, and medications. In
their classic study, Heaton, Smith, Lehman, and
Vogt (1978) found that expert neuropsychologists
could not distinguish the test score summaries of
severe head injury patients from volunteer fakers.
Equally problematic is overweighting self-report
and conducting “diagnosis by clinical history.”
Reliance on subjective cognitive complaints has
little proven ability to predict cerebral status, and
symptoms do not correlate with neurocognitive
test scores (Chelune & Heaton, 1986; Satz et al.,
1998; Gervais, Ben-Porath, & Wygant, 2009).
Neuropsychological testing, like medical lab stud-
ies, was invented to analyze subjective presenta-
tions. The drawbacks of third party records are
manifold, and the fallibilities are outlined by
Cripe (2002). Pitfalls include lack of universal
documentation standards; objectivity versus
subjectivity (CT scan vs. psychiatric diagnosis);
unproven assumption of veridicality; unknown
reliability and validity of past mental health

diagnoses; and overweighting of negative evidence.
The absence of premorbid mental health records
does not prove good mental health. Persons with
antisocial traits, poor insight, or personality disor-
ders are unlikely to seek mental health counseling.
Prospects that social (non-neurological)
influences shaped the data require consideration.
Such exploration provides further insights into
prognosis, separation of neurogenic from psycho-
genic influences, and situational and secondary
gain factors. The history is defined as the story
(or narrative) of the examinee’s problems, from
inception to the present (Albers & Schiffer, 2007).
Data collected from the claimant should include
not only the precipitating event(s) and current
symptoms, but also the evolution (time line) of
complaints, and referral patterns (e.g., saw chiro-
practor or neurosurgeon first?). Cognitive-
attitudinal factors are also important, especially
with regards to provider feedback in litigated
cases. FNs devote some time to exploring the
claimant’s beliefs regarding the nature of their
cognitive problems, their expectancies of out-
come, and the sources for their beliefs. Greater
scrutiny is necessary because the process of
litigation exposes claimants to influences and
experiences not present in straightforward clini-
cal situations.
One source of non-neurogenic influence is
symptom suggestion by authority figures. Direct
coaching by attorneys is a documented occur-
rence (Youngjohn, 1995); the majority of trial
lawyers view it their duty to expose plaintiffs to
psychological test content in preparation for
defense scrutiny (Essig et al., 2001), and well-
meaning neuropsychologists may spoil data by
giving inappropriate warnings about symptom
validity detection (Youngjohn, Lees-Haley, &
Binder, 1999). Other social influences include
education in head injury symptoms through a
“TBI education group,” Internet research (Ruiz,
Drake, Glass, Marcotte, & van Gorp, 2002), and
the mental set known as “diagnosis threat” (Suhr
& Gunstad, 2002). Some plaintiffs may monitor
their every memory act with intense diligence,
resulting in misinterpretation of normal forget-
ting as evidence for a closed head injury.
Adding forensic instruments tailored to the
legal context is often overlooked by FNs. Test
selection is guided by most of the same general
principles as during a regular clinical neuro-
psychological examination, except for one differ-
ence: FNs select tests that answer the legal
question, not just the clinical one. Despite myths
Neuropsychology and the Law 43
to the contrary, there is no legal requirement that
“only fixed batteries” are admissible (Baxter v.
Temple, 2008; Greiffenstein, 2009). Melton et al.
(2007) divide formal psychological tests into three
types, and their categorization is generalizable to
FN practices. Clinical assessment instruments are
tests designed for measurement of clinical con-
structs, but can be co-opted for forensic use if
relevant to a legal question. For example, Wechsler
IQ tests can be used in capital eligibility determi-
nations. Forensically relevant instruments also
measure clinical constructs, but are rarely used in
mental health settings, and the constructs mea-
sured are more prevalent in forensic contexts. The
Hare Psychopathy Checklist Revised is a good
example (Hare & Neumann, 2006). Finally, there
are forensically specific instruments. These tests
measure legal capacities as defined by statute or
case law, and are used strictly in narrowly defined
legal settings. Examples include various trial com-
petency measures. Although these are cognitive
tests that overlap with many recognizable neurop-
sychological constructs, they are never used clini-
cally. The training of FNs puts them in a good
position to use and interpret these instruments
because of their emphasis on cognitive capacities.
The normative basis for tests must be a factor
in selection. A sound normative base provides an
objective means of classifying cognitive scores as
normal, abnormal, deficient, weak or superior.
Commercially available tests with a manual are
preferable, and homemade tests and/or norms are
best avoided. For example, if you assess decision-
making and impulsivity with the Iowa Gambling
Test, rely on T-scores from the manual. Do not
rely on z-scores derived from the small “normal
control” group of a single study (Manes et al.,
2002), like one forensic psychologist did in a high-
stakes criminal case in which one author (MFG)
was involved. Methods are standardized when a
procedure is described with sufficient clarity to
allow different examiners to collect data in the
same manner with minimum error (Grisso, 1988;
Anastasi & Urbani, 1997).
Reliance on tests in common use means tests
used by a least a plurality of the neuropsychology
community; it does not mean test acceptance by
every last neuropsychologist. The best evidence
for community use is published surveys of test
usage. Surveys help the FN in a number of ways.
They can be used to get ideas on what the pre-
ferred tests are for a given question, or they can be
used to justify test selection at the testimony
phase. Good examples of general practice surveys
44 forensic neuropsychology
can be found in Butler, Retzlaff, and Vanderploeg
(1991) and Rabin, Barr, and Burton (2005);
forensic neuropsychology surveys can be found in
Lees-Haley, Smith, Williams, and Dunn (1996)
and Sharland and Gfeller (2007); and good foren-
sic psychology references are Lally (2003) and
Archer, Buffington-Vollum, Stredny, and Handel
(2006). Also useful is a survey of report writing
practices by Donders (2001b, 2001d).
Evidence for test validity is proven incremental
ability to detect cognitive deficits in persons
known to have them (sensitivity) and ruling out
deficits in persons known to be deficit-free (speci-
ficity) when compared to any other available
method (Larrabee & Berry, 2007). Imperfect mea-
sures (errors in prediction) are fine, as long as
there is incremental validity, that is, better overall
hit rate than with guessing or other methods.
Perfection in prediction (or rare errors of predic-
tion) is not a realistic standard; medical doctors
regularly rely on tests with known false positive
and negative errors, such as the PSA and chest
X-rays. It follows that there is no neuropsycho-
logical measure (or battery) demonstrating both
excellent sensitivity and specificity in all imagin-
able clinical situations (Larrabee & Berry, 2007).
Sensitivity and specificity are usually tradeoffs and
depend on many factors, including the base rate of
the target symptom measured and task difficulty.
Diagnostic error management is critical in
forensic cases. The FN aims for tests that show the
best balance between specificity and sensitivity for
the construct that is being measured. The pre-
ferred type of error depends on the goal; there is
no such thing as a single gold standard for errors
of prediction. Always choose the less costly of two
types of diagnostic errors: False positive and false
negative errors. Two practical examples include
the homeowner who would prefer false positive
errors in selecting a smoke alarm, but the female
seeking a mate (who will invest in offspring)
should favor false negatives (Haselton & Buss,
2000). Likewise, brain injury diagnosis should
skew towards false positive errors when data is
mixed/ambiguous, but in effort testing where
malingering is considered, false negative errors are
more desirable. Cutting scores can be adjusted to
reflect the desired error mix. Specificity tends to
be variable, as non-neurological conditions can
affect test scores, for example, abnormal scores in
depressed, older, or intellectually marginal, per-
sons. A defensible forensic test battery should
include both sensitive measures (cognitive perfor-
mance) and specific measures (e.g., aphasia testing
where appropriate). In summary, interpret scores
in a direction of the less damaging error. The
important concluding maxim is this: The nonspeci-
ficty of most neuropsychological tests is the main
reason for never interpreting scores in isolation from
collateral records and history.
The FN should always give symptom validity
tests (SVTs) and effort tests. Much scholarship
was published on this issue since the first edition
of this book, including Boone (2008), Franzen
and Iverson (2006), Greiffenstein and Baker
(2006), Larrabee (2008), Larrabee, Greiffenstein,
Greve, and Bianchini (2007), and Sweet and
Morgan (2009). It is generally accepted that foren-
sic settings contain strong incentives for distort-
ing test scores or interview data (Archer et al.,
2006; Mittenberg, Patton, Canyock, & Condit,
2002; Sharland & Gfeller, 2007; Slick, Tan, Strauss,
& Hultsch, 2004; Sullivan, Lange, & Dawes, 2007).
There is no legitimate reason for omitting these
measures in a forensic context or for avoiding
consideration of the issue during report writing.
The base rate for invalid response styles in liti-
gated brain damage claims is high, even when
stringent criteria for malingering are applied. For
example, Binder and Willis (1991), using the
Portland Digit Recognition Test, reported that
roughly one-third of patients with remote con-
cussion met stringent criteria for malingering.
Larrabee’s (2003) compilation of old data suggests
a base rate of 40% for cognitive invalidity. When
less stringent but still reasonable criteria are
applied, elevated base rate of malingering in
litigated post-concussion syndrome is the rule
and not the exception (Greiffenstein & Baker,
2006; Greiffenstein, 2003; Mathias, Greve,
Bianchini, Houston, & Crouch, 2002). Modestly
high base rates for malingering, defined as from
one-third to two-thirds of a population, provide
maximal diagnostic efficiency and incremental
hit rates for validated SVTs (Mossman, 2000a;
2000b).
There is also good evidence for an inverse
dose-response effect in litigated neurological
injury: The more minor the neurological injury,
the greater the likelihood of response distortion
(Green, Iverson, & Allen, 1999; Greiffenstein,
2003; Greiffenstein & Baker, 2006; Miller &
Cartlidge, 1972; Albers, Wald, Garabrant et al.,
2000). Finally, one should also take a multistrat-
egy approach to examining response distortion
(Sweet, 1999). Poor effort and/or malingering are
not only seen on memory tests. There are other
documented forms of noncompliance such as
 Neuropsychology and the Law 45

exaggeration of motor deficits (Greiffenstein, Assessment: Report Writing Phase

Baker, & Gola, 1996), overidealized premorbid
baseline (Greiffenstein, Baker, & Johnson-Greene,
2002), amplification of somatic problems
(Larrabee, 1998), and excessive subjective com-
plaining (Greiffenstein, Baker, Gola, Donders, &
Miller, 2002). A review of particular SVTs is
beyond the scope of this chapter and is covered in
more detail in another chapter in this volume.
Neuropsychologists should employ proce-
dures to manage potential bias when conducting
neuropsychological evaluations, interpreting
results, and formulating expert opinions. Self
examination and other debiasing procedures have
been discussed extensively elsewhere (Sweet &
Moulthorp, 1999a, 1999b; Lees-Haley, 1999).
Neuropsychologists entering the forensic area for
the first time may treat written reports like clinical
reports. However, there are numerous differences
between the two, including differences in audi-
ence, objectives, vocabulary, level of detail, source
attribution, and treatment of the unspoken
(Derby, 2001; Greiffenstein, 2008; Heilbrun,
Marzcyk, & DeMatteo, 2002; Melton et al., 2007).
The differing matters of style and report content
are summarized in Table 2.5 and discussed in
more detail below.
The most obvious difference in report styles
is audience and the related difference of report
function. The clinician writes for physicians and
mental health professionals, but the FN writes for

TABLE 2.5 DIFFERENCES BET WEEN CLINICAL AND FORENSIC

NEUROPSYCHOLOGY REPORTS

Report Characteristics Clinical Setting Forensic Setting

Audience Physicians, mental health professionals
Audience’s Main Medical Issues: Neurocognitive
Interest diagnosis, prognosis, treatment
Level of Detail Report all meaningful cognitive and
personal characteristics to better
understand patient
Vocabulary Freely use trait labels (“egocentric”),
cognitive deficit terms
(“perseveration”), diagnostic terms
(“dementia”), acronyms (“TIA”)
Controlling Mental Set Write as if the patient’s general welfare
depends on your opinion
Causation Rarely considered, unknown for most
mental disorders
Fact Reporting Treat history as fact unless proven
otherwise, e.g., “The patient became
disabled after the accident”
Functional Patterns Predict activities of daily living
Diagnosis Fit the person to the diagnostic category,
i.e., formal DSM-IV diagnosis
Behavior Observations Typically brief, limited to factors relevant
to administration and scoring of tests
Attorneys, judges, hearing officers, claims
adjustors
Narrow legal issues: Causation, damages,
competency
Report details to establish important facts
and support main inferences; avoid
prejudicial details if not at issue
Use understandable terms, avoid technical
jargon in narrative, although may be
unavoidable when reporting scores.
Both consider general welfare AND write
as if you are under oath; be careful and
definitive
State whether cause of action is a
contributing factor to abnormal
cognitive findings
Stress the attribution of facts, e.g., “The
claimant described himself as disabled
after the accident” or “He reported
subjective disability after the accident.
Provide a nexus, i.e., explain the reasoning
linking test scores to predictions of
altered living skills
Fit the category to the person; describe in
concrete terms (see text for examples)
Longer and more detailed; correlate mental
status with test scores and legal claims
46 forensic neuropsychology
a lay audience with administrative and/or legal
backgrounds. The main report function for a cli-
nician is neurocognitive diagnosis, psychological
diagnosis, prognosis, and treatment. This report
function is invariant across medical referral
sources. In contrast, attorneys, judges, claim
adjustors, and juries are concerned with narrow
issues of law. In disability certification matters, for
example, contract law dictates the scope of the
referral questions, which may not include opin-
ions of treatment. Thus, report functions can vary
widely. In general, the primary function of the FN
report is to offer opinions on the link between
neuropsychological findings and the issue before
the court. In personal injury cases, FNs address
the issue of causation and damages but causation
may not be an issue in probate or criminal cases.
In criminal cases, there are six different types of
competence, including competence to plead
guilty, waive right to counsel, and stand trial
(Grisso, 1988, p. 3). The reader is referred to
Denney’s chapter on criminal contexts in the
present volume. In essence, the FN report writer
needs greater mental flexibility in tailoring the
report to the specific legal issues.
The most important difference between
clinical and forensic reports is the question of
causality. Did the event in question (termed the
“cause of action”) cause any alterations in cogni-
tive (and presumably brain) function? Many juris-
dictions rely on a “proximate cause” criterion,
meaning an act, event, or omission that results in
the damage claims made, though it may not nec-
essarily be the nearest or last cause. There is much
legal controversy about what qualities an agent
must possess in relation to an outcome to deserve
the title “cause” and we will not concern ourselves
with that discussion here. What FN should recog-
nize is that courts are very concerned with simple
causal ideas such as “Did this car accident cause
any cognitive or brain problems”? Most neuro-
psychologists recognize there is rarely a single
cause for any psychological or neuropsychologi-
cal disorder, barring rare neurobehavioral syn-
dromes such as alexia or reduplicative paramnesia.
Neuropsychologists are taught to think in multi-
factorial terms, and clinicians rarely address single
causes in their reports, if they address it at all. But
a forensic setting requires an answer to the ques-
tion in a reasonably certain way. Remember the
standard of proof in personal injury cases is 51%
or better, meaning the FN needs only to state an
opinion that takes the form of more likely than
not. A FN’s statement that “the accident/mold
exposure/toxic substances (is/is not) a factor in
the claimant’s neuropsychological presentation”
represents a nice balance between the need for a
simple causation statement and the need to
consider multiple factors.
Another important difference is characteriza-
tion of fact status. Clinical report writing requires
economy and an assumption of patient self-report
accuracy. Hence, the reporting style may treat
unsupported statements as fact. A common intro-
duction in clinical reports is the following: “The
patient comes for neuropsychological testing 8
months after a closed head injury.” This sentence
assumes “closed head injury” is a valid diagnosis. In
a forensic report, the FN must attribute unsup-
ported “factual sounding” statements to the source
to make it more factual. A more factual restatement
of the lead-in sentence in a forensic context would
be “The claimant comes for neuropsychological
testing, believing/reporting/asserting/recounting
she suffered a closed head injury.” This protects you
(especially plaintiff witnesses) from the accusation
in court that you prejudged brain damage when
you first laid eyes on the patient. Beginning alleged
statements of fact with “The claimant states” or
“reports” is more factual and objective.
Another important difference is the type and
range of detail. In a clinical report, the focus is on
describing all of the meaningful psychological and
cognitive characteristics of the person. In contrast,
the forensic report should focus only on the most
relevant factors that contribute to a neuropsycho-
logical or psychological opinion. Grisso (1988)
discusses the different philosophies of forensic
report writing and recommends “striking a bal-
ance on detail.” The report should include enough
detail to establish important facts or track work-
ing hypotheses; it should not include all of the psy-
chological observations that could be made,
irrespective of how crucial such factors may be in
clinical settings. The mention of a psychologically
meaningful but legally irrelevant characteristic
may introduce bias into the report that is more
prejudicial than probative. When dealing with
emotionally charged details (e.g., sexual orienta-
tion, religiosity, prior crimes), decide whether
they contribute to understanding of the plaintiff ’s
(or criminal defendant’s) legal claims. If sexual
orientation is relevant (in a claim of organic per-
sonality change, for example) note it. If not (pain
disorder claim), strongly consider not reporting.
FN must strive to communicate in plain lan-
guage and limit use of technical terms. One mental
exercise that may be useful to testifying experts is

to develop a “dictionary” of commonly used
jargon that supplies “definitions” that lay people
can understand. This is especially useful prior to
trial. Table 2.6 contains a list of common neurop-
sychological terms. For example, the phrase “the
protocol was characterized by strong persevera-
tive tendencies in response to feedback” can be
translated as “Mr. K showed an abnormal ten-
dency to repeat the same mistake, even when
given clues. This indicates difficulty profiting from
experience”.
The clinical and FN reports also differ on the
importance of behavior observations. The clinical
writer briefly comments on the gross neurological
or cognitive functions necessary to support stan-
dard test administration, for example, does the
respondent have functional vision and hearing?
In forensic settings, behavior observations are
more comprehensive and detailed in order to pro-
mote convergent reasoning and to evaluate social
influences on behavior. Convergent reasoning is
promoted through the correlation of mental
status observations with other data such as test
scores and objective injury characteristics. The
allegation of neuropsychological damages always
include claims of functional deficits, that is,
disruption of daily activities or attitudes deemed
important by society. Examples of functional
impairments include capacity for forming
TABLE 2.6 PROPOSED LIST OF NEUROPSYCHOLOGICAL TERMINOLOGY
TRANSLATED INTO LAYMAN’S TERMS
Concept Technical Definition
Cerebral The superiority of one cerebral
dominance hemisphere for processing specific
tasks
Perseveration Persistence of response set in response
to negative feedback
Executive Cognitive abilities necessary for
Functions goal-directed, error monitoring,
perceptual-motor schemata selection,
and adaptation to a range of
environmental conditions and
demands
Constructional A disturbance in visually guided
dyspraxia constructional activity
Dementia A generalized loss of cognitive functions
resulting from cerebral disease
occurring in clear consciousness
(i.e., absence of confusional state)
Neuropsychology and the Law 47
criminal intent, permanent work disability, and/
or marital problems. A patient’s conduct in the
waiting room would not be mentioned in a rou-
tine clinical report, but an observation of a crimi-
nal defendant reading a magazine in the waiting
room yet scoring at chance levels on the PIAT
Reading Comprehension Test would be relevant
in a competent waiver of Miranda rights issue. On
the other hand, a plaintiff who resists redirection
during the interview by repeating the same
topic during interview and also makes many
perseverative errors on the WCST shows better
clinical correlation.
The approach to formal diagnosis also differs.
In forensic settings, the reader should avoid strict
categorization in the narrative (exclusive of the
formal axial diagnosis) and use more descriptive,
probabilistic sounding statements in describing
neuropsychological characteristics. Fit the cate-
gory to the person, not the person to the category
(Weiner, 1999). For example, in the case of find-
ings favoring the plaintiff position, a conclusory
statement such as “The accident caused closed
head injury syndrome of 5 years’ duration” is not
advisable. Instead, consider a statement such as
“Mrs. Jones present difficulties in recalling new
information and subjective complaints resem-
bling those seen in persons with proven brain
tissue loss after blunt head trauma. The accident is
Layman Definition
The right or left-brain is better at one form of
mental processing than another.
Repeating the same mistake over and over despite
feedback
A group of mental abilities concerned with
decision-making and impulse control. These
abilities stop you from burping loudly in church.
A special difficulty in drawing, copying or building
things, that often seen with right brain damage
A brain disease in which many mental abilities are
lost, even though the patient remains alert and
attentive.
48 forensic neuropsychology
a factor in the present results.” If you discover
findings that favor the defense, consider the fol-
lowing: Make the negative diagnosis conditional,
and then add a positive descriptive statement. For
example, “Although it is not possible for any one-
time examination to rule out closed head injury
symptoms in the past, the present examination
does not contain any evidence for present neu-
ropsychological impairment. Mrs. Jones most
closely resembles persons who are neurologically
normal and enjoy a wide range of intact cognitive,
perceptual, and motor abilities.” In this way, the
neuropsychologist provides differential certainty
depending on time, that is, higher certainty about
the present and lower certainty about the past.
Weiner (1999) describes this language promoting
inter-professional convergence of psychologists’
style of probabilistic statements and attorneys’
“preponderance of the evidence” standards.
A simple diagnosis and formal axial diagnosis
may be sufficient for clinical reports. However, in
a forensic report, providing a diagnosis to address
the causation issue is considered a “mere conclu-
sory comment.” In the example given above of
“closed head injury of 5 years’ duration,” there is
no stated nexus between the event 5 years earlier
and the conclusion. A nexus refers to a network of
lucid links between the cause of action, diagnostic
methods, and the conclusion. In simplest terms,
the FN must explain the reasons the plaintiff still
suffers cognitive impairments so many years
later. Simply diagnosing closed head injury on the
sole basis of obtaining abnormal results after
the incident is not logically supportable. This is
the logical error of post hoc, ergo propter hoc [after
this, therefore because of this] (Larrabee, 1990).
As you prepare your draft, keep these general
objectives in mind:
• Organization
• Detail
• Objectivity
• Priorities
• Persuasion
Organization requires treating every case as a
story, so your writing should flow with a narrative
structure. Begin with an introduction that pres-
ents why you were retained in the first place and
includes the questions you will answer in the nar-
rative. Word them in such a way as they relate to
the questions you know you are answering at the
end. This way, the reader has a sense of closure
about the report he has just read, and why you
have presented the conclusion as you did. An
important caveat that supports a narrative style is
this: Write about a human being, not a set of
scores. The examination should include a vivid
description of the examinee as part of a mental
status examination that leaps from the page in
three dimensions.
Attention to detail means you include those
facts/observations that track the questions, and
supports the reader’s later appreciation of your
conclusion. To maintain objectivity, include
details that help to understand the case, whether it
supports the side retaining you or not. If you feel
you need to account for the problematic points in
the conclusion, do so. Use quotes wherever you
feel it illustrates a particularly informative or
relevant aspect of your evaluation. Importantly,
make sure that you qualify everything the infor-
mant states with words like “reports,” “relates,”
“indicates,” or “notes.” Each is a neutral word
which neither downplays nor supports an infor-
mant’s words. This way you are quietly pointing
out the limits of hearsay in influencing your opin-
ion and supporting the need for corroborating
data. Avoid using a quote that merely quotes
another. That is double hearsay and will be struck
down by courts. Remember to refer to corrobo-
rating sources of information whenever possible,
from records to deposition testimony, whatever
you can utilize as indicative of supporting or
refuting pertinent history.14
Objectivity should be fairly self-evident. An
objective tone is supported by also reporting
details and scores that do not support hypotheses,
by explicitly stating alternative theories you con-
sidered, and avoiding extreme descriptors unless
scores or behaviors are truly extreme. Confirmatory
bias (discussed later) is your biggest enemy, and is
an issue that can scuttle even the best-reasoned
opinion. A commonly encountered example is
the FN who emphasizes weak memory scores
obtained after an accident, and then concludes
these represent post-accident cognitive changes.
But the same FN ignores records showing poor
literacy, limited numerical skill, and a ninth grade
education. This plaintiff may well have sustained a
lingering TBI, but omitting mention of pre-
existing cognitive weaknesses can not only hurt
this neuropsychologist’s credibility, it can also
hurt the plaintiff ’s legitimate injury claim.
However, in an effort to be objective, don’t under-
mine your decisiveness. Lay out your details;
when it comes time to gathering the material into
an interpretation in the conclusion section, be

clear and forceful where you can be. If you have
medical certainty, express it. Part of objectivity is
laying out what information is missing and speci-
fying what additional collateral information
would help to resolve uncertainty.
Priorities become a big issue in more compli-
cated cases. Never lose sight of what you should
really be focusing on in order to educate the reader
about why you came to your conclusions. Work
with the retaining attorney to develop concise
hypothetical questions at the beginning, to stay
on track and prevent the report from getting
unwieldy. Complex cases often distract with many
compelling but peripheral details. Media accounts
of the case may make factual claims that are
untrue, present advocacy as fact, introduce juicy
but irrelevant details, or may channel the views of
advocates trying to inflame the jury pool against
one side of a case. Media accounts of the MMPI-2
Symptom Validity Scale were partly informed by
financially interested parties and their lawyers
(Armstrong, 2008). As you read over your report,
make sure it builds from a neutral stance, so that
by the time the reader gets to the conclusions, it is
obvious not what you are going to say, but why
you are going to say it.
Persuasion means marshalling a sufficient
number of facts, and integrating and interpreting
them with such clarity that the reader is convinced
you made defensible conclusions. Persuasion does
not mean using sophistry or empty eloquence to
bamboozle. Some attorneys use excessive verbiage
to “muddy the record” and their experts may go
along. If you write something in your conclusion
and the facts in your report had not already made
it obvious to the reader, then you either have to
include better explanations in your narrative or
you may have come to the wrong conclusion. Both
of the present authors have many examples of
diagnostic conclusions that leap from the page
precisely because nothing in the results section
prepares the reader. A good example is describing
test scores as being within functional limits, but
still concluding the patient is suffering disabling
brain injury. Another example is reporting poor
memory scores and passed effort tests, but still
concluding the patient is malingering. A large
mismatch between the report body and the sum-
mary conclusions means either key details have
been neglected or the neuropsychologist is not
practicing competent neuropsychology.
Aim to provide a positive theory of the plain-
tiff ’s behavior if your findings are negative for
impairment. What is a reasonable basis for their
Neuropsychology and the Law 49
memory complaints, if not impaired brain func-
tion? Statements about the impact of mood, age,
psychological syndromes, attribution style, physi-
cal status, medication status, and social demand
features can be made if such opinions are grounded
in facts. The following opinion is an example of an
alternative theory of complaints: “Mr. Doe’s
memory complaints are shaped by his sad mood
and significant others’ tendency to over-focus on
any mistake he makes, which results in mistrust of
his thought processes.” In this case, the FN’s evi-
dence for this opinion was a history of remitting/
relapsing depression predating an accident, a cur-
rent spike-2 MMPI-2 profile, an overly solicitous
family, and a speech pathologist that treated low-
average memory scores as evidence for TBI.
The ethical aspects of the report-writing phase
are controlled by Section 9.0 (Assessment) of the
2002 Code (APA, 2002). Ethical standard 9.06
(APA, 2002) implies an ethical reason for relying
on convergent evidence to interpret test scores.
Please refer to Grote’s chapter on ethics in this
volume for a more detailed discussion.
The Trial Phase
This section describes the process of taking and
giving testimony.
Trial Phase: Discovery
Discovery is a preliminary process for compiling
facts relevant to the case. All parties to a suit have
the statutory right to ask for all documents that
form the basis of an opinion, unless those docu-
ments are privileged. Discovery is designed to get
an early look at the basis for the FN’s opinions,
narrow the dispute into main issues, gather perti-
nent personal information, prematurely pin the
expert down, determine what the FN does not
know, and sample the witnesses behavior under
scrutiny. Discovery takes one of two forms: an
interrogatory (a typed list of questions) or a dis-
covery deposition. A discovery deposition can
only be used for impeachment purposes at trial,
meaning it can be used to develop inconsistencies
to address at trial.
Neuropsychologists should expect their entire
file to be subpoenaed. Your complete case file is
discoverable (unless privileged), regardless if you
are a treating or retained neuropsychologist. This
includes interview notes, test forms, computer-
ized scoring reports, electronic correspondence,
records reviewed, notes, and billing statements.
Although practices vary, most states have broad
discovery rules.
50 forensic neuropsychology
Trial Phase: Admissibility
An important element of neuropsychologists’
legal involvement is the admissibility of their
data and opinions. Federal, state, and case law
provide criteria, or “legal tests,” that determine
what evidence is admitted into trial. Courts use
two analytic tools to determine the admissibility
of scientific opinions: The Frye rule and the
Daubert rule.
The Frye rule is presently applied only in 16
states.15 It is also termed the “general acceptance
rule” and originates in a famous case styled as
Frye v. U.S. (1923). For the next 70 years, chal-
lenged experts had to show their method was gen-
erally relied upon by most practitioners in a
particular professional community. The famous
Daubert v. Merrell Dow (1993) Supreme Court
decision replaced Frye in many jurisdictions and
in federal court. Although much has been written
about Daubert, the ruling of law is very simple:
The Federal Rules of Evidence (FRE) are the only
legal basis for judging scientific admissibility in
federal courts. Under the FRE, in order for evi-
dence to be admissible, scientific testimony must
meet two broad criteria: (a) must be scientifically
valid and (b) relevant to the case at hand. In its
obiter dicta (basically, a “discussion section” for
lawyers), the Daubert court offered trial judges a
partial list of guidelines to evaluate scientific “reli-
ability” (validity in our language). Currently, 30
states either codified the FRE, or case law recog-
nized it as applicable. The reader is referred to
Kaufmann’s chapter on evidentiary standards for
an in-depth review. This chapter will only focus
on Rule 702, which states:
If scientific, technical, or other specialized
knowledge will assist the trier of fact to under-
stand the evidence or to determine a fact in
issue, a witness qualified as an expert by knowl-
edge, skill, experience, training, or education
may testify thereto in the form of an opinion or
otherwise, if (1) the testimony is based on suf-
ficient facts or data, (2) the testimony is the
product of reliable principles and methods, (3)
the witness has applied the principles and
methods reliably to the facts of the case.
This means an expert has training in areas that
the average juror or judge is not expected to
understand. The FN assists the juror (or judge) in
either understanding the evidence (e.g., explain-
ing closed head injury) or determining a fact in
issue (e.g., whether the car accident caused a brain
injury in the plaintiff or not). FRE represents a
broad liberalization of the term “expert,” and most
neuropsychologists would have no difficulty being
qualified under this rule. The judge is given
broad discretion in applying admissibility rules.
Understanding admissibility guidelines is crucial
to a productive attorney-neuropsychologist inter-
action, as you must convince the attorney that
your methodology and opinions will survive a
legal challenge. Challenges to neuropsychological
testimony may take three forms: (a) general com-
petence of psychologists to testify, (b) scope of
neuropsychological testimony, and (c) challenges
to particular neuropsychological methods and/or
tests.
Challenges to general competence to testify
are rare. Courts have recognized psychologists as
competent experts since the Jenkins v. United
States (1962) appellate court decision. In Jenkins
the higher court held that mental health experi-
ence and training are most probative. A medical
degree or its absence is insufficient grounds for an
admissibility ruling when a mental health fact is
in legal dispute. Jenkins was cited in subsequent
cases involving neuropsychology evidence. In
Simmons v. Mullen (1974), a Pennsylvania appeals
court relied on Jenkins and the FRE to rule that
neuropsychologists could testify because they had
specialized knowledge about measuring cognitive
change.
Challenges to scope of neuropsychological
testimony are more common but typically involve
only one issue: causation. Can the neuropsycho-
logist reasonably infer brain changes from the
evidence? This body of case law contains mixed
rulings both adverse to and supportive of neuro-
psychological testimony, depending on the court’s
location and type of brain damage claim. Case law
patterns indicate that closed head injury claims
are considered within the scope of expertise of a
neuropsychologist (Hutchison v. American Family
Mutual Insurance, 1994; Valiulis v. Scheffeos
(1989). However, testimonial scope rulings appear
more unfavorable to neuropsychologists in a dif-
ferent context: claims of neurotoxic brain injury.
In this body of law, neuropsychologists’ alleged
ability to infer subtle (i.e., otherwise unobserv-
able) brain changes is regularly challenged, and a
few cases of impact bear mentioning. In Schudel v.
General Electric (1995), plaintiffs proffered neu-
ropsychological evidence for brain damage caused
by organic solvents and PCBs. The 9th Circuit
Federal Appeals Court for the 9th Circuit ruled
neuropsychological testimony is limited to

damages but cannot address physical causation.
In Chandler Exterminators v. Morris (1992), the
Georgia Supreme Court affirmed the exclusion
of a neuropsychologist who linked neurotoxicants
to abnormal test scores.
More likely are challenges to specific neuro-
psychological tests and measures. This type of
challenge questions the scientific basis of one or
more of the expert’s specific methods, measures,
and/or conclusions. For example, a plaintiff
attorney may challenge the use of a particular
malingering detection method, or a defense attor-
ney may challenge reliance on a list of “brain
damage signs.” Challenges to specific methods are
brought under the Frye or Daubert (FRE) rules.
The psychology and neuropsychology com-
munity’s initial reception of the “Daubert trilogy”
was one of mixed feelings tinged with foreboding.
The earliest commentary articles speculated on
Daubert’s impact. Grove and Barden (1999)
warned that a number of diagnoses such as PTSD
and multiple personality disorder would not sur-
vive scrutiny, and Posthuma, Podrouzek, and
Crisp (2002) opined that Daubert poses a serious
challenge to mild head injury cases, and Lees-
Haley, Iverson, Lange, Fox, and Allen (2002)
expected “many inadmissibilties” of MMPI-2
validity scales. Taking a different tack, some com-
mentators saw opportunities to advance narrower
interests. Reed (1996) interpreted Daubert to
mean that only the “fixed” batteries (e.g., Halstead-
Reitan) would survive, but “flexible” test batteries
would be inadmissible. Reitan and Wolfson (2002)
opined most neuropsychological measures are
“lacking” in conformity to Daubert criteria, except
Reitan’s own test battery. Insofar as most neurop-
sychologists adhere to a flexible battery approach
and only a small minority advocate fixed batter-
ies, these authors implied most neuropsycholo-
gists would not receive court work unless they
bought the recommended test battery.
Our view is that Daubert has had minimal to
no impact on neuropsychological practices.
Greiffenstein (2009) and Kaufmann (this volume)
rebutted the idea that “only fixed batteries are
admissible” through a fairer summary of case law.
We agree with Lally (2003) that psychologists
are better positioned to respond to Daubert
challenges than other classes of mental health
professionals. We also agree with Shuman (2001)
that fears of Daubert’s impact on psychology
were over-blown, and showed a misunderstand-
ing of the legal system. Our optimism is also based
on textual analysis of Daubert, combined with
Neuropsychology and the Law 51
cumulative empirical and anecdotal evidence
during 16 years of post-Daubert jurisprudence.
An integrated reading of the Daubert trilogy and
the FRE (1975) indicates the judge’s gatekeeping
role is a liberal mandate, which encourages accep-
tance of even novel and recent methodologies, if
they are defensible on logical and empirical
grounds. Consider this: The Daubert elements are
unweighted and polythetic criteria and they are
not exclusive. This means no single element is
necessary, and any single element or combination
of elements is sufficient to admit evidence.
Practically, this means the trial judge can rely on
only a single element if he chooses, for example,
the Frye “general acceptance” criteria alone.16
Some federal courts have found that evidence is
admissible based on factors that are not included
in Daubert.
There is much empirical evidence for the
nonthreat of Daubert to forensic neuropsychol-
ogy. Neurocognitive symptom validity tests have
survived many Daubert challenges. Mossman
(2003) conducted a LexisNexis™ search in
December 2002 and retrieved 18 published fed-
eral and state cases referring by name to neu-
rocognitive SVTs. Five of these cases involved
application of Daubert reliability factors to use of
neurocognitive SVTs and the courts found such
tests admissible in all cases. More recently, Hoyt
(2009) reviewed a series of 12 cases challenging
the admissibility of the MMPI-2 symptom valid-
ity scale (FBS) over the past decade, concluding
“the fake bad scale is here to stay.” In 2002, there
were 26 federal and state cases in the LexisNexis™
database using the terms “neuropsychology” and
“malingering.” Except for 2006, there has been a
pattern of accelerating growth in these cases cul-
minating in a total of 88 published legal cases in
2009.
Why the failure of dire predictions to come
true? The method skeptics or narrow practice
advocates (those who warn that Daubert will only
favor a narrow range of instruments) seem to
confuse the important legal distinctions between
admissibility and weight. Admissibility is a judge’s
decision that evidence has probative value, that is,
is it relevant, can it determine the outcome of the
case, and should the jury see it? The judge only
analyzes the relevance of the evidence and does
not make value judgments about relative impor-
tance. Hence, a test of modest validity has equal
footing with a test of great validity during an
admissibility hearing because both are probative.
In contrast, “weight” is a jury decision and refers
52 forensic neuropsychology
to perception of the evidence’s importance and
believability after it is admitted. The confusion
between admissibility and weight stems from
Reed’s (1996) commentary piece on a bench trial
result (Chapelle v. Ganger) as proof of his conclu-
sion, but even cursory study of the judge’s written
decision revealed all neuropsychological testi-
mony was admitted.17 Similarly, Reitan and
Wolfson’s (2002) and Russell’s (2007) conclusions
that only fixed test batteries are admissible are
incorrect because it is based on such confusion.
They believe that perceived superiority is relevant
to admissibility, but their arguments for superior-
ity only go to weight.
The FN must still be prepared to cope with
occasional challenges to portions of the test
battery. Challenges to specific neuropsychological
tests take the form of Daubert or Frye hearings
held in limine. This means the court hears evi-
dence pro and con away from the jury. The oppos-
ing attorney files a motion asking the court to
exclude a particular test measure or a particular
conclusion from admission. Most states have
adopted the Daubert standards into their own
rules of evidence, but many states still rely on Frye
or Frye hybrids (e.g., Frye-Davis in Michigan until
2005). The FN helps the retaining attorney pre-
pare the response (or provisions of the motion) by
applying the Daubert criteria to a particular test’s
(or inference’s) knowledge base. The validity and
falsifiability of the WCST can be shown by citing
studies which correlate WCST performance with
frontal activity and/or damage (e.g., Boone et al.,
1999; Pendleton & Heaton, 1982; Robinson,
Heaton, Lehman, & Stilson, 1980; Steinberg,
Devous, & Paulman, 1996) and the sensitivity and
error rate can be shown with Robinson et al.
(1980). The general acceptance of the WCST can
be shown through its mention in commonly used
test compendiums (Spreen & Strauss, 1991) or by
citing test user surveys. For example, Butler,
Retzlaff, and Vanderploeg (1991) reported 73% of
respondents use the WCST routinely. The reader
is referred to Kaufmann’s separate chapter (this
volume) on scientific admissibility law.
Trial Phase: Deposition or Live Testimony
Once the admissibility of neuropsychological
methods is established, the neuropsychologist-
attorney interaction moves to the next step: The
FN offers oral or written opinions under oath for
scrutiny by opposing counsel and the trier of
fact (judge or jury). Sworn testimony can be
offered in written form (interrogatory responses
or affidavit) or in oral form through a deposition
or in the courtroom. A deposition is a form of
legal discovery in which litigants question wit-
nesses to determine what testimony they will offer
at trial. A deposition is a very formal process in
which a court reporter transcribes questions and
answers into a typed record. A “discovery” depo-
sition is conducted solely by the opposing counsel
and represents a preliminary effort to obtain
information about opinions, narrow the dispute
into the most pertinent issues, and to evaluate
potential courtroom demeanor of the FN. A dis-
covery deposition cannot be introduced at trial
except to impeach the witness. A de bene esse
deposition is more commonly referred to as a
“trial deposition,” and it is intended to preserve a
FN’s testimony if he or she is not available to
appear live at trial. Alternatively, but more rarely,
the FN’s live testimony can also be offered at trial
in front of the judge and jury. Rules defining
depositions and governing the use of deposition
testimony vary among the states and the compe-
tent consultant should seek legal advice within
the relevant jurisdiction.
A trial deposition or live trial testimony is
broken into two phases: direct examination and
cross-examination. Direct examination occurs
first and is defined as testimony elicited by the
retaining attorney. The direct examiner first estab-
lishes the FN’s qualifications to testify as an expert.
Questions focus on five broad areas: education,
experience, specialized knowledge, skill, and aca-
demic contribution. Evidence for qualification
includes many forms of evidence, including aca-
demic degrees, neuropsychology coursework at
the graduate school level, nature of pre-doctoral
and post-doctoral training, employment history,
relevant experience, continuing education work-
shops, professional society activity, pro bono ser-
vices, and publications. FNs should prepare
themselves for this approach by briefly outlining
the features of their background that support their
self-designation. Greiffenstein (2002) offered an
objective checklist approach for attorneys to select
neuropsychologists, but FNs can adopt this same
approach to prepare a list of qualifying attributes
for the retaining attorney to use during direct
examination.
Opposing counsel may on occasion challenge
credentials during direct examination by asking
the court to voir dire the FN. Voir dire means, “to
tell the truth” and is a preliminary examination of
competence to testify through additional ques-
tions about credentials. The trial judge then

decides whether your testimony is allowed or not.
Qualification as a witness is rarely a problem for
FNs. In addition, the FRE (1975) 702-705 (and
the related state evidentiary rules) give broad
latitude to trial judges to consider many factors,
including experience in the absence of publica-
tion or board certification. In summary, the voir
dire does not pose a major threat in most cases.
However, opposing attorneys can continue to
emphasize questionable or insufficient credentials
during cross-examination.
The direct examination continues after the FN
has been qualified. The questions are open ended
but designed to elicit brief and simple opinions
favorable to the retaining attorney. Most retaining
attorneys use the FN’s report outline and head-
ings to organize questions, which mirror the same
temporal sequence of steps taken by the FN before
issuing a final report. Cross-examination begins
immediately following the conclusion of direct
examination. The opposing counsel asks ques-
tions from two general categories: (1) questions
designed to elicit weakness or flaws in the FN data
gathering or logic, and (2) questions designed to
prove bias or lack of independence.
Productive attorney-neuropsychologist inter-
actions during trial phase cannot be managed or
controlled in the same way as during any pretrial
stage. The FN’s interactions with retaining and
opposing attorneys are now public. The attorneys
and court rules govern your behavior. Hence, the
FN should focus on their style of interacting with
the judge or jury. The cross-examining attorney
has the right to ask questions and receive respon-
sive answers. Responsive means the answer is rel-
evant; it does not mean you have to give the
answer desired. There is no legal requirement that
FN must answer “yes” or “no,” despite some attor-
neys desire to have you believe this. Brief narra-
tive answers are allowable.
Productive attorney-neuropsychologist inter-
actions depend on the elements of expert witness
control. These are behaviors and attitudes you
have wide latitude in determining. The FN has
control over nonverbal behaviors (demeanor and
gaze); agency (active vs. passive answering),
speech characteristics (pace and volume), speech
content (scope of answers, definitions offered),
manifest attitude (deliberate, unbiased), and gen-
eral style of communication (objectivity, advo-
cacy, educator). The general elements of expert
witness control refer to a consistent style of com-
munication across your entire testimony. While
verbal content of testimony is important, studies
Neuropsychology and the Law 53
consistently show that nonverbal communication
is more persuasive with the jury (Boccacini &
Brodsky, 2002; Cramer, Brodsky, & DeCoster,
2009).
The best general style is defining your role as
one of educating the jury. The corollary of this is
never being an advocate for either party, even as
you defend the neuropsychological methods you
applied in the case. You are not there to persuade,
entertain, advocate, to crusade for justice, pursue
quixotic ideals, or to validate your own sense of
self-importance. Your objectivity will be mea-
sured by how you educate the jury in principles of
neuropsychology and how you applied those
principles to the issue at hand. You advance this
style by responding deliberately without excessive
qualification, patiently explaining definitions in
simple terms without using technical words, and
not making gratuitous assumptions about the fact
finder’s technical knowledge. Be honest about
your experience, knowledge, and the neuropsy-
chological literature. Jurors are likely to come
from more modest backgrounds than the expert,
but they don’t need an advanced degree to recog-
nize puffery, manipulation, and gross violations of
laws of physics when they hear it.
Another stylistic element is maintaining
objectivity. This does not mean you can’t have a
point of view or that you should never be passion-
ate. Despite cherished myths to the contrary, do
not brag that your objectivity is proven by state-
ments such as “I do 50% work for plaintiffs and
50% for defense.” A 50/50 split can easily be
evidence for the opposite: You give a favorable
opinion to the side that reaches the telephone
first. If you commonly give opinions favoring
certain positions over others, this could actually
be more objective if your opinion percentages
approximate the base rate for a given condition,
diagnosis, or phenomenon. For example, if you
happen to find that 40% of minor head injury
litigants show positive malingering signs on
memory tests, this would be more objective given
the high prevalence of malingering in late post-
concussive claimants (Binder & Willis, 1991;
Gianoli, McWilliams, Soileau, & Belafsky, 2000;
Greiffenstein, Baker, & Gola, 1996). For example,
Mittenberg, Patton, Canyock, and Condit (2002)
surveyed forensic neuropsychologists represent-
ing a pool of 33,000+ forensic cases and reported
a 40% base rate of invalid effort. Given the high
prevalence of invalid effort, the FN who never
diagnoses or even suspects invalid effort should
be considered biased. If you find permanent brain
54 forensic neuropsychology
dysfunction in 95% of the mild TBI litigants you
examine, these conclusions may be biased, as they
go against the base rate for residual deficits in
mild head trauma (Binder, Rohling, & Larrabee,
1997). Conversely, if you never find evidence of
permanent brain dysfunction in persons who
have taken over 30 days to follow commands, you
may also show bias, as persisting deficits are
common in persons with less periods of coma
(Dikmen et al., 1995). The point is that witness
bias is not measured by simply calculating the
number of plaintiff versus defense (or prosecution
versus defense) referrals.
Nonverbal behaviors are also important for
attorney-neuropsychologist interactions during
the trial phase. Maintain consistency of demeanor
across both the direct and cross-examination
phases. It is helpful to consider the familiar psy-
chological concept of “examiner characteristics,”
in which the tester’s personality, biological traits,
and nonverbal behavior influence responses to
psychological tests. This applies equally to the
courtroom and entails the characteristics of the
questioning attorney influencing your responses.
That is because direct and cross-examinations
contain entirely different questions, methods, and
aims associated with different personalities. The
direct examination elicits evidence to support an
opinion and the cross-examination elicits testi-
mony that disproves it. The opposing attorney
limits you with closed questions. The FN has no
procedural right to dictate the content of direct or
cross-examination. The FN does have control of
demeanor. This means consistency in tone, pos-
ture, gaze, prosody, and movement. For example,
when retaining attorney’s direct examination is
done, turn in the witness chair and squarely face
the opposing attorney. This signals you are giving
as much attention to the opposing side as you did
the retaining side. Continuing to stare in the old
direction appears dismissive and inattentive.
There is an extensive and evolving scientific
literature on these topics, for example, Neal and
Brodsky (2008), that is beyond the scope of this
chapter,
The FN may also control the scope of answers.
Two types of answers are relevant: passive and
active answers. Passive answering means respond-
ing only to the overt, literal meaning of the ques-
tion. Responding with your name and title when
asked to introduce you is an example. The effec-
tive FN engages in active answering whenever
possible to handle more difficult questions. An
active answer is responsive to the overt question,
but also responds to the latent content, and selec-
tive active responding to neuropsychology con-
tent-specific questions is what differentiates the
effective witness from the less-effective one. This
interchange between a defense attorney and plain-
tiff ’s neuropsychologist shows an active answer in
response to a general question:
Q: So abnormal neuropsychological test scores
are seen in persons with normal brains?
A: It is true that a few abnormal test scores are
common, but Ms. Jones’ high number and
pattern of abnormal scores led to my diagnosis
of brain problems.
In this case, the active answer addressed the
imprecision of the question, namely, ambiguity of
number (How many abnormalities can a normal
person produce?). The latent issue raised by the
question was what criteria differentiate abnormal
brain states from non-neurological explanations.
The answer “yes” may leave misimpressions with
the trier of fact, such as (1) this plaintiff scored
abnormally on only a few measures, (2) the expert
never considered alternative explanations, or
(3) the witness was biased towards finding brain
damage. The point is that active answers are allow-
able, control misimpressions, educate the trier of
fact, and provide a lucid link between general
questions and the specific matter at hand.
Always anticipate difficult questions designed
to trap, embarrass, or impeach you. There are
many popular questions, termed gambits,
designed to make you look ill-informed, stupid,
biased, or out of touch with mainstream neurop-
sychology. While such questions can be legitimate
and such characteristics could accurately apply to
you, this chapter assumes a conscientious and
knowledgeable NP. The following represents a
small list of the most common gambits you should
always be prepared for. These tactics include the
false alternative, learned treatise, upsetting the
witness, and false conceit gambits.
The gambit of false alternatives asks the FN to
choose between two explanations, usually phrased
in an either/or manner. For example, after estab-
lishing that the plaintiff passed effort tests, his
attorney asks, “Now doctor, either my client is
malingering or they are brain damaged, correct?”
This statement assumes (note: latent content) that
malingering and cerebral dysfunction is mutually
exclusive, and the courtroom-unfamiliar neurop-
sychologist may think that courtroom procedure

dictates choosing only those alternatives. The best
response is one that rejects the underlying
premise while simultaneously educating the trier
of fact, for example, “The absence of faking does
not prove brain damage. Good effort only means
the test scores are valid, and Mr. Smith produced
normal memory scores.” Upsetting the witness is
an attempt to raise the frustration level of the
witness. There is a popular maxim that governs
attorney behavior: “If you have the facts on your
side, pound the facts. If you have the law on your
side, pound the law. If you have neither facts nor
law on your aside, pound the table!” Some attor-
neys try to provoke expert witnesses with inap-
propriate assaults in an attempt to elicit an overly
emotional response. When an attorney attacks
(“badgering” or improper argumentative ques-
tioning is legally objectionable by the retaining
attorney), assume your opinions are so unass-
ailable that the attorney has nowhere to go. A
common problem for experts is that not all retain-
ing attorneys will know to object, nor will all trial
judges sustain an objection to unfair questions.
The FN must be prepared to cope with situations
in which attorneys are given unusual latitude. You
cannot offer legal objections yourself.
The FN must recognize the learned treatise
gambit and its variants. This is a line of question-
ing during which the FN is confronted with neu-
ropsychology texts, journal articles, published
commentary, and even interview transcripts with
well-known neuropsychologists. The attorney
tries to get the expert to acknowledge this book/
article/author/sentence/paragraph as “authorita-
tive.” A common question is “Don’t you agree that
Dr. Ima Legend’s book Neuropsychological Testing
for Idiots is authoritative?” or “You have to agree
that Dr. Ima Legend is one of the great authorities
in neuropsychology.” The courtroom-unfamiliar
expert does not know the legal ramifications of
agreeing that a treatise is authoritative: Accepting
a learned treatise means you must agree with every
statement in the document. The eager-to-please
witness who answers “yes” will next be treated to
a list of inconsistencies between his opinion and
the alleged authoritative text.
The general principle is to refuse the gambit.
This is both honest and scientifically defensible
but often difficult to do. Unless the expert is a
polymath and absolute master of a particular
book or paper, you should always refuse to answer
with a simple “yes.” To maintain consistency, your
must even refuse to acknowledge your own publi-
cations as authoritative in the legal sense, even if
Neuropsychology and the Law 55
some expert witness guides advise you against
this. One general approach is to acknowledge a
book’s relative importance or personal usefulness
(“It’s an important text that I sometimes rely
upon…”), while simultaneously denying over-
arching authority (“…but nothing in neuropsy-
chology is authoritative”). The expert may answer,
“That text is one authority in the field, but I have
not recently read every chapter and section con-
tained therein.” Another way is to provide answers
that inform the jury that sound scientific and
clinical practices never rest in any single individ-
ual or any single book. This is particularly true in
neuropsychology. Hence, in response to questions
about a book or specific journal, the FN witness
might respond “With over 100 journals in neu-
ropsychology and neurology coming out every
month, and thousands of articles in general
psychology, no one article is that important.”
In response to the “authoritative person” variant,
reasonable answers may be as follows:
“Thousands of men and women have contrib-
uted to the field of neuropsychology, and I recog-
nize Dr. Legend as one of those contributors.”
Or
“Dr. Legend is an important contributor to
neuropsychology but I don’t necessarily agree
with everything he has written.”
In cases where the opposing attorney wants
you to agree or disagree with a statement he/she
has read, another tactic is to ask for the book/
article/document that the attorney is holding. The
opposing counsel usually offers you a document
containing a highlighted paragraph, sentence, or
in some cases just a half-sentence. Politely demur
and state that although you are able to read, it
would have no meaning unless you could read the
whole chapter. It is very common for an attorney
to read a sentence out of context, even though the
entire paragraph or chapter may make clear the
sentence has a meaning other than the one
intended. Could you get a 60-minute break to
read the whole chapter? In the appropriate con-
text, more courtroom-familiar witnesses can fine
tune the answer to powerfully demonstrate to the
jury that even alleged “authorities” frequently
change their opinion. Going back to the first ques-
tion, an answer might be, “Given that Dr. Lezak
has published many different editions of her book
and updated her opinions, it can’t be authorita-
tive. Which of the updated editions of Lezak did
you have in mind?” However, this is a gambit
where assertiveness does not cause the attorney to
56 forensic neuropsychology
beat a hasty retreat. The attorney may persist in an
effort to make the witness look evasive, pompous,
or out of touch with scholarship. Unlike other
gambits, the FN should be prepared for persistent
questions designed to make you look out-of-
touch.
Courtroom-familiar and knowledgeable
experts face the false conceit gambit. This line of
questioning implies the plaintiff is special and not
subject to the general expectations of persons
with the same claimed etiology. Questions may
focus on length of time in evaluation (“His
treating doctor saw him 25 times, but you just saw
him once?”) and the uncertainties of whether a
particular test or principle applies to this person
(“The Test of Memory Malingering has never
been validated in transsexual railroad workers,
has it?”). The FN’s strategy is to answer these ques-
tions by presenting the bases for generalizing neu-
ropsychological techniques to diverse populations.
Stress the basic commonalities among all patients
from a neurological standpoint. For example, in
the case of memory disorder, you would stress
that all patients irrespective of social class or race
or illness share basic commonalities, including
the fact they have brains with right and left halves,
and the parts of the brain that control memory
formation are basically invariant from one person
to the next with rare exception. Also stress the
representativeness of your test norms. Witness
this interchange:
Q: Isn’t it true that you have never performed
neuropsychological testing on railroad work-
ers exposed to organic solvents, nor have you
published anything about it?
A: Although it is true this is the first time I saw
a railroad worker, neuropsychological tests are
designed for use with a wide variety of patients
with suspected brain disorders.
The expert in this case has accomplished
multiple things: She has answered honestly about
her lack of experience with railroad workers
claiming solvent exposure (responsive to the
surface question). But she also educated the jury
on latent issues such as (a) stressing long and deep
experience with many different kinds of patients,
(b) the generalizability of neurocognitive mea-
sures to different communities, and (c) deflating
the question’s false conceit of the “special plaintiff
understood only by my expert.” She has also pro-
vided a professional “so what” answer, indicating
that the question is unnecessarily tangential and
likely irrelevant.
The trial phase poses its own ethical chal-
lenges. Neuropsychologists must present well-
founded opinions that do not misstate or distort
principles of neuropsychology (Standard 2.04
of the 2002 Code, Basis for Scientific and
Professional Judgments). It is inevitable that some
opinions will be outliers to mainstream practices,
but this is not necessarily unethical. The main-
stream or consensus opinion is not automatically
the best or most valid one. FRE 702-705 combined
with the Daubert (1993), Kumho (1999), and
Joiner (General Electric v. Joiner, 1997) court
decisions were designed to allow novel but poten-
tially provable (“falsifiable”) approaches into the
courtroom.
Sometimes outlying opinions are so
unfounded, and in some instances outrageous,
that appellate courts limit neuropsychologists’
scope of testimony. In the case of Grenitz v. Tomlian
(2003), the Florida Supreme Court withdrew from
earlier legal precedent that gave neuropsycholo-
gists’ broad scope in causation testimony. In
Grenitz, plaintiff ’s expert claimed that the Object
Assembly subtest of a Wechsler IQ test was able to
differentiate in utero from intrapartum brain
damage. Some medical organizations took action
against such testimony on the grounds that testi-
mony is an extension of practicing medicine and
thus subject to oversight. Two neurosurgeons (in
separate jurisdictions) were sanctioned for pur-
portedly misstating practice standards (Albert,
2002). The U.S. Supreme Court upheld the profes-
sional societies’ right to discipline members for
improper courtroom testimony (Austin v. AANS,
2002; also reported by Adams, 2002). To date,
there is no parallel action by any neuropsychology
organization.
Post-Trial Phase
An issue that receives little attention in expert
witness guidebooks is post-trial considerations.
Your involvement should not end after verdict.
This should be a time of reflection. First, never
call the retaining attorney to find out the verdict.
Strong interest in the outcome of a trial means
you have an emotional stake in winning and
losing. Second, engage in an honest self-appraisal
of your methods and testimony. This requires rec-
ollection of the cross-examination. Was the cross-
examination skillful? Did the aggressive questions
uncover genuine weaknesses in your reasoning,
or were they merely designed to assassinate your

character? An honest self-appraisal not only
improves future testimony, it can also inform your
routine clinical work. For example, the author
(MFG) used to rely heavily on qualitative signs as
evidence for brain impairments. After a few
unpleasant depositions, it became evident that
these “signs” were sometimes seen in the context
of normal aggregate scores. Another area for
self-appraisal is reliance on Verbal–Performance
IQ differences. A typical over-interpretation is
“Mr. Doe’s PIQ is 15 points lower than his VIQ,
proving traumatic damage to the right brain.”
Actually, Verbal–Performance IQ splits are the
rule and not the exception among healthy
persons (Kaufman, 1990; Matarazzo, 1972;
Matarazzo, Bornstein, McDermott, & Noonan,
1986). After that point, I (MFG) relied more on a
quantitative approach, using process neuropsy-
chology methods as an additional tool, not a com-
plete approach.
The post-trial phase is the best time for an
“integrity check” (Brodsky, 1999). This is a self-
appraisal of one’s objectivity and fairness.
Maintaining objectivity requires a number of
steps, including awareness of the pull to affiliate
with the retaining side, and double checking for
the error of confirmatory bias. A simple ratio of
plaintiff to defense cases is not compelling evi-
dence for objectivity versus partisanship. It is a
reality that an FN’s career trajectory increasingly
attracts retention by one side more than another.
There are many reasons for this, including word of
mouth, aggressive versus conservative neurodiag-
nostic approaches, and scientist-practitioner
ethos versus pure clinical orientation. In criminal
contexts, many psychologists testify for the
defense because psychologists’ sympathies often
lie with mentally disturbed offenders. Reject the
idea that any kind of “bias” is automatically bad.
All experts have biases towards a type of conclu-
sion or method of analysis, and these should be
readily acknowledged. The human mind was not
designed to be neutral, and there are many built-
in cognitive biases that serve perception, atten-
tion, and decision-making (Haselton & Buss,
2003). There are, however, biases that negatively
influence forensic work product.
One problematic bias common in forensic
psychology is “confirmatory bias.” This is the ten-
dency to search only for evidence consistent with
a diagnosis, but ignore or minimize evidence
inconsistent with a conclusion (Davies, 2003;
Iverson, Brooks, & Holdnack, 2008). A plaintiff ’s
expert who selects only symptoms consistent with
Neuropsychology and the Law 57
a closed head injury from a long list of symptoms,
but ignores the widespread nature of complaints,
is engaging in confirmatory bias by overlooking
other possibilities, such as somatization disorder,
histrionic personality, or malingering. The same
applies to a defense-retained neuropsychologist,
who when confronted with the same list, con-
cludes only malingering. The DSM-IV-TR (APA,
2000) provides a reasonable guide to differential
diagnosis when the FN is confronted with a long
list of symptoms or other challenging presenta-
tions.
Some methods for self-assessment should
be avoided. Colbach (1981) recommended
calculating a Validity Quotient (VQ). This is cal-
culated by dividing the total number of court
decisions into the number of court decisions
where opinion and verdict matched. Hence, if
your opinion and the jury’s have matched every
time, the VQ would be 100%. The present authors
strongly advise against using this method. The
VQ requires calling the retaining attorney to get
the verdict. This is nothing more than the pull of
affiliation, a wish to be “on the winning side.”
Second, the VQ assumes that a legal verdict vali-
dates or invalidates a psychologist’s opinion. But
many factors go into a trier-of-fact’s decision-
making processes, including the competency of
attorneys, the likability of litigants, other expert
witness testimony, liability, and other legal issues
having nothing to do with an FN’s work. Belief in
the VQ may betray underlying grandiosity, that
somehow the FN’s opinion is always the most
critical in determining a fact at issue. If you
strongly believe in the VQ, you may be prone to
the “star witness” mentality.18
The best method for estimating objectivity
is to correlate one’s opinions with known
base rates for certain conditions. Of course,
estimating base rates is art as well as science.
The idea is to determine whether one finds
cognitive dysfunction related to the cause of
action much more often than the base rates allow
or less cognitive dysfunction (or psychopathol-
ogy) than one would expect. One could think
about this issue in the same way attorneys do:
A judge’s basic fairness is not determined if
he sustains plaintiff or defense’s objections in
a 1:1 ratio. That’s not fairness, that’s just score
keeping! Instead, fairness is determined how close
the judge’s rulings adhere to the letter of law.
Hence, a fair judge could still easily rule 90% in
favor of plaintiff and 10% in favor of defense in a
particular case.
58 forensic neuropsychology
CONCLUDING COMMENTS
Practicing competent forensic neuropsychology
requires two integrated approaches: aspirational
behavior and avoidance of committing wrongful
acts (Hess, 1999b). Avoidance of wrongful acts
means the FN provides professional services
that are sensitive to jurisdictional law, with
ethical propriety and moral integrity. Personal
preference may invoke analogies based on the
seven deadly sins, for example, avoiding sloth
by writing timely neuropsychology reports.
Aspirational behavior means constant examina-
tion of each act or report concerning its implica-
tions for personal development, professional
integrity, and our system of justice in civil society.
The aspirational approach encourages excellence
in our profession and science. Some attorneys do
a great service to forensic neuropsychology
practice with heavy scrutiny of our assessment
methods and diagnostic reasoning. A good cross-
examination can reveal genuine inadequacies in
assessment techniques, such as an insufficient
normative base for a test, failure to examine symp-
tom validity, and classification hit rates no better
than base-rate guessing. Cross-examination can
only improve our pursuit of good test instruments
and competent practices. Aspirational goals
include prevention of the misuse of FNs’ work.
Newspapers have been filled with bizarre legal
defense theories in sensational crimes, and some
neuropsychology experts have contributed
regretfully to such defenses. For example, one FN
opined that a mass killer was legally insane
because of “subtle frontal lobe damage,” while
simultaneously ignoring the defendant’s well-
organized efforts to cover up the crime and evade
detection for over a year. State insanity statutes
typically require evidence of severe cognitive
dysfunction or severe emotional dysregulation to
support a conclusion of legal insanity. The respon-
sible FN must not only weigh the body of scien-
tific knowledge, he must apply this knowledge to
all relevant behaviors displayed by a defendant
before agreeing to support an unusual medico-
legal theory.
Table 2.7 represents a distillation of the ideas
in this chapter. It is similar to the “Rules of Road”
tables that the late Ted Blau created for forensic
psychologists (Blau, 1998). The Table contains
both the aspirational and moral underpinnings
mentioned by Hess (1999b). The reader may wish
to add his or her own ideas.
Both budding and experienced FNs may wish
to maintain a basic resource library.
The authors wish to emphasize that an ency-
clopedic knowledge of the law is not necessary to
engage in productive and effective expert witness
work. There are, however, key texts and papers
that are indispensable. Melton, Petrila, Poythress,
Slobogin, and Otto’s third edition of Psychological
Evaluations for the Courts (2007) is a veritable
encyclopedia of forensic knowledge. The book
provides summaries and analysis of landmark
legal cases, demystifies legal terminology, reviews
many forensic assessment instruments that
address cognitive capacities, and devotes much
attention to the ethical and legal details of assess-
ment. The important teaching from this book is
that the FN’s report does not have to be a compre-
hensive evaluation of every last aspect of an exam-
inee’s cognitive function. For example, it is
pointless and potentially harmful if you give a
comprehensive neuropsychological test battery
on a question of competent waiver of Miranda
Rights. Melton et al. (2007) offer no separate
chapter on neuropsychology, but the intelligent
reader can use this book to make extrapolations
to neuropsychology work.
Forensic report writing requires sensibilities
and formatting different from clinical reports.
There are many good casebooks to choose from,
depending on level of experience and the issue to
be addressed. Heilbrun, Marzcyk, and DeMatteo
(2002) casebook is a primer in case studies for
every known forensic context. This includes
worker’s compensation, death penalty mitigation,
competence to be sentenced, and many other con-
texts. Each chapter author is strongly associated
with the diagnostic question, and in some cases,
developed the specialty. The appendix of Melton
et al. (2007) also contains excellent, but briefer
reports. Heilbronner’s (2005) Forensic Neuro-
psychology Casebook data-mines prototypical
cases from the files of the country’s best known
FNs, while Sweet and Morgan (2009) focus solely
on questions of malingering and data validity.
Donders’ (2001a, 2001c) survey details typical
report writing practices within professional
neuropsychology.
Legal libraries should be limited to cases of
impact and pertinent local law. Every neuro-
psychologist should have copies of the Daubert
trilogy. The Daubert, Joiner, and Kumho cases
can be downloaded from Cornell Law School’s
website: http://supct.law.cornell.edu/supct/index.
html. If you are interested in researching federal
and state appellate cases relevant to neuropsy-
chology, the LexisNexis™ service allows relatively
 Neuropsychology and the Law 59

TABLE 2.7 SUMMARY OF FIVE PRINCIPLES OF PRODUCTIVE

AT TORNEYNEUROPSYCHOLOGY RELATIONS, WITH EX AMPLES
Knowledge of Legal Bases
• Understand, accept, and adjust to structural conflicts between legal and scientific outlooks.
• Recognize manageable specific conflicts that arise from time to time and develop specific response strategies,
e.g., third-party observation request.
• Be familiar with the essentials of the Federal Rules of Evidence and Civil Procedure, the Daubert Trilogy,
the Frye decision, and case law applicable to neuropsychological testing.
• Hold strong presumption against third-party observation of testing phase and test manual release, but
final decision to proceed/decline depends on nature of legal action and observation conditions.
Practice Competent Neuropsychology
• Adhere to scientist-practitioner model.
• Data collection is ideally a tripod consisting of outside records, history and behavioral observations,
and test scores.
• Recognize the fallibility of each method in isolation.
• Justify selection of all measures on basis of peer-reviewed studies; admissibility law does NOT require
relying on a fixed test battery.
• Design test battery to target both legal and clinical issues raised by a particular case.
• Avoid use of single or homemade tests, and diagnosis of brain damage on symptoms alone.
Support Board Certification
• Complete appropriate board certification (the authors recommend the oldest, largest, and most-widely
recognized boards associated with the American Board of Professional Psychology (ABPP).
• Acknowledge importance of open peer review and practice standards.
• Reject bogus issues such as “elitism” or “academic–clinical” artificial dichotomies as excuses for avoiding
certification.
Adhere To Ethical Principles
• Understand 2002 Ethics Code both generally and the specific principles relevant to forensic applications.
• View the Specialty Guidelines for Forensic Psychology as a model for desirable behavior.
• Recognize the potential ethical traps associated with each phase of the attorney-neuropsychologist
interaction.
• Avoid “pull of affiliation” by recognizing that you do not have to do everything an attorney
asks you to do.
Be Courtroom Familiar
• Rigorously maintain mental set of “educator to trier of fact” when testifying.
• Maintain consistency of gaze, demeanor, volume, and prosody during both direct and cross-examination.
• Practice “active answering” to questions to educate the jury and avoid misimpressions; no legal authority
requires answering just “yes” or “no.”
• Recognize common legal gambits and develop acceptable means of responding.
• Respond with tactics only when they are genuinely called for; do not overuse.

inexpensive downloading of individual opinions
at http://www.lexisnexis.com/. The recently
published 2003 Federal Rules of Evidence and
Federal Rules of Civil Procedure are available
through West Publishing at http://west.thomson.
com, although there has been little modification
over the first publication in 1975. For those doing
criminal consulting, the 2002 Atkins decision is
important.
Neuropsychologists frequently ask the authors
about specific responses to especially difficult direct
and cross-examination questions. Coping with
cross-examination is partly science, but mostly
art. Stanley Brodsky’s three books (Brodsky, 1991,
60 forensic neuropsychology
1999, 2004) on psychological testimony are essen-
tial tools, especially the first: Testifying in Court:
Maxims for the Expert Witness. They are powerful
tools for providing genuine, responsive, and
respectful answers to the most difficult questions.
The Faust, Ziskin, and Hiers (1991) volume Coping
with Brain Damage Claims provides guidelines for
litigation consultation, such as developing basic
cross-examination questions. The appendices
contain large libraries of stock cross-examination
questions for which every FN should be familiar.
But the book has it biases, such as being strongly
civil-defense oriented in its advice. The material is
also too dated because it predates Daubert,
appeared prior to the revolution in effort and
validity testing, and the book focuses on tests that
are no longer accepted by competent neuropsy-
chologists, for example, Draw-A-Person. In short,
most competent neuropsychologists are skeptics
of the methods used in an earlier era.
Since the first edition, the trend toward neu-
ropsychologists as the preferred brain-behavior
experts in legal cases has become a presumption.
Growth in forensic consulting for neuropsy-
chologists is outpacing every related brain-behav-
ior expertise and that growth is accelerating. The
authors recommend that you be patient, remain
objective, and let your reports speak to the quality
of your work; do not advertise your forensic ser-
vices. Always be a prepared, competent, credible,
and professional witness. Know your client, know
what they need, know what you can and cannot
do for them, and communicate directly and forth-
rightly, even when you know it is something that
may not help their case. Always be true to your
scientist–practitioner training. Neuropsychologists
who practice competently, avail themselves to
forensic consulting, and follow the suggestions in
this chapter, will find that forensic consulting is a
rewarding way to diversify practice and develop
new revenue in an increasingly stagnant/con-
stricted market for general clinical services. In
offering reliable services to the legal profession,
neuropsychology supports the truth-seeking func-
tion of the judiciary, promotes justice, protects the
profession, and serves public policy.
N OT E S
1. Human reasoning, unlike computers, is capable
of abduction: inference to the best explanation, among
many competing ones.
2. The Florida Board of Psychology recently tight-
ened guidelines for marketing specializations and
board certifications
3. Personal attacks are part of the territory in
forensic work. There is an old law school maxim: When
you have the law on your side, pound the law; when
you have the facts, pound the facts; when you have nei-
ther, pound the table.
4. Remittitur is designed to cure an award of
damages that is grossly excessive without the necessity
of a new trial or an appeal.
5. Aggressive attorneys are demanding test manu-
als with greater frequency in some jurisdictions.
Florida is one example.
6. In the first edition, Greiffenstein and Cohen used
the terms “exceptionalism versus legal primacy” camps.
7. However, Judge Woodlock added, “this holding
leaves open the possibility that a more focused and
conditioned disclosure would be acceptable to the
Court. The most common resolution for this type of
dispute has been some compromise between full,
unconditioned disclosure and total exemption from
the Federal Rules of Civil Procedure.” (p. 8). Judge
Woodlock issued a protective order that restricted the
release of psychological test materials in Taylor, even
though the Edison court expressed reservations about
such orders, with the majority noting concern about
intentional violations and the minority acknowledging
problems from inadvertent disclosure.
8. The judge appropriately noted that North
Carolina recognized no test security privilege and that
under conflict of law analysis, North Carolina substan-
tive law controls, absent a specific claim of privilege.
Nevertheless, the judge cited Kaufmann (2009) and an
APA editorial, as important considerations. The judge
ultimately denied plaintiff ’s motion to quash a defense
subpoena for raw test data, and ordered the plaintiff-
retained psychologists to release data to opposing
counsel.
9. A commonly held myth is that only subpoenas
signed by a judge need be honored. The reality is that
in most jurisdictions, judges have delegated much of
their subpoena authority to attorneys. In Michigan for
example, the typed signature of a court clerk is suffi-
cient to render a subpoena valid. That is not to say that
the FN has no rights in response to a subpoena. It is
important to respond to every subpoena, but this does
not mean comply with every demand.
10. In August 2009, the APA Council of
Representatives proposed a change to the Code,
removing some ambiguous language from the section
addressing the “raw data” problem.
11. The majority opinion was written by Scalia,
who noted “attention may wander where the eyes
don’t.” The APA wrote an amicus brief supporting
defendant. This amicus was unusual for a scientific
organization, because it cited only case law, and did not
include any scientific references or psychology practice
standards.

12. Attorney’s perceptions of experts provide good
examples of advocacy. Plaintiff attorneys uniformly
term the neuropsychologists they retain as “treating,
objective doctors,” but those hired by the defense are
“all biased.” Defense attorney’s view “treating” neurop-
sychologists as the biased ones, because they are advo-
cates by nature, and may also have a financial interest in
the outcome of the trial, e.g., the FN has a lien on the
case. In their view, defense experts are more objective
because they are paid irrespective of who wins or loses.
13. The SGFFP are now under revision and may
be in force when this book goes to press. See http://
www.ap-ls.org/aboutpsychlaw/SpecialtyGuidelines.
php for updates.
14. Your extra-test records may be “Bates stamped”
(a numerical page reference used by courts), so put the
Bates number in parentheses after key facts. This makes
it easier to find supporting documents during testi-
mony, rather than struggling to find pages while in the
hot seat.
15. States accepting Frye include Alabama,
Arizona, California, Colorado, the District of Colum-
bia, Florida, Illinois Kansas, Maryland, Minnesota,
Mississippi, New Jersey, New York, Pennsylvania, and
Washington.
16. After hearing Daubert, the Supreme Court
remanded the case back to the trial judge to apply the
new standard to the facts. The trial judge again rejected
plaintiff ’s expert testimony on the same grounds: The
testimony was not valid or relevant for lack of any gen-
eral acceptance. Note that the Frye rule is one of the
Daubert dicta for the trial court to consider. Dicta are
like the discussion section of a paper, but not the formal
ruling of law.
17. Chapelle v. Ganger was a bench trial of a brain
injury claim. The judge’s written decision indicated
that even partial Halstead-Reitan battery protocols
from two other neuropsychologists were admissible.
This fact alone rebuts Reed and Reitan’s assertions.
Defense counsel moved for a Daubert hearing only to
bar the testimony of a vocational specialist who offered
speculative testimony that the minor plaintiff would
never work.
18. A defense attorney once called a co-author
(MFG) to announce the jury awarded plaintiff a large
sum of money. He stated, “After verdict, they said they
liked your down-to-earth manner, and didn’t believe
plaintiff had a significant head trauma. But they really
hated the claims adjustor and my accident reconstruc-
tionist” The point is that doing a competent and ethical
job is not automatically associated with any specific out-
come. Do not judge your work quality by legal outcome.
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Sweet, J. J., Meyer, D. G., Nelson, N. W., & Moberg, P. J.
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Sweet, J. J. & Moulthrop, M. A. (1999a). Self-
examination questions as a means of identifying
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 3
Admissibility of Expert Opinions based on
Neuropsychological Evidence
PAU L M . K AU F M A N N
INTRODUCTION
Clinical neuropsychology is a specialty practice
of psychology that uses unique methods and legally
protected test materials in conjunction with the
brain-behavior knowledge base to evaluate, diag-
nose, and treat individuals with known or sus-
pected neurological disease and/or injury. Lawyers
increasingly seek consultation from neuropsychol-
ogist experts on an expanding set of legal issues, in
part, because clinical neuropsychologists apply a
scientific approach that meets judicial standards
for expert testimony (Larrabee, this volume).
Kaufmann (2009c) recently published a summary
of the growth in forensic neuropsychology con-
sulting, showing that the growth in legal cases
referencing neuropsychology in the Lexis database
is outpacing every related area of brain-behavior
expertise and this growth is accelerating. This
author recently noted a 6% average rate of annual
growth in Lexis cases referencing neuropsychol-
ogy from 2005–2009, with an unprecedented 20%
increase in 2010. Greiffenstein and Kaufmann
(this volume) note the civil, criminal, administra-
tive, probate, and alternative dispute resolution
settings in which neuropsychologists are com-
monly asked to render expert opinions. Kaufmann
(2008) recently detailed the complexities of admis-
sibility of neuropsychological evidence in criminal
cases.1 With the rapidly increasing use of neuro-
psychology in our courts, practitioners of law and
psychology would benefit from understanding the
nature of neuropsychological evidence and the
standards for its admissibility.
In order for neuropsychologists to render
admissible expert opinions, courts must accept
the neuropsychologist as an expert who is capable
of assisting the trier of fact (see Fed. R. Evid. 702)
in adjudicating an issue or controversy confront-
ing the court. Experts who do not assist the jury
are of no value to the court and poorly formulated
opinions may actually be excluded if the expert
testimony results in “unfair prejudice, confusion
of the issues, or misleading the jury, or . . . undue
delay, waste of time, or needless presentation of
cumulative evidence” (Fed. R. Evid. 403). This
chapter begins with a history and description of
key cases that have given rise to the rules for
expert witnesses, with a special emphasis on those
cases involving psychologists. These rules are then
applied to neuropsychological expert opinions in
a set of recurring challenges to the admissibility of
neuropsychological evidence. These challenges
include: 1) battery selection (fixed vs. flexible) as
legally analyzed in Baxter v. Temple (2008),
2) symptom validity science as taken up in a series
of cases involving the MMPI-2 Symptom Validity
Scale (FBS, formerly known as the Fake Bad
Scale), 3) causation opinions with commentary
from Grenitz v. Tomlian (2003) and its final out-
come, and 4) nonpsychologists asserting neurop-
sychological opinions. Florida Frye challenges to
FBS, evolving litigation tactics, related jurispru-
dence, and the smoldering debate over symptom
validity test (SVT) application are summarized,
with recommendations for how neuropsycholo-
gist experts may testify about response bias, effort,
and malingering. The chapter then turns to con-
sider rules and case law relevant to tendering
expert opinions in criminal cases, carefully distin-
guishing between competency and the affirmative
defense of insanity. The Insanity Defense Reform
Act of 1984 and its implications for the scope of
expert testimony are analyzed in a recently
resolved criminal case that relied upon the expert
opinions of a clinical neuropsychologist. These
sections remind professionals that courts
painstakingly avoid philosophical debate to
focus on justiciable issues in actual cases. The
reader is alerted to the persistent controversy
about the proper role, if any, of neuroscience and
 Admissibility of Expert Opinions based on Neuropsychological Evidence
neuroimaging in questions of guilt and punish-
ment. The next section examines research evalu-
ating the impact of Daubert v. Merrell Dow Pharm,
Inc. (1993) and its progeny on admissibility of
expert testimony, with emphasis on neuropsy-
chological evidence. Finally, this chapter con-
cludes with a warning that legislative and judicial
processes are underway that might undermine
the reliability of neuropsychological evaluations
and forensic consulting unless neuropsychologists
advocate for reasonable protections (Howe, Sweet,
& Bauer, 2010) and take active steps to legally
intervene (Kaufmann, 2005; 2009c).
Courts commonly recognize psychologist
experts, but reliance on the board–certified neuro-
psychologist expert is a relatively recent develop-
ment. The next section reviews the history of
forensic psychology consultation in criminal
courts, noting the emergence of neuropsychology
experts who address brain–behavior questions at
issue in litigation.
H I S T O RY
Experience has shown that opposite opinions
of persons professing to be experts may be
obtained to any amount; and it often occurs
that not only many days, but even weeks, are
consumed in cross-examinations, to test the
skill or knowledge of such witnesses and the
correctness of their opinions, wasting the time
and wearying the patience of both court and
jury, and perplexing, instead of elucidating, the
questions involved in the issue.
Winnans v. N.Y. & Erie Railroad Co.
(1859) (p. 101)
Expert testimony must overcome the courts’
caution by clearly assisting the trier of fact.
Following Winnans, other courts expressed simi-
lar hesitations, see Rush v. Megee (1871) (“We are
not enamored with expert testimony, however
procured or presented” p. 73); Whitaker v. Parker
(1876) (“Evidence of experts is of the lowest order
and of the most unsatisfactory character” p. 587).
Clinical psychology did not exist in the nineteenth
century, but courts would have likely refused
to recognize anyone claiming psychological
expertise. Although the science of psychology was
only emerging, practice was well underway by
those called phrenologists, physiognomists,
graphologists, mesmerists, spiritualists, seers,
psychics, mediums, mental healers, and psycho-
logists (Benjamin, 2005).
71
Scientific advances changed skeptical courts,
with Nelson v. Nelson (1958) responding to
Whitaker, writing, “Science of comparing . . . is
much further advanced today than it was 80 years
ago” (p. 770). As the scientific method became
more widely understood and accepted, the meth-
odologies of behavioral and social sciences were
applied increasingly to the study of psychology.
After World War II, training of mental health
practitioners increased with expanded funding
from the U.S. federal government, providing
some support for the Boulder Conference (1949).
The Boulder Conference created the scientist–
practitioner model of training in clinical psychol-
ogy that remains at the core of the profession
(Baker & Benjamin, 2000). The scientist–practi-
tioner model bolsters the credibility of expert psy-
chologists in our courts.
Jenkins v. United States (1962) first addressed
the admissibility of expert testimony by a psy-
chologist as to the existence of mental defect or
organic brain injury. Three psychologists testified
that Mr. Jenkins had a mental disease at the time
of the crime. The trial court instructed the jury to
disregard the testimony of the psychologists
because “a psychologist is not competent to give a
medical opinion as to a mental disease or defect”
(p. 643). On appeal, the reviewing court cited the
greater weight of legal authority finding that
“some psychologists are qualified to render expert
testimony” (p. 644) regarding mental disorders,
referring to concurring dicta2 in an earlier case
(People v. Hawthorne, 1940). For further discus-
sion of Jenkins and its progeny, the interested
reader is referred to Kaufmann (2008).
In an early case recognizing neuropsycho-
logical expertise in a civil proceeding, Simmons v.
Mullen (1974) found that a psychologist was com-
petent to testify “as an expert on organic brain
injury” (p. 897). The following testimony directly
confronts the issue of whether opinions regarding
brain damage are exclusively the domain of
medical professionals.
Q: Doctor, when you formed an opinion that
this girl did have, in addition to some of the
emotional problems which you indicated, that
she did have minimal brain damage.
A: Yes.
Q: Can you state with reasonable medical
certainty whether you have an opinion as to the
cause of this minimal brain damage which you
found; and if so, what that cause would be?
72 forensic neuropsychology
A: Yes. I am just stumbling over your term
“medical.” We have to keep in mind that I am
not a medical person.
Q: I think my question was with reasonable
professional certainty.
A: Okay. Yes, I feel that this youngster’s
minimal brain damage results from the trauma
she received in the accident (p. 897).
Citing Jenkins, the Simmons court noted “it is
not essential that an expert witness be a medical
practitioner to testify on organic problems”
(p. 898). Moreover, a neurosurgeon provided
the court some evidence for such conclusions, as
follows:
Q: Doctor, I wonder if you would explain for
the Court and Jury the relationship of a clinical
psychologist to a neurosurgeon such as your-
self. What does a clinical psychologist do for
yourself [sic]?
A: Well, primarily in our business, if we have a
patient who has complaints, particularly with
those complaints representing the possibility
of emotional disfunction [sic], behavioral dis-
turbance, things that we cannot measure on
the basis of what we can see, things that we
cannot measure on the basis of our detailed
examinations — with that particular history,
we then refer those patients for psychometric
evaluation and request then of our psycho-
logist who is doing the examination whether,
by his battery of tests, he can or cannot tell us
whether he believes there is evidence of distur-
bance as far as brain function is concerned,
whether this would be on the basis of possible
organic disturbance or on the basis of psycho-
logical disturbance.
Q: And is the psychologist properly capable of
determining by his course of tests and his
examination, whether the problem is, the prob-
lem that your patient is having, is primarily
emotional or primarily organic or having to do
with the brain, itself, or a combination of both?
Is that a fair statement?
A: Yes. We feel very strongly that Dr. Romano
can. He has worked with us many, many years
and is one of the two psychologists that, in our
practice over this period of time, we have come
down to, and the only one that we use from the
standpoint of this type of testing, because
I think that this man is most excellent in his
field and we rely heavily on what he reports
to us (p. 898).
Based in part on the reliance of the medical
profession on psychologists to make these
judgments, Simmons concluded that to adopt the
appellant’s view that psychologists are not compe-
tent witnesses to testify on physical matters
“would be to ignore present medical and psycho-
logical practice” (p. 899).
Kaufmann (2009c) notes that courts increas-
ingly rely on neuropsychologists as preferred
brain-behavior-mental-state experts, with growth
trends showing that neuropsychologists are out-
pacing every other forensically related psychiatric
or psychological specialty practice (see Figure 3.1).
This unprecedented growth in forensic neuro-
psychology consulting suggests that practitioners
of law and psychology who want to understand
the nature of neuropsychological evidence and
the standards for its admissibility, should learn
more about how courts recognize expertise. The
next section addresses how courts evaluate the
qualifications of neuropsychologist experts.
Q UA L I F I C AT I O N
OF EXPERTS
Under Federal Rules, courts must evaluate expert
qualifications, and determine the relevance of
the expert opinions to the issue at bar and the
reliability of the bases for those opinions, before
those opinions are admitted into evidence and
heard by a jury. Judges must determine whether
special experience is required to develop these
expert opinions that will assist the jury in resolv-
ing an issue in the case at bar.3 Therefore, consult-
ing neuropsychologists should understand the
evolution of court standards for evaluating
experts as addressed in Frye v. United States
(1923), Daubert v. Merrell Dow Pharm., Inc. (1993)
and its progeny, and Fed. R. Evid. 104 Preliminary
Questions, Fed. R. Evid. 403 Relevance, and
Fed. R. Evid. 702 Testimony of Experts.
In Frye, a defendant convicted of second
degree murder appealed, claiming the trial
court erred because it denied the admission of
expert testimony on a “systolic blood pressure
deception test” (p. 1013). Defense attempts to
admit this expert and his opinions or to conduct
the test in the courtroom were denied. The appel-
late court affirmed the trial judge, quoting the
government’s brief and thereby creating the
following rule:
 Admissibility of Expert Opinions based on Neuropsychological Evidence 73

5500

5000
Published Lexis cases using the term
4500

4000 Neuropsycholo! 2009

Forensic Psycholo!
Federal and State Cases

Foresic Psychia!
3500 Neuropsychia!
Neuropsychology projection 2009
3000 Forensic Psychology projection
Forensic Psychiatry projection
2500 Neuropsychiatry projection

2000

1500

1000

500

0
1979 1984 1989 1994 1999 2004 2009
Five year epochs

FIGURE 3.1: Number of United States federal and state cases using the root terms Neuropsycholo!, Forensic
Psycholo!, Forensic Psychia!, and Neuropsychia! in five-year epochs for the past thirty years used as a basis
for polynomial regression projections for the next fifteen years.

. . . when the question involved does not lie
within the range of common experience or
common knowledge, but requires special expe-
rience or special knowledge, then the opinions
of witnesses skilled in that particular science,
art, or trade to which the question relates are
admissible in evidence (p. 1014).
In a two page unanimous opinion, the appellate
court concluded that the deception test had
not gained “standing and scientific recognition
among physiological and psychological authori-
ties as would justify the courts in admitting expert
testimony” (p. 1014). Stated alternatively, the
test was denied admission in court because it was
not generally accepted in the relevant scientific
community.
In Daubert v. Merrell Dow Pharm, Inc. (1989),
infants and their guardians sued a drug company
to recover for limb reduction birth defects caused
by the mother’s ingestion of the antinausea “morn-
ing sickness” drug Bendectin. Merrell Dow won
on summary judgment4 with the trial judge citing
Frye, the “prevailing school of thought” (p. 572)
regarding Bendectin, and controlling legal autho-
rity that epidemiological studies are the most
reliable evidence of causation in this field of study.
The plaintiffs failed to present “statistically signi-
ficant epidemiological proof that Bendectin causes
limb reduction defects” because their expert
relied, in part, on in vitro animal and chemical
studies (p. 575). The plaintiffs appealed, arguing
the reanalysis of the epidemiological data and the
scientific techniques employed by their experts
were permissible. The unanimous three-judge
Ninth Circuit Appellate Court affirmed the trial
court, again citing Frye and following the prece-
dent set in sister courts, referencing
. . . a well-founded skepticism of the scientific
value of the reanalysis methodology employed
by plaintiffs’ experts; they recognize that “[t]he
best test of certainty we have is good science-
the science of publication, replication, and
verification, the science of consensus and peer
review. P. Huber, Galileo’s Revenge: Junk Science
in the Courtroom 228 (1991) (p. 1131).
The Ninth Circuit suggested in vitro studies
were junk science, affirming the trial court
decision to ignore this new scientific evidence
because it failed Frye’s general acceptance test.
74 forensic neuropsychology
The plaintiffs appealed and the U.S. Supreme
Court granted certiorari.5
In a landmark decision that forever changed
the scope of expert testimony, the Supreme Court
found that the general acceptance test in Frye
had been superseded by Fed. R. Evid. 702, thereby
requiring all federal courts to admit any “scien-
tific, technical, or other specialized knowledge”
that assists the trier of fact to understand the
evidence.6 “General acceptance” is not a necessary
precondition for the admissibility of scientific
evidence under the Federal Rules of Evidence.
A 7–2 majority also held that District Court
judges (gatekeepers) had the duty to evaluate the
admissibility of expert testimony. However,
the Honorable Chief Justice William Rehnquist
parted company on the issue of the judge’s role,
writing
I do not doubt that Rule 702 confides to the
judge some gatekeeping responsibility in decid-
ing questions of the admissibility of proffered
expert testimony. But I do not think it imposes
on them either the obligation or the authority
to become amateur scientists in order to
perform that role (p. 600-01).
With candor, Chief Justice Rehnquist acknowl-
edged being “at a loss” to understand what is meant
when it is said that the scientific status of a theory
depends on its “falsifiability” and he predicted
other federal judges would be too. Nevertheless,
the Ninth Circuit decision was reversed and the
case was remanded for further proceedings.
In the interests of justice and judicial economy,
the Ninth Circuit decided to conduct the newly
required Daubert analysis of Fed. R. Evid. 702,
framing the question in this “brave new world” as
follows: “How do we figure out whether scientists
have derived their findings through the scientific
method or whether their testimony is based on sci-
entifically valid principles?” (p. 1316). In the end, a
unanimous Ninth Circuit found that the plaintiff
expert failed Rule 702 requirements and Daubert’s
holding because the plaintiff presented only experts’
qualifications, their conclusions, and their assur-
ances of reliability. The original summary judg-
ment rendered six years earlier was affirmed and
the Daubert plaintiffs received due process, equal
protection, and justice, but no compensation,
because the scientific evidence offered by their
expert failed to show with a preponderance of the
evidence that Bendectin caused the birth defects.
The Court clarified Daubert and broadened its
impact in two subsequent cases, General Electric
Co. v. Joiner (1997) and Kumho Tire Co. v.
Carmichael (1999). In Joiner, a city electrician,
who was diagnosed with lung cancer, brought suit
against the manufacturer of polychlorinated
biphenyls (PCBs) and manufacturers of electrical
transformers and dielectric fluid, alleging expo-
sure caused his cancer based on expert testimony.
The District Court judge excluded the plaintiff ’s
expert testimony finding it “subjective belief or
unsupported speculation” (p. 140) and Joiner
appealed. The Eleventh Circuit Appellate Court
applied a stringent standard of review, reversing
the trial court and finding the judge erred in
excluding the expert testimony. The U.S. Supreme
Court intervened to reverse the Eleventh Circuit,
thereby affirming and strengthening the gatekeep-
ing function of the trial court, directing appellate
courts not to review a trial judge’s decision regard-
ing expert admission unless the judge committed
a clear abuse of discretion. Basically, appellate
courts were ordered to show great deference to
gatekeeper judges in District Courts and to not
disturb the decisions of the trial judge regarding
the admissibility of expert testimony in the
absence of gross error.
In Kumho Tire, a vehicle overturned when a
right rear tire blew out, killing one passenger and
injuring others. The plaintiffs sought to admit the
testimony of a tire failure analyst regarding his
visual and tactile inspection of the tire, based on
the theory that in the absence of at least two of
four specific physical indicators, tire failure must
have been caused by a defect. The defendant
moved to exclude the tire analyst testimony, claim-
ing the methodology failed to satisfy Fed. R. Evid.
702 requirements. The trial court applied Daubert
and the judge excluded the tire analyst after find-
ing the methodology employed was insufficiently
reliable; plaintiff Carmichael appealed. The
Eleventh Circuit held that the trial court erred in
applying Daubert, believing that it only applied to
scientific testimony. The U.S. Supreme Court
reversed the Eleventh Circuit and clarified that
Daubert factors apply to the testimony of engi-
neers and other experts who are not scientists.
Experts may also be evaluated and admitted to tes-
tify based on skill, experience, and other special-
ized knowledge, not only scientific knowledge.
In 2002, holdings from the Daubert “trilogy”
of cases were used to amend Rule 702 and codify
these U.S. Supreme Court decisions into the
 Admissibility of Expert Opinions based on Neuropsychological Evidence
current rules governing expert testimony. Rule
702 reads as follows:
If scientific, technical, or other specialized
knowledge will assist the trier of fact to under-
stand the evidence or to determine a fact in
issue, a witness qualified as an expert by knowl-
edge, skill, experience, training, or education,
may testify thereto in the form of an opinion or
otherwise, if (1) the testimony is based upon
sufficient facts or data, (2) the testimony is the
product of reliable principles and methods,
and (3) the witness has applied the principles
and methods reliably to the facts of the case.
(Fed. R. Evid. 702)
The test for when expert testimony may
be used is determined on the basis of assisting
the trier. Such opinions are excluded when
they are unhelpful, and therefore superfluous and
a waste of time. (Fed. R. Evid. 702 Comments).
The next section shows how these rules are
applied to a neuropsychologist expert in a recent
civil case.
B AT T L E O F T H E
E X P E RT S OV E R
ADMIS SIBILITY OF
NEUROPSYCHOLOGICAL
EVIDENCE
Within 12 years of Simmons (1975), neuropsy-
chology identified some emerging concerns
(Schwartz, 1987; Satz, 1988; Rothke, 1992) regard-
ing the qualifications of neuropsychologist
experts and the scope of opinions. Neuropsy-
chologists began tracking early decisions regard-
ing admissibility of expert opinions (Richardson
& Adams, 1992). Despite the clear history of
admissibility of expert opinions based on neuro-
psychological evidence, courts have confronted
cases and controversies in which psychologist
experts have taken diametrically opposed posi-
tions on the admission of certain types of opin-
ions based on methodological assumptions
underlying the basis for those opinions. These
most common challenges to the admissibility of
expert neuropsychologist opinions, include
motions to exclude evidence based on: 1) battery
selection (fixed vs. flexible), 2) application of
symptom validity science in neuropsychological
evaluations, 3) causation testimony beyond the
scope of expertise, and 4) expert unqualified to
render neuropsychological opinions.
75
Battery Selection (Fixed vs. Flexible
and the Boston Approach)
Although there have been a number of lower
court cases that have uniformly supported the
use of flexible batteries in forensic consulting
(Chapple v. Gangar, 1994; People v. Sebastianelli,
1998; Minner v. American Mortg. & Guar., 2000),
fixed battery advocates continue to promote fixed
battery superiority in forensic neuropsychology
(Hom, 2008; Russell, 2007). More recent scientific
studies have shown equivalent or superior validity
of flexible batteries to fixed battery (i.e., Halstead-
Reitan) approaches (Larrabee, 2008; Larrabee,
Millis, & Meyers, 2008).
In Baxter v. Temple (2005), the defense filed a
motion in limine7 to exclude the testimony of a
Barbara Bruno–Golden, EdD as insufficiently
reliable under Daubert. During the evidentiary
hearing, Dr. Bruno–Golden described the Boston
Process Approach (BPA) to hypothesis testing in
the neuropsychological evaluation of a child
exposed allegedly to lead poisoning. The defen-
dants argued successfully that Dr. Bruno–Golden’s
testimony should be excluded because the BPA
has not been subject to peer review and publica-
tion, has no known or potential error rate, and
is not generally accepted in the appropriate scien-
tific community. A review of hearing testimony
shows how a trial judge used Daubert factors
to exclude expert neuropsychological evidence
and the cross–examination provides instruction
for how to avoid such outcomes (Desmond,
2007).
All three neuropsychologists, Drs. Bruno–
Golden, Sandra Shaheen, and David Faust, testi-
fied that the Boston Process methodology
employed was untested (Baxter v. Temple (2005),
p. 8). Dr. Bruno–Golden added that the BPA that
she employs in forensic examinations, “has never
been . . . and cannot be tested, because it varies
from practitioner to practitioner.” (p. 9) [emphasis
added]. In fact, Dr. Bruno–Golden testified that
she “could not recall if she had ever administered
the same test battery” (p. 9) on the thousands of
other patients she evaluated during her career.
The Baxter trial court ruled that the BPA as
employed by Dr. Bruno–Golden cannot be and
has not been tested in this case.
All three neuropsychologists testified that the
BPA methodology employed was not subjected to
peer review, nor described in published articles.
Dr. Bruno–Golden referenced a professional
position paper supporting the application of the
76 forensic neuropsychology
BPA that Dr. Faust noted was not in a peer-
reviewed publication. Dr. Shaheen referred to
many learned treatises on the general acceptance
of the BPA in clinical neuropsychology practice,
yet admitted that Dr. Bruno–Golden’s specific
methodology had not been subject to peer review
or described in published articles. Finally,
Dr. Bruno–Golden admitted she had not previ-
ously used the methodology employed and it was
likely that no other clinician had either. Therefore,
the Baxter trial court found the BPA as employed
in this case had not been subject to peer review
and publication.
No evidence was offered on a known or
potential error rate for the BPA. At one point,
Dr. Bruno–Golden testified that she ignored
standardized instructions regarding time con-
straints on some tests in order to “test the limits”
of the child’s performance. Neither Drs. Bruno–
Golden nor Shaheen offered any evidence on the
reliability of testing the limits. Dr. Faust pointed
out that any variation in the standardized instru-
ctions destroys the normative comparisons of the
child’s performance to like–aged peers, making it
impossible to determine an error rate or interpret
the results. Moreover, although selected individ-
ual tests have known error rates, when Dr. Bruno–
Golden modified the BPA she created what
Dr. Faust described as an “idiosyncratic combina-
tion, if not hodgepodge of multiple influences.”
(p. 11). The court detailed some departures from
standardized techniques. Dr. Faust concluded the
methodology employed was “not scientifically
validated . . . founded on guesswork, speculation,
and conjecture, which sometimes flies directly in
the face of scientific literature.” (p. 11). Hence,
the Baxter trial court ruled the methodology
employed by Dr. Bruno–Golden did not have a
known or potential error rate.
In concluding its analysis, the Baxter trial
court drew a distinction between appropriate
scientific literature for clinical assessment and
“a ‘forensic’ approach to assessing children with
lead poisoning” (p. 13). Dr. Faust described how
the role of the expert neuropsychologist changes
depending on whether a case is a clinical or foren-
sic referral. This important distinction between
the roles of clinical provider and forensic exam-
iner has been frequently described (Greenberg &
Shuman, 1997; Heilbrun, 2001). Although most
authorities agree that clinical and forensic roles
are irreconcilable and every effort should be made
to avoid the dual role (Greenberg & Shuman,
2007), others’ approaches are more situational
(Woody, 2009) and a minority even suggest that
the roles are potentially compatible (Heltzel,
2007). Dvoskin (2002) chastised forensic evalua-
tors as “illogical” and “ignorant” for suggesting
that providing treatment presents some conflict of
interest with the “purity of their objective assess-
ments” (p. 537). In the end, neuropsychologists in
forensic practice should always employ objective
methods that allow them to be unbiased truth–
seekers and must exercise care in all professional
work, not just forensic consulting
The Baxter trial court held that the evidence
overwhelmingly showed that Dr. Bruno–Golden’s
methodology was not sufficiently reliable for
forensic analysis (Desmond, 2007). The trial court
judge found the evidence failed to meet any of
Daubert’s flexible factors. Therefore, the defen-
dant’s motion in limine was granted, Dr. Bruno–
Golden’s testimony was excluded, and the jury
never heard her opinions in the original trial. The
plaintiff appealed and the New Hampshire
Supreme Court certified three questions for
judicial review, asking whether the trial court
erred when excluding: 1) the neuropsychologist’s
testimony based on the Boston Process Approach,
2) the IQ test testimony, and 3) the pediatrician’s
testimony that reasonably relied upon the neuro-
psychologist’s report.
In a thorough analysis of neuropsychological
test administration errors and a unanimous
decision, the New Hampshire Supreme Court
reversed the trial court on the first question and
vacated the subsequent questions as moot. The
Baxter court reasoned, “the Daubert test does not
stand for the proposition that scientific knowl-
edge must be absolute or irrefutable” (citing State
v. Dahood, 2002). Referring to the trial court’s
conclusion, it “focused upon the plaintiff ’s failure
to demonstrate that the specific battery–the entire
series of tests viewed as a whole–employed by
Dr. Bruno-Golden in this case was, or could not
be, tested, was subject to peer review and publi-
cation, or has a known or potential error rate.”
(p. 174). In its review, the court found that the
Daubert factors “do not constitute a definitive
checklist or test” (Kumho Tire v. Carmichael,
1999), but even if they did, “the BPA meets three
of four Daubert factors” (p. 184). The Baxter court
expressly rejected the battery as a whole argu-
ment, finding “that the individual tests he or she
administered as part of the battery, not the battery
as a whole, have been tested, have been subject to
peer review and publication, and have a known or
potential error rate” (p. 184). The Baxter court
 Admissibility of Expert Opinions based on Neuropsychological Evidence
wrote, “we reject the defendant’s assertion that
Dr. Bruno-Golden’s methodology, the BPA as a
flexible battery approach, is not a sufficiently reli-
able methodology to assist the fact finder in under-
standing the plaintiff ’s neuropsychological status.”
(p. 187). The case was remanded back to the trial
court with the instruction to admit Dr. Bruno-
Golden’s opinions that were based on the BPA.
The Baxter court relied, in part, on an amicus
brief (co-authored by Greiffenstein and Sweet)
submitted by the American Academy of Clinical
Neuropsychology (AACN). Justices referred to
the AACN brief frequently during oral arguments,
raising questions about the standard of care for
clinical neuropsychology. In its brief, AACN drew
an analogy between the specialty practices of
clinical neuropsychology and clinical neurology,
arguing that neurologists do not “conduct either
an invariant exam procedure or order an invariant
set of diagnostic tests for each and every patient”
(p. 9). AACN asserted “that administering the
same set of tests to all patients and litigants,
regardless of the known or suspected condition is
uninformed and inappropriate practice” (p. 9).
Further, AACN added “a standardized battery
runs counter to an acceptable standard of care in
neurology” and “we know of no area of specialty
or subspecialty in clinical medicine in which
a routine, invariant battery of tests across all
medical conditions being evaluated would be
acceptable practice” (p. 9).
Although not entirely clear from the brief,
AACN was apparently advocating for a flexible
battery standard of care for clinical neuro-
psychology. The flexible battery approach is the
predominant form of practice, for certain popula-
tions and referral questions, but the fixed battery
method remains a respectable minority practice
in clinical neuropsychology. In what is probably
the best example of the application of Daubert
factors to neuropsychological methodology, the
Baxter case nicely illustrates how federal courts
and a majority of state courts would likely address
questions of admissibility based on battery selec-
tion. Baxter also shows that neuropsychology
is in early stages of addressing complex questions
about standards of care for the profession.
Although the New Hampshire Supreme Court
resolved concerns about the admissibility of flexi-
ble batteries in forensic practice, the Baxter trial
court has not weighed the opposing opinions
because the second trial has not yet been heard
(Hanna, August 8, 2010). Indeed, Baxter has
been delayed by state budget cuts resulting in
77
allegations of unconstitutional delay of justice
(Baxter v. State, 2010).
Application of Symptom Validity Testing
Science in Neuropsychological Evaluations
The application of symptom validity science in
neuropsychology is not new (Benton & Spreen,
1961) and it will not go away. The modern era of
scientific investigation of symptom validity
was introduced with the examination of faking
believable deficits in neuropsychological testing
(Heaton, Smith, Lehman, & Vogt, 1978; Pankratz,
Fausti, & Peed, 1975), but probably began in
earnest after descriptions of symptom validity
testing (SVT) (Pankratz, 1979; Pankratz, Binder,
& Wilcox, 1987). For the past twenty years,
neuropsychology has seen a proliferation of
research designs investigating symptom validity
and an explosion of peer-reviewed scientific
research on malingering. As exemplified in the
Frye, effort to introduce a physiologically based
“deception” test some 85 years ago, there is a
lengthy history of assessment of deception and
malingering in clinical practice detailed elsewhere
(Rogers, 2008). However, the competent forensic
consultant is well advised to carefully compare
and contrast lay opinion about deceit with expert
opinion regarding response bias, effort, and symp-
tom validity. Astute comparisons of symptom
validity with deceit yield a deeper appreciation of
an important boundary between the role of the
expert and the province of the trier–of–fact. The
scientific evidence supporting SVT application in
neuropsychology practice is overwhelming and
widely accepted (Boone, 2007; Larrabee, 2007,
this volume; Morgan & Sweet, 2008).
The application of SVT science in neuro-
psychological evaluations is an increasingly
common practice and a more recent source of
challenge to expert neuropsychological opinions.
The problem of symptom validity and effort test-
ing has become so prominent that professional
neuropsychological associations have published
positions on this topic (NAN, 2005; AACN, 2007)
and the AACN recently convened a conference
(2008) that set forth a Consensus Conference
Statement on the Neuropsychological Assessment
of Effort, Response Bias, and Malingering
(2009). The jurisprudence of SVT science has
been hotly debated in our courts (detailed
below), scientific journals (Butcher et al., 2008;
Ben-Porath, Greve, Bianchini, & Kaufmann,
2009a; Williams, et al. 2009; Ben-Porath, Greve,
Bianchini, & Kaufmann, 2009b), continuing
78 forensic neuropsychology
education workshops (Kaufmann, 2006; 2007;
2009a), and a recent American Bar Association
Conference (Kaufmann, 2009b).
Legal opposition to the application of SVT
science in neuropsychological practice has evolved
over the past decade, with early challenges being
confronted in court (Batzel v. Gault, 2002) and
described in subsequent nonscientific advocacy
writings in legal newsletters (Creager, Shea, &
Larner, 2002), advocacy groups, and blogs. Other
plaintiff attorneys took note and began opposing
SVT admissibility, arguing that experts were
inappropriately engaging in determination of the
truthfulness and credibility of the plaintiff. SVT
science has clearly collided with evidence law and
the burden is on the expert to demonstrate the
reliability and relevance of its application in
neuropsychology, and to present results in testi-
mony that does not intrude upon the province of
the court (Kaufmann, 2009c).
A common tactic used to restrict application
of SVT science is a motion in limine, in which an
attorney asks the court to exclude SVT evidence
from being heard by a jury. In civil cases, motions
to exclude evidence of malingering are most com-
monly filed by plaintiff attorneys, whereas in
criminal cases the defendant is usually seeking to
keep out evidence of malingering. Attorneys are
advancing legitimate arguments regarding the
admissibility of SVT science for consideration by
the court. Although arguments to exclude SVT
science may take a variety of forms, most are
based on the rules of evidence and standards
for expert testimony, asserting that SVT science
is: 1) more prejudicial than probative; 2) confus-
ing, rather than helpful, to the jury; 3) inadmissi-
ble character evidence; 4) inadmissible hearsay
evidence; 5) wrongfully intruding into the prov-
ince of the jury; or 6) not generally accepted by
the relevant scientific community.
The first three arguments rely upon Federal
Rule of Evidence 401 and the definition of
relevance, as follows:
“Relevant evidence” means evidence having
any tendency to make the existence of any fact
that is of consequence to the determination of
the action more probable or less probable than
it would be without the evidence.
Essentially, all relevant evidence is admissible,
unless privileged. However, Federal Rule of
Evidence 403 requires courts to balance other
factors when resolving admissibility.
Although relevant, evidence may be excluded
if its probative value is substantially outweighed
by the danger of unfair prejudice, confusion of
the issues, or misleading the jury, or by consid-
erations of undue delay, waste of time, or need-
less presentation of cumulative evidence.
The judge in Williams v. CSX Transportation,
Inc. (2007) weighed these concerns and deter-
mined that the probative value of the MMPI-2
Symptom Validity Scale (formerly and hereinafter
“FBS”) was outweighed by its prejudicial effect,
commenting that the term “faking bad” was overtly
prejudicial. In balancing the relevance of SVT
science, Williams placed greater weight on the
name of the scale rather that its reliability. Other
Florida judges have disagreed (Nason v. Shafranski,
2008) allowing expert testimony based on FBS,
but restricting use of the term malingering.
Symptom validity science involves system-
atically designed studies using psychometric tests
and sophisticated statistical techniques that are
beyond the ken of most jurors, demonstrating the
need for an expert to assist the trier of fact.
However, if an expert cannot adequately explain
the science and gets drawn into extended testi-
mony about, for example, specificity, sensitivity,
negative predictive value, likelihood ratios, and
other receiver operating characteristic (ROC)
curve analysis, a judge may find such testimony
more confusing than helpful. Although it is very
important for an expert to understand his or her
methodology thoroughly, accurate and compre-
hensive explanation all of the subtle complexities
of a science may not necessarily enhance expert
credibility. Courts may exclude testimony that is
more confusing than helpful to the jury.
The inadmissible character evidence argument
derives from the relevance question from Federal
Rule of Evidence 404, as follows:
Evidence of a person’s character or a trait of
character is not admissible for the purpose of
proving action in conformity therewith on a
particular occasion.
The complicated exceptions to this rule in
criminal cases are beyond the scope of this chap-
ter, but in civil proceedings, character evidence is
generally inadmissible unless character is at issue
(e.g., defamation). An elevated FBS indicates that
the examinee was likely over-endorsing symp-
toms—a fact that a plaintiff attorney can miscon-
strue as the expert calling the plaintiff a fake, a
 Admissibility of Expert Opinions based on Neuropsychological Evidence
fraud, or a liar. One good response to this inten-
tionally inflammatory tactic is to answer in the
negative and simply point out that an elevated
FBS is just one indicator of symptom invalidity
(over-reporting) and allow the jury to draw its
own conclusions.
Some plaintiff attorneys have advocated for
exclusion of SVT science based on the hearsay
rule (Creager, Shea, & Larner, 2002), suggesting
that reliance on another examiner’s test scores
constitutes hearsay data. This argument fails to
recognize the common expert exception to the
hearsay rule, allowing the expert to use such
information reasonably relied upon by experts in
that particular field (Federal Rule of Evidence
703). Hearsay objections are rarely successful in
excluding expert testimony.
Respecting juror conclusions is the basis for
the fifth argument against FBS admissibility.
Judges make decisions about admissibility of
evidence, and generally, juries weigh the credi-
bility of that evidence. In the end, the jury decides
the credibility of the plaintiff ’s claim, not an
expert witness. Experts must express appropriate
opinions within the scope of their expertise
in a manner that is helpful to the jury (Federal
Rule of Evidence 702). However, experts must
not state legal conclusions that potentially invade
the province of the jury. In this regard, Federal
Rule of Evidence 704 is a source of confusion, as
follows:
No expert witness testifying with respect to the
mental state or condition of a defendant in a
criminal case may state an opinion or inference
as to whether the defendant did or did not have
the mental state or condition constituting an
element of the crime charged or of a defense
thereto. Such ultimate issues are matters for the
trier of fact alone.
Some attorneys misapply this rule in civil pro-
ceedings, while others over-extend its reach by
suggesting that experts cannot testify about their
data when those data are directly relevant to a
matter that a jury must decide. In many respects,
the “ultimate issue” rule is abandoned when the
expert witness testimony is demonstrably helpful
to the jury. Expert opinions based on SVT science
are helpful to the jury considering questions of
symptom over-reporting (“fake-bad”) in criminal
and civil proceedings or symptom under-report-
ing (“fake-good”), in child custody disputes or
mental health commitment proceedings.
79
Having addressed the relevance-based argu-
ments used in efforts to exclude SVT science, the
final argument questions the reliability of expert
opinions. Again, the best case examples come
from Florida involving FBS. This strategy for
excluding FBS uses the standards for evaluating
experts as described in section III of this chapter.
Here, the judge plays the key role in determining
reliability of the methods employed by expert wit-
nesses. Briefly, a judge may deny the admission of
evidence in a Frye jurisdiction by simply finding
that the methodology is not accepted in the
relevant scientific community. The judge in
Vandergracht v. Progressive Express (2005) made
such a finding and excluded the MMPI-2 FBS
because there was not “ample evidence that the
test is accepted by his peers.” Surveys of current
SVT science application in neuropsychological
evaluations, not available at the time of the hear-
ing (e.g. Sharland & Gfeller, 2007), would have
effectively addressed the judge’s concern.
Attorneys must be cognizant that zealous
advocacy for their clients should be balanced by
their professional responsibility to exercise candor
before the court. Recent examples of these com-
peting forces, observed in motion practice from
forensic neuropsychology, involve challenges to
the admissibility of the FBS (Vandergracht v.
Progressive Express, 2005; Williams v. CSX
Transportation, Inc., 2007; Davidson v. Strawberry
Petroleum, Inc., 2007; Stith v. State Farm, 2008;
UpChurch v. Broward Co. School Board, 2008;
Limbaugh-Kirker v. Decosta, 2009) and from those
cases that were not successful in excluding such
testimony (Nason v. Shafranski, 2008; Solomon v.
TK Power, 2008). However, the orders in these
Florida cases cannot be neatly categorized. For
example, although the Decosta judge excluded
FBS after a lengthy Frye challenge that was with-
drawn during pretrial motions then re-introduced
at trial, all other SVT evidence was allowed and
the plaintiff was shown to be exaggerating symp-
toms.
In Sharrer & Sharrer v. Sunscape Landscape
Nursery, Inc. et al. (2009), FBS testimony was
excluded, as was all testimony regarding malinger-
ing. The expert neuropsychologist was allowed to
testify about performance validity, defined as the
assessment of whether an accurate measure of
plaintiff ’s actual abilities was obtained. This testi-
mony included discussion of how SVTs are devel-
oped based on simulation and known groups
investigations, showing how simulators as well as
persons with known invalid performance perform
80 forensic neuropsychology
in ways that are atypical for persons with actual
neurologic, psychiatric, or developmental prob-
lems. Although testimony about the FBS was pro-
hibited, testimony was allowed comparing the
plaintiff ’s standard validity and clinical scale pro-
file to various clinical groups (depression, chronic
pain, spinal cord injury, moderate and severe TBI,
and multiple sclerosis) and to a profile of examin-
ees with known invalid performance. The expert
further testified that when a particular examinee
shows multiple SVT failures, it is a strong indica-
tion that test performance is invalid. In such
circumstances, the expert testified that poor per-
formances were, more likely than not, the product
of invalid performance, whereas normal range
scores were likely an underestimate of actual level
of ability. In this fashion, the expert neuropsychol-
ogist was able to effectively communicate that the
plaintiff was producing invalid data, without dis-
closing the assessment of probable malingering
made in the original examination report.
Generally, SVT evidence is not challenged
(Ben-Porath, Greve, Bianchini, & Kaufmann,
2009a), but even when it is, SVT science is
routinely admitted (United States v. Bitton, 2008;
Jackson v. Mason, 2009; Johnson v. Rockwell
Automation, 2009).8 Despite a few isolated Florida
trial court rulings excluding MMPI-2 FBS
(reviewed above), Decosta reflects the shifting
plaintiff tactics that purportedly belie an underly-
ing debate about timing of SVT challenges (Hsieh,
2008). With more recent rulings allowing FBS
into evidence on pre-trial motions to exclude,
plaintiff attorneys have started withdrawing such
motions, only to re-introduce them at trial, a
strategy designed to hamper effective defense of
the motion to exclude. A common impeachment
strategy used at deposition and trial attempts to
examine the expert on each and every item of the
MMPI-2 FBS in an effort to use content of the
items to discredit the expert. These facial attacks
may score short–term gains with the court and/or
jury, if the court allows the plaintiff advocate to
use such a strategy and the expert is ill–prepared.
Recently, experts have successfully used the law to
pre-empt these attacks before they can take place.
Some Florida judges recognize that an item-by-
item cross examination not only wastes the time
of the court and wearies the patience of the jury,
but also that Florida regulation bars release of
psychological test material to nonpsychologists
(Fla. Admin. Code Ann. r. 64B19–18.004(3);
Fla. Admin. Code Ann. r. 64B19–19.005(3)).
In these cases,9 the judge ordered that raw data
and psychological test materials cannot be released
to nonpsychologists. In Sierra, the defense expert
neuropsychologist discovered that the plaintiff
expert released the protected material to the
plaintiff counsel in violation of the judge’s order.
Such action can result in contempt findings and
may raise ethical questions. For more information
regarding the best practice for protecting psycho-
logical test materials see Greiffenstein and
Kaufmann (this volume) and Kaufmann (2005;
2009c). The implications of these Florida FBS
decisions remain hotly debated (Williams et al.,
2009; Ben-Porath, Greve, Bianchini, & Kaufmann,
2009b; Kaufmann, Larrabee, & Bigler, 2010).
However, in response to Hoyt’s (2009) question,
“Is the fake bad scale test here to stay?” the answer
in almost all jurisdictions is a resounding yes. The
same can be said for SVT science in general.
Causation Opinions Beyond the Scope of
Neuropsychological Expertise
Generally, psychologists who conduct assess-
ments testify about tests, test results, and their
interpretation of those results (Buckler v. Sinclair
Refining Co., 1966; Ross v. State, 1980; Executive
Car & Truck Leasing, Inc. v. DeSerio, 1985; Minner
v. American Mortgage & Guaranty Co., 2000).
Nevertheless, psychologists who offer opinions
regarding the physical causes of injury, based on
their assessments, are sometimes challenged, with
most courts conducting a fact-specific inquiry
before recognizing expertise and admitting psy-
chologist opinions. A majority hold that neurop-
sychologists are qualified to render opinions about
the physical causes of brain injury (Kinsey v. King,
1982; Madrid v. Univ. of Ca., 1987; Valiulis v.
Scheffeos, 1989; Fabianke v. Weaver ex rel. Weaver,
1988; Sanchez v. Derby, 1989; Hutchinson v.
American Family Mut. Ins., 1994; Cunningham v.
Montgomery, 1995; Huntoon v. TCI Cablevision,
1998; Landers v. Chrysler Corp., 1998; Adamson v.
Chiovaro, 1998; Bonner v. ISP Technologies, Inc.,
2001; Rustenhaven v. American Airlines, Inc., 2003;
Sanders v. Nike, 2004; Wiles v. Dep’t of Educ.,
2008), though a minority restrict or bar neuropsy-
chologists from rendering causation testimony
(Krevitz v. Savoy Heating and Air Conditioning
Co., 1981; G.I.W. Southern Valve v. Smith, 1985;
Lugo v. Citicorp Mortgage, 1994; Bergeson v. Ray,
1998; In re: Breast Implant Litigation, 1998;
Louderback v. Orkin Exterminating Co., 1998).
Comparing these two sets of decisions shows that
courts tend to admit neuropsychological expert
opinions on causation in car accident TBI cases,
 Admissibility of Expert Opinions based on Neuropsychological Evidence
but more readily exclude causation opinions from
neuropsychologists in cases involving various
toxic exposures. Psychologist expert opinions
about damages are commonly accepted without
challenge, but the court’s differential exclusion of
certain causation opinions seems reasonably
based on the neuropsychologist’s insufficient
expertise in toxicology. Expert neuropsychologist
opinions about causation are also excluded when
relying on untested or unproven technologies,
for example, QEEG (In re: Breast Implant
Litigation, 1998; John v. Im, 2002). When neurop-
sychologists offer opinions that fall within their
scope of expertise, courts generally allow causa-
tion testimony.
A resurgent minority have found that neuro-
psychologists offering opinions about the physical
causes of injury are operating outside the scope of
psychology practice (John v. Im, 2002; Grenitz v.
Tomlian, 2003; McCarthy v. Atwood, 2005;
Guzman v. 4030 Bronx Blvd. Assoc. L.L.C., 2008).
In Grenitz, the Florida Supreme Court confronted
the scope of neuropsychology practice when an
expert, Barry Crown, PhD, ABN, proffered opin-
ions that Jacob Tomlian’s brain damage “was
brought about by an oxygen deprivation experi-
ence at the intrapartum level or in the neonatal
period” (p. 1003). Although this medical mal-
practice case was complicated by a statutory
change in the definition of psychology practice
that took place during the pendency
of the appeal, Dr. Crown’s testimony illustrates
an important boundary of neuropsychologist
expertise, as follows:
Q: [Plaintiff ’s counsel]. Can you rule out injury
occurring during the 24- to 34-week period?
A: [Dr. Crown]. Yes, to the extent that—that
his functioning includes those aspects of the
brain that are the last to develop; and, in fact,
his highest score on object assembly involves
that kind of visual motor processing, yes.
Q: As a neuropsychologist, how can you
do that?
A: As I said, there are functions that were tested
that he scored—Actually, his highest score on
one test was in that area, and that’s the last area
of the brain that actually develops.
Q: Do you have an opinion within a reasonable
degree of neuropsychological probability as to
whether Jacob sustained a hypoxic injury at the
24- to 34-week period?
81
A: I believe that it was after that.
Q: And the basis for that opinion, sir?
A: The basis is that there appears to be an intact
brain based on neuropsychological function-
ing, that there wasn’t a delay in total brain
development, and that, in fact, rather than a
delay, there’s an impairment and that would
have come much later in the process.
Q: More likely than not was Jacob’s injury—did
Jacob’s injury occur during the intrapartum
period when Dora was at Bennett Hospital on
May 11th?
A: Yes. (p. 1011–1012).
After analyzing the scope of psychology practice
under the statute, the Court concluded “Thus, the
neuropsychologist was permitted to testify with
regard to the etiology (brain damage) of the
behavior he evaluated. He should not have been
permitted to testify as to the medical causation of
the organic brain damage itself ” (p. 1003). Despite
a split opinion on some issues, the Court unani-
mously noted that Dr. Crown exceeded his area of
expertise with the dissent writing ‘the field of
psychology being related to behavior, and behav-
ior is not studied or known in utero.’ The dissent
reasonably argued any error introduced by
Dr. Crown’s testimony was harmless because both
parties presented expert testimony of pediatric
neurologists on the causation question. In the
end, the plaintiff ’s neurologist expert was appar-
ently persuasive, with the jury finding the hospital
(85%) and obstetrician (15%) negligent and
awarding the plaintiff $30 million–the largest
medical malpractice verdict awarded in Broward
County, Florida (Tomlian v. Grenitz, 2008).
Despite what some may view as a setback for
neuropsychologist causation opinions, even
Grentiz disagreed with a “categorical rule that a
neuropsychologist can never testify as to the cause
of organic brain damage” (p. 1010). Based on cur-
rent jurisprudence in this area, courts are much
more willing to admit neuropsychologist brain
injury causation testimony in TBI car accident
cases.
Experts Unqualified to Render
Neuropsychological Opinions
Some courts have excluded physicians from
rendering expert neuropsychological opinions
(see proffered testimony of Kaye Kilburn, MD in
Downs v. Perstorp Components, Inc., 1999; Goeb v.
82 forensic neuropsychology
Tharaldson, 2000; Ellis v. Appleton Papers, Inc.,
2006). However, most courts follow the general
rule that “any person whose profession or voca-
tion deals with the subject at hand may testify as
an expert” (Hagen v. Swenson, 1975, p. 162).
A New York judge held that selected social work-
ers were qualified to offer expert neuropsychologi-
cal opinions, finding the practice of psychology
and social work “wholly equal and the same”
(People v. R.R. & G.A., 2005, p. 544). Ultimately,
most courts admit neuropsychologist expert testi-
mony and the value of expert evidence is addressed
under cross examination and weighed by the jury.
In criminal litigation involving questions of
mental illness, psychologists are recognized as
experts in matters of competence, insanity,
criminal culpability, and mitigation, with few
exceptions.10 Although the modern trend toward
broader recognition of neuropsychologist expert
opinions in criminal cases is apparent, isolated
courts may still apply the traditional rule that only
physicians can offer expert medical testimony.
Courts remain cautious about the science of
brain-behavior relations and are skeptical about
its application to resolve cases and controversies
(Brown & Murphy, 2010; Pardo & Patterson, 2010;
Appelbaum, 2009; Khoshbin & Shahram, 2007;
Pettit, 2007; Keckler, 2006; Morse, 2006, Redding,
2006; Kulynych, 1997). Although many judges
may be ignorant of the science, they rightfully
are concerned with balancing the probative value
of neuropsychological evidence against its preju-
dicial effect, while being mindful of the risks
associated with juror confusion (Fed. R. Evid.
403). Criminal courts cannot resolve long-stand-
ing philosophical debates about free will and
determinism; such matters are nonjusticiable
issues. However, even though the jurisprudence
of neuropsychological expertise in criminal litiga-
tion is not as long as other mental health experts,
nor as well developed, judges increasingly admit
the brain–behavior science of neuropsychologist
experts into their courts.
Although the rules of evidence for expert wit-
nesses apply in civil and criminal litigation, pro-
cedural rules and burdens of proof are markedly
different. In civil proceedings, the plaintiff must
prove its case with a “more likely than not” pre-
ponderance of the evidence, whereas in criminal
cases the state carries a much heavier burden to
prove guilt beyond a reasonable doubt. Careful
analysis of modern jurisprudence shows the piv-
otal role of the neuropsychologist expert in assist-
ing the trier of fact to understand the mental
condition of a defendant as it may relate to con-
siderations of competence, insanity, culpability,
and mitigation. Before considering the current
and continuing application of neuropsychology in
criminal litigation, it is important to understand
some basic concepts of criminal law, and some
rules of evidence and procedure in criminal
proceedings. In criminal litigation, competency
must be distinguished from the affirmative defense
of insanity in order to understand admissibility
standards for neuropsychological evidence.
In 1899, the Sixth Circuit determined that the
Fourteenth Amendment due process clause pro-
hibited criminal proceedings against a mentally
incompetent person (Youtsey v. United States,
1899). Although history provides different defini-
tions of insanity that are reviewed elsewhere
(Denney, chapter addressing criminal responsi-
bility in the current volume; Denney & Sullivan,
2008), after John Hinckley shot President Ronald
Reagan, his Press Secretary James Brady, and two
law enforcement personnel, Congress changed
the federal standard for an insanity defense,
heightening the defendant’s burden of proof. The
Insanity Defense Reform Act (IDRA) places the
burden on the defendant to prove that he or she
was unable to appreciate the “nature and quality
or the wrongfulness” of his or her acts as a result
of a “severe mental disease or defect” at the time
of the crime (18 U.S.C. § 17). In order to meet this
burden, the defendant must present clear and
convincing evidence11 (§ 17(b)). In contrast, the
test for competency is whether the party has “suf-
ficient present ability to consult with his lawyer
with a reasonable degree of rational understand-
ing—and whether he has a rational as well as fac-
tual understanding of the proceedings against
him” (Dusky v. United States, 1960, p. 402). Thus,
while insanity is relevant only to the time of the
crime, competency is relevant throughout the
entire legal proceeding, including understanding
of Miranda warnings, entry of a plea, waiver of
counsel, nature of trial proceedings, and punish-
ments. Consequently, the consulting expert must
understand the rules governing and distinguish-
ing competence and the insanity defense.
RU L E S G OV E R N I N G
COMPETENCY
AND THE INSANITY
DEFENSE IN CRIMINAL
PROCEEDINGS
Generally, prohibitions against subjecting an
incompetent person to trial extend from arrest
 Admissibility of Expert Opinions based on Neuropsychological Evidence
until imposition of the sentence (18 U.S.C. § 4244;
United States v. Johns, 1984). Retrospective com-
petency determinations, although disfavored,
may be conducted provided that a meaningful
hearing of the issue remains possible (p. 957).
Moreover, the issue of a criminal defendant’s
mental capacity to proceed may be raised at any
stage of the litigation (Howard v. State, 1985),
whether by the defense, the government, or the
court (State v. Broom, 1995).
Once competency is placed at issue, the defen-
dant constitutionally is entitled to a hearing (Pate
v. Robinson, 1966). Competency hearings do not
determine whether the defendant is competent,
but rather whether there are reasonable grounds
for the court to believe that the defendant may be
incompetent (Calloway v. State, 1995). However,
the mere fact that a defendant is pleading not
guilty by reason of insanity does not require the
court to order a competency hearing (State v. Lee,
1983). The fact that competency has been put in
doubt also does not require the court to order a
mental examination (State v. Clemons, 1997).
A defendant must file pretrial motions if
planning to introduce expert testimony relating
to a mental disease or defect, or to any other
mental condition bearing on the issue of guilt
(Fed. R. Crim P. 12.2(b)). However, the court
may, in its discretion, allow a defendant to file
notice of intent to rely on the insanity defense at a
later time (Fed. R. Crim P. 12.2(a)). There is
a split of authority12 as to whether the Rule 12.2(b)
notice is sufficient for the court to order a mental
examination (United States v. Banks, 1991) or
whether the defendant expressly must place
competency at issue or file intent to rely on the
insanity defense (United States v. Marenghi, 1995).
These jurisdictional variations yield different
defense strategies. For example, a defendant who
claims the presence of a mental condition negates
an element of the crime may not necessarily be
required to undergo a state mental examination.
In some jurisdictions, the defendant may present
expert testimony about his or her mental condi-
tion without being required to undergo an inde-
pendent examination by the state, so long as that
defendant has not placed competency or insanity
at issue.
Recognizing that competency to proceed can
be raised by either party or the court at any stage
of the proceedings, competency may become an
issue at the time of issuance of Miranda warnings,
entry of a plea, standing trial, sentencing, and
punishment.
83
Miranda Warnings
Waiver of the Fifth Amendment right to remain
silent raises the first issue of competency, in that
such waiver must be made “knowingly, voluntarily,
and intelligently” (Miranda v. Arizona, 1966, p.
444). Moreover, waiver of the Sixth Amendment
right to consult with an attorney must use the
same standard and the right to counsel can be
invoked at any time during the proceeding. Indeed,
the government has a high burden to show com-
petent waiver if they intend to use statements
made by a suspect during custodian interrogation
conducted in the absence of an attorney (p. 503).
However, that governmental burden does not nec-
essarily require an express written or oral state-
ment of waiver (North Carolina v. Butler, 1979).
Entry of a Plea
Competency to enter a plea applies the afore-
mentioned Dusky “sufficient present ability”
standard. No higher standard of competency
applies to entry of a plea than that which is
required for standing trial (Miles v. Stainer, 1997).
However, if evidence presents a substantial
question of the defendant’s sanity at the time of
the offense, then the court must assure that the
defendant: 1) is fully availed of alternative pleas,
2) comprehends the consequences of failing to
assert an insanity defense, and 3) exercises a free
choice (Frendak v. United States, 1979). Further,
even if counsel indicates that the defendant
waives a viable insanity defense, the court must
ascertain through independent inquiry that
waiver is voluntary and intelligent before such
waiver can be accepted (People v. Gettings,
1988). Finally, defendants pleading not guilty by
reason of insanity must be advised of the likeli-
hood of involuntary commitment for mental
illness if the plea is successful (Morrison v. United
States, 1990).
Stand Trial
The Dusky “sufficient present ability” test of com-
petency involves the defendant’s ability to com-
municate with his attorney and to understand the
nature of the proceedings. Stated alternatively, it is
fundamental to our system of criminal justice to
prohibit subjecting to trial a person whose “mental
condition is such that he lacks the capacity to
understand the nature and object of the proceed-
ings against him, to consult with counsel, and to
assist in preparing his defense” (United States v.
Renfroe, 1987, p. 766). The capacity to assist in
preparing a defense includes understanding court
84 forensic neuropsychology
procedures and roles (accused person, attorneys,
judge, jury), and the ability to recall relevant
events, produce evidence, testify, confront hostile
witnesses, and project a sense of innocence (Drope
v. Missouri, 1975, p. 172). Essentially, incompetent
persons are not really present in the courtroom,
even though they physically appear.
Punishment
Although the basic premise that insane individu-
als should not be punished while “insane” applies
to all punishments (18 U.S.C. § 4245(e)), it is
rarely invoked except for execution. In yet another
inherently confusing choice of terminology, here
the term insane actually refers to competency to
face execution. The Eight Amendment prohibi-
tion against cruel and unusual punishment bars
execution of insane individuals (Ford v.
Wainwright, 1986), and also is prohibited under
state laws. However, the standard for legal insan-
ity applied to execution is not the same as suffer-
ing from a mental illness (Billiot v. State, 1995).
Although intelligence is a relevant factor that
courts must weigh, mental impairment and brain
damage (Shaw v. Delo, 1992) do not preclude exe-
cution necessarily, so long as the inmate possesses
the mental awareness required for execution. In
some jurisdictions, sufficient competence for exe-
cution only requires that the defendant under-
stand execution proceedings, know that it is a
punishment, and appreciate why he is being pun-
ished (Rector v. Clark, 1991).
Individuals with mental retardation can be
found competent to stand trial, yet a death sen-
tence does not pass Constitutional muster and is
barred as cruel and unusual punishment under
the Eighth Amendment (Atkins v. Virginia, 2002).
The Court reasoned that individuals with mental
retardation have diminished capacity that reduces
their personal culpability. Similarly, the Court has
held states cannot impose the death penalty on
juveniles under the age of eighteen years (Roper
v. Simmons, 2005), due to the diminished cul-
pability of psychological immaturity. Capital pun-
ishment is reserved for those offenders who
commit the most serious crimes and the death
penalty is only for those whose extreme culpabil-
ity makes them “the most deserving of execution”
(Atkins, p. 319).
THE INSANITY DEFENSE
REFORM ACT
A small minority of jurisdictions abolished the
insanity defense by statute (State v. Beam, 1985;
State v. Korell, 1984). There is no fundamental
Constitutional right to assert an insanity defense,
even in capital murder cases (State v. Card, 1991).
However, such statutes do not preclude all consid-
erations of a defendant’s mental state during
criminal proceedings. Courts have acknowledged
the “constantly shifting adjustment” of tension
between the “evolving aims of the criminal law
and changing religious, moral, philosophical, and
medical views of the nature of man” (p. 1085).
Uncertainty regarding the proper treatment of the
criminally insane has resulted in wavering stan-
dards and inconsistent application by our courts.
After Hinkley, Congress passed IDRA defining
the circumstances when an “otherwise culpable
defendant is excused for his conduct because of
mental disease or defect” (18 U.S.C. § 17), but it
does not limit evidence offered to negate specific
intent13 (United States v. Frisbee, 1985, p. 1220).
Under IDRA, evidence of mental abnormality
proving lack of mens rea14 is admissible, although
such evidence cannot be used to prove diminished
responsibility or diminished capacity (United
States v. Pohlot, 1987). Although “persistent con-
fusion” remains in the application of terms like
diminished responsibility and diminished capac-
ity in determining guilt, IDRA attempted to care-
fully delineate the proper use of mental health
evidence as it relates to legal excuse and criminal
culpability (United States v. Cameron, 1990).
Cameron summarized how IDRA altered the
use of mental health evidence in federal criminal
trials, as follows: 1) eliminated the volitional
“diminished capacity” element of the insanity
defense (§ 17(a)), 2) eliminated all other affirma-
tive defenses or excuses based on mental disease
or defect (§ 17(a)), 3) required the defendant to
show clear and convincing evidence of insanity
(§ 17(b)), 4) limited the use of expert psycholo-
gical testimony regarding ultimate issues (Fed. R.
Evid. 704(b)), and 5) linked a “not guilty by reason
of insanity” verdict directly to federal civil com-
mitment proceedings (§ 4242(b)). Notwithstand-
ing the statutory language or congressional intent
behind IDRA, federal courts have struggled with
statutory interpretation and its application to
criminal cases (Cameron, p. 1062).
Cameron suggested that federal court decisions
are erratic with no less than three approaches
to diminished capacity. Some courts view “dimin-
ished responsibility” and “diminished capacity” as
interchangeable terms meaning that mental
health evidence will be admitted on the issue of
specific intent. Other courts agree the terms are
 Admissibility of Expert Opinions based on Neuropsychological Evidence
interchangeable, but they contend that such desig-
nations do not narrow the use of psychiatric evi-
dence solely to the question of specific intent. This
second group applies both terms “to excuse, miti-
gate, or lesson the defendant’s moral culpability”
due to “psychiatric compulsion or inability or fail-
ure to engage in normal reflection” (p. 1062).
Essentially, this approach views these diminish-
ments as a partial legal excuse. Finally, other courts
distinguish diminished responsibility and dimin-
ished capacity. They claim that only diminished
capacity aims at negating specific intent, while
diminished responsibility refers to showing that
“the accused suffered from an abnormality of mind
that substantially impaired his mental responsibil-
ity” (p. 1062). Current jurisprudence on these mat-
ters remains unsettled.
Modern neuroscience and neuroimaging
technology are adding to the confused jurispru-
dence of diminished capacity, in the form of the
neuropsychological signs and symptoms collec-
tively described as frontal lobe syndrome. Frontal
lobe syndrome has given rise to the frontal lobe
defense (FLD) in criminal cases (State v. Rogers,
2000), which some predict will play an increasing
role when representing brain-injured defendants
(Redding, 2006). A New York Times article (Rosen,
2007) proclaimed, “Neuroscientific evidence will
have a large impact not only on questions of guilt
and punishment, but also on the detection of lies
and hidden bias, and on the prediction of future
criminal behavior.” A subsequent Lexis search15
revealed that functional magnetic resonance
imaging (fMRI) findings have been raised, but
not yet admitted in a U.S. criminal trial, even as
some speculate the threat of neuroimages has
prompted more favorable plea agreements (Rosen,
2007). Popular media increasingly speculates
about how neuroimaging may be “redefining
criminal culpability” (Haederle, 2010). These
“Orwellian” theories of brain function and neu-
roimaging techniques are already appearing in
legal cases, as scientists produce enhanced brain
images that are dramatically highlighted with vivid
hues indicating areas of heightened or suppressed
brain activity. Some legal scholars and commenta-
tors agree that the influence of neuroimaging is
bound to spread and may threaten the underpin-
nings of criminal law, even as most predict that the
law will continue to hold individuals accountable
for wrongful conduct (Erickson, 2010).
However, expert opinions based on functional
neuroimaging may be used to by either party to a
dispute. India is the first country to convict a
85
defendant accused of murder, relying in part on
neuroimaging EEG technology.
In June 2008, police in Maharashtra, India,
took 24-year-old student Aditi Sharma into
custody as a suspect in the murder of her
former fiancé, Udit Bharati. Sharma and Bharati
had been living together in Pune when Sharma
met another man and eloped with him to Delhi.
The following year, Sharma returned to Pune,
where, according to prosecutors, she asked
Bharati to meet her at a McDonald’s and laced
his food with arsenic. Bharati died from the
poisoning. Sharma insisted she was innocent.
Police read Sharma her rights and asked
her to sit for a brain imaging test. Sharma
agreed to the test. Officers strapped her onto a
high-tech gurney and fastened electrodes to
her head. The sensors measured electrical
brainwaves in response to targeted stimuli.
Investigators read Sharma first-person state-
ments that corresponded to their theory of the
crime, as well as neutral statements to help the
software distinguish between Sharma’s actual
remembrance and her normal cognition.
Sharma said nothing in reply, but the sensors
were able to measure and display her brainwave
patterns to confirm that she knew some of the
statements were true and that some were false.
“I bought arsenic,” they said. And, “I met Udit at
McDonald’s.” For an hour, Sharma did nothing.
But the parts of her brain where memo-
ries are thought to be stored lit up on the screen
when she heard these statements. At the
murder trial, the brain scans were admitted
into evidence. These neuroscientific test results
persuaded Judge S.S. Phansalkar-Joshi that
Sharma had “experiential knowledge” of having
committed the murder. Sharma was convicted
and sentenced to life in prison.16
In a second case from England alleging
Munchausen by proxy, fMRI data were admitted
in an effort to bolster the innocence of a female
caretaker accused of poisoning a child (Spence
et al., 2008). The interested reader is directed to a
series of papers published after a Neuroscience,
Law & Government Conference (Moriarty,
2008).17
Although a number of investigators believe
neuroimaging used in conjunction with neuropsy-
chological techniques may be applied increasingly
to assist the trier of fact (Bigler, 2001), courts are
cautious about admitting expert testimony based
86 forensic neuropsychology

on neuroimages (also see the chapter on neuro-
imaging by Ricker in the current volume). The fail-
ure of magnetic resonance imaging (fMRI) lie
detection science under Daubert was predicted
because of the gap between experimental findings
and practical application (Alexander, 2006).
Alexander’s prediction has been vindicated in
U.S. courts thus far. In March, 2009, an attempt to
admit fMRI images to bolster claims of innocence
was withdrawn in a San Diego County case with
sealed records alleging sexual abuse of a minor.
Figure 3.2 provides an excerpt from the No Lie
MRI report. More recently, fMRI lie detection has
failed to meet the judicial standards under Frye in
New York state courts (Wilson v. Corestaff Services,
2010) and under Daubert in a Tennessee federal
court (United States v. Semrau, 2010). Despite
these rebuffed attempts to admit expert opinions
based on fMRI neuroimaging, civil plaintiffs and
criminal defendants are likely to persist in efforts
to use newly emerging functional neuroimaging
technology to bolster claims. Admission of expert
testimony based on functional neuroimaging,
when used to evaluate witness credibility, would
likely draw challenges under the First, Fourth,
Fifth, Sixth, Seventh, and Fourteenth Amendments
of the U.S. Constitution.
Even the most enthusiastic promoters of the
legal applications of functional neuroimaging
currently urge caution when using such evidence
in criminal cases, because the scientific basis for
such is very limited, as follows:
. . . the role of FLD in violent behavior, a note of
caution must be sounded. These studies, still
relatively few in number, often include only a
small number of subjects, lack control groups,
or find ‘considerable overlap between the values
of patient and control groups in studies of the
size, shape, or metabolic activity of different
brain regions.’ Moreover, to date, there are no
standard criteria available for differentiating
between normal and abnormal scan results or
for quantifying the extent of brain damage.
(Redding, 2006, p. 63)
Others are less diplomatic in their criticism of
neuroimaging evidence, suggesting that “brain
overclaim syndrome”18 often afflicts those enam-
ored by fascinating new theories in the neurosci-
ences (Morse, 2006). Morse concludes, “brains do
not commit crimes, people commit crimes”
(p. 397), seemingly unconvinced they are materi-
ally the same and absolutely unwilling to yield
personal accountability under the law in what he
describes as a “fundamental psycholegal error”
(p. 397). Prominent cognitive neuroscientists have
started to address these questions, asking,
Should psychopaths, a group that makes up
about 20% of our high-security male prison
population, be considered as suffering from
a brain disorder that prevents them from
forming an empathetic response and under-
standing (even comprehending) the feelings of
others? If so, do we want to excuse them under
insanity or diminished capacity doctrines and
thereby judge them as exculpable and let them
go? Do we want the state to house them
in a different kind of facility? The issues seem

FIGURE 3.2: Published excerpt from No Lie MRI report recently contemplated, then withdrawn, from a
San Diego County child custody dispute, illustrating how physiologically based Lie Detection technology is
fundamentally different than the application of SVT science in neuropsychological evaluations.
To illustrate how SVT science is not attempting to detect lies or discern truth as noted above.
Contrast to common language usage of SVT science in neuropsychological evaluation.
“Three independent examiners conducted three separate MMPI-2 administrations that demonstrated profound response bias consistent
with symptom exaggeration. All evaluations demonstrated a pattern of symptom reports that are essentially never seen, except in patients
who are seeking compensation in litigation. Other embedded measures were consistent with exaggerated memory complaints. Reanalysis
of existing neuropsychological raw data demonstrate multiple indications of atypical performance and suboptimal effort during three
neuropsychological evaluations.”
 Admissibility of Expert Opinions based on Neuropsychological Evidence
endless. We are at a major crossroads.
(Gazzaniga, 2008)19
Workshops at professional conferences are begin-
ning to address these vexing ethical, legal, and
social questions (Kaufmann & Wagner, 2010;
Blair, 2010; Morse, 2010), even as the scientific
literature expands rapidly. Legal commentary
continues to identify the “well intentioned, but
misguided reductionism” (Brown & Murphy,
2010, p. 1191) of those who “seem all too willing
to accept a view of personhood that invariably
trivialized the ability of individuals to exert con-
trol over their own behaviors, in favor of one
which reduces humanity to the indiscriminate
ebb and flow of chemicals between neurons”
(Erickson, 2010, p. 33). Although neuroscientists
may view a person and their brain as one and the
same for scientific investigation, such a perspec-
tive is irrelevant to criminal law because describ-
ing physiology that may provide explanation of
multifactorial causes does not excuse conduct.
Nevertheless, Brown and Murphy (2010) include
an appendix “checklist for judges confronted with
functional neuroimaging evidence” in full antici-
pation “that the validity and probative value of
fMRI will improve in the future” (p. 1207).
Definition by exclusion is another way to grasp
diminished capacity–by distinguishing it from
competency and insanity. Unlike a finding of
incompetency, diminished capacity does not delay
criminal proceedings, nor is it an affirmative
defense. However, even when a defendant, who is
found competent to stand trial, fails to show clear
and convincing evidence of insanity, or cannot
prove that diminished capacity negated the mens
rea component of a crime, his mental condition
may still be relevant in mitigating punishment.
Consequently, when the battle of neuropsycholo-
gists experts does not yield a favorable verdict for
the defendant, testimony used by the defense to
argue incompetence, insanity, or diminished
capacity may be resurrected to reduce a sentence
or avoid the death penalty.
In light of these complex, inconsistent, and
confusing legal standards, how can neuropsychol-
ogists provide meaningful expert testimony to
assist the trier of fact in resolving guilt or inno-
cence? Knowing the differing legal standards for
insanity and competency in the relevant jurisdic-
tion is essential for neuropsychological consulting
on criminal cases, but such understanding is moot
if the clinical neuropsychologist fails to appreciate
and fulfill the requirements for recognition as an
87
expert and rendering expert testimony to the
court. Therefore, the next section will take the rel-
evant case law and rules governing experts, sum-
marized in the third section of this chapter and
apply them to a recently resolved federal case,
challenging the scope of a neuropsychologist’s
expertise.
A P P L I C AT I O N O F
A D M I S S I B I L I T Y S TA N D A R D S
IN A CRIMINAL CASE
United States v. Jose Santos-Bueno (2006) illus-
trates the current standards of admissibility for
neuropsychological evidence as applied in a fed-
eral criminal case. Here, the government filed a
motion in limine, to exclude the expert testimony
of a neuropsychologist regarding the impact of a
brain injury on the defendant’s cognitive abilities.
Mr. Santos-Bueno was charged with transport-
ing illegal aliens in violation of the Immigration
and Nationality Act (8 U.S.C. § 1324(a)(1)(A)(ii)).
The defense introduced expert neuropsychologist
testimony to rebut the government’s evidence that
Mr. Santos-Bueno formed the requisite mental
state to commit the crime. The neuropsychologist’s
testimony challenged “the accuracy and reliability
of inculpatory statements” made by the defendant
to law enforcement following his arrest (p. 2).
Essentially, the defense asserted that Mr. Santos did
not have the requisite state of mind to infer that
passengers were aliens and that he was excessively
vulnerable to suggestions during questioning, due
to his cognitive disabilities. The government sought
to exclude the expert testimony on three grounds:
1) preclusion under IDRA, 2) insufficient reliability
and relevance under Fed. R. Evid. 702 and Daubert,
and 3) probative value of the expert testimony is
outweighed substantially by its potential to mislead
and confuse the jury under Fed. R. Evid. 403.
Pleading in the alternative, the government also
sought to have their own expert examine the defen-
dant under Fed. R. Crim. P. 12.2(c)(1)(B),20 should
the court decide to admit the defense expert.
Federal court authority to review this motion
derives, in part, from Fed. R. Evid. 104
(a) Preliminary Questions of Admissibility, and
(b) Relevancy Conditioned on Fact, as follows:
(a) Preliminary questions concerning the
qualification of a person to be a witness,
the existence of a privilege, or the
admissibility of evidence shall be
determined by the court, subject to the
provisions of subdivision (b). In making
88 forensic neuropsychology
its determination it is not bound by the
rules of evidence except those with respect
to privileges.
(b) When the relevancy of evidence
depends upon the fulfillment of a
condition of fact, the court shall
admit it upon, or subject to, the
introduction of evidence sufficient to
support a finding of the fulfillment of the
condition.
As the gatekeeper of admissibility as outlined
under Daubert, the Honorable Judge F. Dennis
Saylor conducted a pre-trial evidentiary hearing
and rendered an opinion on January 5, 2006.
In analyzing the statutes and evidence, Judge
Saylor concluded that only two of four elements
of 8 U.S.C. § 1324(a)(1)(A)(ii) were at issue, that
is: 1) Did Mr. Santos-Bueno act “knowing or in
reckless disregard of the fact that an alien has
come to . . . the United States in violation of
law” and 2) Did Mr. Santos-Bueno act “willfully in
furtherance of the alien illegal presence” in the
United States? (p. 11). The government attempted
to prove these two elements and the defense was
to rely on the testimony of an expert neuropsy-
chologist to rebut their proof. David Gansler,
PhD, ABPP-CN offered testimony that Mr. Santos-
Bueno suffered a brain injury six months before
the crime, which caused persistent and significant
cognitive deficits. Dr. Gansler was prepared to tes-
tify people with defendant’s condition “are known
to be vulnerable to suggestion” (p. 10). The defense
argued that statements allegedly made by Mr.
Santos-Bueno during a police interview were
unreliable and untrue. In evaluating the admissi-
bility of this testimony, Judge Saylor asked whether
such evidence is: 1) precluded under IDRA,
2) admissible under Rule 702 and Daubert, and
3) excluded under Rule 403.
Neuropsychologist Testimony
not Precluded by the Insanity
Defense Reform Act
The Insanity Defense Reform Act provides an
affirmative defense when showing clear and con-
vincing evidence of insanity (IDRA at §17), but
precludes “the use of non-insanity” psychiatric
evidence pointing toward exoneration or mitiga-
tion of an offense (United States v. Cameron, 1990,
p. 1066). Congress intended to preclude “dimin-
ished capacity” testimony by restricting the use of
defendant’s supposed “psychiatric compulsion or
inability or failure to engage in normal reflection”
(p. 1061). However, the IDRA does not preclude
the use of such evidence “to negate a requisite state
of mind” that is an element of the alleged criminal
offense (United States v. Schneider, 1997, p. 201).
Some appellate courts admit diminished capacity
testimony only for “specific intent” crimes, because
it is difficult or rare that a mental condition could
negate a “general intent” requirement (United
States v. Santos-Bueno, 2006, p. 14). However,
there is no agreement whether transportation of
illegal aliens is a specific or general intent crime,
nor did the defense attempt to use this distinction.
Rather, the defense simply asserted that
Mr. Santos-Bueno did not have the required
mental state because he did not draw the neces-
sary inferences that the van passengers were
illegal aliens. Consequently, the court held that
the IDRA simply did not apply to the neuro-
psychologist’s expert opinions.
Neuropsychologist Testimony
meets Daubert and Rule 702 Standards
for Admissibility
Next, the court turned to Daubert and Fed. R.
Evid. 702, which codifies the requirements for
admissibility of expert testimony in federal courts.
District courts have broad gatekeeping discretion
in this inquiry—a process of evaluating the
reliability and relevance of expert testimony
(Kumho Tire Co. v. Carmichael, 1999, p. 141).
Courts may use a flexible approach and enjoy
“substantial discretion” in determining whether
to admit or exclude expert testimony (General
Electric Co. v. Joiner, 1997). Although the govern-
ment neither challenged the scientific reliability of
the evidence nor Dr. Gansler’s qualifications to
conduct an appropriate evaluation or render an
expert opinion, the court must conduct a prelimi-
nary assessment.
Reliability of Neuropsychologist
Testimony
In Daubert, the Supreme Court determined that
Fed. R. Evid. 702 superseded the holding in Frye v.
United States (1923) and set a new standard for
admissibility of novel scientific evidence. Federal
rules allow expert testimony “if scientific, techni-
cal, or other specialized knowledge” will assist the
trier of fact (p. 589). Rule 702 provides that a wit-
ness may qualify as an expert based on “knowledge,
skill, experience, training, or education.” However,
courts must evaluate expert testimony and an
expert may testify only if: 1) the testimony is based
upon sufficient facts or data, 2) the testimony is the
 Admissibility of Expert Opinions based on Neuropsychological Evidence
product of reliable principles or methods, and
3) the witness applied the principles and methods
reliably to facts in the case (Fed. R. Evid. 702).
Although declining to establish a definitive
checklist, the Court examined whether the theory
and methods used: 1) were generally adopted by
the scientific community (Frye “general accep-
tance” test), 2) were subject to peer review and
publication, 3) can be or have been tested, and
4) have a known and acceptable error rate
(Daubert, p. 597).
Although the government evidence did not
challenge the scientific reliability of the neuro-
psychological evaluation, Judge Saylor concluded
that “the reasoning and methodology applied by
Dr. Gansler in drawing conclusions” appears reli-
able (Santos-Bueno, p. 24). Dr. Gansler’s reliance
on standardized psychological tests, for example,
the Wechsler Adult Intelligence Scale–III,
although not infallible, as a tool for assessing cog-
nitive function “is not seriously disputed in this
case” (p. 24). Accordingly, the court held that
Dr. Gansler’s testimony regarding cognitive abili-
ties were reliable sufficiently under Daubert and
Rule 702, and were not excluded.
Relevance of Neuropsychologist
Testimony
In addition to Fed. R. Evid. 702 governing expert
testimony, the criminal court also addressed
Fed. R. Evid. 704, as follows:
No expert witness testifying with respect to the
mental state or condition of a defendant in a
criminal case may state an opinion or inference
as to whether the defendant did or did not have
the mental state or condition constituting an
element of the crime charged or of a defense
thereto. Such ultimate issues are matters for the
trier of fact alone.
Here, all parties stipulated that Dr. Gansler may
not offer any opinions on whether Mr. Santos-
Bueno “actually knew (or recklessly disregard
[ed])” that the van passengers were illegal aliens
(p. 23). However, because the defense offered
Dr. Gansler’s opinion only in rebuttal to the
government’s proof of actual knowledge, Rule 704
does not apply.
While conceding the reliability of neuro-
psychological methodology, the government chal-
lenged the relevance of the neuropsychological
evaluation and expert testimony about cognitive
abilities. In addition to arguing that the cognitive
89
abilities of defendant were irrelevant, the balanc-
ing of relevance was the more essential analysis
under Daubert and the Federal Rules. As such, the
Santos-Bueno court asked whether the probative
value of the expert testimony “to the extent that
any exists—is substantially outweighed by its
potential to mislead or . . . confuse the jury”
(p. 23). However, this legal analysis also relies, in
part, on Fed. R. Evid. 403.
Neuropsychologist Testimony Does not
Mislead or Confuse the Jury
Although a court may find neuropsychological
evidence reliable and relevant under Daubert and
Rule 702, such evidence may be excluded if its
value to the court does not outweigh its potential
to mislead or confuse the jury. In addressing this
question, the court applied Fed. R. Evid. 403, as
follows:
Although relevant, evidence may be excluded
if its probative value is substantially outweighed
by the danger of unfair prejudice, confusion of
the issues, or misleading the jury, or by consid-
erations of undue delay, waste of time, or need-
less presentation of cumulative evidence.
(Fed. R. Evid. 403)
In balancing these factors, the court must
decide whether the proposed expert testimony
“could improperly suggest . . . the abolished
diminished capacity defense is available” or that
Mr. Santos-Bueno is “entitled to sympathy and
possible nullification” (p. 26). Psychiatric evidence
“presents an inherent danger” of distracting the
jury from their task of evaluating the govern-
ment’s proof of each element of the alleged offense.
In this case, there was concern as to whether
Dr. Gansler’s testimony may improperly open up
the jury to theories of defense that do not exist
under current law or provide an erroneous
justification for the alleged crime (p. 26).
Consequently, Judge Saylor limited the scope of
Dr. Ganlser’s testimony to those expert opinions
addressing how Mr. Santos-Bueno’s cognitive
disabilities impacted his factual inferences, or lack
of such inferences, regarding whether the van
passengers were illegal aliens. Further, the Judge
excluded any opinions about “alleged difficulty in
exercising judgment, his impaired ability to appre-
ciate the consequences of his actions, and . . . to
‘execute appropriate plans of action’” as being out-
weighed by the potential to mislead or confuse the
jury (p. 27).
90 forensic neuropsychology
Then, the court proceeded to apply a similar,
although briefer, analysis to evaluate the admi-
ssibility of neuropsychological evidence and
Dr. Gansler’s opinion on the defense claim the
Mr. Santos-Bueno was more vulnerable to sugges-
tion due to his head injury. Judge Saylor expressed
“grave concern about both the scientific reliability
and the relevance of Dr. Gansler’s statement” about
enhanced vulnerability to suggestion (p. 29). The
court granted the defense an additional week to
supplement the record on this question.21
Santos-Bueno illustrates current application of
standards for admissibility to neuropsychological
evidence in a recent federal criminal case.
Although the court applied Daubert in its analysis
of Dr. Gansler’s proposed testimony, the court
does not, nor should it, provide a thorough under-
standing of the significant impact of Daubert on
the use of expert testimony in criminal cases. The
next section focuses on the broader trends and
far-reaching implications of Daubert and its prog-
eny on the standards for admissibility of expert
testimony.
T H E I M PA C T O F D AU B E R T
ON ADMIS SIBILITY OF
EXPERT TESTIMONY IN
C R I M I N A L L I T I G AT I O N
Research demonstrates that greater judicial scru-
tiny after Daubert was increasingly fatal to civil
cases, with 90% of summary judgments going
against the plaintiff (Dixon & Gill, 2002). That is,
testimony from plaintiff experts was more readily
excluded. In contrast, there has been little change
in admission rates for expert evidence in criminal
litigation at the trial and appellate level (Groscup,
Penrod, Studebaker, Huss, & O’Neil, 2002).
Further, the setting of a standard for appellate
review in Joiner had little impact on the admissi-
bility of expert testimony in criminal litigation.
Nonetheless, Daubert and its progeny prompted
greater scrutiny of experts by criminal court judges
and brought about many changes to the manner in
which expert testimony is evaluated. Groscup et al.
(2002) note a few general trends in criminal appel-
late cases as briefly summarized below.
Since Daubert, relevance of expert testimony
was discussed at greater lengths in criminal appel-
late decisions, suggesting that courts spend more
time analyzing the Federal Rules or applying the
Daubert factors. Specifically, judges spent more
time scrutinizing expert evidence under Fed. R.
Evid. 702. However, judges also devoted more
time to analyzing Fed. R. Evid. 104 (permitting
pre-trial determinations), apparently because
Daubert reminded that judges have an obligation
to do pretrial assessments of the reasoning and
methodology of experts. Although there were
increased references to Daubert, Groscup et al.
(2002) noted no concomitant increase in analysis
of its four suggested factors. Increasingly, courts
are trying to dispose of admissibility issues in Rule
104 hearings as a result of Daubert.
Not surprisingly, Daubert also caused greater
discussion of Frye, if for no other reason than to
distinguish the holding. Even though Daubert
and its progeny were superseded by the 2002
amendment to Rule 702, the discussion of Frye
remains relevant because a minority of states (16)
still use its general acceptance standard, including
CA, NY, FL, IL, and AZ (Lustre, 2004). Groscup
et al. (2002) reported a decreased use of the gen-
eral acceptance standard in jurisdictions adopting
Daubert, and an increase in reliance on its falsifi-
ability, peer review, and error rate criteria. As
courts have adjusted to the gatekeeping function,
courts spent less time analyzing Daubert when
disposing of expert admissibility issues.
In a result with greater implications for clini-
cal neuropsychology, scientific expert evidence is
treated differently than medical-mental health,
technical, or business evidence. In addition to
lengthier discussions of Daubert, court consider-
ation of Rules 104, 403, and the Frye general
acceptance test were much longer and more influ-
ential on admissibility for scientific expert opin-
ion. Obviously, these rules existed before Daubert,
but results show greater scrutiny of scientific
expert opinions on key evidentiary rules, in addi-
tion to the Daubert factors of falsifiability, peer
review, and error rate. This elevated scrutiny has
led to greater exclusion of scientific expert testi-
mony when compared with medical-mental
health testimony. Clinical neuropsychologists are
trained in a scientist-practitioner training model
and may be retained to offer expert opinions as
scientists or board-certified providers of medical–
mental health services. Results show that when
the expert’s opinion is viewed as scientific, Daubert
factors must be met in order for the court to admit
the expert evidence. For most other experts, pre-
sentation of information addressing Daubert is
probably unnecessary. Courts tend to rely more
heavily on whether the expert testimony will assist
the trier of fact (Rule 702) and that its probative
value outweighs its prejudicial effect (Rule 403).
Medical-mental health practitioners seeking
expert qualification should be more prepared to
 Admissibility of Expert Opinions based on Neuropsychological Evidence
discuss their indicia of expertise, for example,
education, experience, specialty, board certifica-
tion, and so forth, rather than their own research
or an existing body of research.
Courts increasingly rely on neuropsychologist
experts to assist the jury in resolving certain legal
claims (Kaufmann, 2005; 2009c). However, legal
scholars generally avoid the legal implications of
neuroscience in our courts (Greely, 2006), with
only six published articles using the terms “neuro-
science” or “neuroimaging” in their titles (p. 607).
However, a more recent Lexis search22 revealed 62
law review and bar journal articles, with 52 of
those published in the last 3.5 years. As noted in
the recent cases from California, New York, and
Tennessee (federal), neuroimaging techniques for
detecting deceit are no better than lie-detectors,
with neither technique being sufficiently reliable
for admission (Keckler, 2006). Thirteen years ago,
few neuroimaging findings were considered
specific enough to address legal questions of
cognitive or volitional impairment (Kulynych,
1997). Although neuroimaging has advanced rap-
idly, a carefully conducted neuropsychological
evaluation remains a more reliable and legally rel-
evant source of information about an individual’s
level of functioning because neuropsychological
tests have much better normative data (also see
the chapter by Ricker in the current volume).
Indeed, it is on the basis of reliable and valid nor-
mative data that neuropsychological tests meet
the requirements of admission under Daubert
and the Federal Rules (Kaufmann, 2005; 2008).
Lawyers may believe that a neuroimage pic-
ture is worth a thousand words, but the general
public does not seem to carry an inherent bias
toward greater reliance on neuroimages than neu-
ropsychological test results (Guilmette, Kennedy,
Weiler, & Temple, 2006). However, students
ascribe greater explanatory power to neurosci-
ence publications that use the phrase “brain scans
indicate” and present neuroimages, masking oth-
erwise problematic explanations (Weisberg et al.,
2008). Another recent study noted that under-
graduate students tend to rate sham scientific
articles as “better written” if the article included
neuroimages (McCabe & Castel, 2008). The risk
of undue prejudice has recently prompted some
commentators to suggest that trials using neu-
roimages may require special jury instructions or
hiring court-appointed experts to assist judges to
“fortify the gate” (Compton, 2010). But these sci-
entific reports and legal commentary do not com-
pare neuropsychological evaluations from actual
91
cases that commonly incorporate structural
neuroimaging studies when rendering clinical
formulations. It is routine practice for clinical
neuropsychologists to use neuroanatomical find-
ings when drawing inferences about brain-behav-
ior relations and when rendering expert opinions.
To date, there are no studies comparing the rela-
tive persuasiveness of expert opinions based on
neuropsychological evaluations presented with
and without functional neuroimages, even as it is
widely presumed that neuroimages have a preju-
dicial impact on jury deliberations (Brown &
Murphy, 2010).
In summary, Daubert assigned and Joiner
reinforced the gatekeeping role of the trial court
judge in determining the admissibility of expert
testimony, thereby raising the level of scrutiny of
experts and the basis for their testimony. Daubert
also partially defined a road map, in the form of
flexible factors, for experts to follow in order to
have their testimony admitted and ultimately
heard by the trier of fact. Santos-Bueno showed
how careful attention to evidentiary and proce-
dural rules in a criminal proceeding, including
Daubert factors, allows expert neuropsychologists
to be recognized by the court in a preliminary evi-
dentiary hearing. Ultimately, Dr. Gansler’s expert
neuropsychological opinions were admitted as
sufficiently reliable and relevant to assist the jury.
WRONGFUL DISCLO SURE
OF PSYCHOLOGICAL
T E S T S T H R E AT E N S
T H E A D M I S S I B I LT Y O F
NEUROPSYCHOLOGICAL
OPINIONS
At the same time that clinical neuropsychology
has experienced unprecedented growth in foren-
sic consultation, discovery rules and isolated court
decisions threaten the validity of neuropsycho-
logical methods (Kaufmann, 2005; 2009c).
Specifically, the strong public policy underlying
test security (Detroit Edison Co. v. NLRB, 1979), as
applied to clinical cases (Chiperas v. Rubin, 1998),
is being threatened by the overly zealous discov-
ery demands of litigation. Standardized psycho-
metric tests used during forensic evaluations
provide the best technology available to assist the
jury in resolving certain legal claims (Kaufmann,
2005). Wrongful disclosure of psychological test
materials allows opportunistic litigants and their
attorneys to “review test protocols, obtain test
items, discover answers, and ‘cheat’ on the tests in
the future” (p. 100), thereby risking the validity of
92 forensic neuropsychology
future applications of neuropsychological meth-
ods in our courts (also see Wetter & Corrigan,
1995; Youngjohn, 1995; Youngjohn, Lees-Haley,
& Binder, 1999; Abeles, 2001; Rüsseler et al.,
2008). Recent articles provide specific recommen-
dations for minimizing the risks associated with
wrongful disclosure (Prohaska & Martin, 2007;
Kaufmann, 2009a; Morrell, 2009). In keeping
with the theme of this chapter, such wrongful dis-
closure could possibly lead judges to exclude neu-
ropsychological evidence in pre-trial hearings,
because opinions based on tainted data would not
be sufficiently reliable under Daubert. In Detroit
Edison, the U.S. Supreme Court ordered that such
materials should be released only to psychologists
in order to “insure [sic] the future integrity of the
tests” (p. 308).
Although about 20 states have acted to protect
psychological test materials from wrongful dis-
closure, potentially harmful court decisions
caused concerned professionals to create the
“Group Protecting the Integrity of Psychological
Examinations” (hereinafter, G–PIPE) Berman v.
Kuckarski, (2006). G–PIPE consists of individual
practitioners, neuropsychology credentialing
boards, and state psychological associations who
are concerned about negative consequences of
test disclosure on the objectivity, fairness, and
integrity of neuropsychological evaluations and
practice. G-PIPE also includes test developers,
publishers, marketers, and distributors who are
concerned about copyright infringement, trade
secret protection, and other intellectual property
rights associated with their tests. G-PIPE has
addressed challenges to the integrity of neuropsy-
chological evaluations posed by third-party
observers/recording devices (hereinafter, TPO)
and compliance with court orders protecting the
integrity of test materials.23
Currently, Florida places the burden of proof
on the party seeking to avoid a TPO during
a psychological evaluation (Broyles v. Reilly, 1997).
In Broyles, the court set forth a two-part test
requiring: 1) case-specific reasons why a TPO is
disruptive to the evaluation, and 2) no other qual-
ified provider in the area is willing to conduct the
evaluation in the presence of a TPO. This legal test
was developed originally for medical legal exami-
nations, and G-PIPE argues that psychological
evaluations are distinguishable because they
employ psychometric tests. G-PIPE advocates that
the party seeking the TPO have the burden to
show case-specific reasons why a TPO should be
allowed. In a related Florida case, G-PIPE sought
to amend a protective order requiring the return
of a videotape made during a psychological evalu-
ation (Fla. Dept. of Trans. v. Piccolo, 2007).
Ultimately, neither of these cases were successful
in modifying the Broyles v. Reilly rule, but efforts
continue with the Florida Psychological
Association and the legislature (Howe, Rice, &
Hoese, 2007). For more recent information on the
harmful effects of TPO and the most effective
responses for challenging litigation tactics, see
Grieffenstein and Kaufmann (this volume) and
Howe and McCaffrey (2010).
In a unanimous decision, a California
appellate court held that copyright protection
does not preclude a test recipient from obtaining
their answers and the test questions after complet-
ing a mental examination using psychometric
tests (Carpenter v. Yamaha Motor Corp., 2006).
The court also found that a test recipient could
obtain the names of the tests before the examina-
tion and—with the assistance of counsel, psychol-
ogist, or other expert—could object to certain
tests if deemed inappropriate for the purposes of
the mental examination. Although the Carpenter
court acknowledged that disclosure of test materi-
als before the examination “could affect the integ-
rity of the tests” (p. 267), this appellate panel failed
to appreciate that test identification before exami-
nation posed a risk. While remanding the case for
further proceedings due to deficiencies in the
record, Carpenter saw no threat in providing test
names because “actual test questions are a care-
fully guarded secret among the publishers and
examiners” (p. 268). Yet in Detroit Edison, all of
the justices recognized the risk of test disclosure,
with the majority commenting that protections
afforded by restrictive orders were not persuasive
(p. 314), and the minority commenting on the
harm associated with inadvertent disclosure
(p. 324). In the end, the U.S. Supreme Court has
found a better balance in clarifying the strong
public policy underlying test security, ordering
that psychometric tests should only be released to
psychologists. Subsequent state courts (Fla. Dept.
of Trans. v. Piccolo, 2007) and federal courts
(Taylor v. Erna, 2009; Lumsden v. United States of
America, 2010) continue to explore the contours
of the Detroit Edison psychologist nondisclosure
privilege/duty to safeguard psychological test
materials. The reader is directed to Greiffenstein
and Kaufmann (this volume) for solutions to the
“raw data” problem.
The Florida and California TPO cases show
how easily a court could disclose psychological
 Admissibility of Expert Opinions based on Neuropsychological Evidence
test materials into the public domain, thereby
compromising the integrity of neuropsychologi-
cal practice and forensic consultation. This
chapter has demonstrated the importance of pro-
tecting psychological test materials, standardized
instructions, and normative comparisons in
developing neuropsychological evidence and
rendering reliable opinions in court. Precedent-
setting court decisions may sway the public
policy debate away from test security, in favor of
evidentiary discovery rules, such that courts will
increasingly find neuropsychological opinions
unreliable. Wrongful disclosure of psychological
test materials is a looming threat to the admissi-
bility of neuropsychological evidence in our
courts, prompting more aggressive legal advocacy
efforts by G-PIPE and within AACN (Kaufmann,
2009c).
CONCLUSIONS
Three out of every four reported cases referencing
neuropsychology have been adjudicated in the
past decade. This rapid increase in use of neuro-
psychology to assist juries shows that neuropsy-
chologist expert opinions meet the criteria for
admissibility under Daubert and the Federal
Rules. As such, courts are admitting neuropsy-
chologist expert opinions on essential questions
in administrative, probate, civil, and criminal
cases. Standardized, norm-referenced psycho-
metric tests provide the most reliable and valid
procedures for addressing questions involving the
mental condition of the civil plaintiff and the
criminal defendant. Unlike other mental health
professionals, psychologists use objective psycho-
logical tests as part of a scientific methodology to
refine their impressions when formulating expert
opinions (Kaufmann, 2005; 2009c). Applying the
unique brain-behavior knowledge base, neurop-
sychologists use psychological tests in conjunc-
tion with neurologic findings and neuroimaging
techniques in a scientific enterprise that assists
the trier of fact to resolve certain legal claims.
Neuropsychological methods fulfill Daubert and
Frye requirements and the board-certified neu-
ropsychologist versed in the constitutional and
judicial foundations of forensic consultation shall
continue to provide an important expert service.
That is, the forensic neuropsychologist expert
shall offer admissible neuropsychological evi-
dence that is more probative than prejudicial of
the ultimate issues of civil liability and criminal
responsibility.
93
Although the law seeks every rational means
for ascertaining the truth, public policy must
promote the truth-seeking function of the judi-
ciary by protecting psychological test materials
from wrongful disclosure in a manner that serves
all parties and the profession, while preserving
justice in our courts.
N OT E S
1. Extended excerpts from Kaufmann, P. M.
(2008). Admissibility of neuropsychological evidence
in criminal cases: Competency, insanity, culpability,
and mitigation. In R. L. Denney & J. P. Sullivan (Vol.
Ed.), Clinical Neuropsychology in the Criminal Forensic
Setting. New York: Guilford Press are contained herein
with the publisher’s permission.
2. Statements of opinion or belief considered
authoritative because they are made by the court.
Compare to holding, which is “a court’s determination
of a matter of law pivotal to its decision; a principle
drawn from such a decision.” Black’s Law Dictionary
(7th Edition). Dicta may be persuasive, but do not set
precedent. Holdings create binding precedent within
the applicable jurisdiction of the court.
3. Current case being heard by the court.
4. There is no genuine issue of material fact upon
which the plaintiff could prevail as a matter of law. The
trial judge rendered a verdict for Merrill Dow based on
briefs without a trial.
5. The most common mechanism used by the U.S.
Supreme Court, in which it chooses to hear a case by
order directing a lower court to deliver the case record.
6. However, about 16 states still use a Frye type of
standard, including CA, NY, FL, IL, and AZ.
7. A motion to limit or exclude allegedly prejudi-
cial evidence presented to the judge or during a trial.
8. See Hoyt, T. D. (Fall, 2009). Is the fake bad scale
test here to stay? Mass Torts, 8(1), 14–15, 23. citing Nejo
v. Tamaroff Buick Honda Isuzu Nissan, 88 Fed. App’x
881, 885 (6th Cir. Feb. 23, 2004); Thomas v. Sec’y of
Health and Human Servs., No. 98–1185, 1998 WL
516815, at *1 (7th Cir. Aug. 17, 1998) (unpublished);
Carovski v. Jordan, No. 06CV716S, 2008 WL 1805813,
at *1 (W.D.N.Y. Apr. 18, 2008); Adams v. Astrue, No.
06–5132-CV-S-JCE-SSA, 2008 WL 508683, at *3 (W.D.
Mo. Feb. 21, 2008); Eubanks v. Astrue, No. 03–427-
WDS, 2008 WL 515001, at *6 (S.D. Ill. Feb. 22, 2008);
Cummins v. Unumprovident Ins. Co., No. 04–339-A,
2007 WL 4104275, at *11 (M.D. La. Nov. 15, 2007);
Contreras v.United States, No. 1:03-CV-360, 2004 WL
3457632, at *7 (W.D. Mich. Oct. 26, 2004); Spurgeon v.
Barnhart, No. 2:02 CV 29 DDN, 2003 WL 25734676,
at *5 (E.D. Mo. Sept. 16, 2003); Sochor v. State, 883 So.
2d 766, 779 (Fla. 2004); Posey v. Singletary, 795 So. 2d
1249, 1259 (La. App. 2001); Muhammed v. State, 46
94 forensic neuropsychology
S.W.3d 493, 508 (Tex. App. 2001); See also Chuk, S. R.
(2009). NOTE: It’s (Not) Bad, It’s (Not Bad), you know
it: The growing acceptance of the “Fake Bad Scale.”
Villanova Law Review, 54, 479–513.
9. Campbell v. Papell, Florida 12th Circuit, Sarasota
County (March 19, 2009 Order denying release of raw
data and psychological test materials to the plaintiff
attorney); see also Sierra v. Reyes Florida 13th Circuit,
Hillsborough County (February 16, 2009 Order deny-
ing release of raw data).
10. See Foster, S., Qualification of NonMedical
Psychologist to Testify as to Mental Condition or
Competency, 72 A.L.R.5th 529 (1999); citing Russell v.
State, 775 So. 2d 866 (Ala. CIM. App. 1997); People v.
Noble, 42 Ill. 2d 425, 248 N.E.2d 96 (1969); State v.
Alexander, 252 La. 564, 211 So. 2d 650 (1968); Saul v.
State, 6 Md. App. 540, 252, A.2d 282 (1969),; Span v.
Bees, 23 Md. App. 313, 327 A.2d 801 (1974); People v.
Diaz, 51 N.Y. 2d 841, 433 N.Y.S. 2d 751, 413 N.E. 2d
1166 (1980); Com v. Williams, 270 Pa. Super. 27, 410
A.2d 880 (1979); State v. Williams, 278 Md. 180, 361
A.2d 122 (1976); Saul v. State, 6 Md. App. 520, 252
A.2d 282 (1969).
11. Intermediate evidentiary standard that exceeds
the preponderance of the evidence standard used in
civil litigation, but less than the beyond a reasonable
doubt standard used in criminal litigation. Therefore,
although the defendant has the burden to show that
insanity is highly probable, the defense is not required
to prove it beyond the shadow of a doubt.
12. Courts in different jurisdictions operate under
different legal precedent and rules.
13. Specific intent refers to the state of mind
required to accomplish a precise criminal act that can
be negated by intoxication or insanity.
14. Mens rea means guilty mind or the state of
mind that the prosecution must prove beyond a rea-
sonable doubt in order to secure a conviction.
15. Conducted on July 3, 2010.
16. See Anand Giridharadas, Brain Scan a New
Wave in Criminal Evidence, INT’L HERALD TRIB.,
Sept. 8, 2008, at 1; Anand Giridharadas, India’s Novel
Use of Brain Scans in Courts is Debated, N.Y. TIMES,
Sept. 14, 2008, at A8.
17. See http://www.uakron.edu/law/lawreview/
v42/v42num3.dot, for series of nine papers on
neuroimaging applications and the law, last visited
July 5, 2010.
18. Morse describes the speculative claims of some
practitioners about the implications of neuroscience
for criminal responsibility that cannot be conceptually,
empirically, or legally sustained; recommending “cog-
nitive jurotherapy” as the treatment of choice for brain
overclaim syndrome.
19. See The Law and Neuroscience Project at www.
lawandneuroscienceproject.org; last visited July 5,
2010.
20. Rule allowing the court to order the defen-
dant to be examined by a government expert after
the defendant provides notice of intent to intro-
duce expert evidence relating to a mental disease or
defect.
21. Defense counsel reported that the admission
of neuropsychological evidence was pivotal in the gov-
ernment’s offer to let her client plea guilty to a lesser
offense, that is, conspiracy to transport illegal aliens,
being sentenced to time already served and avoiding
immediate deportation (personal communication).
22. Conducted July 15, 2011.
23. For more information on G-PIPE, contact
Laura Lee Shaw Howe, JD, PhD.
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100 forensic neuropsychology
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 4
Ethical Practice of Forensic Neuropsychology
CHRISTOPHER L. GROTE AND BENJAMIN A. PYYKKONEN
Neuropsychologists have at least two reasons to
be aware of the unique ethical dilemmas that can
present in the “legal” arena: the increasing
percentage and number of forensically related
referrals made to our profession, and the vastly
increased number of resources available to
practitioners seeking out published guidance or
position papers on these topics. This chapter
reviews: 1) how the number of forensic referrals,
involvement of neuropsychology in the courts,
and ethics position papers have increased tremen-
dously in just the last few years; 2) how the “ethics
of neuropsychology” fits into the larger context of
assessment guidelines promulgated by organiza-
tions, some of which are not exclusively populated
by neuropsychologists; 3) the continued impor-
tance of issues related to the release of psycholo-
gical raw data, and; 4) common ethical dilemmas
that can present in forensic neuropsychological
evaluations, as illustrated by actual case examples
encountered by the authors.
T R E N D S I N AVA I L A B L E
REFERRALS AND
RESOURCES ON ETHICAL
PRACTICE
Recent neuropsychology practice surveys report
continued growth in the practice of forensic neu-
ropsychologists. The survey conducted by Rabin,
Barr, and Burton (2005) of the National Academy
of Neuropsychology (NAN), APA Division 40,
and International Neuropsychological Society
(INS) members reported that legal work accounts
for 32% of the referrals to these same neuropsy-
chologists, a significant increase compared to ear-
lier surveys. This same survey reported as many as
68.3% of all neuropsychologists reported receiv-
ing referrals from attorneys. Further, reimburse-
ment rates in forensic neuropsychology can
approach 100% of the billed amount and at rates
which can be considerably higher than those
offered by commercial insurers or government
payers such as Medicare. It is not surprising then
that these referrals will increase not only because
of the valuable information they can bring to the
courtroom, but because neuropsychologists will
seek out and welcome such cases both for finan-
cial and research purposes. Kaufmann’s recent
review (2009) points out that 71% of Lexis refer-
ences for “neuropsycholo-” occurred in just the
last ten years, and that the ‘growth of legal cases
referencing neuropsychology is outpacing every
related area of brain-behavior expertise and this
growth is accelerating’ (p. 1131).
Given that neuropsychologists can increas-
ingly expect to have forensic cases constitute a
part of their practice, it might be considered a
relief for most and a “burden” for a few, that “igno-
rance of the law” can no longer be offered as an
excuse for not knowing how to anticipate or
potentially resolve ethical dilemmas that may
arise during such cases. When the senior author
of this chapter was preparing for his ABCN exams
in the mid 1990s, there were very few articles,
chapters, or books on the ethics of neuropsychol-
ogy. Instead, one relied primarily on the APA
ethics code, and just a few relevant publications
that were specific to neuropsychological practice.
Five to ten years later, during the writing of this
chapter for the first edition of this book, there
were quite a few more resources available to the
interested clinician or scientist. Dr. Shane Bush
certainly was a leader in this development, and
the interested reader would do well to simply seek
out his publications for thorough reviews of a
number of contemporary issues in the ethics of
forensic neuropsychology (e.g., Bush & Drexler,
2002). What has transpired in more recent years,
however, is increased awareness of and efforts by
organizations in neuropsychology to publish posi-
tion papers on topics related to ethics in forensic
neuropsychology. Reference to the website for the
102 forensic neuropsychology
American Academy of Clinical Neuropsychology
(www.theaacn.org) lists 12 position papers devel-
oped just in the last five years, all of which could
be considered as regarding ethical practice. More
specifically, AACN has asked experts, either on
their own or in collaboration with others, to
review the literature and to offer guidelines on
topics such as working with minority populations,
the proper assessment of effort and bias
(Heilbronner et al., 2009), practice guidelines, and
disclosure of psychological raw test data. Of
particular interest is a compendium prepared
by Dr. Bush of neuropsychology-related ethics
references (Bush, 2007). This 24-page document
lists hundreds of citations, nearly all published
in the last decade, arranged over a dozen or so
topics. In addition, the National Academy of
Neuropsychology (NAN) has also long been active
in developing and publishing papers related to
competent and ethical practice. Many of these
were pioneering efforts, in that they date to the
late 1990s and early 2000s, but have been added to
in subsequent years, including unique topics such
as the secret recordings of evaluations. These
papers are also easily accessed via the Internet at
www.nanonline.org.
Given these expanded resources, no practic-
ing neuropsychologist can be absolved for claim-
ing lack of awareness of potential ethical problems
or how they might be best resolved. These
increased resources are entirely appropriate given
the unique demands of the forensic neuropsycho-
logical evaluation. This is both appropriate and
necessary, for at least two reasons. First, neurop-
sychologists have to be constantly vigilant of the
need to produce unbiased and appropriately
informed opinions if courts can be expected to
rely on our opinions. Failure to maintain this neu-
trality could instead lead others to view us as mer-
cenaries whose opinions might be influenced by
the needs of those who retain us in adversarial
cases. Second, neuropsychologists may not be
fully aware of all the potential ethical and legal
implications that arise when their reports are used
in forensic settings. Their graduate education and
training may have focused only on more general
ethical issues, such not having sexual relation-
ships with patients (note: the term “patient” will
be used throughout this chapter instead of client,
claimant, or litigant; of course, use of this term is
not meant to imply that a treating or doctor-
patient relationship exists during a forensic neu-
ropsychological examination). Previous training
in ethics may not have specifically focused on
those issues related to forensic neuropsycholo-
gical practice, such as informed consent for assess-
ment, release of raw data, or obstacles to presenting
unbiased and fully informed opinions in forensic
cases.
PLACING THE ETHICS OF
NEUROPSYCHOLOGY IN
CONTEXT
It appears to be that very few “unethical” neurop-
sychologists commit blatantly grievous acts such
as engaging in romantic or sexual liaisons with
clients, embezzling from employers, or like poten-
tial felonies. Instead, most perceived transgres-
sions involve incompetent practice (Grote, Lewin,
Sweet, & van Gorp, 2000). Of course, “compe-
tence” can be in the eye of the beholder and may
not be easily agreed upon, especially in cases that
are being litigated. Nonetheless, the following sec-
tion reviews ways in which various organizations
have commented on this issue.
Competency Requirements
“Professional competence is the foundation of
ethical practice” (Bush, 2007, page 37). Incom-
petent practice precludes ethical practice.
Therefore, it is entirely appropriate and useful to
identify the basic competency requirements for
the ethical practice of forensic neuropsychology.
The following will delineate competency require-
ments for ethical practice in three areas with
successively increasing demands: 1) clinical
assessment, 2) neuropsychological assessment,
and finally, 3) forensic neuropsychological
assessment. Naturally, more space will be spent
discussing competency demands for forensic
neuropsychological assessment.
Competency Requirements for
Clinical Assessment
Basic test user qualifications were most clearly
identified in official APA policy in a position
paper for the American Psychological Association
(APA) published in 2001 (Turner, DeMers, Fox, &
Reed, 2001). The basic qualifications represent the
final results of the APA’s Task Force for Test User
Qualifications (TTFUQ) to identify APA policy.
This policy statement identifies two categories of
test user qualifications: a) generic psychometric
knowledge with widespread application to the
majority of tests, and b) qualifications specific
to the application of particular tests in specific
settings. The basic psychometric knowledge iden-
tified in this APA policy statement includes an
 Ethical Practice of Forensic Neuropsychology
understanding of item response theory; descrip-
tive statistics; reliability and measurement
error; validity and meaning of test scores; norma-
tive interpretation of test scores; selection of
appropriate tests; test administration procedures;
ethnic, racial, cultural, gender, age, and linguistic
variables; and the use of tests with individuals
with disabilities. This policy also recommends
that theses skills are best and most ethically devel-
oped under the supervision of “appropriately
experienced professionals.” Unfortunately, the
qualifications of such professionals are not clearly
delineated in this policy statement. In addition to
these basic psychometric requirements for test
user qualifications, this policy paper identifies
a number of specific qualifications related to
specific contexts. Five general categories of test
use are identified, including: (a) classification,
(b) description, (c) prediction, (d) intervention
planning, and (e) tracking. Although neuropsy-
chological assessment is not identified in this
policy statement, these are the exact applications
of clinical neuropsychology. Moreover, while neu-
ropsychological assessment is not specifically
listed, the forensic context is specifically delin-
eated in this policy paper and will be discussed
below.
Specific Requirements for Competent
Neuropsychological Assessment
Numerous attempts have been made to identify
or describe the qualifications of a competent
neuropsychologist. In this vein, training para-
digms have been developed, with the most com-
plete being the Houston Conference guidelines
on specialty education and training in clinical
neuropsychology (http://www.theaacn.org/
position_papers/Houston_Conference.pdf ).
These guidelines indicate that practice in clinical
neuropsychology requires basic clinical training
to include proficiencies in statistics, psychopa-
thology, psychometric theory, and lifespan devel-
opment, among other critical areas. In addition to
this foundational generalist training, these guide-
lines identify the need for foundational under-
standings of the brain-behavior relationship,
including (a) functional neuroanatomy; (b) neu-
rological and related disorders including their
etiology, pathology, course and treatment;
(c) non-neurologic conditions affecting central
nervous system functioning; (d) neuroimaging
and other neurodiagnostic techniques; (e) neuro-
chemistry of behavior (e.g., psychopharma-
cology); and (f) neuropsychology of behavior.
103
The application of this understanding of brain-
behavior relationships in concert with the afore-
mentioned generalist training represents the
foundational building blocks for the practice of
competent clinical neuropsychology. The Houston
Conference guidelines then identify specific areas
of expertise requisite to competent practice of
clinical neuropsychology, including an under-
standing of neuropsychological assessment, inter-
vention, research design, professional issues and
ethics, and the practical implications of neuro-
psychological conclusions.
A comprehensive update and review of the
APA ethics code (American Psychological
Association, 2002) can be found in Ethical Decision
Making in Clinical Neuropsychology (Bush, 2007).
Within this review a chapter is dedicated to com-
petence. Specific APA ethics codes related to com-
petence in clinical neuropsychology include
standards related to boundaries of competence,
maintaining competence, and understanding the
bases for scientific and professional judgment.
The application of these ethical codes can func-
tion as a useful guide and omnibus in the applica-
tion of the Houston Conference guidelines to
competent practice in clinical Neuropsychology.
Additional Requirements for
Competency in Forensic Practice
Given the unique nature of the forensic practice of
clinical neuropsychology, certain competency
requirements emerge; namely, competent man-
agement of raw data and its release, and informed
consent (i.e., the person assessed is not afforded
the same rights of confidentiality or the results).
The existing APA ethics code is applicable in these
circumstances and provides some guidance in this
regard.
R E L E A S E O F R AW D ATA
No doubt the reader of this chapter has already
been alerted to the fact that the 2002 ethics code
has altered policy regarding release of raw data.
The ethics code change probably most relevant to
the practice of forensic neuropsychology is found
in Standards 9.04 (Release of Raw Data) and 9.11
(Maintaining Test Security). The current product
is a more liberal interpretation than the 1992
code (American Psychological Association, 1992;
2003) in determining to whom, and when, a psy-
chologist must release “raw data.” The 1992 code
prevented release to others who were ‘not quali-
fied’ to use the raw data. This was a vague descrip-
tion that led to frequent debate about who was or
104 forensic neuropsychology
was not qualified to examine raw data. There was
also dissension regarding the 1992 interpretation
of ‘raw data’ and whether this referred to test
forms, test materials, test scores, or some combi-
nation of these elements. As a result, some neu-
ropsychologists reportedly refused to release
copies of patient’s test results/forms to other
licensed psychologists because they were not
board certified by a particular organization or
perhaps even because of some personal enmity
between the two psychologists.
The 2002 code makes it a bit clearer as to what
psychologists should do when asked for their files,
although these requests will have to be balanced
against one’s interpretation of HIPAA and appli-
cable laws in one’s state of practice. Further, the
2002 code draws a distinction between raw data
and test materials. The 2002 Standard 9.11
(Maintaining Test Security) states that “psycholo-
gists make reasonable efforts to maintain the
integrity and security of test materials,” these
being defined as “manuals, instruments, proto-
cols, and test questions or stimuli and does not
include test data as defined in Standard 9.04.” This
seems to suggest that psychologists should not
freely release things such as the WAIS Block
Design drawings and blocks, the WMS Spatial
Span blocks, or test protocols containing the actual
test items (e.g., the word list for the California
Verbal Learning Test-II). The differentiation of
test data and materials is discussed at length in a
2003 position paper from the National Academy
of Neuropsychology (www.nanonline.com),
which is a follow-up to their first paper on Test
Security (National Academy of Neuropsychology,
2000). This update further discusses the confusion
arising from Standard 9.04 and Standard 9.11.
True raw test scores or calculated test scores that
do not reveal test questions do not require test
security protection, per this position paper update.
However, the new 2002 revised APA Ethics Code
does not address the very practical problem of
releasing data which imply or reveal test ques-
tions. As recommended in the original test secu-
rity position paper (National Academy of
Neuropsychology, 2000), when the court orders
release of raw data that include test protocols con-
taining test stimuli, the expert neuropsychologist
should request a protective order containing the
following language: The test materials will not be
circulated beyond those directly involved in the
case, no unauthorized copies or reproductions
will be made, the presentation of the test materials
in the courtroom will be minimized to the extent
possible, exhibits and courtroom records contain-
ing test materials will be protected or sealed, and
all test materials will be destroyed or returned
upon the completion of the case.
A position paper and a review paper were also
published by the AACN on the topics of releasing
and protecting raw data. These can either be
retrieved through their website (www.theaacn.
org), or through the papers published in The
Clinical Neuropsychologist (Attix, Donders,
Johnson-Greene, Grote, Harris, & Bauer, 2007;
Kaufmann, 2009). These papers indicate the com-
plexity of these issues, which is further discussed
in chapter 2 of the current volume. However, it
does seem to be the case that “test materials” are
rarely, or never, requested by nonpsychologists.
Second, the standard only requires “reasonable
efforts” to not release these materials, and does
not make it clear what this means. Some psychol-
ogists may interpret this to mean they only need
to explain their potential concerns about misuse
of the materials to a nonpsychologist before
releasing them, while other psychologists might
instead insist on a court order. Regardless of these
quibbles, it is clear that Standard 9.04 has greater
relevance concerning the release of test materials
or raw data. It states:
(a) The term test data refers to raw and
scaled scores, client/patient responses to
test questions or stimuli, and
psychologists’ notes and recordings
concerning client/patient statements
and behavior during an examination.
Those portions of test materials that
include client/patient responses are
included in the definition of test data.
Pursuant to a client/patient release,
psychologists provide test data to the
client/patient or other persons identified
in the release. Psychologists may refrain
from releasing test data to protect a
client/patient or others from substantial
harm or misuse or misrepresentation of
the data or the test, recognizing that in
many instances release of confidential
information under these circumstances is
regulated by law
(b) In the absence of a client/patient release,
psychologists provide test data only as
required by law or court order.
Standard 9.04 is more liberal than what was
in the 1992 code in that it is fairly clear in telling

psychologists to release copies of test forms
when directed to by patients or their attorneys.
One might attempt to argue that “substantial
harm” might result because of this release, but this
might be a stretch, especially in light of the new
HIPAA regulations. Of course, psychologists who
practice in states such as Illinois and Iowa, which
have laws restricting the release of raw data to
nonpsychologists, will not be affected by either
the new APA ethics code or by HIPAA. An article
in the January 2003 APA Monitor states that state
law supersedes HIPAA, and of course both of
these would trump the APA ethics code in those
situations where the code conflicts with state or
federal law. It is also important to know that
HIPAA is not applicable when raw data was
collected in the process of legal or administrative
When Should Raw Data Be Released?
Has patient or their attorney
requested release?
Yes
Is raw data to be sent to
another psychologist?
No
Has a court order directed
you to release raw data?
No
Does state law prohibit
release of raw data to
non-psychologist?
No
Was raw data collected as
part of legal or
administrative proceeding?
No Ye
HIPAA is
relevant
Can you clearly
demonstrate substantial
harm will be done if
data is released?
Yes No
Release Data
FIGURE 4.1: Flowchart of data release.
Ethical Practice of Forensic Neuropsychology 105
proceeding (Fisher, 2003). Federal Law 45 CFR 45
164.508 and 164.524[(a)(1)] is part of the HIPAA
legislation, and states that “Patients do not have
the right of access to information compiled in rea-
sonable anticipation of, or for use in, a civil, crim-
inal, or administrative action, or procedure.”
In terms of release of raw data, it has been
written that state law takes precedence over
HIPAA, and that HIPAA in turn supersedes any
ethical codes (Daw Holloway, 2003a). Figure 4.1
attempts to provide an overview of steps that
clinicians may want to consider in determining
if or when to release copies of their raw data. It
illustrates that a patient, their attorney, or a court
must request or order this release; it is difficult to
imagine circumstances under which this release
could otherwise occur. However, if a patient has
No
Do not
release data
Ye
s
Release data
Yes
Yes Do not
release data
s
HIPAA is
not relevant
Can you clearly
demonstrate substantial Yes Do not
harm will be done if release data
data is released?
No
Release Data
106 forensic neuropsychology
requested this release, and a court has not ordered
the release, the clinician must then determine
whether the state in which they are practicing has
any legislation regarding this issue. An informal
survey of colleagues indicated that at least four of
the United States, and one Canadian Province,
each prohibit the release of raw data to non-
psychologists. The cited legislation for each juris-
diction is as follows: Illinois (Section 3 c) of
(740 ILCS 110) of the Mental Health and
Developmental Disabilities Act of the State of
Illinois); Florida (chapter 490; 64 B19–18.004(3);
Iowa (Section 1 228.9); Texas (Title 22, Part 21,
Rule 465.22); Alberta (Health Information Act
Section 11(1)(e). Colleagues from other states,
including Utah, Hawaii, Arizona, and Oregon,
responded that their states had no such restric-
tions on the release of raw data to nonpsycholo-
gists. This obviously is not a comprehensive
listing, so it is incumbent upon a practicing psy-
chologist to check with their state psychological
association, or otherwise be aware of state legisla-
tion regarding this issue. Assuming that a psy-
chologist is not prohibited from releasing raw data
to nonpsychologists, the next step in this process
would be to determine if the request is related to a
court or administrative proceeding. If it is not
related, then HIPAA does apply. This is important,
because HIPAA does not appear to allow for the
concept of “substantial harm or misuse” of the
data to be an excuse to not send the data (Fisher,
2003). That is, a psychologist’s concern that the
data will somehow be misused cannot serve as a
reason to not send it in non-legal cases. The excep-
tion to sending raw data to a patient extends to
test protocols which contain the actual test stim-
uli, which are excluded from HIPAA release
requirements due to the “trade secret” exemption
provision. On the other hand, if the request for
raw data is related to a court or administrative
proceeding, then HIPAA does not apply. Should
there be a substantial reason to believe the data
would be misused in such a scenario, they would
be justified in attempting to withhold it. Of course,
this refusal may not be the last word, as an attor-
ney might be successful in obtaining a court order,
which of course would trump any of the psychol-
ogist’s reasons for not sending the data along.
Again, if such a court order for release is obtained,
the expert neuropsychologist should attempt to
obtain language in the order protecting the test
protocols containing actual test stimuli, such
that these are used only for the specific case in
litigation, and prevented from other disclosure,
including becoming part of the record of the
case. Obviously, this is a complicated situation
and clinicians should proceed cautiously, consult
with colleagues, and document their reasons for
responding or failing to respond to requests for
copies of their raw data. Chapters 2 and 3 provide
further discussion of the issue of test security.
O B S TA C L E S T O T H E
ETHICAL PRACTICE
OF FORENSIC
NEUROPSYCHOLOGY
It is not enough to be well intentioned, or to view
oneself as “ethical,” to avoid ethical dilemmas
and inappropriate outcomes in forensic neuro-
psychology. One cannot necessarily rely on one’s
common sense, or the opinion of a referring party,
as to the correct course of action in ethically
questionable situations. Another problem is that
many questions or problems can’t be anticipated
in advance of their occurrence, and one may have
little time to seek consultation from colleagues or
to think one’s way through the problem. Therefore,
the rest of this chapter is intended to serve as
a reference guide for ethical dilemmas that one
reasonably might expect to encounter in forensic
neuropsychology cases. These are based on situa-
tions and actual questions and comments encoun-
tered by the author and colleagues. These are now
presented in roughly the same order that they
would occur in the evolution of a forensic neurop-
sychological evaluation. That is, this discussion
will initiate with dilemmas likely encountered with
the first contact with a referring party, and con-
clude with issues related to deposition or trial tes-
timony. References to the relevant sections of the
2002 Ethical Principles are made for each section.
COMEPETENCE
(ES 2 COMPETENCE;
2 . 0 1 B O U N DA R I E S O F
COMPETENCE)
“Will you provide opinions on this child
custody case?”
Psychologists should agree to be retained only on
those cases where their education, training, and
knowledge are sufficient for them to offer expert
opinions on the issues at hand. At a minimum,
this would require them to have knowledge of the
relevant literature and sufficient supervised and/or
recent clinical experience with the type of patient/
problem being referred. Neuropsychologists
 Ethical Practice of Forensic Neuropsychology
typically have a doctorate in clinical psychology,
and as such usually have had experiences in other
areas besides neuropsychology. This might allow
them to serve as experts in cases involving chronic
pain, psychopathology, child custody, or a host of
other issues, but they should make sure of their
ongoing competence before agreeing to be
retained. Psychologists and nonpsychologists
alike might refer to the “definition of a neuro-
psychologist” papers promulgated either by
Division 40 (Clinical Neuropsychology) of the
American Psychological Association (1989) or by
the National Academy of Neuropsychology
(2001) to help determine who might have the
necessary credentials to offer a neuropsycholo-
gical opinion. Both definitions seem to agree that
board certification may be or is the best evidence
of specialized training and knowledge in neuro-
psychology.
M E T H O D O F R E TA I N E R
(ES 3.06 CONFLICT OF
INTEREST; 6.04 FEES
AND FINANCIAL
ARRANGEMENTS; 6.07
REFERRALS AND FEES)
1) “Will you work on lien?” 2) “Will you work
for a reduced fee?”
Since plaintiff lawyers typically don’t collect a fee
from a client until a settlement or jury verdict has
been awarded, they sometimes will ask experts to
wait to get paid. Besides not knowing when this
will occur, the psychologist may not even know if
they will get paid. It is difficult to imagine how an
expert can maintain their neutrality, say in front
of a jury, if they know that none of their fees will
be paid unless the plaintiff receives a favorable
verdict. Similarly, disability insurance companies
or defense litigators may sometimes ask an expert
to “cap” their bill for a less-than-usual amount.
Although this may not be as problematic as
working on lien, it is not without its own set of
problems. Working for less than your usual fee
may tempt one to cut corners and not do as
thorough a job as is necessary or typical. On the
other hand, psychologists should also consider
doing pro bono work for impoverished clients.
One should carefully think such things through
and try to ensure that their work will remain of
the highest quality and not be tainted by the
manner of retainer before agreeing to one of these
alternative financial arraignments.
107
SUGGESTIONS OF BIAS,
COLLUSION (ES 2.04 BASES
FOR SCIENTIFIC AND
PROFES SIONAL
JUDGMENTS)
“Will you be able to hit a home run on this case?”
It is the rare attorney who is so psychopathic or
aggressive as to make an up-front suggestion to a
potential expert that only a certain opinion is
being sought, but it happens. It is more common
for an attorney or insurance company representa-
tive to inquire about a professional’s training and
experience. Questions about board certification,
work setting and experience, and familiarity with
a particular clinical issue are entirely appropriate
and should be welcomed. However, in some cases
the attorney may drop subtle or not-so-subtle
hints that certain opinions are being sought.
It may be the case that an attorney is naive and
inexperienced and that they can be quickly dis-
abused of your willingness to go along for the ride.
Of course, some attorneys are not naive about such
issues, and these might be refused one’s services.
Attorneys are not the only possible source of
bias in a forensic neuropsychological examina-
tion. As reviewed in a chapter by Sweet, Grote,
and van Gorp (2002), both the neuropsycholo-
gical expert and the patient may also introduce
elements of unfairness or preconceived notions
of outcome of an evaluation. The interested
reader might review Sweet and Moulthrop’s (1999)
article on ways one might attempt to identify bias
in one’s own work. The subsequent commentary
and critique of this article by Lees-Haley (1999),
as well as Sweet and Moulthrop’s response to
Lees-Haley, provide a range of complementary
and contradictory views.
REVIEW OF RECORDS/
E X A M I N AT I O N O F PAT I E N T
(ES 9.01 BASES FOR
AS SES SMENT)
“Don’t worry Doctor, we’ll tell you what you
need to know about this case.”
Neuropsychologists unfamiliar with their role
may not fully appreciate their duty to exhaust
all reasonable means to understand a case
before they reach their opinion. They need to be
pro-active in asking for and receiving appropriate
background information. These might include
108 forensic neuropsychology
school and work records to estimate premorbid
functioning, or deposition transcripts of the
patient’s collaterals to determine their view of
how a person’s daily life has been affected by an
accident or illness. Medical records can be volu-
minous in these cases, but the forensic neuro-
psychologist should routinely attempt to review
things such as ambulance and police records, the
statements of witnesses, as well as emergency
room, hospital, and imaging records. Psycholo-
gists should not passively rely on the judgment of
the retaining party to determine which records
will be sent. Attorneys or insurance companies
might send only a subset of a voluminous group
of records to a psychologist for review, and it may
be the case that these are sufficient for the psycho-
logist to understand the situation. If they are not
sufficient, it is the psychologist’s duty to ask for
additional records, which may or may not be
available. If they are not available or not sent
for some other reason, the psychologist should
document this in their records and report, and
note the effect that this lack of information had on
their opinion.
In most cases, a decision needs to be made as
to whether the psychologist is going to request to
do their own examination of a patient. This
request for examination will often be agreed to by
a retaining party, but in some cases this request
may not be granted. This could be because certain
deadlines have passed or the patient’s attorney is
somehow successful in refusing to accede to
such a request. It should be noted that failure to
personally examine a patient does not mean that a
psychologist cannot produce opinions. Ethical
Standard 9.01c addresses this in acknowledging
that in some situations an individual examination
is not warranted or necessary for opinions.
Obviously, psychologists will typically have to
offer a more limited range of opinions in cases
where they only review records and have not seen
a patient, but again, they are not precluded from
offering any opinions. The primary point is that
psychologists need to determine what must be
reviewed or done in order for them to arrive at
their opinions. They should not rely on the
opinions of retaining or opposing parties to deter-
mine this. Obstacles should be fought against,
and if the result is unsuccessful (records or patient
not examined) the effect of this needs to be
incorporated into the report.
“Doctor, please provide your opinion about this
person’s mental health even though you will not
have the opportunity to examine them.”
At times, attorneys will want the input of neuro-
psychologists even though they know there will
not be an opportunity for an independent medi-
cal evaluation. The reasons for this “denial” of
evaluation can vary, but may include legal strategy
on the part of the attorney, an unwillingness to
pay fees associated with a clinical evaluation, the
passage of a court-imposed deadline of the time
by which the evaluation could have been con-
ducted, or that the person in question simply isn’t
required to present themselves for an evaluation.
Since the number of reason for nonevaluation
can vary so widely, so does an appropriate response
on the part of the consulting neuropsychologist.
Obviously, we don’t have to be co-opted or other-
wise participate in schemes initiated by attorneys
based on their procrastination, cheapness, or lack
of attention to detail. To do so without disclaimer
would put a neuropsychologist at risk of issuing
incomplete or incorrect opinions and accordingly
put one at risk of complaints of incompetent
practice from the examined client. However, at
times there may be legitimate or unavoidable
circumstances in which a client is indeed unavail-
able for examination. While it might be preferen-
tial for some to simply “just say no” to any
consultation request that doesn’t allow for per-
sonal examination, such automatic denial may
preclude the court from benefiting from at least a
partial or preliminary analysis by a competent
neuropsychologist. It is not difficult to imagine
scenarios wherein a neuropsychologist’s review of
records could make a difference in the court’s
understanding of a client’s mental or cognitive
health. As long as the neuropsychologist had
wanted to (but couldn’t) examine a client, had
some reasonable method of determining their
opinion, and expressed the limitations of their
opinion because of the lack of ability to conduct
an examination, it would seem that they acted
within the bounds of ethical conduct.
S A F E G UA R D I N G
PSYCHOLOGICAL TESTS (9.04
R E L E A S E O F R AW D ATA )
“We’ll let you test our patient only if we tape your
evaluation.” “Send your complete file to us.”
Attorneys have a duty to represent their client’s
interests, and they do not have to be objective or
even “friendly” in how they do this. They often
will voice active suspicion of opposing experts
and imply that only a biased incompetent expert
could have arrived at certain opinions. Sometimes
 Ethical Practice of Forensic Neuropsychology
they may feel this way even before the patient is
evaluated and go to great lengths to insure that an
evaluation will be done “fairly.” Therefore, they
may attempt to obtain court orders that allow the
examination to be videotaped or audiotaped.
Demands might be made to allow an attorney or
their representative (such as another psychologist
or a court reporter) to sit in on the evaluation.
At the end of the evaluation, attorneys might
insist that copies of all test materials be sent to
them. Any of these scenarios should cause the
psychologist to invoke Ethical Standard 9.04.
Test data should not be released to nonpsycholo-
gists unless there’s good reason to (see Figure 4.1
and earlier discussion). In the case of a post-
evaluation request for raw data, it is nearly inevi-
table now that requested raw data will have to be
copied and sent to someone else. However, this
does not mean that psychologists need to agree to
infringements on the evaluation itself. While it
may be that attorneys are sincerely interested in
ensuring that only appropriate interviewing and
testing is being conducted, it seems equally if not
more likely that such requests are meant to intimi-
date the evaluating psychologist, perhaps even to
the point of withdrawing from the case for ethical
concerns or because of the unpleasantness of being
monitored by an adversarial party. Psychologists
should attempt to educate others about the nega-
tive impact that this third-party observation may
have on the obtained results. Position papers from
the National Academy of Neuropsychology
(Axelrod et al., 2000) and the American Academy
of Clinical Neuropsychology (2001), as well as
other sources (Constantinou, Ashendorf, &
McCaffrey, 2002) can be cited in such instances,
and previously have caused judges to disallow an
invasion of the evaluation process. However, since
some states may allow an attorney to be present
during any independent medical evaluation, the
psychologist must be prepared for this and have
ready a series of responses for different scenarios.
It may be that, if forced, a neuropsychologist would
agree to allow an attorney to quietly sit behind a
client during the interview or testing. Such a stance
may be the best that can be hoped for in certain
cases. However, it is difficult to imagine how a psy-
chologist would allow this observer to interfere
with the evaluation process, such as by interrupt-
ing with questions, comments, or derisive sneers
and snorts. It is also difficult to imagine situations
in which a psychologist might allow recording
equipment during the administration of psycho-
logical tests, unless there was some sort of agree-
ment or protective order that prohibited release or
109
further use of these recordings. Additional details
on ways to handle requests for release of raw data
or test materials can be found in another position
paper put out by the National Academy of Neuro-
psychology (www.nanonline.org).
R A N G E A N D D E TA I L O F
I N T E RV I E W ( E S 9 . 0 1 B A S E S
FOR AS SES SMENT)
“I’m only answering the interview questions that
I think are relevant.”
It may not be unusual for patients to come to an
independent medical evaluation with the feeling
that the evaluating psychologist is there to help
them no matter what (if referred through their
attorney) or there to hurt them no matter what (if
referred by their insurer or an opposing attorney).
Attempts to convince them of the evaluator’s neu-
trality might be attempted, but still might be
answered by the patient with scorn or disbelief. In
any event, the patient’s attitude should not deter-
mine the number, range, or type of questions asked
of them. Despite attempts to build some rapport,
some patients may go on to refuse to answer inter-
view questions. This could range from an isolated
question or two to a steadfast refusal to answer any
all-forthcoming questions. In such situations the
neuropsychologist must determine if the informa-
tion is needed for them to arrive at opinions being
asked of them. If the information indeed is needed
(as will probably be the case, since the question
was asked in the first place), the clinician then has
the dilemma of determining how to proceed. It
might be possible to persuade the patient into con-
tinuing with the interview by pointing out the rel-
evance of the questions. Alternatively, the question
might be asked either later in the interview or
rephrased in another way that the patient does not
find objectionable. However, the neuropsycholo-
gist should not refrain from terminating an evalu-
ation if it appears that the client’s resistance is so
high as to keep one from obtaining the needed
background information.
R E L AT I O N S H I P S W I T H
LITIGANTS AND CLAIMANTS
(ES 9.03 INFORMED CONSENT
IN AS SES SMENTS)
“Doctor, will you send me a copy of my report?”
It might seem self-evident that litigants and
claimants understand the reason they’re being
110 forensic neuropsychology
referred for a forensic neuropsychological assess-
ment, as one could presume they’ve been informed
by their attorney or insurance company about
this. Since one can’t make such an assumption, it
is incumbent upon a neuropsychologist to explain
the circumstances of the assessment. This debrief-
ing minimally should include an explanation that
the patient is being referred for an independent
medical evaluation (IME) and not for treatment.
Patients need to understand that there are limits
to confidentiality and that a report detailing the
results will be written. They also need to under-
stand that feedback won’t be offered to them
unless the neuropsychologist is authorized to do
so. Litigants should have an opportunity to ask
questions. The patient’s understanding of the
evaluation might be memorialized by having
them sign some sort of IME waiver or disclaimer.
However, since some litigants have been fore-
warned “to not sign anything,” it is also acceptable
to have a verbal explanation and consent, which is
then documented by the psychologist. In some
states such as Florida, written informed consent is
required for any psychological service. In such
states, the retaining attorney should be made
aware of the need for informed consent prior to
the date of evaluation, so that the informed con-
sent form can be forwarded to opposing counsel
for review prior to the examination.
The ethics code requires psychologists to make
a determination of whether a patient is competent
prior to obtaining informed consent. If there is
some reason to doubt this (and the basis for this
doubt will probably have to be documented some-
where), then the patient may need to only give
assent. This seems to be a less-stringent criterion
than consent. The former may be generally inter-
preted as primarily presenting information to a
patient and allowing the patient to ask questions
or have the opportunity to make objections
known. However, it may not always be required
that the patient make some sort of indication that
he or she understands and agrees to proceed with
the assessment if it appears that the patient lacks
the ability to do so. In contrast, patients who ini-
tially are presumed or known to be competent
would be required to give consent, meaning that
there is some indication both that they understand
what is proposed and they have agreed to this.
How much detail should neuropsychologists
provide in explaining what will happen if a patient
is assessed, and how should this be documented?
This is not spelled out by the ethics code and could
not be, given the inevitable problems that would
occur if a “one-size-fits-all” solution had been
attempted on what will obviously be a compli-
cated and diverse range of situations.
One possible solution has been proposed by
the Board of Directors of the National Academy
of Neuropsychology. Their official statement on
informed consent in clinical neuropsychology
practice (National Academy of Neuropsychology,
2003a), approved in October 2003, includes both
a flowchart indicating for which situations either
assent or consent should be obtained, as well as a
sample template for informed consent. The last
document explains some of what the patient
should expect during the evaluation (e.g., inter-
view, memory testing), foreseeable risks such as
frustration or fatigue, estimated fees and length of
evaluation (including that patients are ultimately
responsible for the fee), and limits of confidenti-
ality. Presenting such a document to a patient,
and the patient eventually signing it, has some
obvious merits, particularly in that it provides a
strong counterclaim to any later possible patient
claims that he or she did not know what to expect.
A subsequent position paper on independent and
court-ordered neuropsychological evaluations
includes an example of an informed consent form
for this particular type of evaluation (National
Academy of Neuropsychology, 2003b). This docu-
ment forewarns the examinee regarding tests of
symptom validity in such a manner as to minimize
potential for detection of these procedures;
specifically, the examinee is advised to answer
questions as accurately as they can; for example,
when discussing their problems they are not to
minimize major problems, nor are they to exag-
gerate lesser concerns. Moreover, they are informed
that they are expected to give their best effort
during testing, clarifying that they are not expected
to get every answer or problem correct, for no one
ever does, but must give their best effort. Last, they
are advised that part of the examination will
address the accuracy of their responses as well as
the degree of effort that they exert on the tests.
INFORMED CONSENT
F O R S E RV I C E S O F
AN INTERPRETER (ES 9.03,
SECTION (C))
“Doctor, this claimant does not speak English.
Will you please evaluate this patient for me?”
Non-English-speaking persons continue to
constitute a sizable percentage of the population
 Ethical Practice of Forensic Neuropsychology
of many American cities and regions. This is due
in part to new immigrants coming to America,
but also because some persons do not become
fluent in the English language even after having
been in the United States for years or decades.
These factors make it important that psycholo-
gists realize that the last revision of the APA Ethics
Code mandates that informed consent is also
required for services of an interpreter. This has
been separated out here because this seems to be
an issue different from what is usually considered
a routine part of obtaining informed consent for
assessment. Ethical Standard 9.03 states that
“Psychologists using the services of an interpreter
obtain informed consent from the client/patient
to use that interpreter, ensure that confidentiality
of test results and test security are maintained,
and include in their recommendations, reports,
and diagnostic or evaluative statements, including
forensic testimony, discussion of any limitations
on the data obtained.” Also relevant is Section
9.02(c): “Psychologists use assessment methods
that are appropriate to an individual’s language
preference and competence, unless the use of an
alternative language is relevant to the assessment
issues.”
These standards bring to mind issues raised by
Artiola and Mullaney (1998) and others (LaCalle,
1987) that discuss the evaluation of patients
who come from a different culture or who speak
a different language than the evaluator. There is
no doubt that such patients should, when possi-
ble, be referred to clinicians who speak the same
first language as the patient. Also, the clinician
should attempt to use assessment instruments
developed and normed for the appropriate ethnic
group. Ponton and Leon-Carrion (2001), for
example, have written extensively on how to
evaluate Hispanic patients appropriately.
It is less clear, however, what to do if a clini-
cian cannot find an appropriate colleague for
referral. This problem is especially acute in large
cities such as Chicago or New York, where the
clinician is likely to encounter patients who speak
Urdu, Mandarin, or myriad other languages.
It is unlikely that these clinicians will have access
to colleagues who either speak these languages
or have appropriately normed testing materials
available.
What should be done in such circumstances?
Although it may be tempting simply to tell a refer-
ent that “It can’t be done,” this runs the risk of
denying clients appropriate services. Obviously,
responses at the other end of the spectrum may be
111
equally inappropriate. That is, proceeding as if the
patient is fluent in English and is familiar with
“majority” American culture and not describing
the limits of the evaluation in one’s report is just as
likely to lead to an inappropriate outcome. Instead,
each referral of this type will dictate various
ways of proceeding, which might range from
referral to a colleague, to judicious and limited
evaluation, to refusal to accept the referral even in
the absence of referring elsewhere.
If a clinician elects to proceed with the use of
an interpreter, the ethical standard does serve
as a warning that patients must agree to this, and
the interpreter must be cautioned against the
inappropriate release of information to non-
authorized others concerning either information
about the patient or the specifics of a test’s items
or content. Clinicians should also be cautious
about asking friends or relatives of the friend to
stand in as interpreters because their lack of
objectivity may interfere with accuracy. Patients
might also be reluctant to disclose personal
information fully in interviews if a friend or
relative is serving as an interpreter.
“Doctor, you are ordered by this court to have
your evaluation videotaped through a one-way
mirror, but you are not to notify the examined
client about such taping.”
While attempting to preclude the presence of a
third party observing or videotaping the exami-
nation of a child because of the potential biasing
effects on the examination, a judge proposed (and
immediately ordered) what he thought to be a
sensible compromise: The videotaping would take
place, but behind a one way mirror. This would
ostensibly kill two birds with one stone: The plain-
tiff ’s attorney is granted his/her wish of monitor-
ing the examination and the potential of scaring,
alarming, or biasing the child with videotaping
equipment and technicians is removed by means
of a secret recording. At first glance, this might
seem like an acceptable and preferred solution,
but upon further analysis, it is not. As described
in a recent NAN position paper (Bush et al., 2009),
the problem is that of deception. By not inform-
ing the client of an essential component of the
evaluation (the videotaping) one is engaged in
an activity undermining the client’s (or the
client’s guardian’s) ability to be informed of the
context of the evaluation and how it is being
conducted. Beside the primary problems involved
in deceiving a client, it is not difficult to further
112 forensic neuropsychology
imagine other complications that could arise
during a secret videotaping. These could include
the client making a “confession” meant only
for the ears of the neuropsychologist but instead
being recorded for all eternity and anyone
authorized to review the tape. Also, the client
might well detect the presence of the supposedly
undetected videographer by hearing them through
the wall or wandering into the taping room. Of
course, the angry and bewildered reaction that
might understandably result from such detection
would certainly and negatively affect any chances
of a valid examination being conducted post-
discovery.
PERFORMING A
C O M P E T E N T E VA L UAT I O N
(ES 9.01 BASES FOR
A S S E S S M E N T, 2 . 0 3
M A I N TA I N I N G
COMPETENCE)
“You don’t need to give my client a malingering
test. I can tell you he’s honest.”
As earlier reviewed, neuropsychologists should
not enter into cases in which they do not have
proper expertise. This would include awareness of
recent developments in the field and knowing
some of the seminal papers about issues being
discussed. For instance, the papers by Dikmen
et al. (1995) and Binder (Binder, 1997; Binder,
Rohling, & Larrabee, 1997) and the book by
McCrea (2007) are extremely important contribu-
tions in how to diagnose and understand mild
traumatic brain injury, but it is evident that many
neuropsychologists are unfamiliar with these
papers, and seem to have no greater understand-
ing of this topic than what they might have learned
in graduate school years or decades ago (also see
chapter 9, this volume). Similarly, some clinicians
have argued that tests of effort, or “malingering
tests,” don’t need to be given since they can assess
this by virtue of their observation of the patient,
or because that area of research isn’t well devel-
oped in their opinion. Such comments, of course,
run counter to empirical research (Grote et al.,
2000; Sweet, 1999; Youngjohn, Spector, & Mapou,
1998; chapter 5 this volume). Some of these same
clinicians also have argued that it is appropriate to
give tests that have not been re-normed in over 50
years. The basis for such claims seems quite thin.
The point is that our clinical work is based on
scientific investigations, and these are ongoing.
Clinicians have a responsibility to keep up
with developments in their field. Failure to make
reasonable efforts to do so may well justify charges
of failure to adhere to the standards of one’s field
and to maintain one’s competence.
A C C U R AT E A N D F U L L
REPORTING OF FINDINGS
(ES 9.01 BASES FOR
AS SES SMENT; 9.10
EXPLAINING AS SES SMENT
R E S U LT S )
“Doctor, please don’t mention that my client
was once arrested. It has nothing to do with
this case.”
“Doctor, don’t include my wife’s IQ scores
in your report. Her employer has no need to
know them.”
A neuropsychological interview is just as, if not
more than, important than any test that might be
administered (Lezak, Howieson, & Loring, 2004).
These interviews need to assess a broad range of
factors that will assist the neuropsychologist
in placing the test data in proper context. Both
clinical and forensic patients should routinely be
asked questions about their families of origin;
educational attainment and achievement; previ-
ous medical, psychiatric and substance abuse
histories; and so on. It is not unusual for such
interviews to reveal potentially embarrassing
details that a client, or their attorney, would prefer
not go into a report. Of course, this possibility
should have been discussed beforehand during
the informed consent for assessment, and these
details need not be reported if they don’t contrib-
ute to an understanding of the patient’s neuropsy-
chological status. However, the neuropsychologist
should remember that they are ultimately respon-
sible for providing a full and correct neuro-
psychological opinion, and they may not be able
to arrive at such opinions if they agree to omit
relevant biographical details.
ACCURACY IN TESTIMONY
(ES 9.06 INTERPRETING
A S S E S S M E N T R E S U LT S )
“Doctor, please don’t mention that you found scor-
ing errors that would help my opponent’s case.”
As entire texts (Brodsky, 1999) have been written
to provide extensive detail on how to prepare for
 Ethical Practice of Forensic Neuropsychology
and conduct oneself in giving expert testimony,
this review will give detail for just one component
of testimony—that of giving full and honest opin-
ions about one’s findings. Testifying at deposition
or in court can be very stressful and unnerving,
especially if the retaining attorney attempts to
coach or even bias your testimony beforehand.
In most cases, attorneys will ask to meet with their
retained expert for 15 to 60 minutes prior to a
deposition. This typically will involve some dis-
cussion of their expert’s findings and opinions,
including what the expert might say in response
to likely questions from the deposing attorney.
However, the occasional attorney might attempt
to convince the expert to withhold certain opin-
ions if possible. This could include the discovery
of scoring errors made by another psychologist,
and the realization that accurate scoring could
be seen as “helping the opposition.” Of course, a
forensic neuropsychologist cannot ignore this
data, and must inform the retaining attorney of
their opinions, even if the opinions are based on
errors not yet discovered by others in the case.
P ROT E C T I N G T H E P U B L I C
(ES 1.05 REPORTING
E T H I C A L V I O L AT I O N S )
Psychologists will sometimes encounter reports or
opinions from colleagues whose work seems to be
so riddled with error, or without any reasonable
scientific foundation, that it raises a question as to
whether that colleague is acting in a competent
and ethical manner. Reaching a decision about
whether to contact the colleague, or perhaps even-
tually reporting the colleague to a regulatory or
professional organization, can be difficult. The
psychologist should determine whether the per-
ceived differences in opinions or work products
simply reflect an honest difference in opinion or
whether a colleague’s work can be viewed by others
as representing a significant threat to patients or
the public good. Previous reviews (Deidan &
Bush, 2002; Grote, Lewin, Sweet, & van Gorp,
2000) have detailed when and how a psychologist
might proceed in such situations. Obviously, friv-
olous or harassing complaints should never be
made, but it is recommended that psychologists
take appropriate steps when they perceive that a
colleague has acted in a grossly incompetent or
unethical manner.
It is also recommended that one not contact
another psychologist, or file a complaint,
until incident litigation has fully resolved.
Although there may be emergent situations where
113
immediate reporting is required, more typically a
complaint filed in the midst of ongoing litigation
could be perceived as a tactic of intimidation or
harassment. A 2003 position paper from the
American Academy of Clinical Neuropsychology,
published in The Clinical Neuropsychologist,
detailed this issue.
S U M M A RY
This chapter has reviewed the increasing use of
neuropsychologists by courts, the vastly increased
availability of position papers and other publica-
tions on the ethical practice of forensic neuro-
psychology, the context in which these ethics are
grounded, and the continued importance of the
protection of raw data/test materials.
It is hoped that this review will contribute to
the ethical practice of this burgeoning subfield,
as it is gratifying to see the inroads made by our
profession both in the application of our craft and
in the vastly increased attention being made by its
members to provide the public well-validated and
ethical services.
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The Clinical Neuropsychologist, 21, 232–38.
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Axelrod, B., Barth, J., Faust, D., Fisher, J., Heilbronner,
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 5
Assessment of Malingering
G L E N N J. L A R R A B E E
This chapter reviews definitions of malingering,
research designs for investigation of malingering,
and discusses various symptom validity tests and
response bias procedures developed to identify
the presence of malingering. The primary purpose
is to provide a conceptual understanding of the
construct of malingering rather than offer a
detailed review of the procedures developed for
detection of malingering. Detailed reviews of
these procedures are provided by Boone (2007a)
and Larrabee (2007), and the edited case book by
Morgan and Sweet (2009) provides an extensive
bibliography of various measures of symptom
validity and response bias. Last, the American
Academy of Clinical Neuropsychology (AACN)
has published a consensus statement on the
neuropsychological assessment of effort, response
bias, and malingering (Heilbronner, Sweet,
Morgan, Larrabee, & Millis, 2009).
DEFINITION OF
MALINGERING
Accurate neuropsychological evaluation is based
on test procedures that are reliable, yielding con-
sistent and stable scores, and valid, producing true
measures of the abilities and traits that we assume
we are measuring; thus, tests of attention should
yield reliable and valid assessments of attention,
and tests of memory should yield reliable and
valid measurement of memory function. Test pro-
cedures that have proven reliability and validity,
however, may yield scores that are not reliable or
valid measures for the individual examined; in
other words, these test performances are not an
accurate measure of the examinee’s actual level of
ability. In these instances, questions about the
accuracy of patient performance arise because
of significant inconsistencies in test data
(Iverson & Binder, 2000; Larrabee, 1990). These
may include inconsistencies between neuropsy-
chological domains (e.g., impaired attention with
normal memory); inconsistencies between
neuropsychological test scores and the suspected
etiology of brain dysfunction (e.g., impaired
IQ with normal memory in alleged hypoxic brain
injury); inconsistencies between neuropsy-
chological test scores and medically documented
severity of injury (e.g., performance at levels char-
acteristic of those associated with prolonged coma
in a patient who had a blow to the head without
loss of consciousness); and inconsistencies between
neuropsychological test scores and behavioral
presentation (e.g., failure on measures of recent
and remote memory contrasted with the ability,
during interview, to report an accurate clinical
history). Analysis of inconsistencies, as well as
consistencies in performance helps define a second
type of validity: performance validity.
Inconsistencies in test scores often are the
result of variable effort and motivation. Variable
motivation can be secondary to factors outside
the patient’s conscious intent or control, such as
depression, anxiety, or conversion disorder, or
may result from conscious, intentional response
distortion such as occurs in factitious disorder or
malingering (Iverson & Binder, 2000; Larrabee,
1990). Factitious disorder and malingering
share intentional, volitional distortion or misrep-
resentation of symptoms, but differ in that the
motivation for factitious disorder is the psycho-
logical need to assume a sick or disabled role
(Diagnostic and Statistical Manual of Mental
Disorders, fourth edition [DSM-IV], American
Psychiatric Association, 1994). In contrast, malin-
gering is the intentional production of false or
grossly exaggerated physical and psychological
symptoms for external incentives such as obtain-
ing monetary compensation or avoiding criminal
prosecution (DSM-IV, American Psychiatric
Association, 1994; Rogers, 2008).
Rogers (1997a; 2008) discussed various
explanatory models of malingering, including

(a) mentally disordered (pathological), (b) antiso-
cial/criminological, and (c) adaptational. The
adaptational model, first proposed by Rogers
in 1990 (1990a, 1990b), considers would-be
malingerers as engaging in a cost–benefit analysis
when confronted with an assessment perceived
as indifferent or in opposition to their needs.
In this model, malingering is more likely to occur
when the context is adversarial, the personal
stakes are very high, and there are no other
perceived viable alternatives.
Rogers (1997a) noted that descriptive data
generally support the adaptational model, with
higher prevalence of malingering in adversarial
settings (forensic vs. nonforensic) or when per-
sonal stakes are particularly high (e.g., avoiding
military combat or succeeding in personal injury
litigation). Rogers considered the adaptational
model as providing “the broadest and least
pejorative explanation of malingering” (Rogers,
1997a, p. 8). As a consequence, clinicians may be
less likely to ignore evidence of malingering
because a person does not fit more judgmental
criteria (Iverson & Binder, 2000). The cost–benefit
analysis underlying the adaptational model also
allows gradations of malingering (mild, moder-
ate, severe) and better fits the definition of
malingering as involving either fabricated or exag-
gerated deficits.
Malingering can occur in one of three patterns
in neuropsychological settings (Iverson &
Binder, 2000; Larrabee, 2000): (a) false or exag-
gerated reporting of symptoms (Larrabee, 1998;
Nelson, Sweet, & Demakis, 2006; Wygant et al.,
2007); (b) intentionally poor performance on
neuropsychological tests (Binder & Willis, 1991;
Mittenberg, Rotholc, Russell, & Heilbronner,
1996); or (c) a combination of symptom exaggera-
tion and intentional performance deficit (Heaton,
Smith, Lehman, & Vogt, 1978; Larrabee, 2003a).
Extensive research exists on specialized proce-
dures to detect malingering, such as the Portland
Digit Recognition Test (PDRT; Binder & Willis,
1991) the Test of Memory Malingering (TOMM;
Tombaugh, 1996), and Word Memory Test (WMT;
Green, Lees-Haley, & Allen, 2002), as well as
research identifying patterns of malingering on
standard clinical tests (Mittenberg, Aguila-
Puentes, Patton, Canyock, & Heilbronner,
2002) and fabrication and exaggeration of symp-
toms on the Minnesota Multiphasic Personality
Inventory-2 (MMPI-2; Butcher et al., 2001;
Lees-Haley, 1992; Lees-Haley, English, & Glenn,
1991).
Assessment of Malingering 117
Drawing on the work of Rogers (1990a,
1990b), Pankratz and Binder (1997), Greiffenstein
and colleagues (Greiffenstein, Baker, & Gola,
1994; Greiffenstein, Gola, & Baker, 1995), and
Nies and Sweet (1994), Slick, Sherman, and
Iverson (1999) have proposed diagnostic criteria
for malingered neurocognitive dysfunction
(MND). This is defined by Slick et al. (1999) as the
volitional exaggeration or fabrication of cognitive
dysfunction for the purpose of obtaining substan-
tial material gain (e.g., compensation for injury)
or avoiding or escaping legally obligated formal
duty (e.g., prison, military) or responsibility
(e.g., competency to stand trial).
The Slick et al. (1999) criteria require consid-
eration of separate criteria including (A) presence
of a substantial external incentive, (B) consider-
ation of evidence from neuropsychological
testing, (C) evidence from self-report, and
(D) behaviors meeting necessary criteria from B
and C are not fully accounted for by psychiatric,
developmental, or neurological factors. Evidence
from neuropsychological testing (B) includes defi-
nite negative response bias, defined as below
chance performance (p < .05) on one or more
forced-choice measures of cognitive function,
whereas probable response bias involves perfor-
mance on one or more well-validated psychomet-
ric tests or indices consistent with feigning.
Evidence from neuropsychological testing also
includes discrepancies between test data and pat-
terns of brain functioning, discrepancies between
test data and observed behavior, discrepancies
between test data and reliable collateral reports,
and discrepancies between test data and docu-
mented background history.
The Slick et al. (1999) indicators of evidence
from self-report (C) include self-reported history
discrepant with documented history, self-reported
symptoms discrepant with known patterns of
brain functioning, self-reported symptoms dis-
crepant with behavioral observations, and self-
reported symptoms discrepant with information
obtained from collateral informants. Self-reported
evidence of malingering also includes evidence of
exaggerated or fabricated psychological dysfunc-
tion based on well-validated validity scales or
indices from measures such as the MMPI-2.
The Slick et al. (1999) criteria for definite
MND include (A) presence of a substantial
external incentive, (B1) definite negative response
bias (e.g., worse-than-chance performance on
forced-choice testing), and (D) behaviors that
meet necessary criteria for definite negative
118 forensic neuropsychology
response bias that are not fully accounted for by
psychiatric, neurological, or developmental
factors. The criteria for probable MND include
(A) presence of a substantial external incentive;
(B) two or more types of evidence from neuro-
psychological testing, excluding definite negative
response bias or one type of evidence from
neuropsychological testing, excluding definite
negative response bias, and (C) one or more types
of evidence from self-report; and (D) behaviors
that meet necessary neuropsychological testing
criteria and self-report that are not fully accounted
for by psychiatric, neurological, or developmental
factors. The criteria for possible MND include
(A) presence of a substantial external incentive;
(C) evidence from self-report; and (D) evidence
from self-report is not fully accountable by psy-
chiatric, neurological, or developmental factors,
or criteria for either definite or probable MND are
met, but the D criteria (psychiatric, neurological
or developmental factors) cannot be ruled out.
Slick et al. (1999) urged thorough consider-
ation of differential diagnoses before concluding
that a person is malingering. They recommended
that a “reasonable doubt” strategy be applied to
decisions about the probability that a patient is
malingering, keeping in mind the limitations of
assessment methodology and the cost of false-
positive errors.
Bianchini, Greve, and Glynn (2005) have
extended the Slick et al. (1999) diagnostic criteria
for MND to malingered pain-related disability
(MPRD). Similar to MND, the criteria for MPRD
require an A criterion for presence of a substantial
external incentive, and E criteria for ruling out
presence of a viable legitimate neurologic, psychi-
atric, or developmental explanation for pain
symptom portrayal. Bianchini et al. (2005) also
make the important point that malingerers have
an end goal of demonstrating disability, a goal
that can be met not only by demonstration of
impairment of functional capacity on physical
examination (B criteria) or pain scale endorse-
ment (D criteria), but a goal that can also be met
by intentional underperformance on measures of
cognitive ability (C criteria; see Myers & Diep,
2000, for an example). Bianchini et al. introduce
the new criterion of “compelling inconsistency,”
which occurs when there is a discrepancy in the
way a patient presents when knowingly being
evaluated in contrast with when they are unaware
of being evaluated, such that it is reasonable to
believe the patient is purposefully controlling the
difference. Similar to the MND criteria of Slick
et al. (1999), the MPRD criteria allow a gradation
of certainty regarding diagnosis, ranging from
definite to probable to possible MPRD. Definite
MPRD is defined either by presence of signifi-
cantly worse-than-chance performance on two-
alternative forced choice testing, or presence of
one or more compelling inconsistencies, in the
presence of an external incentive, and absence of
alternative neurologic, psychiatric, or develop-
mental explanations. Probable MPRD is defined
by presence of external incentive, and two or more
types of “probable” evidence from criteria B, C, or
D, in the absence of alternative clinical explana-
tions. Possible MPRD is defined by external incen-
tive, only one type of evidence (exclusive of
worse-than-chance or compelling inconsistency)
from criteria B, C, or D and absence of alternative
explanations, or by the patient who meets a diag-
nosis sufficient for MPRD, with the exception that
the E criteria for absence of significant neurologic,
psychiatric, or developmental conditions cannot
be met. These criteria are also discussed in the
chronic pain chapter by Greve, Bianchini, and
Ord in the present volume.
Larrabee, Greiffenstein, Greve, and Bianchini
(2007) reviewed the diagnostic criteria for MND
and MPRD, noting several common features of
evidence supporting symptom or performance
invalidity. First, symptom report and test perfor-
mance are atypical in pattern or degree of deficit
for expected findings in bona fide neurologic,
psychiatric, or developmental disorders. Second,
the diagnostic criteria for both MND and MPRD
require presence of multiple indicators of symp-
tom exaggeration or performance invalidity, and
that there are no viable alternative explanations
for these atypical symptom endorsement or exam-
ination performance patterns. Larrabee et al.
(2007) observe that it is the combined improba-
bility of findings, in the context of external incen-
tive, without any viable alternative explanation
that establishes the intent of the examinee to
malinger.
RESEARCH DESIGNS FOR
I N V E S T I G AT I O N O F
MALINGERING
Rogers (1997b; 2008) reviewed basic research
designs for evaluation of malingering, including
the case study approach, simulation studies,
known-group designs, and differential prevalence
designs. The case study approach was used by
Pankratz, Fausti, and Peed (1975) in the evalua-
tion of hysterical deafness and by Hiscock and

Hiscock (1989) in their initial demonstration of
the validity of their Digit Memory Test (DMT).
Denney (1996) also employed a case study design
in the evaluation of claimed remote memory loss
in criminal defendants professing amnesia for the
events contemporaneous with the alleged crime.
Although these authors employed a single-case or
multiple-single-case approach, all three investiga-
tions relied on the normal approximation to the
binomial—applied to two-alternative, forced-
choice testing—that could be used to generate
probabilities of malingering (this approach is
discussed in greater detail in the section on
forced-choice symptom validity testing).
Simulation studies typically involve use of
noninjured persons who are provided with
instructions to attempt to feign deficit success-
fully in an imaginary litigation scenario. Rogers
(1997b) noted the main problem with these types
of studies is generalizability. That is, will the find-
ings in normal individuals simulating malinger-
ing generalize to the real-world setting, in which
the financial stakes are considerably larger and
involve real potential for financial gain? Rogers
(1997b) recommended a design strategy by which
four groups are studied: (a) simulating nonclini-
cal subjects, (b) honestly responding nonclinical
subjects, (c) honestly responding clinical subjects,
and (d) clinical subjects simulating greater impair-
ment than they really experience. Note that this
strategy should increase generalizability of the
results over studies that merely employ simulating
and nonsimulating nonclinical subject groups.
A number of neuropsychological investiga-
tions have contrasted simulators with groups of
subjects who have genuine clinical disorders, fre-
quently suffering from moderate-to-severe trau-
matic brain injury (TBI). Heaton et al. (1978) used
this approach, which has also been employed by
Mittenberg and his group in their investigations
of profiles of malingering on the Wechsler Adult
Intelligence Scale–Revised (WAIS-R; Wechsler,
1981), Halstead-Reitan Battery (HRB; Reitan &
Wolfson, 1993), and Wechsler Memory Scale–
Revised (WMS-R; Mittenberg, Azrin, Millsaps, &
Heilbronner, 1993; Mittenberg et al., 1996;
Mittenberg, Theroux, Zielinski, & Heilbronner,
1995; Wechsler, 1987).
The differential prevalence design is rarely
used and poses several problems of interpretation.
In this design, a group known to have a higher
base rate of malingering is investigated and con-
trasted with a group not suspected of having an
elevated rate of malingering. An example of this is
Assessment of Malingering 119
the Binder and Rohling (1996) meta-analysis of
litigating and nonlitigating closed injury. As
Rogers (1997b) pointed out, very little is learned
from differential prevalence designs because we
do not know who is dissimulating in each group
and how many are dissimulating in each group.
The fourth type of research design is the
known-groups design, also known as the criterion
groups design (Heilbronner et al., 2009). This
requires a two-part approach: establishing the
criterion groups (bona fide patients and malin-
gerers) and conducting a systematic analysis of
similarities and differences between the criterion
groups. This research design has benefited signifi-
cantly from the specification of diagnostic criteria
for malingering by Slick et al. (1999), which
provide stronger confidence in creating the
criterion groups. These criteria for malingering
have been employed by Greve, Bianchini, Mathias,
Houston, and Crouch (2002) to contrast the
performance of subjects who had probable MND
with that of persons who had moderate-to-severe
TBI. I (Larrabee, 2003b) employed the Slick et al.
(1999) criteria to compare and contrast perfor-
mance on the MMPI-2 as well as on a select
number of standard neuropsychological test
procedures in subjects with definite or probable
MND and subjects who had suffered moderate
and severe TBI (Larrabee, 2003a). As Rogers
(1997b) noted:
Employment of known-groups comparisons
addresses fully the clinical relevance of dis-
simulation research. First, the research
typically is conducted in clinical or other pro-
fessional settings where dissimulation is
expected to occur. Second and more impor-
tant, the persons engaging in dissimulation are
doing so for real-world reasons. (p. 416)
When using a clinical comparison group to
contrast performance either with a normal sub-
ject group simulating malingering or with a
known group of malingerers, it is important that
the clinical group not include malingering sub-
jects. This is particularly problematic when the
clinical group includes persons who themselves
are in litigation. One cannot merely assume that a
group of subjects with a bona fide condition such
as moderate or severe TBI are performing at their
best. Rohling, Binder, and Langhinrischen-
Rohling (1995) found that patients in chronic
pain in litigation averaged 0.48 pooled standard
deviations higher on pain scales than those not in
120 forensic neuropsychology
litigation, a value quite close to the .47 effect size
found by Binder and Rohling (1996) in contrast-
ing the neuropsychological performance of
TBI patients in litigation versus the performance
of nonlitigating TBI patients. Thus, when using
a compensation-seeking clinical control group,
this group must itself be carefully screened for
malingering.
SPECIALIZED TESTS
OF RESPONSE BIAS FOR
DETECTION OF
MALINGERED
NEUROCOGNITIVE
DEFICITS
Several specialized tests of response bias for detec-
tion of malingered cognitive deficit have been
devised, dating to Rey’s 15-item and dot-counting
procedures developed over 40 years ago (Lezak,
Howieson, & Loring, 2004; Rey, 1964). In modern
times, these procedures fall in two categories:
(a) tasks that appear to measure a cognitive
ability, but are so simple that even persons with
significant neuropsychological deficits can per-
form perfectly or near perfectly (e.g., Rey 15-Item
Test); and (b) tests based on forced-choice stimu-
lus presentation, which can be evaluated for
worse-than-chance performance using the normal
approximation to the binomial theorem, usually
referred to as symptom validity testing (SVT;
e.g., PDRT, Binder & Willis, 1991).
Simplistic Tests Performed
Normally by Brain-Injured Persons
The Rey 15-Item Test (Rey, 1964) is probably
the best-known task typically performed normally
by brain-injured persons, so that poor perfor-
mance may be considered a result of reduced
motivation. The 15 redundant stimuli (e.g., quan-
titatively equivalent Roman and Arabic numerals;
upper- and lowercase identical letters of the
alphabet; see Lezak et al., 2004) are presented for
10 seconds, then withdrawn, with the subject
asked to draw as many of the items as he or she
can recall. Various cutoffs have been recom-
mended, but performance is typically considered
motivationally suspect at 67% or less (Greiffenstein
et al., 1994; Lee, Loring, & Martin, 1992; Lezak
et al., 2004). The Rey 15-Item Test has been
criticized as having poor sensitivity to the
presence of malingering (Iverson & Binder, 2000;
Sweet, 1999). Others have questioned both
sensitivity and specificity (e.g., elevated level of
false-positive errors in patients with genuine
impairment secondary to amnestic disorder,
dementia, or severe psychiatric disorder;
Schretlen, Brandt, Krafft, & Van Gorp, 1991).
Because of these problems, it has been recom-
mended that the test not be the sole measure of
effort and motivation (Iverson & Binder, 2000),
and that the test should not be used in truly
amnestic populations or with patients suffering
severe psychopathology (Schretlen et al., 1991).
A meta-analysis of the 15-Item Test (Vickery,
Berry, Inman, Harris, & Orey, 2001) reported an
average specificity (i.e., correct identification of
clinical patients as not malingering) of 92.5%
(based on eight studies), average sensitivity (i.e.,
correct detection of malingerers as malingering)
of 43.3% (based on seven studies), and average hit
rate of 70.5% (based on six studies).
Two modifications of the 15-Item Test have
appeared (Boone, Salazar, Lu, Warner-Chacon, &
Razani, 2002; Griffin, Glassmire, Henderson, &
McCann, 1997). Griffin et al. eliminated the
sequence of three geometric patterns and three
lowercase letters on the original Rey 15-Item Test
and replaced them with two numerical sequence
stimuli redundant with the numerical sequences
on the original 15-Item Test. The sensitivity and
specificity of the revised “Rey-II” were evaluated
in honest and dissimulating college students and
honest and dissimulating nonlitigating clinical
groups of board-and-care residents (clinical
groups included those with schizophrenia and
developmental disability and elderly persons
needing residential care). Performance on the
Rey-II was contrasted with performance on
the original 15-Item Test (with the exception of
not having a condition of a dissimulating clinical
group on the original 15-Item Test). Griffin et al.
found that both quantitative and qualitative scores
on the Rey-II were superior in discriminating
genuine from poor effort in the college students
(qualitative scores had 100% specificity and 69%
sensitivity; quantitative scores had 97% specificity
and 73% sensitivity). These values were lower in
the college students for the original 15-Item Test
for qualitative scores (100% specificity, 57% sensi-
tivity) and quantitative scores (98% sensitivity,
40% specificity). In the clinical population admin-
istered the Rey-II, qualitative score specificity was
75%, with sensitivity of 71%.
The modification of the 15-Item Test devel-
oped by Boone, Salazar, et al. (2002) maintains the
original stimuli and format of the 15-Item Test,
but adds a recognition trial administered follow-
ing the standard drawing-from-recall condition.

The recognition trial presents Rey’s 15 original
stimuli with 15 numeric, geometric, and alpha-
betic foil stimuli on one page. The subject is then
instructed to look at the page, which includes “the
15 things that I showed you as well as 15 items
that were not on the page,” and circle the things
they remember from the page they previously
viewed. Scoring includes (a) recall correct,
(b) recognition correct, (c) false-positive recogni-
tions, and (d) a combination score computed as
recall correct plus recognition correct minus
false-positive recognitions (combined score).
Boone, Salazar, et al. (2002) evaluated the
sensitivity and specificity of the Rey 15-Item
Plus Recognition trial in four groups of subjects:
(a) a litigating group with independent evidence
of suspect effort, (b) a clinic patient group (non-
demented mixed neurological and psychiatric
patients), (c) learning-disabled college students,
and (d) normal control subjects (mean age 61.3
years). These authors found the best combination
of sensitivity and specificity for the combined
(recall plus recognition minus false-positive)
score, yielding a sensitivity of 71.4% and specific-
ity of 91.7–93.9%. In addition, Boone et al. identi-
fied four false-positive errors never made by clinic
or learning-disabled patients and rarely (by one
subject) by the normal controls.
Of suspect-effort cases, 14% made at least one
of the false-positive recognition errors compared
with 0.02% of the three groups of normal-effort
subjects. Boone, Salazar, et al. (2002) noted that,
although these four errors were not frequent in
the suspect-effort group, they may serve as virtual
pathognomonic signs of noncredible performance
when present (i.e., the presence of these signs
would have nearly 100% positive predictive value
for noncredible performance).
The Boone, Salazar, et al. (2002) investigation
showed that addition of a recognition trial to the
15-Item Test improved both sensitivity and speci-
ficity compared to the traditional version of the
test as well as to the other recent modification of
the test stimuli (Griffin et al., 1997). Indeed,
Boone, Salazar, et al. noted that the combined
score raised sensitivity by 50% relative to recall
alone and maintained high specificity.
Boone and Lu (2007) have cross-validated the
Rey 15-Item Test with recognition, using 90 addi-
tional noncredible patients and 105 comparison
patients. Using an E score cutoff of <20 yielded a
specificity of 85.7% (comparing favorably with the
original derivation sample specificity of >91%)
but sensitivity declined from 71% in the original
Assessment of Malingering 121
study to 55.6% on cross-validation. Boone and Lu
speculated that the decline in sensitivity may be
the product of increased sophistication of proba-
ble malingerers regarding effort tests, and/or rep-
resent the effects of compromised test security.
Additional procedures for evaluation of effort
that are sufficiently simple so that nonlitigating
clinical patients can perform adequately include
Rey’s Dot-Counting Test (Boone et al., 2002;
Lezak et al., 2004; Rey, 1964; Youngjohn, Burrows,
& Erdal, 1995), and the b Test (Boone et al., 2000).
The Dot-Counting Test requires the subject to
count dots presented on index cards as quickly as
possible. Some of the dots are grouped, whereas
others are not grouped. A person taking as long or
longer to count grouped dots as they did to count
ungrouped dots is displaying motivationally
suspect performance (Lezak et al., 2004).
Vickery et al. (2001) included the Dot-Counting
Test as one of the tasks in their meta-analysis of
measures of effort. These authors found that the
Dot-Counting Test was equivalent in mean effect
size to the 15-Item Test in separating subjects
showing poor effort from those demonstrating
adequate effort. Both the Dot-Counting Test and
Rey 15-Item Test yielded smaller effect sizes than
the DMT (Hiscock & Hiscock, 1989), the PDRT
(Binder & Willis, 1991), and the 21-Item Test
(Iverson, Franzen, & McCracken, 1991). Sensitivity
and specificity values could not be computed for
the Dot-Counting Test by Vickery et al. because of
inconsistencies in scoring procedures.
Subsequent to the Vickery et al. (2001) meta-
analysis, Boone, Lu, et al. (2002) published Dot-
Counting Test data on large samples of persons
with suspect effort, as well as on a large sample of
clinical subjects. Using an E score based on
ungrouped counting time plus grouped counting
time and number of errors, sensitivity was 100%
in a criminal forensic sample and 75% in a civil
litigation sample, with specificity of at least 90% in
the clinical groups. Boone and Lu (2007) con-
ducted a cross-validation of the Dot Counting
Test E score on 91 litigation/compensation-seek-
ing subjects failing other symptom validity test
procedures, compared to 111 clinical patients and
found little change in specificity (validation
sample = >90%; cross-validation sample = 89.2%)
or sensitivity (validation sample = 75%, cross-
validation sample = 72.5%).
The b Test (Boone, Lu, et al., 2000; Boone,
Lu, & Herzberg, 2002) requires subjects to
circle all the lowercase b’s in a 15-page booklet,
discriminating the b’s from the q’s, p’s, d’s, and
122 forensic neuropsychology
those lowercase letters with diagonal stems. Boone
et al. (2000; 2002) compared the b Test perfor-
mance of litigating subjects suspected of malin-
gering to the performance of nonlitigating
learning-disabled subjects; older depressed sub-
jects; nonlitigating individuals with moderate and
severe closed head injury (CHI), left or right
hemisphere cerebrovascular accident, or schizo-
phrenia; and normal elderly. Boone et al. (2002)
have also developed an E score for the b Test based
on weighted combinations of omission errors,
commission errors, and average time per stimulus
page. The b Test E score cutoffs are provided for
the various clinical groups above. Patients with
bona fide severe traumatic brain injury perform
the best, whereas patients with stroke or schizo-
phrenia perform the worst, necessitating higher
E score cutoffs to maintain a reasonable specific-
ity. Comparing a group of litigants with suspect
effort/probable malingering to all of the clinical
cases combined yields a sensitivity of 73.6%
and specificity of 85.1%, at an E score cutting
score of <120 (for valid test performance).
Measures of Response Bias and
Symptom Validity Based on
Forced-Choice Testing
The application of forced-choice methodology
and the normal approximation to the binomial to
evaluate validity of test performance represents a
major advance in the evaluation of malingering
(Binder, 1990; Binder & Pankratz, 1987; Hiscock
& Hiscock, 1989). In a forced-choice task (e.g.,
identifying whether one has been touched once or
twice; identifying which of two 5-digit numbers
was presented previously), it is conceivable that
someone could perform at chance level, consis-
tent with zero ability. If, however, someone per-
forms significantly worse than chance, based on
application of the normal approximation to the
binomial theorem, the assumption can be made
that they had to know the correct answer to per-
form at such an improbably poor level. At extreme
levels of probability (e.g., .05 or .01), it can be
argued that such an improbable performance is
tantamount to admission of malingering
(Larrabee, 2000).
The formula for the uncorrected z approxima-
tion to the binomial is
z = ( X − NP )/ NPQ
where X is the patient’s score correct, N is the
number of test items, and P and Q are the expected
proportions of right and wrong answers, respec-
tively. In a two-alternative task, P = Q =.5; in
a four-alternative task, P = .25, Q = .75. A one-tail
test is the most appropriate, given the suspected
intent of producing suppressed scores (Larrabee,
1992). Since the binomial distribution involves a
discrete variable and the normal distribution is
for a continuous variable, a correction factor of .5
is recommended to maximize correspondence
with the normal curve (for x falling below NP, the
0.5 is added to x; for x falling above NP, the 0.5 is
subtracted from x; Siegel, 1956).
Note that because the formula for the normal
approximation to the binomial is based on the
standard normal (z) distribution, forced-choice
tests can be constructed “on the spot” for a par-
ticular patient. Pankratz et al. (1975) constructed
a subject-specific forced-choice test for evaluating
feigned deafness, and Pankratz, Binder, and
Wilcox (1987) did the same for evaluation of
exaggerated somatosensory deficits. Denney
(1996) demonstrated that three criminal defen-
dants suspected of malingering remote memory
impairment in the context of evaluation for
competency to proceed to trial performed at
significantly worse-than-chance level on correct
identification of facts relevant to the alleged
offenses, presented in two-alternative, forced-
choice format.
A variety of SVTs utilizing the forced-choice
format have been published. Many used prese-
ntation of individual sequences of digits to the
subject, who after some period of time must
then “recognize” the multidigit number in a two-
alternative, forced-choice format: DMT (Guilmette,
Hart, & Giuliano, 1993; Hiscock & Hiscock, 1989);
PDRT (Binder, 1993; Binder & Kelly, 1996; Binder
& Willis, 1991); Victoria Symptom Validity Test
(Grote et al., 2000; Slick, Hopp, Strauss, & Spellacy,
1996); or Computerized Assessment of Response
Bias (CARB; Conder, Allen, & Cox, 1992).
Other procedures use words as test stimuli,
including the 21-Item Test, in which the subject is
presented with a list of 21 items they must freely
recall, followed by two-alternative, forced-choice
testing (Iverson, Franzen, & Mc-Cracken, 1991,
1994). The Word Memory Test (WMT) requires
the subject to learn a list of several word pairs
presented over two trials, followed by immediate
and then delayed forced-choice recognition of
one word from each word pair, with additional
yes/no recognition and paired associate, followed
by free-recall trials (Green, Iverson, & Allen, 1999;
Green, Rohling, Lees-Haley, & Allen, 2001;

Iverson, Green, & Gervais, 1999; Green, Lees-
Haley, & Allen, 2002).
There is also a visual memory malingering
measure based on two-alternative, forced-choice
recognition of easily encoded visual stimuli, the
Test of Memory Malingering (TOMM; Rees,
Tombaugh, Gansler, & Moczynski, 1998;
Tombaugh, 1996). Berry and colleagues (Inman
et al., 1998) have developed the Letter Memory
Test, a procedure for evaluating effort based on
recognition of arrays of three, four, and five con-
sonants presented in forced-choice format involv-
ing two, three, or four choices (note that each
stimulus length is tested in two-, three-, or four-
alternative format so that stimulus length is fully
crossed with number of alternatives). Last,
Frederick (1997) developed a forced-choice mea-
sure of nonverbal and verbal abilities, the Validity
Indicator Profile (VIP; also see Frederick, Crosby,
& Wynkoop, 2000; Frederick, Sarfaty, Johnston, &
Powel, 1994).
The two-alternative, forced-choice memory
analog tests (CARB, DMT, PDRT, 21-Item Test,
TOMM, Victoria Symptom Validity Test, and
WMT) can be scored for worse-than-chance
performance using the normal approximation to
the binomial. In addition, these procedures can be
scored on the basis of empirically derived cutoff
scores that minimize false-positive identification
in nonlitigating groups of clinical patients because
it has been found that many litigants suspected of
malingering do not perform at levels that are sig-
nificantly worse than chance; for example, Greve,
Binder, and Bianchini (2009) found that below
chance performance (p <0.05, one-tailed) on any
of the various trials of the PDRT, WMT, or TOMM
occurred at frequencies of 6.2%, 7.1% and 2.6%,
respectively. Typically, forced choice tasks are
sufficiently easy that the majority of nonlitigating
neurological patients can perform extremely
well (e.g., for the Letter Memory Test and DMT,
the average correct scores for nonlitigating neuro-
logical patients were 99.5% and 99.3% correct,
respectively, contrasted with 54.8% and 64.4%
correct, respectively, for normal community
volunteers faking head injury; see Inman et al.,
1998; for the TOMM, the majority of nonlitigat-
ing neurological and psychiatric patients scored
above the cutoff of 90% correct, see Rees et al.,
1998; Tombaugh, 1996).
For the VIP, Frederick developed a more
elaborate performance curve analysis based on
item difficulty. On the VIP, items are randomly
presented as to item difficulty level. In scoring,
Assessment of Malingering 123
item difficulty is taken into account so that
persons are expected to do less well as the task
becomes more difficult. Departures from this
expectation, particularly reversal of errors with
better performance on more difficult than on
easier items, are associated with a motivated
performance deficit.
Studies of the comparative sensitivity of SVTs
are beginning to appear. Vickery et al. (2001) con-
ducted a meta-analysis of the DMT, PDRT,
21-Item Test, 15-Item Test, and Dot-Counting
Test. The DMT was the most sensitive, separating
honest and dissimulating responders by approxi-
mately 2 SD, whereas the 21-Item Test and PDRT
had effect sizes of approximately 1.5 SD and 1.25
SD, respectively. In contrast, effect sizes were
equivalent, and the smallest, for the 15-Item and
Dot-Counting Tests, approximately 0.75 SD.
Vickery et al. (2000) also conducted sensitivity
and specificity analyses. Based on four studies, the
DMT had a specificity of 95.1% and a sensitivity
of 83.4%; the PDRT had a specificity of 97.3%,
sensitivity of 44%, and combined hit rate of 71.2%
based on two studies. The 15-Item Test had a
specificity of 92.5%, sensitivity of 43.3%, and
combined hit rate of 70.5% based on a range of six
to eight studies. The 21-Item Test had a specificity
of 100%, sensitivity of 22%, and combined hit rate
of 60.7% based on four to six studies.
Vickery et al. (2000) noted that the sensitivity
of the 21-Item Test could be improved by using a
more liberal cutoff score than that originally
proposed by the 21-Item Test authors. Vickery
et al.’s study was weighted more heavily with
noninjured dissimulators than studies using a
known-group design employing actual clinical
malingerers, which may limit the generalizability
of their findings. These authors recommended
against the use of any one measure, in isolation, as
a malingering screening device because of the
less-than-perfect sensitivities of the tests they
reviewed.
Subsequent to the review by Vickery et al.
(2001), Bianchini, Mathias, Greve, Houston, and
Crouch (2001) reported a higher sensitivity (77%)
for the PDRT, with a specificity of 100% in a
known-group design discriminating clinical
malingerers from subjects with moderate and
severe CHI. Inman and Berry (2002) found that
the Letter Memory Test and DMT attained the
highest hit rates for identification of malingering
in college students with and without history of
mild head injury who took the tests following
instructions for good effort versus instructions to
124 forensic neuropsychology
deliberately perform poorly. The DMT had a
specificity of 100%, sensitivity of 64%, and overall
hit rate of 82%; the Letter Memory Test had a
specificity of 100%, sensitivity of 73%, and overall
hit rate of 87%, compared to the 21-Item Test and
15-Item Test, which had sensitivities of 2% and
5%, respectively, and a specificity of 100% each.
The classification results for the DMT and Letter
Memory Test were also superior to the use of
malingering cutoff scores or formulas for Reliable
Digit Span (RDS; cf. Greiffenstein et al., 1994;
100% specificity, 27% sensitivity, 65% combined
hit rate); Seashore Rhythm Test (Reitan & Wolfson,
1993) errors greater than 8 (Trueblood & Schmidt,
1993; 98% specificity, 27% sensitivity, 64% com-
bined hit rate); Rey Auditory Verbal Learning Test
(AVLT; Rey, 1964) recognition less than 8
(Greiffenstein et al., 1994; 100% specificity, 16%
sensitivity, 60% combined hit rate); Digit Symbol
(Wechsler, 1981) scale score less than 5 (cf.
Trueblood, 1994; 100% specificity, 2% sensitivity,
53% combined hit rate); and the Bernard,
McGrath, and Houston (1996) Wisconsin Card
Sorting Test (WCST; Heaton, Chelune, Talley, Kay,
& Curtiss, 1993) discriminant function (100%
specificity, 9% sensitivity, 58% overall hit rate).
Greve, Ord, Curtis, Bianchini, and Brennan
(2008) compared the diagnostic accuracy of the
PDRT, TOMM, and WMT for discrimination of
probable TBI malingerers and probable pain
malingerers from nonmalingering patients with
bona fide TBI, and bona fide chronic pain.
Employing receiver operating characteristic
(ROC) analyses, Greve et al. found that the PDRT,
TOMM, and WMT had equivalent area under
curve (AUC) maximum values for discriminating
the TBI malingerers from TBI patients (PDRT
Easy AUC = 0.89; TOMM Trial 1 AUC = 0.85;
WMT IR AUC = 0.86), and for discriminating
chronic pain malingerers from chronic pain
patients (PDRT Total AUC = 0.78; TOMM Trial 1
AUC = 0.76; WMT Consistency AUC = 0.83).
AS SES SMENT OF
MALINGERING USING
AT Y P I C A L P E R F O R M A N C E
PAT T E R N S O N S TA N D A R D
NEUROPSYCHOLOGICAL
TESTS
Detection of malingering through the presence
of atypical performance patterns on standard
neuropsychological tests is the basis of the
performance inconsistency approach discussed in
the section on the definition of malingering
(Larrabee, 1990; 2000; Slick et al., 1999). Test
patterns should make “neuropsychological sense”
(Larrabee, 1990); hence, a patient with impaired
attention should not have above average memory
(Mittenberg et al., 1993); a patient with impaired
Wechsler Adult Intelligence Scale, Third Edition
(WAIS-III; Wechsler, 1997a) Digit Span at a level
characteristic of dementia should not have
above average WAIS-III Vocabulary (Mittenberg
et al., 1995, 2001); a patient with very poor Grip
Strength (Reitan & Wolfson, 1993) should not
perform above average on the Grooved Pegboard
(Lafayette Instrument, P.O. Box 5729, Lafayette,
IN; Greiffenstein, Baker, & Gola, 1996).
Mittenberg, Aguila-Puentes, et al. (2002)
referred to multiple variable pattern analysis
as neuropsychological profiling of symptom
exaggeration and malingering. The authors
credited Heaton et al. (1978) with the first demon-
stration that patterns of neuropsychological test
performance could discriminate 16 non-injured
dissimulators from 16 nonlitigating patients
with moderate-to-severe CHI. Using the WAIS
(Wechsler, 1955) and HRB, discriminant function
analysis correctly classified 100% of the dissimu-
lators and patients with CHI. Based on the
MMPI (Hathaway & McKinley, 1983) alone, only
one subject in each group was misidentified.
Significant univariate differences were found on
the WAIS Digit Span, and for HRB tests including
Category Test errors, Tactual Performance
Test Total Time, Memory and Location, Finger
Tapping, Finger Agnosia, suppressions, and the
Hand Dynamometer.
Mittenberg et al. (1996) replicated the Heaton
et al. results with an HRB discriminant function
contrasting noninjured dissimulating subjects
from nonlitigating subjects with CHI (mild,
moderate, and severe TBI). Significant univariate
differences were found on Category Test errors,
Tactual Performance Test Total Time, Speech
Sounds Perception Errors and Seashore Rhythm
Correct, Trails B, Finger Tapping, Sensory Suppre-
ssions, Finger Agnosia, and Finger Tip Number
Writing.
Patterns of performance indicative of poor
effort have also been reported on individual neu-
ropsychological tests, such as poor recognition
memory on the AVLT (Binder, Villanueva,
Howieson, & Moore, 1993; Boone, Lu, & Wen,
2005); and poor recognition memory on the
California Verbal Learning Test (CVLT; Delis,
Kramer, Kaplan, & Ober, 1987; Millis, Putnam,
Adams, & Ricker, 1995). More complex patterns
 Assessment of Malingering 125

characteristic of intentional underperformance

TABLE 5.1 PERFORMANCE OF
including atypical recall and recognition have
LITIGANTS WITH DEFINITE OR
been developed for the second edition of the
CVLT, the CVLT-2 (Delis, Kramer, Kaplan, & PROBABLE MALINGERED
Ober, 2000; Wolfe et al., 2010), and for the AVLT NEUROCOGNITIVE DYSFUNCTION AND
(Barrash, Suhr, & Manzel, 2004). Atypical error CLINICAL PATIENTS ON
patterns on problem-solving tests such as the NEUROPSYCHOLOGICAL TESTS
WCST (Bernard et al., 1996; Suhr & Boyer, 1999) SENSITIVE TO MALINGERING
and Category Test (Tenhula & Sweet, 1996) have
Test MNDa Clinical p Effect
also been identified. Patientsb Sizec
I (Larrabee, 2003a) found that scores on Benton
Visual Form Discrimination (VFD; Benton, Sivan, VFDd
Hamsher, Varney, & Spreen, 1994), Finger Tapping M 26.39 29.89 .0005 1.02
(FT), RDS, Wisconsin Card Sorting Failure-to- SD (4.58) (2.25)
Maintain Set (FMS), and the Lees-Haley Fake Bad FTe
Scale (FBS; Lees-Haley, English, & Glenn, 1991) M 69.27 83.85 .005 .70
on the MMPI-2 were useful in discriminating liti- SD (27.95) (13.78)
gants with definite or probable MND from patients RDSf
with moderate/severe TBI and various neurologi- M 7.15 9.78 .0005 1.33
cal and psychiatric disorders. Table 5.1 presents SD (1.82) (2.11)
the test data for litigants with MND and for Clinical FMSg
Patients (TBI, depression, and various neurologi- M 1.29 .56 .005 .67
cal conditions). These data, the aforementioned SD (1.36) (0.84)
studies, and the discriminant function analyses of FBSh
Mittenberg and colleagues (Mittenberg et al., M 26.95 16.48 .0005 1.99
1993, 1995, 1996) suggested that standard test pro- SD (5.36) (5.22)
cedures particularly sensitive to poor effort are
a
MND = 24 litigants with definite and 17 probable litigants with
tests of sensorimotor function, attention, recogni- neurocognitive dysfunction
tion memory, and problem solving. b
Clinical patients = 27 moderate/severe TBI, 14 psychiatric and 13
A set of symptom validity scores has been mixed neurologic diagnosis
c
Effect size: in pooled SD units.
developed for the WAIS-IV (Wechsler, 2008) and d
VFD = Benton Visual Form Discrimination
WMS-IV (Wechsler, 2009) as part of The e
FT = Finger Tapping combined right and left hand raw scores
f
RDS = Reliable Digit Span
Advanced Clinical Solutions (ACS; Holdnack and g
FMS = Wisconsin Card Sorting Test Failure to Maintain Set
Drozdick (2009). The ACS includes a chapter on h
FBS = MMPI-2 Symptom Validity Scale
assessment of suboptimal effort based on five
scores: Reliable Digit Span from WAIS-IV, the
recognition trials of Logical Memory, Verbal can choose test performance cutoffs identifying 2,
Paired Associates, and Visual Reproduction, and 5, 10, 15, and 25% of the combined clinical sample
the score from a newly developed free-standing (i.e., false alarm rates of 2% to 25%), then check
SVT, the Word Choice Test (a two alternative, the corresponding percent of the simulators (i.e.,
forced choice word recognition procedure similar sensitivity values for detection of feigning), and
to the verbal part of the Recognition Memory Test the percentage of the “no stimulus” group who
of Warrington). Data are provided on the perfor- achieve these scores. Data are also provided as to
mance of the WAIS-IV and WMS-IV clinical the percentage of clinical subjects who are mis-
groups (e.g., TBI, temporal lobectomy, etc.) on identified as showing poor effort, and percentage
these measures, as well as the performance of a of simulators correctly identified, based on mul-
group of 50 healthy simulators, and 50 healthy tiple positive test indicators (e.g., 2, 3, 4, or 5
subjects taking the Word Choice Test, Logical scores exceeding a particular cutoff ).
Memory, Verbal Paired Associates, and Visual Miller et al. (2011) evaluated the diagnostic
Reproduction recognition tests without having sensitivity of the five ACS scores to feigned
been exposed to the stimuli during the learning impairment, using 39 healthy individuals simulat-
trials for these tests (i.e., recognition memory is ing TBI, and 45 nonlitigating subjects with actual
tested without the subject having been presented moderate and severe TBI. Logistic regression
with the to-be-remembered stimuli). The examiner including the five ACS variables yielded an area
126 forensic neuropsychology
under curve (AUC) of .95, showing outstanding
discrimination (Hosmer & Lemeshow, 2000).
A second logistic regression that removed the
Word Choice Test, showed a statistically signi-
ficant change compared to the full model includ-
ing Word Choice, providing strong support for
including Word Choice in the full model. Word
Choice, by itself, showed excellent discrimination,
with an AUC of .84. Effect sizes (Cohen’s d) were
1.03 for Reliable Digit Span, .21 for Logical Memory
Recognition, .67 for Verbal Paired Associates
Recognition, 1.81 for Visual Reproduction Reco-
gnition, and 1.38 for Word Choice.
Motivational Impairment on
Motor Function Tests
Binder and Willis (1991) contrasted the neurop-
sychological test performance of ten subjects with
mild CHI with low motivation on the PDRT (15
or less of 36 on the “hard” items or 30 or less of 72
total items) with that of 19 subjects with mild CHI
scoring 23 or higher on the “hard” PDRT. The
poorly motivated subjects with mild CHI per-
formed significantly lower than the normally
motivated subjects with mild CHI on the Finger
Tapping and Grooved Pegboard Tests.
Greiffenstein et al. (1996) compared the Grip
Strength, Finger Tapping Test, and Grooved
Pegboard performance of 54 subjects with mod-
erate-to-severe CHI who also had unambiguous
motor abnormalities on standard neurological
examination (note that dense hemiplegics were
excluded) with the performance of 131 litigating
patients with post-concussion syndrome (PCS)
who performed on at least one motor function
score poorer than T40 using the normative data
of Heaton, Grant, and Matthews (1991). The sub-
jects with moderate-to-severe CHI showed the
expected pattern of performing best on Grip
Strength and worst on the Grooved Pegboard
Test, whereas the PCS subjects performed poorest
on Grip Strength and better on Finger Tapping
and the Grooved Pegboard. In particular, the most
significant PCS/CHI differences were on Grip
Strength. Although the PCS subjects had higher
scores on MMPI Scales 1, 2, 3, and 7 than the sub-
jects with moderate-to-severe CHI, consistent
with heightened reports of depression, anxiety,
and physical symptoms in the PCS group, these
MMPI scales did not correlate with motor perfor-
mance in the PCS group. The authors suggested
that the low Grip Strength scores of their PCS
litigants were consistent with malingering, but
not necessarily proof of malingering.
Rapport, Farchione, Coleman, and Axelrod
(1998) attempted a replication of the Greiffenstein
et al. (1996) motor function results with Grip
Strength, Finger Tapping, and the Grooved
Pegboard. These authors, using naive and coached
noninjured college student dissimulators and
noninjured college student controls, did not
replicate the Greiffenstein et al. results. Although
the dissimulators were provided with descriptions
of effects of spinal cord injury and mild head
injury, they were not specifically advised to
perform poorly on the motor function tests. This
may explain the differences between the Rapport
et al. (1998) results and those of Greiffenstein
et al., who used actual litigating patients chosen
for presence of reduced motor function scores.
Finger Tapping scores are also available from
the Heaton et al. (1978) and Mittenberg et al.
(1996) studies contrasting noninjured dissimula-
tors with nonlitigating patients with CHI. Despite
18 years of difference between these two investi-
gations, conducted in Denver, Colorado (Heaton
et al., 1978), and Ft. Lauderdale, Florida
(Mittenberg et al., 1996), there is a striking simi-
larity in dominant plus nondominant raw score:
The Heaton et al. dissimulators averaged 63.1 taps,
and the Mittenberg et al. dissimulators averaged
63.0 taps.
Arnold et al. (2005) reported separate score
distributions on Finger Tapping for males and
females, and determined that the best discrimina-
tor of probable malingerers from bona fide clini-
cal groups was the dominant hand performance.
For females, a dominant hand score of <29 yielded
a sensitivity of 61% and specificity of 92%; while
for males, a dominant hand score of <36 had a
sensitivity of 50% with a specificity of 90%.
Interestingly, when the male and female data are
combined for the dominant- plus nondominant-
hand raw scores, the optimal cutting score for dis-
criminating probable malingerers from clinical
patients was 63 for a sensitivity of 49% and speci-
ficity of 90%. These values are nearly identical to
those reported by me (Larrabee, 2003a), support-
ing the generalizability of findings from both
investigations.
Table 5.2 displays average Finger Tapping data
for dissimulating and head-injured subjects in the
Heaton et al. (1978) and Mittenberg et al. (1996)
studies; the Rapport et al. (1998) dissimulators;
a group of dissimulators from Orey, Cragar, and
Berry’s (2000) study; a group of subjects with
MND from Binder and Willis’s (1991) study;
my (2003a) subjects with definite MND and
 Assessment of Malingering 127

TABLE 5.2 COMBINED DOMINANT PLUS

NONDOMINANT FINGER TAPPING SPEED FOR
HEADINJURED, SIMULATING, AND MALINGERING
SUBJECTS

Subject Group

Study Traumatic Simulatorsa MNDb

Brain Injury

Heaton et al. (1978)c

M 80.2 63.1 —
SD (21.4) (17.1) —
Mittenberg et al. 1996)d
M 75.6 63.0 —
SD (20.4) (32.7) —
Binder & Willis (1991)e
M — — 71.89
SD — — (16.5)
Rapport et al. (1998)f
M — 60.0 —
SD — (19.2) —
Orey et al. (2000)g
M — 64.19 —
SD — (18.67) —
Larrabee (2003b)h
M 78.37 — 70.97
SD (13.64) — (26.72)
Arnold et al. (2005)i
M 85.24 — 68.37
SD (16.06) — (17.88)
a
Simulators = Noninjured persons simulating impairment
b
MND = Malingered Neurocognitive Deficit
c
Heaton et al. = 16 simulators, 16 Traumatic Brain Injury (TBI)
d
Mittenberg et al. = 80 simulators, 80 TBI
e
Binder & Willis = 10 MND
f
Rapport et al. = 31 simulators
g
Orey et al. = 26 simulators
h
Larrabee = 27 TBI, 24 MND
i
Arnold et al. = 24 TBI, 77 MND

moderate-to-severe TBI; and the Arnold et al.
(2005) probable malingerers and moderate/severe
TBI patients. Greiffenstein (2007) has reported
similar data for combined (right plus left hand)
Finger Tapping data in samples of simulators,
known groups, and clinical patients, including
many of the studies reported in Table 5.2, as well
as additional clinical bench mark data for clinical
patients with known neuromotor dysfunction
secondary to such conditions as multiple sclero-
sis, Huntington’s disease, and cerebrovascular
disease. In the data reviewed by Greiffenstein
(2007), the lowest mean combined (right plus left
hand) Finger Tapping scores are seen in patients
with Huntington’s disease (48), multiple sclerosis
(60), and cortical dementia (62), from a series
reported by Butters, Goldstein, Allen, and
Shemansky (1998). Last, Arnold and Boone
(2007) provide a helpful appendix summarizing
data from a variety of studies contrasting either
dissimulating subjects with clinical cases, or
known-groups of probable malingerers contrasted
with relevant clinical groups (e.g., moderate/
severe TBI) for several motor function tasks
including grip strength, the Grooved Pegboard,
and Finger Tapping.
128 forensic neuropsychology
Digit Span and Malingering
Mittenberg et al. (1995) found that the simple
difference score between Vocabulary and Digit
Span age-scaled scores worked almost as well as a
discriminant function analysis employing seven
WAIS-R subtests in discriminating noninjured
dissimulators from nonlitigating patients with
CHI. Mittenberg et al. (2001) replicated this result
using the WAIS-III, subjects with CHI, nonin-
jured dissimulators, and a group of litigants iden-
tified as probable malingerers by virtue of current
functioning IQ more than 15 points below esti-
mated premorbid level of function. Trueblood
and Schmidt (1993) recommended consideration
of malingering when the age-scaled score for Digit
Span was less than 7.
Suhr and Barrash (2007) reviewed research
contrasting performance of simulators or proba-
ble malingerers to clinical comparison samples
including chronic pain and TBI. A Digit Span
age-corrected scaled score of <5 was associated
with sensitivities ranging from 25% to 47%
(median = 30%), and specificities ranging from
94% to 100% (median = 98%). The review by
Babikian and Boone (2007) also supports a cut-
ting score of <5 on Digit Span age-scaled score as
associated with >90% specificity, but sensitivity
was low, ranging from 19% to 32%. Babikian and
Boone (2007) observed that raising the Digit Span
age-scaled score cutoff to <6 increased sensitivity
from 36% to 47%, while limiting false positives to
10%, with the exception of stroke patients, who
had a 14% false positive rate (per Heinly, Greve,
Bianchini, Love, & Brennan, 2005). In a study sub-
sequent to these two reviews, Greve et al. (2007)
reported sensitivity of 46% and specificity of
97% for a WAIS-III Digit Span age-scaled score of
<6 for discriminating between probable malinger-
ers with neurotoxic claims and nonmalingering
patients with toxic exposure.
Greiffenstein et al. (1994) developed a proce-
dure for evaluating effort based on the WAIS/
WAIS-R/WAIS-III Digit Span Subtest: Reliable
Digit Span (RDS). This is computed by summing
the longest string of digits repeated without error
over two trials under both forward and backward
conditions. As an example, Greiffenstein et al.
noted that a patient who passed both trials of
three digits forward and both trials of two digits
backward, but failed one trial at four digits
forward and one trial at three digits reversed,
would have an RDS of 5. Greiffenstein et al.
reported a sensitivity of 70% and specificity of
73% for an RDS of 7 or less in discriminating
probable malingerers from patients with TBI
and a sensitivity of 68% and specificity of 89% for
an RDS of 7 or less in discriminating probable
malingerers from subjects with persistent PCS.
Meyers and Volbrecht (1998) replicated
the RDS findings of Greiffenstein et al. (1994).
In a comparison of 47 litigants with mild brain
injury and 49 nonlitigants with mild brain injury,
only 4.1% of nonlitigants had an RDS of 7 or less,
contrasted with 48.9% of litigants. In my (Larrabee,
2003a) investigation, an RDS score of 7 or less
correctly identified 50% of litigants with definite
MND and 93.5% of persons with moderate and
severe TBI.
In a unique investigation, Etherton, Bianchini,
Ciota, and Greve (2005) administered the Digit
Span subtest to three groups of undergraduates:
1) a group undergoing a cold-pressor test,
2) a group following standard instructions, and
3) a group simulating pain-related memory deficit
in pursuit of personal injury litigation. There were
no differences in RDS performance between the
group undergoing cold-pressor testing and the
group tested on standard Digit Span instructions,
and no subject in either group had an RDS of 7 or
less. By contrast, 65% of the simulator group had
RDS of 7 or less.
Suhr and Barrash (2007) and Babikian and
Boone (2007) have also reviewed published
research on RDS. Suhr and Barrash reported
sensitivities ranging from 19.6% to 71%, and
specificities ranging from 71.6% to 100% for an
RDS score of <8, concluding that an RDS cutoff of
<7 was a solid recommendation, but that a cutoff
of <8 might also indicate malingering, particu-
larly in the presence of other malingering indica-
tors to help minimize false positives and with
consideration of the nature and severity of the
neurological injury (see Larrabee, 2003a).
Babikian and Boone (2007) computed a weighted
average sensitivity of 68% for probable malinger-
ers in the studies they reviewed, but weighted
average specificity of 81% for moderate/severe
TBI, noting a further drop in specificity for stroke
and for a general neurological sample, using an
RDS cutoff of <8. Babikian and Boone (2007)
observed that lowering the RDS cutoff to <7
caused a drop in sensitivity to probable malinger-
ing, ranging from 38% to 57% in the studies they
reviewed, but that specificity was 88% or higher
using this cutoff, with the exception of stroke
patients (Heinly et al., 2005).
Contemporaneous with the Suhr and Barrash
(2007) and Babikian and Boone (2007) reviews,

Greve et al. (2007) investigated RDS in neurotoxic
claimants classified as probable malingerers,
nonmalingering neurotoxically exposed patients,
and patients with history of TBI or chronic pain.
RDS <8 was associated with a sensitivity of 54%
and specificity of 89%. Lowering the RDS cutoff
to <7 reduced sensitivity to 46% but improved
specificity to 97%.
Measures of Recognition Memory
Several investigators have reported dispropor-
tionate impairment in recognition memory in
probable malingerers. Binder et al. (1993) found
significantly lower Rey AVLT recognition scores
in litigants with mild TBI failing the PDRT than
in nonlitigating head-injured patients. Suhr,
Tranel, Wefel, and Barrash (1997) also reported
poorer AVLT recognition scores for probable
malingerers in comparison to patients with head
injury, depression, or somatization disorder.
Binder, Kelly, Villanueva, and Winslow (2003)
found that litigating subjects with mild TBI with
good motivation outperformed litigating subjects
with mild TBI who had poor motivation on the
recognition trial of the AVLT. The poorly moti-
vated litigants with mild TBI were also outper-
formed on AVLT recognition by a group of
normally motivated nonlitigating patients with
moderate-to-severe TBI. Atypical patterns of rec-
ognition play a prominent role in the Exaggeration
Index (EI) developed for the AVLT by Barrash
et al. (2004). Four of the seven atypical perfor-
mance patterns comprising the EI are based on
clinically atypical patterns of recognition memory
performance, including worsening recognition,
learned words not recognized, recalled words not
recognized, and exceedingly poor recognition.
Millis et al. (1995) found that litigants with
mild TBI with poor motivation produced lower
scores on CVLT Recognition Hits and
Discriminability than did patients who had mod-
erate or severe TBI. Coleman, Rapport, Millis,
Ricker, and Farchione (1998) replicated these
findings with a normal subject simulation design,
although the effect was attenuated when the sub-
jects were provided with cues on how to elude
detection as a malingerer.
The CVLT-II (Delis et al., 2000) contains an
optional forced choice recognition task as a mea-
sure of symptom validity. Root, Robins, Chang,
and Van Gorp (2006) found that a total correct of
14 or less out of 16 on forced choice recognition
had a sensitivity of .44 and specificity of .93, and
that scores of 11 or less were associated with 100%
Assessment of Malingering 129
specificity (no false positives) in discriminating
forensic examinees with valid data from
those with invalid data consistent with the
presence of probable malingering (on the basis
of failure of TOMM and/or VIP). Wolfe et al.
(2010) found that a logistic regression based on
CVLT-II Long-Delay Free Recall, Total Recog-
nition Discriminability (d′) and Total Recall
Discriminability, discriminated well between
litigants/claimants with alleged mTBI failing at
least two SVTs in a manner consistent with
probable malingering, and nonlitigating patients
with moderate or severe TBI. The receiver operat-
ing characteristic area under curve was .83, and
sensitivity was .49 at a specificity of .90.
Donders and Strong (2010) attempted to
cross-validate the Wolfe et al. (2010) logistic
regression, employing passing or failing the WMT
as the “gold standard” for presence of invalid effort
using a sample of mild, moderate, and severe TBI.
Although there was a significant association
between pass/fail on both the WMT and CVLT-II
logistic regression, the CVLT-II false positive rates
were much higher than originally reported by
Wolfe et al. (2010). To achieve .90 specificity,
Donders and Strong had to raise the CVLT-II
logistic regression cutoff to .67, resulting in
a sensitivity of .375. This contrasts with specificity
of .90 and sensitivity of .49 associated with a
cutoff score of .6245 in the Wolfe et al. (2010)
investigation. Donders and Strong reported
significant correlations between all three CVLT-II
validity indicators and duration of coma, con-
trasted with no significant correlations between
the WMT scores and coma or between CVLT-II
forced choice scores and coma. The authors noted
this demonstrated that the CVLT-II scores com-
prising the invalid effort equation measure factors
related to cognitive ability rather than serving
only as measures of invalid effort. They concluded
that investigators use great caution in applying
the Wolfe et al. (2010) formula, prior to further
independent replication, and recommended the
more conservative cutoff of .67, along with admin-
istration of other SVTs in addition to the CVLT-II
logistic regression for invalid effort.
Poor performance on recognition memory in
association with poor motivation has also been
reported for the Rey Complex Figure Test (Corwin
& Bylsma, 1993; Osterrieth, 1944; Rey, 1941);
Warrington Recognition Memory Test
(Warrington, 1984), and recognition tasks/scores
on the Wechsler Memory Scale III (WMS-III;
Wechsler, 1997b). Meyers and Volbrecht (1999),
130 forensic neuropsychology
using a differential prevalence design, found
that litigants (primarily those with mild TBI)
produced memory error patterns characterized
by poor recognition performance on the Rey
Complex Figure Test, in contrast to nonlitigating
individuals with mild TBI, who did not show evi-
dence of poor recognition. Lu, Boone, Cozolino,
and Mitchell (2003) found that a combination
score based on copy plus true positive minus
atypical recognition errors discriminated suspect
effort cases from a variety of clinical cases on the
Rey Complex Figure Test. Millis (1992, 1994) and
Millis and Putnam (1994) have shown that litigat-
ing subjects with mild TBI performed more poorly
on the Recognition Memory Test, more so on
Words than on Faces, in comparison to nonlitigat-
ing subjects with moderate and severe TBI.
Subsequently, Kim et al. (2010) found both the
total correct score for Warrington Words (sensi-
tivity of 88.9%, specificity of 91.9%), and the total
time to complete the recognition memory task
(sensitivity of 65.5%, specificity of 90.7%) discrim-
inated well between subjects with external incen-
tive who had failed at least two independent SVTs
from subjects who had failed at most one SVT.
Other recognition memory procedures are
also sensitive to detection of poor effort. Glassmire
et al. (2003) found that poor performance on
WMS-III Faces I was characteristic of noninjured
persons trying to simulate impairment, as well as
characteristic of participants with moderate and
severe TBI attempting to dissimulate impairment.
Finally, Langeluddecke and Lucas (2003) found
that WMS-III delayed auditory recognition
memory tasks successfully discriminated a group
of litigating subjects with mild TBI with probable
MND from a group of litigating individuals with
mild TBI with good motivation as well as from a
group of litigating individuals with severe TBI. I
(Larrabee, 2008a) developed embedded SVT
scales for the Continuous Visual Memory Test
(CVMT; Trahan & Larrabee, (1988) and the
Continuous Recognition Memory Test (CRM;
Hannay, Levin & Grossman, 1979), identifying
those CVMT or CRM items typically failed by
litigants performing significantly less-than-chance
on the PDRT, which were typically passed by
patients with moderate or severe TBI. Sensitivity
for the CVMT SVT was 83% with specificity at
88.9%, with CRM SVT scores showing a sensitiv-
ity of 87.5% at a specificity of 93%. Although spec-
ificity remained high on cross validation with
neurologic and psychiatric patients (93% for
CVMT, 96% for CRM), sensitivity dropped
substantially (35% for CVMT, 52.9% for CRM) in
litigants failing at least two SVTs but not at values
that were significantly worse-than-chance. These
data show that both the CVMT and CRM SVT
scales were more sensitive to detection of definite
than probable malingering.
Measures of Problem-Solving Ability
Persons identified as malingering also performed
poorly and in neurologically atypical patterns of
performance on measures of problem solving
such as the WCST (Heaton et al., 1993) and the
Category Test of the HRB. Bernard et al. (1996)
found that noninjured simulators produced
poorer performance ratios on Categories relative
to Perseverative Errors on the WCST in compari-
son to patients with TBI or other central nervous
system disorders.
Suhr and Boyer (1999) found that student
simulators as well as probable malingerers could
be discriminated from nonlitigating subjects
with mild and moderate TBI on the basis of
WCST Categories and FMS, with a lower ratio
of Categories to FMS in the malingering groups.
I (Larrabee, 2003a) found that FMS alone worked
more effectively than the Suhr and Boyer discrim-
inant score based on Categories and FMS in dis-
criminating litigants with definite MND from
patients with moderate and severe TBI.
Greve and Bianchini (2002) found an unac-
ceptably high false-positive rate for both the
Bernard et al. (1996) and Suhr and Boyer (1999)
WCST discriminant function equations in dis-
criminating simulating normal college students
from patients with TBI, various neurological con-
ditions, and substance abuse. In another investi-
gation, Greve et al. (2002) improved the sensitivity
and specificity of WCST malingering indicators
by combining multiple indicators (e.g., Bernard
et al., 1996, criteria and Suhr & Boyer, 1999, crite-
ria), including “unique” errors on the WCST as
another variable sensitive to malingering. These
authors also provided different cutoffs for the
Bernard et al. (1996) and Suhr and Boyer (1999)
functions that minimized false-positive errors in
discriminating probable malingerers from patients
with TBI with adequate motivation.
King, Sweet, Sherer, Curtiss, and Vanderploeg
(2002) found varying degrees of classification
accuracy for the Bernard et al. (1996) and Suhr
and Boyer (1999) WCST classification formulas,
as well as for a logistic regression formula devel-
oped by King et al. that employed FMS, Categories
Achieved, and Percent Conceptual Responses.

Overall, these formulas worked well; however,
King et al. found classification limitations in
association with chronicity and severity of the
reported TBI and advised against use of any single
WCST insufficient effort criterion in isolation.
Subsequently, Greve, Heinly, Bianchini, and Love
(2009), using samples of mTBI and moderate/
severe TBI plus a large clinical sample, found that
most WCST scores were not effective in discrimi-
nating litigants with invalid SVT performance
from those with valid SVT performance, with the
exception of FMS, and the Suhr and Boyer (1999)
and King et al. (2002) logistic regressions. At
100% specificity (0% false positives), FMS had a
sensitivity of 16%, which was clearly superior to
that of the Suhr and Boyer (1999) formula, 8%,
and King et al. (2002) formula, 5%. Greve et al.
offered three possibilities for the limited sensitiv-
ity of WCST scores to malingering: 1) there are
large individual differences in all WCST scores in
the normative population; 2) measures of execu-
tive dysfunction, like the WCST, are very sensitive
to acquired brain impairment, so that persons
with legitimate impairment may perform in the
same range as those who show evidence of malin-
gering; and 3) persons who are malingering do
not perform atypically on the WCST as they do
not perceive the test as relevant or reflecting the
type of impairment they think is a consequence of
traumatic brain injury.
Indicators of insufficient effort suggestive
of malingering have also been developed for
the Category Test. Tenhula and Sweet (1996)
performed a double cross-validation study con-
trasting normal subjects simulating impairment
on the Category Test with performance on the
Category Test of normal subjects performing
optimally and with nonlitigating patients with
severe TBI. A number of Category Test indicators
showed good discrimination of the simulating
malingerers from the normal and severe TBI
groups, including Total Number of Errors, Items
from Subtests I and II, “Bolter et al.” items (Bolter,
Picano, & Zych, 1985; items rarely missed by
patients with bona fide brain damage), Number of
Errors on Subtest VII, and Number of “Easy”
items (items rarely missed by the group with
severe TBI, similar to the Bolter et al. items). The
best sensitivity (75.6%) and specificity (98.1%)
were associated with number of errors on
Subtests I and II.
In a replication study that also investigated the
effects of coaching on feigned performance,
DiCarlo, Gfeller, and Oliveri (2000) also found
Assessment of Malingering 131
that the number of errors on Subtests I and II
was consistently the most accurate malingering
indicator regardless of degree of coaching or
presence of TBI. Sweet and King (2002) provided
further review of Category Test validity indicators
with case examples and recommendations for
use.
Greve, Bianchini, and Roberson (2007) evalu-
ated the sensitivity and specificity of a variety of
Booklet Category Test scores in discriminating
litigants with invalid SVT performance consistent
with probable malingering from those TBI
patients with valid test performance, and from a
clinical group with various neurological disorders
but who did not have any external incentives.
They found that the total error score was the most
accurate indicator overall, with the effectiveness
of the other indicators related to injury severity.
Greve et al. also compared their results to those of
Tenhula and Sweet (1996), using the cutoff scores
from this earlier investigation, and found that in
their sample, the false positive rates were higher
than those reported by Tenhula and Sweet. When
Greve et al. adjusted their cutoffs to yield false
positive rates equivalent to those reported by
Tenhula and Sweet, the sensitivity was substan-
tially lower than that reported by Tenhula and
Sweet. Moreover, total errors on Category Subtests
I and II, found by both Tenhula and Sweet (1996)
and Dicarlo et al. (2000) to be the most effective in
discriminating malingering from TBI patients
was a poor discriminator in Greve et al. (2007),
with a sensitivity of 15% at a false positive rate of
4% using a cutoff of 2 or more errors.
D E T E C T I O N O F S Y M P TO M
E X A G G E R AT I O N
Forensic neuropsychological evaluation entails
both direct examination of the litigant/defendant,
including interview, testing, and behavioral
observation, as well as record review. These
sources of information are then integrated by the
forensic neuropsychologist. The direct part of the
evaluation includes interviewing, testing of neu-
ropsychological abilities, and quantification of
symptom report through interview (including
structured interview); use of symptom checklists;
and use of formal self-report instruments such as
the MMPI-2 (Butcher, Graham, Ben-Porath,
Tellegen, Dahlstrom, & Kaemmer, 2001) or pain
scales such as the McGill Pain Questionnaire
(MPQ; Melzack, 1975). Obviously, a litigant/
defendant can control both the degree of effort
exerted on testing and the number and magnitude
132 forensic neuropsychology
of reported symptoms. Consequently, the forensic
examiner must be able to discriminate legitimate
from exaggerated symptom report.
The present review of measures of symptom
report will focus selectively on the MMPI-2.
Although there are many other measures of symp-
tom report, the MMPI-2 has the greatest research
database of any omnibus personality scale. Berry
and Schipper (2007) reviewed a number of scales
for detection of feigned psychiatric symptoms
during forensic neuropsychological examinations
on a variety of what they termed “quality control
indicators,” including adequate number of
publications, operating characteristics from
appropriate samples, convergence in operating
characteristics, appropriate predictive power,
independent cross-validation, and neurologic
control groups. Only the FBS from the MMPI-2
and the Structured Interview of Reported
Symptoms (SIRS; Rogers et al., 1992) met all seven
criteria (note though, that the SIRS neurologic
group was a group with mental retardation rather
than acquired neurologic deficit). Two scales met
all criteria with the exception of not having a neu-
rologic control group: the Negative Impression
scale and Malingering Index from the Personality
Assessment Inventory (Morey, 1991), and the
Total Score from the Miller Forensic Assessment
of Symptoms Test (Miller, 2001).
The most widely used symptom report scale in
forensic neuropsychology is the MMPI/MMPI-2
(Lees-Haley, Smith, Williams, & Dunn, 1996). The
MMPI and MMPI-2 have long played a role in
assessment of malingered symptom report (Berry,
Baer, & Harris, 1991; Graham, 2006; Greene, 2000;
Rogers, Sewell, & Salekin, 1994). The prototypic
MMPI scale for detection of malingering is the
Infrequency or F scale, which was originally
derived by selecting items endorsed by 10% or less
of the normal adult sample (Graham, 2006). The
MMPI-2 (Butcher et al., 1989) includes the F scale,
as well as the Fb scale, developed for items occur-
ring on the second half of the MMPI-2, again
endorsed by 10% or less of the normal adult
sample, using the same methodology as that used
to develop F. In addition, the MMPI-2 includes
measures of response inconsistency, including the
Variable Response Inconsistency scale (VRIN), a
measure designed to detect response inconsis-
tency as the reason for significant elevations at a T
score of 100 or more on F or 90 or more on Fb. A
second consistency score, True Response
Inconsistency scale (TRIN), measures the ten-
dency to respond either “True” or “False” in an
indiscriminant manner. The MMPI/MMPI-2
also include measures such as the F-minus-K
index, Obvious–Subtle difference scores, and
Dissimulation-Revised scales, which are sensitive
to malingering of psychiatric disorder (Greene,
2000). Of all the scales, F is one of the most effec-
tive in discriminating valid from invalid psychiat-
ric profiles (see Berry et al., 1991).
Following the publication of the MMPI-2
(Butcher et al., 1989), Arbisi and Ben-Porath (1995)
developed the Infrequency-Psychopathology
Scale, F(p), by selecting MMPI-2 items endorsed
by 20% or less of hospitalized psychiatric patients
as well as infrequently endorsed by 20% or less of
MMPI-2 normal subjects. In a subsequent inves-
tigation, Arbisi and Ben-Porath (1998) found that
F(p) outperformed F in distinguishing between
psychiatric patients performing honestly and
those attempting to fake bad.
Gass and Luis (2001) demonstrated that the
sensitivity of F(p) to symptom exaggeration was
reduced by the presence of four items from the L
scale of the MMPI-2. These authors showed that
these four items actually measured defensiveness,
not exaggeration, and recommended removal of
the items from the F(p). A shortened version of
F(p) that omitted the four L scale items was
found to be superior to the original F(p) as a
measure of symptom exaggeration. In a subse-
quent study, Arbisi, Ben-Porath, and McNulty
(2003) found that the original F(p) scale contain-
ing the four L scale items was more effective in
identifying malingering than was the revised
version suggested by Gass and Luis (2001). The
F(p) scale was included as a standard validity scale
in the revised edition of the MMPI-2 (Butcher
et al., 2001).
Despite demonstration of the sensitivity of F,
Fb, F(p), F minus K, and other MMPI-2 scores
such as the sum of Obvious-Subtle difference, and
Dissimulation-Revised scores to detection of exag-
gerated psychiatric symptomatology (Rogers et al.,
1994), these MMPI-2 validity scales may not be
sensitive to exaggeration of symptoms in personal
injury settings for litigants pursuing neuropsycho-
logical claims. Indeed, Greiffenstein et al. (1995)
found that F, total sum of Obvious-Subtle differ-
ence, and F minus K did not discriminate probable
malingerers from subjects with TBI and from
those with persistent PCS despite the presence of
significant group differences on several measures
of neuropsychological malingering, including the
Rey 15-Item Test, Recognition Word List, AVLT
Recognition score, RDS, and PDRT-27.

Lees-Haley and colleagues (Lees-Haley et al.,
1991; Lees-Haley, 1992) recognized a different
pattern of symptom reporting in personal-injury
litigants and developed a scale that would be sen-
sitive to personal-injury exaggeration, the FBS.
The FBS was constructed on a rational content
basis, taking into consideration unpublished fre-
quency counts of malingerer’s MMPI-2 test data
and responses that fit a model of goal-directed
behavior with a focus of (a) appearing honest;
(b) appearing psychologically normal except
for the influence of the alleged cause of injury;
(c) avoiding admitting preexisting psychopathol-
ogy; (d) attempting to minimize the impact of
previously disclosed preexisting complaints;
(e) minimizing or hiding pre-injury antisocial or
illegal behavior; and (f) presenting a degree of
injury or disability within perceived limits of
plausibility. The FBS contains 18 items scored in
the “True” direction and 25 items scored in the
“False” direction.
Greene (1997) presented data to show that the
FBS did not correlate strongly with F (0.14), Fb
(0.26), or F(p) (0.08), in contrast to significant
correlations between F, Fb, and F(p) that averaged
.75 for normal subjects and patients with mental
disorders. Most of the FBS items occurred on
MMPI-2 Scales 1 and 3, with six on Scale 1, seven on
Scale 3, and seven appearing on Scales 1 and 3. One
FBS item appeared on L, one on K, four on F, four on
Scale 2, two on Scale 4, four on Scale 6, three on
Scale 7, six on Scale 8, and three on Scale 0 (note that
there is some item overlap on more than one scale).
Lees-Haley et al. (1991), using an FBS cutoff
of 20 or higher, found that 24 of 25 (96%) of per-
sonal injury claimants assessed as malingering
emotional distress were correctly classified, with
18 of 20 (90%) claimants assessed as presenting
genuine injuries correctly classified. Subsequently,
Lees-Haley (1992) found sensitivity and specific-
ity values of 75% and 96%, respectively, using an
FBS cutoff of 24 or higher for males and 74%
and 92%, respectively, for a cutoff of 26 or higher
for females, for discriminating pseudo-post-
traumatic stress disorder (PTSD) claimants from
claimants with legitimate emotional distress.
I (Larrabee, 1998) found that 11 of 12 litigants
with independent objective evidence of malinger-
ing on tasks such as the Rey 15-Item Test and
PDRT produced elevated scores (≥24 for males,
≥26 for females), whereas only 3 had elevated
F scales (T > 69 for the MMPI, T > 64 for the
MMPI-2), despite T scores on Scales 1 and 3 that
exceeded scores for chronic pain samples (Keller &
Assessment of Malingering 133
Butcher, 1991). In addition, the sample of probable
malingerers produced scores on Scale 3 that excee-
ded those produced by noninjured persons simulat-
ing somatoform disorder on the MMPI-2 (Sivec,
Lynn, & Garske, 1994). These data were used to pro-
pose a somatic malingering profile on the MMPI-2,
characterized by FBS scores of ≥24 for males and
≥26 for females, with T scores of ≥80 on Scales Hs
and Hy (conservative) or ≥80 on Hy (liberal).
In a subsequent investigation, I (Larrabee,
2003c) found that the FBS was significantly more
sensitive to detection of symptom exaggeration
than F, Fb, or F(p) in 33 litigants with definite or
probable MND. Moreover, the MMPI-2 profiles
of the definite/probable malingerers were charac-
terized by significantly higher elevations on Scales
1, 3, and 7 than scores produced by a variety of
clinical groups, including those with nonlitigating
severe CHI, multiple sclerosis, spinal cord injury,
chronic pain, and depression. The definite and
probable malingerers also produced significantly
higher elevations on Scales 2 and 8 than were pro-
duced by all clinical groups, with the exception of
the depressed clinical patient group. I (Larrabee,
2003c) contrasted the neuropsychological malin-
gering profile obtained, with elevations on the
FBS and Scales 1, 2, 3, 7, and 8, with the Graham,
Watts, and Timbrook (1991) profile for simulated
psychiatric disturbance, which was characterized
by significantly elevated F and significant eleva-
tions on Scales 6 and 8. These data were inter-
preted as showing at least two patterns of
malingering on the MMPI-2: malingered injury
and malingered severe psychiatric disturbance.
Miller and Donders (2001) found that litigat-
ing patients with mild TBI produced higher FBS
scores than nonlitigating patients with mild TBI
and were twice as likely to produce FBS scores
that fell beyond 23 for males and 25 for females.
The finding that both the litigating and nonlitigat-
ing individuals with mild TBI produced more sig-
nificant elevations on the FBS than nonlitigating
patients with moderate-to-severe TBI led Miller
and Donders to recommend caution in using the
FBS solely as an indicator of symptom exaggera-
tion. The authors recommended that elevated FBS
scores be interpreted as suggesting the likelihood
that something other than acquired cerebral
dysfunction was accounting for maintaining
the patient’s symptomatology. In this vein, they
recommended that elevated FBS scores be supple-
mented with other data demonstrating invalid
performance before concluding that a person is
malingering.
134 forensic neuropsychology
Martens, Donders, and Millis (2001) repli-
cated the Miller and Donders (2001) results, dem-
onstrating higher FBS scores for litigating subjects
with mild TBI in comparison to subjects with
moderate or severe TBI. They also showed a sig-
nificant association between the FBS and mea-
sures of invalid effort derived from the CVLT.
Prior psychiatric history was associated with ele-
vations on the FBS in subjects with mild TBI,
including those who were not litigating, indicat-
ing that invalid response set alone was not the sole
explanation of elevated FBS scores. Not a single
patient with moderate or severe TBI produced
invalid scores on both the FBS and CVLT, rein-
forcing the suggestion that use of multiple inde-
pendent criteria to determine the presence of
invalid response set improved diagnostic accu-
racy for malingering (Slick et al., 1999; Sweet,
1999).
Greiffenstein, Baker, Gola, Donders, and
Miller (2002) compared groups of litigating
patients with mild TBI with atypical symptom
history/outcome, litigating individuals with mod-
erate-to-severe TBI, and nonlitigating individuals
with moderate-to-severe TBI. Setting specificity
at 80% for the litigating individuals with moder-
ate-to-severe TBI resulted in an FBS cutting score
above 23 and identified 57% of atypical litigants
with mild TBI, but only 4% of nonlitigating indi-
viduals with moderate-to-severe TBI. Although
Greiffenstein et al. (2002) could not exclude litiga-
tion status as a potential factor in FBS elevation in
their litigating group with moderate-to-severe
TBI, there was some evidence that FBS scores
were related to neurological abnormalities in the
litigating patients with moderate-to-severe TBI
(e.g., the FBS correlated positively with the pres-
ence of anosmia and residual motor impairment).
Of interest, the FBS correlated significantly with
three measures of invalid neuropsychological test
performance, including the PDRT-27, Rey 15-Item
Test, and Rey’s Word Recognition List, in the liti-
gating subjects with atypical mild TBI, but the
FBS did not correlate with these measures in
the litigating group with moderate-to-severe TBI.
The FBS also correlated significantly with a
Symptom Improbability Rating Scale score within
the litigating sample with atypical mild TBI.
Meyers, Millis, and Volkert (2002) developed
a composite, weighted validity index for the
MMPI-2 based on the T score for F, the raw
F-minus-K difference, F(p), Dissimulation Scale–
Revised, Es (Ego Strength), sum difference of
Obvious and Subtle scores, and the FBS. These
authors were able to discriminate litigating
patients with chronic pain with cognitive com-
plaints from nonlitigating patients with chronic
pain with cognitive complaints using their weig-
hted index. Moreover, the empirically derived
cutoff score that had 100% specificity (i.e., identi-
fied none of the nonlitigating patients with
chronic pain) identified 36% of the litigating
patients with chronic pain and 86% of noninjured
persons attempting to simulate chronic pain
impairment. FBS scores greater than 24 identified
42% of the litigating patients with chronic pain,
whereas only 16% of the nonlitigants scored in
this range. No nonlitigating patient with chronic
pain scored over 29 on the FBS.
Aguerrevere, Greve, Bianchini, and Meyers
(2008) developed a revised version of the Meyers
Index for the MMPI-2 that omitted both the
Obvious minus Subtle score and the Dissimula-
tion Scale-Revised, since these two scales are no
longer provided in the commercially available
scoring program from Pearson. Litigants claiming
TBI classified with probable malingered neu-
rocognitive dysfunction were discriminated from
nonmalingering TBI subjects equally well by the
original Meyers Index (receiver operating charac-
teristic [ROC] area under curve [AUC] of .780)
and by the abbreviated Meyers Index (ROC AUC
= 0.781). Similarly, litigants with chronic pain
classified with malingered pain-related disability
were discriminated from nonmalingering chronic
pain subjects equally well by the original Meyers
Index (AUC = 0.923) and the abbreviated Meyers
Index (AUC = 0.923). The reader should note that
AUC values of .9 or greater provide outstanding
discrimination (Hosmer & Lemeshow, 2000).
I (Larrabee, 2003b) found that the FBS was
superior to F, Fb, F(p), Meyers’s Weighted Validity
Index, F minus K, Dissimulation Scale–Revised,
Obvious–Subtle difference, and Es in discriminat-
ing 26 litigants with definite MND (worse than
chance on the PDRT) from 29 patients with mod-
erate or severe TBI. In a combined sample of defi-
nite and probable MND plus the TBI subjects, the
FBS was the only MMPI-2 validity scale that cor-
related significantly with the PDRT. The FBS also
correlated significantly with all other MMPI-2
validity scales except for F(p) and F minus K, but
correlated most strongly with Es and Meyers’s
Index. The FBS correlated significantly with
MMPI-2 clinical scales 1, 2, 3, 6, 7, 8, and 0, with
the strongest correlations occurring with 1, 2, 3,
and 7. An FBS cutoff score above 20 or 21 pro-
vided optimal classification of the malingering

and head-injured groups, with a sensitivity of .808
and specificity of .862. None of the subjects with
moderate-to-severe TBI scored higher than 30 on
the FBS, with only 3% (one subject) scoring higher
than 25. I concluded that the data were consistent
with the presence of different dimensions of
exaggeration on the MMPI-2, extending the find-
ings in my (Larrabee, 2003c) investigation. These
data were seen as consistent with the demonstra-
tion by Lanyon (2001) of MMPI-2 dimensions
of (a) exaggerated psychiatric symptoms and (b)
exaggerated health concerns in a mixed forensic
sample (child custody evaluees, personal injury
litigants, and criminal defendants; note that a third
dimension not relevant to the present discussion
was also obtained: exaggeration of virtue).
Ross, Millis, Krukowski, Putnam, and Adams
(2004) reported a sensitivity of .90 and specificity
of .90 using an FBS cutoff of 21 or higher or 22 or
higher to discriminate 59 probable malingerers
from 59 nonlitigating patients with moderate and
severe TBI. None of their nonlitigating subjects
with moderate-to-severe TBI scored higher than
26 on the FBS (100% specificity).
In an investigation that included the subjects
from my studies (Larrabee, 1998, 2003b, 2003c) as
well as additional clinical and malingering sub-
jects, the FBS was the single most sensitive mea-
sure for discriminating definite MND from
moderate and severe TBI compared with other
measures of motivational impairment derived
from Benton VFD, FT, RDS, and Wisconsin Card
Sorting FMS (Larrabee, 2003a). The FBS remained
the most frequently failed validity indicator in a
cross-validation discriminating litigants with prob-
able MND from groups of nonlitigating psychiat-
ric and neurological patients (also see Table 5.1).
The FBS has also been shown by others to be
sensitive to the presence of symptom exaggera-
tion in mixed personal injury samples. Posthuma
and Harper (1998) found the FBS was elevated in
a sample of personal injury litigants contrasted
with FBS scores produced by a child custody liti-
gant sample. Tshushima and Tshushima (2001)
found that only the FBS significantly discrimi-
nated a sample of personal injury litigants from a
sample of clinical patients, and the FBS also had
the largest effect size contrasting the personal
injury group with a group of job applicants under-
going employment screening. Greve, Bianchini,
Love, Brennan, and Heinly (2006) found that a
variety of MMPI-2 validity scales worked well at
detecting malingering in TBI, including FBS, Fb,
DS-r, the Meyers Index, and ES, when specificity
Assessment of Malingering 135
was set at 95%. At a malingering base rate of .40,
positive predictive powers (i.e., probability of
malingering) were over .80 for F (0.83), Fb (.89),
FBS (0.88), DS-r (0.90), Meyers Index (0.84), K
(0.80), and ES (0.93). The reader should note that
lower T score cutoffs (>80) were used for F and Fb
based on malingering versus nonmalingering
comparisons in this study, compared to what is
typically recommended in the test manual (e.g.,
100 for F, 110 for Fb; Butcher et al., 2001).
Bianchini, Etherton, Greve, Heinly, and Meyers
(2008) also found that a variety of MMPI-2 valid-
ity scales differentiated litigants with malingered
pain-related disability from chronic pain patients
without evidence of malingering, as did the Hs
and Hy scales of the MMPI-2. FBS demonstrated
the largest effect size for discriminating between
nonmalingering chronic pain and those with defi-
nite malingered pain-related disability, d = 2.4,
followed by the Meyers Index, d = 2.2, and
Fb, d = 2.1. Consistent with the findings of other
investigators, FBS raw scores ≥30 were associated
with essentially zero false positives.
The sensitivity and specificity of the FBS
decline when investigated in psychiatric settings.
Rogers, Sewell, and Ustad (1995) found that F, Fb,
F minus K, and F(p) were superior to the FBS in
correct identification of psychiatric outpatients
taking the MMPI-2 under honest or simulated
malingering conditions. In the honest condition,
the FBS had a 21.1% false-positive rate, with only
a 48.5% sensitivity in the malingered condition.
Rogers et al. (1995) commented that their results
did not necessarily demonstrate the invalidity of
the FBS, which they observed may be more sensi-
tive in context-specific (e.g., personal injury) or
diagnosis-specific (e.g., PTSD) circumstances.
Correlations of the FBS with other measures
of symptom validity support the construct valid-
ity of the FBS. Slick et al. (1996) reported more
significant correlations of the FBS with the
Victoria Symptom Validity Scale than were found
for the F scale. Martens et al. (2001) reported a
significant association between the FBS and per-
formance invalidity measures developed from the
California Verbal Learning Test. Greiffenstein
et al. (2002) found significant associations between
the FBS and a Symptom Improbability Rating
Scale, Grip Strength, Finger Tapping Speed,
PDRT-27, Rey 15-item Test, and Rey Word List in
a sample of probable malingerers showing atypi-
cal outcome for mild TBI. I reported a significant
association between the FBS and the PDRT
(Larrabee, 2003b), and the FBS was frequently
136 forensic neuropsychology
associated with other performance invalidity
measures derived from standard clinical tests
including Benton Visual Form Discrimination,
Finger Tapping, Reliable Digit Span, and the
Wisconsin Card Sorting Test FMS score in sam-
ples of both definite and probable malingerers
(Larrabee, 2003a). The FBS was also associated
with Reliable Digit Span performance in a sample
of probable pain malingerers (Larrabee, 2003d).
Two studies have appeared that are critical of
the FBS as a measure of symptom exaggeration.
Butcher, Arbisi, Atlis, and McNulty (2003) con-
cluded that the FBS had an unacceptably high rate
of false-positive identification in clinical groups,
overidentified malingering in a personal injury
sample, and showed poor internal consistency.
Butcher et al. studied six subject samples; four
samples were obtained from the National
Computer Systems (NCS) database (profiles sent
in by clinicians for NCS scoring/interpretation),
including psychiatric inpatients, individuals in a
correctional facility, general medical patients, and
those with chronic pain. Another sample was
from a large tertiary care Veterans Affairs medical
center, with a sixth sample that included personal
injury litigants.
Butcher et al. (2003) did not report the per-
centage of subjects involved in compensation or
litigation actions in the psychiatric, chronic pain,
general medical, or Veterans Affairs samples and
did not report the context in which the MMPI-2s
were conducted in the correctional facility (e.g.,
competency to proceed to trial, criminal respon-
sibility, consideration for early release). Moreover,
Butcher et al. did not report results on measures
of exaggeration and symptom validity that were
independent of the MMPI-2 for their correctional
facility or personal injury samples. Hence, speci-
ficity values based on true false positives cannot
be computed; sensitivity values, absent indepen-
dent assessment of malingering in the correctional
facility and personal injury samples, also cannot
be computed. At best, elevated scores in the per-
sonal injury sample can serve as base rate indica-
tions of the frequency of malingering, assuming
the FBS is a valid indicator of symptom exaggera-
tion. Considered in this light, the rates of exag-
geration of 24.1% for males (FBS > 23) and 37.9%
for females (FBS > 25) reported by Butcher et al.
(2003) are well within previously reported base
rates of malingering in neuropsychological per-
sonal injury evaluations (59%, Greiffenstein et al.,
1994; 42%, Grote et al., 2000; 49%, Meyers &
Volbrecht, 1998).
The Butcher et al. (2003) article actually con-
tained data supporting the construct validity of
the FBS. These authors performed a content anal-
ysis identifying five groups of items: (a) somatic
symptoms, (b) sleep disturbance, (c) tension or
stress, (d) low energy/anhedonia, and (e) denial of
deviant attitudes or behaviors. Although Butcher
et al. criticized the FBS as having poor internal
consistency, the median Cronbach α of .62 for all
six subject samples is quite similar to the Cronbach
α of .64 for males and .63 for females for the F
scale reported in the MMPI-2 manual (Table D-7,
p. 97; Butcher et al., 1989). Of particular interest,
the Cronbach α was .85 for the personal injury
sample, showing that the five content areas of the
FBS identified by Butcher et al. are highly interre-
lated in personal injury litigants compared to
lower values in patients with chronic pain (0.47)
and general medical patients (0.58). Last, Butcher
et al., in their Table 4, showed that the FBS corre-
lated most strongly with MMPI-2 Scales 1, 2, 3, 7,
and 8, which are the MMPI-2 scales most likely to
be elevated in personal injury probable malinger-
ers (Boone & Lu, 1999; Larrabee, 1998, 2003b,
2003c; Ross et al., 2004).
Bury and Bagby (2002) compared the MMPI-2
validity scales of a sample of patients diagnosed
with PTSD to samples of university students
completing the MMPI-2 under standard instruc-
tions and under four conditions of exaggeration:
(a) faking PTSD; (b) coached on PTSD symptoms
only; (c) coached on MMPI-2 validity scales only;
and (d) coached on both PTSD symptoms as well
as MMPI-2 validity scales. These authors found
that the family of F scales, particularly Fb and
F(p), consistently produced the highest overall
classification rates and relatively stable estimates
of positive and negative predictive power (NPP)
across the different malingering conditions. In
contrast, the authors found that the FBS was
ineffective and failed to produce significant group
differences between the PTSD claimants and
the research participants in each of the fake PTSD
conditions.
The Bury and Bagby (2002) article suffers,
however, from a “fatal” research design error:
100% of their clinical PTSD sample was seeking
continuation or reinstatement of compensation
from the Workplace Safety and Insurance Board
of Toronto, Ontario, Canada. In addition, Bury
and Bagby did not assess their clinical sample for
evidence of symptom exaggeration/test perfor-
mance invalidity on measures that were indepen-
dent of the MMPI-2. This is a critical design error
 Assessment of Malingering 137

that invalidates their conclusions. Indeed, Bury
and Bagby stated: “In the context of these incen-
tives, symptom exaggeration is expected, and the
comparatively low classification rates may be a
result of the presence of individuals in the work-
place PTSD comparison sample who were actu-
ally exaggerating or malingering their condition”
(pp. 482–483).
The authors (Bury & Bagby, 2002) went on to
state that there was evidence in their clinical PTSD
sample that some of the claimants were likely
exaggerating their symptoms. Hence, the FBS may
well have been a poor discriminator of the clinical
PTSD sample because a sizable proportion of the
sample was malingering. This interpretation is
supported by review of Table 1 on page 476 of the
Bury and Bagby article, which shows a mean FBS
of 26.31 for their clinical PTSD sample, a value
that is well within the range of mean FBS scores
produced by analogue malingerers and suspected
malingerers (Lees-Haley, Iverson, Lange, Fox, &
Allen, 2002; see Table 5.3).
Greiffenstein, Baker, Peck, Axelrod, and
Gervais (2004) found that the FBS had good sensi-
tivity, specificity, and positive predictive power
(PPP) in discriminating 48 nonlitigating patients
suffering psychological trauma following events
such as completed rape or serious injury (mutila-
tion/traumatic amputation) from 57 litigants with
atypical symptom report seeking compensation for
psychological damages following relatively minor
events (e.g., minor frights not meeting DSM-IV
“gatekeeper” criteria for major trauma). In con-
trast, the F family (F, Fp, and F minus K) showed
poor discriminant utility. Logistic regression
yielded optimal FBS cutting scores of 21 for males
and 26 for females. FBS scores greater than 30 for
females and greater than 29 for males were associ-
ated with 100% positive predictive power for detec-
tion of implausible psychological trauma claims.
There have been two meta-analyses published
on the use of the FBS in civil forensic practice
(Nelson, Hoelzle, Sweet, Arbisi, & Demakis, 2010;
Nelson, Sweet, & Demakis, 2006). Nelson et al.

TABLE 5.3 FBS SYMPTOM VALIDIT Y SCALE

ENDORSEMENT BY CLINICAL PATIENTS,
SIMULATORS, AND MALINGERERS

Subject Group

Study Clinical Simulators Malingerers

Patients

Lees-Haley et al. (1991)a

M 15.7 25.0 27.6
SD (4.11) (8.5) (4.65)
Lees-Haley (1992)b
M 18.2 — 27.2
SD (5.3) — (5.2)
Larrabee (2003)e
M 15.67 — 26.15
SD (6.02) — (5.41)
Ross et al. (2004)d
M 14.61 — 28.61
SD (4.65) — (5.12)
a
Lees-Haley et al.: 25 Clinical Ss with emotional distress following personal injury;
67 noninjured Ss simulating emotional reaction to injury; 25 Ss malingering after
personal injury
b
Lees-Haley: 64 clinical Ss with emotional distress following injury; 55 Ss malingering
PTSD.
c
Larrabee: 29 clinical patients with moderate/Severe TBI; 26 litigants with definite
malingered neurocognitive dysfunction
d
Ross et al.: 59 Ss with moderate/severe TBI, and 59 litigants with probable malingered
neurocognitive dysfunction.
138 forensic neuropsychology
(2006) reported the largest grand effect size for
the FBS (0.96) followed by Obvious-Subtle (0.88),
Dissimulation-Revised-2 (DS-r-2; .79), F–K
(0.69), and F Scale (0.63). In a subsequent meta-
analysis, Nelson et al. (2010) included an addi-
tional 13 investigations, which when added to the
original set of 19 analyses from Nelson et al.
(2006), yielded a total of 32 studies, representing
2,218 over-reporting subjects, and 3,123 compari-
son subjects. Effect size remained large for the
FBS, d = 0.95, exceeded only by the DS-r-2 (d =
1.03) and Obvious-Subtle score (d = 1.00). The
largest FBS effect sizes were in investigations
including malingered TBI (d = 1.28), and gender
was found to be a significant moderating variable,
leading the authors to suggest that differential
cutoff scores be considered for men versus women.
Nelson et al. (2010) concluded that the updated
meta-analysis continued to support use of the FBS
as a validity measure, noting that FBS was partic-
ularly effective when effort was known to be insuf-
ficient and assessment occurred in the context of
traumatic brain injury.
Wygant et al. (2007) have published a unique
investigation of the relationship between context
of evaluation, symptom validity testing, and
MMPI-2 validity and clinical scales. These authors
found that the FBS was associated with symptom
validity test failure (TOMM and/or WMT) in
both civil and criminal forensic settings. The only
significant association of symptom validity test
failure with the F family of MMPI-2 validity scales
was in the criminal forensic setting, in association
with elevation on Fp. Both the civil litigants and
criminal defendants elevated RC1 and FBS, but
only the criminal defendants elevated Fp and RC8.
Wygant et al. concluded that criminal defendants
demonstrated a more global pattern of exaggera-
tion and feigned cognitive impairment, whereas
civil litigants restrict exaggeration to somatic
complaints and feigned cognitive impairment.
The extensive publications that have appeared
supporting the validity of the FBS correlate well
with the results of a survey conducted by Sharland
and Gfeller (2007) who found that the FBS was
the third most widely used measure of symptom
validity in a poll of NAN professional members
and fellows. Greiffenstein, Fox, and Lees-Haley
(2007) provide a comprehensive review of the FBS
research, and a summary table showing the fre-
quency distribution of FBS scores in 1,052 clinical
subjects, including those with moderate and
severe TBI, psychiatric patients, medically ill
patients, substance abusers, nontraumatic brain
diseases, and epilepsy. An FBS of ≤22 occurred in
90.3% of these clinical subjects, 95% had FBS of
≤25, and 99.7% scored ≤29. Greiffenstein et al.
offer detailed, empirically based recommenda-
tions for use and interpretation of the FBS, includ-
ing joint use with other MMPI-2 validity scales,
consideration of a general threshold score of ≥23
(90% specificity), and consideration of a variety
of moderating variables, including gender and
pre-existing psychiatric history, injury severity,
and medical history. They advise never to use FBS
alone; rather, it should be combined with other
data. Scores of 30 and above were noted to have a
99–100% posterior probability of indicating pro-
motion of suffering across all settings, and the
FBS was particularly useful in neuropsychological
settings wherein complaints of somatic dysfunc-
tion, cognitive symptoms, and nonpsychotic emo-
tional symptoms are common.
The FBS was added to the formal scoring
program for the MMPI-2 in September, 2006,
following a review conducted by the University of
Minnesota Press (Ben-Porath, Graham, & Tellegen,
2009). Ben-Porath et al. (2009) have prepared a
monograph detailing the development and
research results for the FBS, now known as the
Symptom Validity Scale (but still referred to by the
letters FBS). Ben-Porath et al. also offer interpre-
tive recommendations for the use of the FBS.
Other MMPI-2 invalidity scales have been deve-
loped subsequent to the FBS, including the Resp-
onse Bias Scale (RBS; Gervais, Ben-Porath, Wygant
& Green, 2007), and the Henry-Heilbronner Index
(Henry, Heilbronner, Mittenberg, & Enders, 2006).
Additionally, a revised version of the MMPI-2, the
MMPI-2-RF has been published (Ben-Porath &
Tellegen, 2008) which contains a new validity
scale, Fs, designed to capture somatic complaints
that are rarely endorsed in a medical population.
The MMPI-2-RF represents a major advance in the
evolution of the MMPI, and has been totally
restructured with the goal of creating purer clinical
scales with reduced item overlap, resulting in a
338-item version of the test with the core clinical
scales comprised of the Restructured Clinical
Scales (also available on the standard MMPI-2).
Validity scales include revised versions of VRIN
and TRIN, F, Fb, and Fp, with a new frequency
of endorsement analysis for the revision of F-r.
The four L scale items that previously occurred on
Fp have been dropped. FBS was reduced to those
30 items still remaining on the MMPI-2 RF.
The RBS was developed by using multiple
regression analysis to identify 28 MMPI-2 items

that discriminated between non-head-injury dis-
ability claimants who passed or failed the WMT,
CARB, TOMM (for over half the claimants), and
Medical Symptom Validity Test (MSVT; Green,
2004), for a minority of claimants (Gervais et al.,
2007). The RBS correlated significantly with
the FBS, r = 0.65, F and Fb, r = 0.67, and with Fp,
r = 0.36. The RBS added significant incremental
variance when entered following the F-family and
FBS scores, but none of the other response exag-
geration scales added significant incremental vari-
ance when the RBS was entered first in regression
equations that predicted failing performance on
the WMT, TOMM, CARB, or MSVT. Gervais et al.
found a larger Cohen’s d for the RBS (0.92) than
for the FBS (0.61). Cohen’s d was .63 for F, 1.00
for Fb, and .57 for Fp. At an RBS cutoff score of
16 or more, sensitivity was .48 at a specificity of
.89, defining the invalid performance group on
the basis of failing both the WMT and MSVT. At
the score of 17 or greater recommended by Gervais
et al., sensitivity dropped to .41 at a specificity of .95
in those failing both the WMT and MSVT.
Nelson, Sweet, and Heilbronner (2007) con-
trasted samples with external incentive versus no
incentive (differential prevalence design) on sev-
eral MMPI-2 validity scales, including the FBS
and an older version of the RBS. The RBS yielded
the largest effect size (d = 0.65), followed closely
by the FBS (d = .60). The RBS correlated highly
with the FBS (r = 0.74). By contrast, the effect
sizes were .22 for F, .01 for Fb, and .05 for Fp.
Nelson et al. suggested that the RBS and FBS may
represent a similar construct of symptom validity
and may outperform other MMPI-2 validity scales
in discriminating patient groups with and without
secondary gain.
Wygant et al. (2010) evaluated the association
of RBS scores with pass/fail performance on the
WMT and/or TOMM in both criminal and civil
forensic samples. RBS was correlated with most of
the validity scales and clinical scales in both
samples, but the correlations were higher with
the F family and RC8 in the criminal compared to
the civil forensic sample. Although RBS had a
large effect size in discriminating criminal foren-
sic subjects who failed SVTs from those who did
not, with a d = 1.48, F family scales yielded higher
values of d (Fp = 1.65; F = 1.61), with MMPI-2-RF
F-r and Fp-r yielding effect sizes of 1.48 and 1.46,
respectively. In the civil forensic sample, RBS
yielded the largest effect size, d = 1.24, though
not meaningfully different than the values of FBS
(d = 1.18), Fs (d = 1.14), and FBS-r (d = 1.13).
Assessment of Malingering 139
Employing logistic regression analysis to predict
pass/fail SVT performance, RBS did not add to
the discrimination provided by the MMPI-2 over-
reporting scales in the criminal forensic sample,
but did account for a significant increase in
prediction over and above the MMPI-2 over-
reporting scales in the civil forensic sample.
Wygant et al. concluded that the RBS was associ-
ated with SVT failure in both criminal and civil
forensic samples.
Smart et al. (2008) utilized classification tree
analysis with Optimal Data Analysis (CTA with
ODA), to determine which MMPI-2 validity and
clinical scales discriminated between examinees
failing SVTs and those passing SVTs, with a
sample including subjects evaluated in secondary
gain contexts (disability claim, personal injury
litigation) and those examined in clinical con-
texts. RBS and Hy were the only MMPI-2 vari-
ables selected by the CTA with ODA analysis,
with cutoff scores of <16.5 RBS (raw score) identi-
fying valid SVT performance, as well as RBS
scores > 16.5 but with Hy <79.5. Invalid SVT per-
formance was associated with RBS >16.5, and Hy
> 79.5. When RBS was excluded from the MMPI-2
scales that were subjected to analysis, Hy replaced
RBS as the primary node in the hierarchical tree
(i.e., most salient variable for discrimination of
pass/fail SVT status), with additional discrimina-
tion provided by Pa, Fb, K, and Fp. FBS did not
enter into the final classification model, nor did it
enter into the model based on RBS and Hy. These
data support the validity of the RBS, at a cutoff
score identical to the RBS raw score of ≥17 pro-
posed by Gervais et al. (2007) and demonstrate
that Hy also has a major contribution to detection
of invalid SVT performance, consistent with the
role Hy played in the somatic malingering profile
proposed by me (Larrabee, 1998).
Henry et al. (2006) derived the 15-item Henry-
Heilbronner Index (HHI) from both the 43-item
FBS and the 17-item Pseudoneurologic Scale
(PNS) of Shaw and Matthews (1965). Using logis-
tic regression, the authors compared the ability of
the FBS, PNS, and a combined FBS-PNS scale to
discriminate a group of 45 litigation/compensa-
tion-seeking examinees, defined as meeting Slick
et al. (1999) criteria for either definite or probable
malingered neurocognitive dysfunction from a
group of 74 nonlitigation, non-compensation-
seeking TBI patients, the majority with mTBI. All
three scales discriminated between the head-
injured and probable malingering groups, with
the FBS and the combined FBS-PNS performing
140 forensic neuropsychology
better than the PNS. Further item analysis yielded
15 items that best discriminated the two groups,
with the HHI comprised of nine FBS items, four
PNS items, and two items shared by FBS and PNS.
A score of 8 or higher had a sensitivity of .80 and
a specificity of .89. A principal components analy-
sis of the HHI showed that it comprised one dom-
inant factor, including mostly physical items,
leading Henry et al. to characterize the scale as a
“pseudosomatic index,” which they contended
may be a purer measure of somatic malingering
than the FBS and MMPI-2 scales Hs and Hy, as
identified by me (Larrabee, 1998).
Whitney, Davis, Shepard, & Herman (2008)
evaluated the prediction of failure on the TOMM
by the RBS, FBS, F family scales, HHI, and Fptsd
scale (Elhai, Ruggiero, Frueh, Beckham, Gold, &
Feldman, 2002). In a VA sample wherein 24 passed
the TOMM and 22 failed, only the RBS, Fb, and
HHI significantly discriminated the groups, with
the RBS and HHI showing large effect sizes of .98
and .90, respectively. Scores on TOMM trials 1, 2,
and Retention all correlated with the RBS and
HHI, but not at all with FBS. Multiple regression
predicting TOMM pass/failure showed that
no scale added to the prediction of TOMM
performance beyond the prediction based upon
RBS alone. Last, the RBS had an ROC area under
curve of .75. Whitney et al. found that an RBS
cutoff score of 19 or higher had a sensitivity
of .23 and a specificity of .96. The best likelihood
ratio, however, was associated with an RBS cutoff
score of 17 or higher, at which sensitivity was
.50 with specificity of .92. It is noteworthy that
this cut score of 17 matches the optimal cutoff
score originally published by Gervais et al. (2007),
and also reported and recommended by Smart
et al. (2008).
I (Larrabee, 2008, February) compared the
diagnostic classification of the RBS, FBS, FBS-r,
HHI, F, Fp, Fptsd, and Fs in the discrimination of
a group of definite and probable malingerers from
a group of clinical patients with moderate and
severe TBI and various neurologic and psychiatric
diagnoses. FBS (d = 1.99), RBS (d = 1.91, FBS-r (d
= 1.85), and the HHI (d = 1.77) yielded very large
effect sizes, as well as large ROC area under curve
values (0.917, .901, .900, and .892, respectively).
When the various validity scales were predicted
by four embedded/derived SVT scores (Benton
Visual Form Discrimination, Combined Finger
Tapping, Reliable Digit Span, and Wisconsin Card
Sorting Test Failure-to-Maintain-Set), RBS
showed the highest R2 value, .436, followed by
FBS-r (0.363), HHI (0.270), Fs (0.270), and FBS
(0.258). Logistic regression showed that both
RBS and FBS (or FBS-r) added significantly to
discrimination of the malingering and clinical
samples, with no other validity scale adding to
the discrimination provided by RBS and FBS (or
RBS and FBS-r). Overall, these data support the
validity of the RBS, FBS, FBS-r, and HHI, although
the HHI does not appear to add additional useful
information to that provided by RBS and FBS/
FBS-r. These results differ from those of Whitney
et al. (2008), likely due to larger sample size in the
Larrabee (2008, February) study, the fact that the
Larrabee study used a civilian rather than a vet-
eran population, and the Larrabee investigation
compared litigants/clamainants who met Slick
et al. (1999) criteria for either definite or probable
malingered neurocognitive dysfunction, whereas
the Whitney et al. study discriminated between
subjects who either passed or failed the TOMM.
In other words, the Larrabee investigation con-
trasted malingering versus clinical patient samples
whereas the Whitney et al. study evaluated pass/
fail performance on a single SVT.
In summary, there appear to be at least two
types of malingering detected by the MMPI-2. In
the first, scores are elevated on F and the F scale
derivatives, including Fb, F(p), and F minus K,
with extreme elevations on MMPI-2 clinical
Scales 6, 8, and RC8 (Graham, 2006; Greene, 2000;
Wygant et al., 2007; Wygant et al., 2010). This pat-
tern is consistent with exaggeration of severe psy-
chopathology and likely occurs with greater
frequency in settings in which suffering psychosis
may mitigate external consequences such as con-
viction of crimes or compulsory military service.
The second type of malingering detected by the
MMPI-2 is exaggeration of health and physical
injury symptoms in the context of personal injury
litigation in general, and litigation for neuropsy-
chological claims specifically. This is character-
ized by elevations on the FBS, RBS, and HHI, as
well as by elevations on Scales 1, 2, 3, 7, and 8.
Last, as with any measure of exaggeration or
performance invalidity, diagnostic certainty
increases with the presence of abnormal scores on
other independent indicators (Larrabee, 2003b;
Martens et al., 2001; Slick et al., 1999; Sweet,
1999). Per the work of Donders and colleagues
(Martens et al., 2001; Miller & Donders, 2001),
preexisting psychiatric history can be a mitigating
factor in nonlitigating individuals with mild TBI,
and per Greiffenstein et al. (2002), presence of
anosmia or residual motor impairment can be a

mitigating factor in evaluating the FBS scores of
litigating patients with moderate and severe TBI.
ADDITIONAL DIAGNO STIC
C O N S I D E R AT I O N S
The diagnosis of malingering in the individual
case, using the Slick et al. (1999) criteria, involves
relying on psychometric measures of response
bias. These measures are associated with various
degrees of sensitivity (to the true presence of
response bias) and specificity (accurate detection
of the absence of response bias). The diagnostic
accuracy of response bias procedures in the indi-
vidual case also depends on the base rate or
frequency of malingering in the forensic popula-
tion. Given information on sensitivity, specificity,
and base rate, one can compute for individual
measures of response bias the PPP, or probability
that someone with a positive score is truly
malingering, and NPP, or probability that some-
one with a negative score truly is not malingering
(Baldessarini, Finklestein, & Arana, 1983; also see
chapter 1, this volume).
Two articles provide converging support for a
40% prevalence of malingering in litigating claim-
ants with mild TBI. Mittenberg, Patton, Canyock,
and Condit (2002) surveyed members of the
American Board of Clinical Neuropsychology
who did forensic work and in personal injury liti-
gants with mild TBI found base rates of malinger-
ing of 38.5% unadjusted for referral source,
increasing slightly to 41.24% when adjusted for
referral source. Additional information obtained
in this survey showed that the board-certified
respondents typically employed several sources of
information similar to the Slick et al. (1999) crite-
ria for probable MND, strengthening the likely
accuracy of the base rate obtained by Mittenberg,
Patton, et al. The base rate figures obtained by
Mittenberg, Patton, et al. for litigants with mild
TBI are quite close to the base rate of malingering
in mild TBI as I reported (Larrabee, 2003a) based
on my review of 11 studies (Binder & Kelly, 1996;
Frederick et al., 1994; Greiffenstein et al., 1994;
Grote et al., 2000; Heaton et al., 1978; Meyers &
Volbrecht, 1998; Millis, 1992; Millis et al., 1995;
Rohling, Green, Allen, & Iverson, 2002; Trueblood
& Schmidt, 1993; Youngjohn et al., 1995), which
identified 548/1,363 persons (40%) who showed
motivated performance deficit suggestive of
malingering. Of additional interest, Mittenberg,
Patton, et al. (2002) also provided adjusted base
rates of malingering for several other alleged con-
ditions, including 38.61% for fibromyalgia (FM)
Assessment of Malingering 141
or chronic fatigue, 33.51% for pain or somatoform
disorders, 29.49% for neurotoxic disorders, and
25.63% for electrical injury.
The Mittenberg, Patton et al. (2002) and my
(Larrabee, 2003a) base rates for malingering of
40% for litigants with mild TBI and Mittenberg,
Patton, et al.’s malingering base rate of 33.51% for
pain or somatoform disorders are quite consistent
with the results of the Carroll, Abrahamse, and
Vaiana (1995) investigation of the costs of excess
medical claims for automobile personal injuries.
Carroll et al. analyzed “soft” (i.e., sprain/strain)
and “hard” (i.e., fractures) injury claims as a func-
tion of compensation system per state (e.g., tort
system, dollar no-fault, and verbal no-fault) and
found that 35–42% of all medical costs submitted
in support of auto injury claims were excessive.
Other studies have provided further support for
a base rate of malingering of 40% or more in set-
tings with external incentive. Ardolf, Denney,
and Houston (2007) found that of those persons
referred for pre-trial pre-sentencing neuropsy-
chological evaluation, 21.9% met Slick et al. (1999)
criteria for definite malingering, and 32.4% met
criteria for probable malingering, for a combined
definite/probable rate of 54.3%. Van Hout,
Schmand, Wekking, and Deelman (2006) found
that 57.2% of a sample with suspected neurotoxic
injury failed at least one of three SVTs. Greve et al.
(2006) reported a malingering prevalence of 40%
(33.3% probable, 6.7% definite) in persons claiming
exposure to occupational and environmental sub-
stances. All of these investigations were of subjects
who had known external incentives. The consis-
tency of these base rates led my colleagues and I to
propose a new “magical number”: 40% plus or
minus 10, as representative of the base rate of invalid
neuropsychological testing in settings with external
incentive (Larrabee, Millis, & Meyers, 2009).
The review of SVTs published by Vickery et al.
(2001), covering data obtained on the DMT,
PDRT, Rey 15-Item Test, 21-Item Test, and Dot-
Counting Test, showed an average sensitivity of
56.0%, average specificity of 95.7%, and average
hit rate of 76.8%. These data showed findings
characteristic of most SVTs or measures of
response bias: The specificity is set at a high value
to minimize the occurrence of false-positive
errors, that is, misidentifying someone as a malin-
gerer who is not truly malingering. The conse-
quence of setting specificity high is that sensitivity
is low; that is, using the Vickery et al. (2001) data,
on average 44% of persons who truly are malin-
gering go undetected.
142 forensic neuropsychology
Computation of PPP and NPP, using the aver-
age sensitivity and specificity values reported by
Vickery et al. (2001) and malingering base rate of
40%, yields a PPP of .897 (proportion of true pos-
itives to true positives plus false positives) and an
NPP of .765 (proportion of true negatives to true
negatives plus false negatives) for a single failed
SVT. These data show that the probability of truly
identifying malingering when test scores exceed
the cutoff is higher than the probability of
correctly detecting the absence of malingering.
Consequently, negative findings on SVTs are poor
at ruling out the presence of malingering; in
contrast, greater confidence can be afforded
positive findings on SVTs (Bianchini, Mathias, &
Greve, 2001; Faust & Ackley, 1998; Slick et al.,
1999). Thus, a clinician doing a forensic assess-
ment does not merely tally the number of passes
and failures on SVTs and conclude malingering or
absence of malingering based on which outcome
has the greatest number of tallies.
Actually, using multiple criteria for assessment
of malingering is supported on a statistical basis,
both for improving sensitivity and for keeping
constant or increasing specificity (Iverson &
Franzen, 1996; Larrabee, 2003a; Martens et al.,
2001; Orey, Crager, & Berry, 2000; Vickery et al.,
2004). An example of this, using a known-group
design, is one of my studies (Larrabee, 2003a).
This investigation derived cutoff scores on five
tests for discriminating litigants with definite
MND from patients who had moderate or severe
TBI: Benton VFD, FT, RDS, WCST FMS, and the
Lees-Haley FBS from the MMPI-2. The sensitivity
and specificity, respectively, of the individual tests
at specific cutoff scores were .48 and .931 for VFD,
.40 and .935 for FT, .50 and .935 for RDS, .48 and
.871 for FMS, and .808 and .862 for FBS. Evaluating
all possible pairwise combinations of scores
exceeding cutoff (e.g., FT and RDS; FMS and FBS;
etc.) resulted in a sensitivity of .875 and specificity
of .889. Evaluating all possible three-way combi-
nations reduced sensitivity to .542 (still higher
than the individual sensitivities for VFD, FT, RDS,
and FMS), but resulted in 100% specificity (i.e., no
false-positive scores), a value better than that
achieved by any individual test.
Vickery et al. (2004) reported similar results in
a simulation design in which noninjured persons
and persons with moderate-to-severe TBI com-
pleted testing under conditions of standard as well
as malingering instructions. Sensitivity dropped
as a function of the number of scores falling in
the range of motivational impairment increased,
whereas specificity increased as a function of the
number of motivationally impaired scores. Perfect
specificity was achieved at three or more test
failures, the same result I reported (Larrabee,
2003a). Subjects with three or more test failures
had 100% PPP for malingering regardless of the
base rate. Persons with two or more test failures
had PPP of .952 and NPP of .808 at a malingering
base rate of 40% in the Vickery et al. investigation.
These values, obtained with a simulation design,
can be compared to the PPP of .913 and NPP of
.921 I reported (Larrabee, 2003a) in a known-group
design for discriminating definite and probable
MND from moderate-to-severe TBI, psychiatric,
and neurological patients, employing two or more
test failures at a malingering base rate of 40%.
Victor, Boone, Serpa, Buehler, and Ziegler
(2009) reported results that were quite similar to
my findings (Larrabee, 2003a) and the results of
Vickery et al. (2004). Employing four embedded/
derived indicators (derived from the Rey-
Osterrieth Complex Figure Test, Auditory Verbal
Learning Test, Finger Tapping, and Reliable Digit
Span) to discriminate probable malingerers from
a mixed neurologic and psychiatric sample, Victor
et al. obtained a sensitivity of 83.8% and specificity
of 93.9% for failure of any two indicators, and a
sensitivity of .514 with a specificity of .985 for
failure of any three indicators. These values for
failure of any two or failure of any three matched
quite closely the data from my earlier investiga-
tion (Larrabee, 2003a) and the results of Vickery
et al. (2004); specifically, the best overall hit rates
were with two failed indicators, and failure of
three indicators was associated with essentially no
false positives (no cases in my investigation or that
of Vickery et al., 2004; one case in Victor et al.,
2009). Moreover, Victor et al. also found that the
hit rates for two failed indicators matched the hit
rates when all four indicators were entered as con-
tinuous variables in a logistic regression, the same
as I reported for failure of any two indicators com-
pared to a logistic regression based on the five
indicators in my investigation (Larrabee, 2003a).
My finding of improved sensitivity and con-
stant or improved specificity (Larrabee, 2003a) by
aggregating scores across multiple measures of
malingering is understood as a function of the
rarity of test scores exceeding malingering cutoffs
for truly impaired patients in combination with
regression to the mean. My (Larrabee, 2003a)
investigation included 27 subjects with moderate
or severe TBI, 13 nonlitigating patients with vari-
ous disorders affecting the central nervous system,

and 14 patients with psychiatric disorders, pri-
marily major depressive disorder, yielding a total
of 54 clinical patients. The performance of these
54 patients on VFD, FT, RDS, FMS, and FBS was
analyzed for this chapter to determine mean per-
formance and standard deviations for this mixed
clinical sample. Then, z scores were determined,
relative to the clinical sample, for scores on the
five malingering indicators beyond the empirical
cutoffs for malingering. The average z score for
these cutoffs, collapsed across all five malingering
indicators, was 1.57 SD beyond the clinical group
mean (showing an average false-positive rate per
test of 5.8%). The average intercorrelation (using
Fisher’s z transformation) of the five malingering
indicators was .175. Thus, based on regression to
the mean and the average z score associated with
the malingering cutoffs, the predicted value of
performance on any given test given a perfor-
mance at a z score of 1.57 on another malingering
indicator was (0.175)(1.57) or a z score of .274, a
value substantially below the average z score of
1.57 associated with performance invalidity. Thus,
although a clinical patient may on rare occasion
(5.8%) obtain a score beyond the cutoff for malin-
gering on any one of the five malingering indica-
tors I identified (Larrabee, 2003a), it is not likely
that two scores will exceed the cutoff.
Boone and Lu (2003) made a similar point
related to the probability of multiple scores exceed-
ing cutoff for malingering in nonmalingering clini-
cal patients. They observed that specificity is
typically set at .90 to keep false-positive identifica-
tion at a minimum. Assuming the tests are not
strongly correlated (see the above discussion),
Boone and Lu noted that the overall false-positive
rate for six “failed” effort measures could be as low
as 1 in 1 million (0.1 × 0.1 × 0.1 × 0.1 × 0.1 × 0.1).
Applying this reasoning to the Slick et al. (1999)
criteria for probable response bias, the probability
of a false-positive score for two tests exceeding
cutoff for malingering, each with a specificity of .90
with no correlation between the two tests in a non-
litigating clinical sample, is (0.1 × 0.1) or .01. Boone
and Lu (2003) conclude that rather than inflating
(false positive) error, administering several inde-
pendent and well-validated effort techniques serves
to substantially increase diagnostic accuracy.
The finding of increased probability of malin-
gering as a function of multiple failed SVTs is
supported by the methodology of chaining of like-
lihood ratios (Grimes & Schulz, 2005; also see
Chapter 1, this volume). The positive likelihood
ratio is obtained by dividing the sensitivity at a
Assessment of Malingering 143
particular cutoff score by the false positive rate
that is associated with that same cutoff score. For
example, to use values typical of most SVTs which
show sensitivities of .50 at specificities of .90
(Vickery, et al. 2001), a sensitivity of .50 is divided
by the false alarm rate of .10 (1–specificity, or
1–.90) to obtain a likelihood ratio of 5.0. One can
then premultiply this likelihood ratio by the base
rate odds of malingering, to obtain the posttest
odds of malingering. Per data cited in this chapter,
a value of .40 is a widely replicated base rate of
malingering. This is converted to base rate odds
by the formula odds ÷ 1–odds, or .40 ÷ 1–.40 or
.67. Premultiplying the likelihood ratio of 5.0 by
the base rate odds of .67 yields a posttest odds of
3.35. These posttest odds can then be used as the
new odds of malingering, which can be used to
premultiply the likelihood ratio based on a second
independent SVT. Assuming that the second SVT
has the same operating characteristics as the first
one (i.e., sensitivity of .50 at specificity of .90), the
new posttest odds after applying this second, inde-
pendent SVT are 3.35 × 5.0 or 16.75. Applying a
third, independent SVT with the same operating
characteristics gives posttest odds of 16.75 × 5.0 or
83.75. At any point in this chain of likelihood
ratios, the posttest odds can be converted back to
probabilities of malingering by the formula odds
÷ odds + 1; for example, after applying one SVT,
the probability of malingering is 3.35 ÷ 4.35 or .77;
after two failed SVTs, the probability of malin-
gering is 16.75 ÷ 17.75 or .94; after three failed
SVTs, the probability of malingering is 83.75 ÷
84.75 or .99. The reader will notice that the values
for failure of two and failure of three SVTs closely
approximate the values reported by me (Larrabee,
2003a), Vickery et al. (2004), and Victor et al.
(2009), based on the actual empirical data.
Moreover, chaining of likelihood ratios shows
that even at low base rates of malingering, for
example, .10, multiple SVT failure leads to poste-
rior probabilities over .90. In my paper (Larrabee,
2008b), failure of one SVT with a sensitivity of
.50 and specificity of .90 yields a posterior proba-
bility of malingering of .36 at a base rate of malin-
gering of .10, as might be expected in a low
base-rate condition, even using an indicator with
a low false-positive rate of .10. Failure of a second
independent SVT with the same operating char-
acteristics (sensitivity of .50, specificity of .90) at a
base rate of .10 now yields a posterior probability
of malingering of .74. Failure of a third indepen-
dent SVT at a base rate of .10 now yields a poste-
rior probability of .93.
144 forensic neuropsychology
It is important to note that all of the computa-
tions discussed in the preceding two paragraphs
assume independent SVTs, producing cutoff
scores that are each associated with sensitivities of
.50 and specificities of .90. These values will
change as a function of differing likelihood ratios
and base rates, and the probabilities generated by
chaining of likelihood ratios will be inflated if the
SVTs are correlated rather than independent
(Grimes & Schulz, 2005). Inflated probabilities as
a function of correlated SVTs did not occur when
I analyzed my own data by direct empirical meth-
ods (which would allow for SVT intercorrelation)
versus using chaining of likelihood ratios
(Larrabee, 2008b). This was because the SVT
intercorrelation averaged .175, as reported earlier
in this section of the current chapter.
The accumulating empirical evidence subse-
quent to the seminal article by Slick et al. (1999)
provides statistical support for these criteria, in
particular, the criteria for definite and probable
malingering. My colleagues and I (Larrabee,
Greiffenstein, Greve, & Bianchini, 2007), demon-
strated that significantly worse-than-chance per-
formance showed definite intent to perform
poorly, and that groups defined by the Slick et al.
criteria for probable malingering did not differ
from those defined by criteria for definite malin-
gering (other than by the presence of worse-than-
chance performance in the definite malingering
samples). To show that intent underlies worse-
than-chance performance, we compared the
performance of groups of litigants/claimants
with worse-than-chance performance to that of
noninjured persons simulating impairment. In
making this comparison, the simulators are
known to be intentionally manipulating their test
performance because they have been instructed
to do so. Consequently, showing equivalent or
worse SVT performance (independent of the
original forced choice SVT chosen for group
formation) by litigants with worse-than-chance
performance compared to simulators would
support intent on the part of the definite malin-
gerers. For example, performance on Reliable
Digit Span (RDS; one of the best studied SVT
indicators) yielded a pooled mean of 6.89 and
standard deviation of 3.03 for 138 simulators
(Inman & Berry, 2002; Etherton, Bianchini, Ciota,
& Greve, 2005; Strauss, Slick, Levy-Bencheton,
Hunter, MacDonald, et al., 2002). Corresponding
data for a pooled sample of 77 definite malinger-
ers (Etherton, Bianchini, Ciota, Heinly, & Greve,
2006; Etherton, Bianchini, Greve, & Heinly 2005;
Heinly, Greve, Bianchini, Love, & Brennan, 2005;
Larrabee, 2003a) yielded a mean RDS of 7.11
and standard deviation of 2.47, which was not
significantly different from the pooled simulator
performance. Data are also available regarding
exaggerated symptom report on the MMPI-2 FBS.
Pooled FBS data on 72 simulators (Bianchini,
Etherton, Greve, Heinly, & Meyers, 2008; Dearth,
Berry, Vickery, Vagnini, Baser, et al., 2005) yielded
an FBS mean of 25.7, with a standard deviation
of 6.4. This was actually significantly lower
(p <0.01) than pooled data on 72 definite malin-
gerers (Bianchini et al., 2008; Greve, Bianchini,
Love et al., 2006; Larrabee, 2003b), yielding a
mean of 28.5 and standard deviation of 4.66.
Hence, the definite malingerers showed more
exaggeration than a noninjured group of persons
intentionally producing injury-associated symp-
toms on the MMPI-2.
My colleagues and I (Larrabee et al., 2007)
next explored the similarity of performance of
litigants/claimants meeting criteria for probable
malingering to that of litigants/claimants meeting
criteria for definite malingering. Heinly et al.
(2005) found no differences on Digit Span-based
scores, including Reliable Digit Span and the
Digit Span scaled score in comparisons of the
performance of probable versus definite malin-
gerers. Similarly, Greve, Bianchini, Love, et al.
(2006) found no differences in a number of differ-
ent MMPI-2 validity scales, including the FBS
(e.g., mean FBS was 26.9, SD = 6.4 for 31 probable
malingerers, vs. mean FBS of 29.8, SD = 3.9 for 14
definite malingerers). I (Larrabee, 2003a) found
no differences in test scores contrasting the
performance of 17 probable malingerers and
24 definite malingerers on Benton VFD, com-
bined (dominant and nondominant hand) Finger
Tapping, Reliable Digit Span, Wisconsin Card
Sorting Test Failure-to-Maintain set, and FBS.
Moreover, I found no significant differences
between the performances of the probable and
definite malingerers on four other sensitive neu-
ropsychological measures including Controlled
Oral Word Association, Trail Making B, Verbal
Selective Reminding, and the CVMT.
In a very unique investigation, Bianchini,
Curtis, and Greve (2006) demonstrated a dose-
response relationship between the magnitude of
potential compensation and failure on tests sensi-
tive to malingering. They compared three groups
of patients varying in level of potential compensa-
tion: a) a no-incentive group, b) limited incentive
as provided by Louisiana Workers’ Compensation

law, and c) high incentive as provided by federal
law. Severity of brain injury was also analyzed as a
factor, comparing patients with mild TBI to those
with moderate/severe TBS. For every SVT indica-
tor examined, mTBI patients covered by federal
law showed considerably higher rates of positive
findings and diagnosable malingering than
patients covered by state law. By contrast, patients
with moderate/severe TBI showed a general
incentive effect (i.e., those with external incentive
failed SVTs at a higher rate than in the no-
incentive group, but this rate did not differ in fed-
eral vs. state disability settings). Similar findings
of more pronounced compensation effect in mild
versus severe TBI have been reported by Binder
and Rohling (1996).
In summary, we (Larrabee et al., 2007)
contended that the lack of difference between
definite malingerers and simulators (who are
known to be producing false deficits and exagger-
ated symptoms) further demonstrates “intent” as
the motivation for performing significantly
worse-than-chance. Second, the lack of differ-
ences in performance and symptom report when
comparing probable to definite malingerers (with
the exception of performance on two-alternative
forced choice testing) establishes the validity of
the Slick et al. (1999) probable malingering crite-
ria. Last, the dose-response existing between SVT
failure and malingering diagnosis demonstrated
by Bianchini et al. (2006), and Binder and col-
leagues meta-analytic work on compensation
effect sizes in TBI (0.47, Binder & Rohling, 1996)
and chronic pain (0.48, Rohling, Binder, &
Langhinrischen-Rohling, 1995) establishes the
role that external incentive plays in motivating
malingering behavior in settings with external
incentive.
We concluded our review of the criteria for
malingering by offering several empirically based
recommendations (Larrabee et al., 2007). First,
given the data showing the effect on posterior
probability of diagnosis by aggregating multiple
positive indicators, we suggested that presence of
any two positive indicators was sufficient for a
diagnosis of probable malingering, provided there
was a setting with external incentive and no pri-
mary explanation of poor performance as a func-
tion of neurologic, psychiatric, or developmental
factors. As shown in my paper on aggregating
likelihood ratios (Larrabee, 2008b), failure of two
independent SVTs associated with cut scores
having sensitivity to malingering of .50 and speci-
ficity of .90, in a setting of external incentive with
Assessment of Malingering 145
base rate of malingering at .40 has a posterior
probability of malingering of .94. Additionally,
per earlier discussion in this chapter of classifica-
tion statistics, specificities of 1.00 are associated
with a positive predictive power of 1.00 (true pos-
itives/true positives + 0 false positives). Per the
results of Vickery et al. (2004), Victor et al. (2009),
and my own work (Larrabee, 2003a), failure of
three independent SVTs is essentially associated
with zero false positives and a 1.00 probability of
malingering. Boone (2007b) makes the same con-
clusion relating the presence of three failed SVTs
to the diagnosis of definite noncredible neurocog-
nitive performance (note that an important excep-
tion to this rule, as pointed out by Meyers &
Vollbrecht, 2003, is the patient who requires a
24-hour supervised living setting). Consequently,
failure of three independent SVTs in the context
of external incentive and unexplained by neuro-
logic, psychiatric, or developmental factors is
diagnostically equivalent to the worse-than-
chance performance characteristic of definite
malingering. In this regard, the reader should
note that failed SVT performance at 100% speci-
ficity is not conceptually equivalent to the active
avoidance of the correct response that is associ-
ated with significantly worse-than-chance perfor-
mance on two-alternative forced choice testing.
In our review of diagnostic criteria, we also
recommended that C criteria (subjective com-
plaint) be given equal weight (Larrabee et al.,
2007). In the original Slick et al. criteria, evidence
of exaggeration of symptoms or inconsistent or
atypical symptom report alone, on multiple inde-
pendent indicators, could only result in a diagno-
sis of possible malingering. Our recommended
change to allow multiple, independent measures
of symptom exaggeration to define probable
malingering corrects the original asymmetry
between criteria for feigned neuropsychological
test performance and exaggerated symptoms.
Whereas it is the current author’s experience that
most persons defined as malingering both feign
deficit and exaggerate symptoms, there are smaller
subgroups who either feign performance or exag-
gerate symptoms, but do not do both. Again, the
requirement for symptom report is that there be
multiple independent indicators (i.e., multiple
elevated validity indicators on the MMPI-2 would
only count as one independent indicator; evi-
dence from independent personality tests or
symptom rating scales must be evident to count
towards the criteria for multiple independent
indicators of symptom exaggeration).
146 forensic neuropsychology
As we observed in our review of the criteria
for malingering (Larrabee et al., 2007), the clini-
cian does not need to make an inference of intent;
rather, intent is demonstrated by the presence of
multiple, highly improbable events. The research
reviewed in the present chapter, as well as in recent
reviews of malingering (Boone, 2007; Larrabee,
2007), shows that individual SVT measures,
whether they be free-standing or embedded/
derived, have cutoff scores that are rare in patients
with bona fide clinical disorder, either in terms of
extreme levels of performance abnormality, or
atypical nature of performance (e.g., recognition
worse than recall, or attention worse than
memory). The additional requirement for the
presence of multiple positive scores on indepen-
dent SVTs thus results in multiple rare/atypical
performances and/or symptom endorsements.
Known group/criterion group designs evaluating
the effects on diagnostic probability of positive
scores on multiple independent SVTs (Larrabee,
2003a, 2008b; Vickery et al. 2004; Victor et al.
2009) statistically support this interpretation of
intent; that is, the probability of malingering
increases from one to two to three positive SVT
findings, such that diagnostic probability is in the
.90 range for two SVT failures and essentially 1.00
for the presence of three indicators.
TESTIFYING ABOUT
MALINGERING
As discussed by Kaufmann (Chapter 3, this
volume), testifying about malingering can be
challenging. A key issue to keep in mind is that
one cannot comment upon the truthfulness or
credibility of the examinee. This includes describ-
ing symptom exaggeration as lying. How can this
be handled? I have found that keeping to the Slick
et al. (1999) MND or Bianchini et al. (2005)
MPRD definitions is very helpful, for they objec-
tify the definition of malingering and the criteria
for determining its presence. Describing malin-
gering as exaggeration and/or fabrication of defi-
cits in the context of external incentives is
preferable to the DSM-IV definition of malinger-
ing as “. . .the intentional production of false or
grossly exaggerated. . .” (p. 739; italics added).
When being cross examined on a diagnosis of
malingering, opposing counsel may try to have
you use the terms “lying,” “false,” or “not telling
the truth.” Avoid these terms, referring back to the
original definition.
When discussing symptom validity results,
certain data can be placed into perspective in such
a way as to drive home the point of how atypical
the performance is; for example, when discussing
a derived or embedded procedure for which there
are data obtained on a noninjured simulator
group, performance can be described as “similar
to the performance of noninjured persons
attempting to feign impairment, who themselves
perform differently than patients with severe trau-
matic brain injury.” The same can be done with
symptom report; for example, in Larrabee (2003c)
I present MMPI-2 data for a probable malinger-
ing sample, as well as for samples of patients with
chronic pain, major depressive disorder, severe
TBI not in litigation, multiple sclerosis, and spinal
cord injury (the majority of whom were quadri-
plegic). It is compelling when the data for the case
on which you are testifying produce MMPI-2
primary clinical scale scores falling above the
mean scores for the probable malingering sample,
which themselves are higher than those produced
for the bona fide clinical samples presented in the
same article.
On occasion, a judge may prohibit you
from any testimony about malingering. In such a
circumstance, one can still comment on the
validity of the examinee’s neuropsychological
examination results. What I have done (also see
Kaufmann, chapter 3) is testify that neuropsy-
chological evaluation involves interviewing and
testing (including both symptom report measures
such as the MMPI-2, and performance on various
tests of abilities, such as memory and intelligence).
The tests we use are valid measures of the abilities
we are assessing, showing decrements in patients
who have lesions in their brains, and correlation
with external criteria such as the ability to safely
drive a motor vehicle. In addition to the validity
of the test, the validity of a particular patient’s per-
formance must be evaluated, so that we know we
are obtaining an accurate measure of their actual
abilities. I then describe how we determine perfor-
mance validity, including studies wherein a group
of simulators (noninjured persons trying to per-
form poorly in an attempt to mimic brain injury
or illness) is compared to groups of patients with
objectively documented severe brain injury, or
severe psychiatric or developmental problems.
The simulators end up performing atypically for
common neurologic, psychiatric, and develop-
mental problems, and it is this differing pattern of
performance or symptom endorsement that allows
determination of the validity of test performance.
Examples can be offered such as grossly over-
reported symptoms far in excess of what is seen in

actual clinical disorders, or patterns of perfor-
mance not seen in brain-injured patients, such as
poor attention with normal memory. These proce-
dures developed to address validity of perfor-
mance are called symptom validity tests. Additional
studies are done in which litigants with multiple
SVT failures are compared to nonlitigating clini-
cal groups with bona fide neurological and/or psy-
chiatric disorders, further establishing valid versus
invalid patterns of performance. Testimony can
then convey that when a particular examinee
shows multiple symptom validity failures, it is a
strong indication that test performance is invalid.
In such circumstances, poor performances are
more likely the result of invalid performance,
whereas normal-range scores are themselves an
underestimate of actual level of ability.
FUTURE DIRECTIONS
The 1990s characterized a veritable explosion in
research on malingering, culminating with the
publication of the Slick et al. (1999) criteria for
malingered neurocognitive dysfunction. The area
of identification of poor effort on specialized tests
of response bias (e.g., PDRT, CARB, WMT,
TOMM) and identification of atypical perfor-
mance patterns on standard clinical tests (e.g.,
Mittenberg’s work on the WAIS-R/III, WMS-R,
HRB) is better defined than the area of assessment
of exaggerated symptom report, particularly in
the area of personal injury litigation.
It is particularly noteworthy that there is very
little research on malingering of chronic pain,
despite the near total reliance on self-report instru-
ments for assessment of chronic pain. Indeed,
Turk and Melzack (2001) did not review malinger-
ing in the second edition of their Handbook of
Pain Assessment. This is particularly important
given Mittenberg et al.’s (2002) results showing a
base rate of malingering of 38.61% for FM/chronic
fatigue and 33.51% for pain/somatoform disor-
ders, values consistent with Meyers et al.’s (2002)
data that yielded a base rate for malingering of
36% determined from scores produced on their
MMPI-2 weighted validity index by a large sample
of litigating chronic pain patients.
Gervais et al. (2001) found that 30% of patients
with FM receiving disability failed either the
CARB or WMT, with the failure rate increasing to
44% in patients with FM seeking disability. These
values were contrasted with CARB/WMT failure
rates of 0% in rheumatoid arthritis and 4% in
patients with FM not receiving disability. A later
paper reporting on the derivation of the Response
Assessment of Malingering 147
Bias Scale (RBS, Gervais et al., 2007) used a sample
that was comprised of over 50% chronic pain and
orthopedic injury, with over 50% either referred
by the Workers Compensation Board or attor-
neys, selecting RBS MMPI-2 items that distin-
guished examinees passing SVTs from those
failing SVTs. These data provide evidence for SVT
failure in chronic pain cases seen in the context of
external incentive. Similar data have been pub-
lished by Bianchini, Greve, and colleagues for
both symptom exaggeration (Bianchini et al.,
2008) and SVT failure (Greve et al., 2008).
I (Larrabee, 2003d) compared the pain scale
endorsement of 29 litigants with definite or proba-
ble MND who also complained of pain and had
FBS scores of at least 22 to published data on patients
with chronic pain for the MPQ (Melzack, 1975;
Mikail, Dubreuil, & D’Eon, 1993); Pain Disability
Index (Tait, Chibnall, & Krause, 1990); and Modified
Somatic Perception Questionnaire (MSPQ; Main,
1983). At a specificity of .90 (i.e., a score only
achieved by fewer than 10% of patients with chronic
pain, from samples that were not characterized by
compensation-seeking versus non-compensation-
seeking status or screened for malingering), the
sensitivities were .21 for the MPQ, .59 for the Pain
Disability Index, and .90 for the MSPQ. In particu-
lar, the MSPQ showed high sensitivity at high spec-
ificities (sensitivity values were .86 and .69,
respectively, at specificities of .95 and .99).
Subsequently, Brasseux, Greve, Gianoli,
Soileau, and Bianchini (2008) found a significant
association between performance on computer-
ized dynamic posturography (CDP) and degree of
symptom endorsement on the MSPQ, further
supporting the validity of the MSPQ as a measure
of somatic symptom exaggeration. Patients who
had aphysiologic sway patterns on CDP were
more likely to have higher MSPQ scores. Brasseux
et al. concluded that patients with both aphysio-
logic CDP and high MSPQ scores were more
likely to be exaggerating their balance-related
complaints and deficits.
Another area that has seen limited research is
the area of subtypes of malingering. The majority
of specialized tests of response bias follow memory
paradigms (e.g., PDRT, CARB, WMT, TOMM),
with the exception of the VIP, Dot Counting, and
the b Test. Yet, research investigations contrasting
simulating or known groups of malingerers to
patients with moderate or severe TBI showed
atypical performance on measures of perception,
motor function, attention, and problem solving
(Greiffenstein et al., 1996; Heaton et al., 1978;
148 forensic neuropsychology
Larrabee, 2003a; Mittenberg et al., 1993, 1995,
1996). I have identified subtypes of malingering
through cluster analysis that showed specific
impairment on (a) memory, perception, and
motor function; (b) symptom exaggeration; (c)
motor function and symptom exaggeration; (d)
problem solving; and (e) perception and problem
solving (Larrabee, 2004a). These data highlight
the need for additional measures of malingering
of motor dysfunction, impaired perception, and
abnormal problem solving. I also identified,
through cluster analysis, two basic types of
MMPI-2 profiles present in a large sample of per-
sonal injury litigants with MND: subtype varia-
tions on a somatoform exaggeration profile
(characterizing the majority, 88%, of profiles) and
a subtype profile showing exaggeration of severe
psychopathology (Larrabee, 2004b).
Related to the issue of subtypes of malingering
is whether or not malingering occurs along a con-
tinuum of symptom report and performance on
measures of ability, as opposed to representing the
presence of a distinct category of persons who are
not just quantitatively different but also qualita-
tively different from nonmalingering clinical
examinees. This question has been addressed with
taxometric analysis, which allows determination
as to whether the data being analyzed varies only
along a continuum, referred to as dimensional
latent structure, or varies due to the presence of a
true dichotomy between valid and invalid perfor-
mance, referred to as taxonic latent structure
(Meehl & Yonce, 1994; 1996; Ruscio, Haslam, &
Ruscio, 2006). Three papers have found evidence
for a discrete category or taxon of malingering.
Strong, Greene, and Schinka (2000) found evi-
dence of a taxon for the F and Fp scales of the
MMPI-2 in two samples, one from an inpatient
psychiatric hospital, and the other from a VA hos-
pital that included a wide range of patients, nearly
50% of whom were being evaluated for disability
claims. In a follow-up investigation with a crimi-
nal forensic sample, Strong, Glassmire, Frederick,
and Greene (2006) found evidence for a taxon
based on MMPI-2 Fp endorsement. The unique
feature of this investigation was that they utilized
a sample suspected to contain subgroups of severe
psychopathology resulting in lack of competency
in the criminal setting, as well as a subgroup feign-
ing incompetency. Last, Frazier, Youngstrom,
Naugle, Haggerty, and Busch (2007) found evi-
dence for a taxon based on a taxometric analysis
of VSVT performance, in a large, general clinical
sample, without any external incentive.
Three investigations employing taxometric
analysis of both symptom report and SVT perfor-
mance have failed to find evidence of a malinger-
ing taxon, rather, demonstrating that symptom
endorsement/SVT performance showed evidence
of dimensional latent structure. Walters et al.
(2008) evaluated the latent structure of the six
nonoverlapping primary scales of the SIRS, as well
as the MMPI-2 F, Fp and Dissimulation (Ds)
scales. In both criminal and civil forensic samples,
the SIRS showed evidence of dimensional rather
than taxonic structure. Similarly, F, Fp and Ds
showed evidence of dimensional structure.
Walters, Berry, Lanyon, and Murphy (2009) per-
formed a taxometric analysis of three factor
scales extracted from the Health Problem Over-
statement scale in a large (n = 1,050) outpatient
mental health sample, and a criminal and civil
(child custody or disability) sample (n = 194). The
taxometric analyses supported a dimensional
rather than taxonic latent structure. Last, Walters,
Berry, Rogers, Payne, and Granacher (2009) inves-
tigated the latent structure of a civil forensic sample
that was administered the TOMM, Letter Memory
Test, and VSVT. Again, evidence was found for a
dimensional rather than a taxonic latent structure.
Referring to their earlier work (Walters et al.,
2008), Walters, Berry, Rogers, et al. (2009) noted
that both feigned mental disorder and feigned
cognitive disorder appeared to be supported by
dimensional constructs, but this did not mean
that these two categories of feigning were sup-
ported by the same dimension or dimensions.
They also noted the need for evaluation of a third
domain, that of feigned medical complaints
(a topic addressed by Walters, Berry, Lanyon &
Murphy, 2009, reviewed above). Ascertaining
whether these three domains fall along a common
dimension or dimensions requires test data on all
three domains from a large sample of subjects
with the incentive to feign in all three domains.
Walters recommended consideration of explor-
atory or confirmatory factor analysis to determine
the number of dimensions underlying the con-
structs and whether different domains of feigning
and their respective detection strategies share
common dimensions. Walters, Berry, Rogers et al.
(2009) concluded that there is no evidence yet for
or against a general feigning construct that encom-
passes all domains and detection strategies.
This last observation regarding domains of
malingering and detection strategies is particu-
larly pertinent to the research reviewed in the
present chapter. There are at least two areas of

symptom over-reporting: over-reporting of severe
psychiatric symptoms (faking crazy) and over-
reporting of health, cognitive, and injury symp-
toms (faking hurt), with multiple domains of
invalid neuropsychological test performance,
including motor function, attention, memory, and
problem-solving skills. The multivariate nature of
both symptom over-reporting and invalid test
performance may be why three studies found tax-
onicity (Frazier et al., 2007; Strong et al., 2000;
Strong et al., 2006) and three did not (Walters
et al., 2008; Walters, Berry, Lanyon, et al., 2009;
Walters, Berry, Rogers, et al., 2009): none of these
investigations evaluated more than one test or one
test domain in the taxometric analyses that they
conducted. Measures included either scales from
the MMPI-2, SIRS, single SVTs such as the VSVT,
or three SVTs from the same test domain: memory
paradigm forced choice procedures (VSVT,
TOMM, and Letter Memory Test).
Moreover, patterns of test performance may
vary by the context in which malingering can
occur. As shown by Wygant et al. (2007), SVT fail-
ure was associated with the FBS and RC1 (mea-
sures sensitive to exaggerated physical, cognitive,
and nonpsychotic emotional distress) and with Fp
and RC8 (measures of exaggerated psychosis) in a
criminal forensic setting, whereas only the FBS
and RC1 were associated with SVT failure in a
civil forensic setting. Collecting a large civil and
criminal forensic sample, employing the full range
of SVT and self-report validity scales, with multi-
ple indicators of each domain, would appear to be
necessary to truly answer the question of whether
these measures of symptom exaggeration and
response bias show dimensionality versus taxo-
nicity, a design also recommended by Walters,
Berry, Rogers, et al. (2009). Certainly, the cluster
analyses referenced above suggesting the presence
of subgroups of malingerers (Larrabee, 2004a, b,
February), and the different contingencies of pass/
fail on five different SVTs reported in my earlier
investigation (Larrabee, 2003a), suggest that there
may well be discrete subgroups of malingerers; if
discrete subgroups exist, it stands to reason that a
single primary or multiple primary taxons of
malingering can exist, and these can be demon-
strated by taxometric analysis.
Since Slick et al.’s (1999) observation that
almost no research exists on the coexistence of
legitimate neuropsychological dysfunction with
poor effort or malingering, cases have started to
appear in the literature (Bianchini, Greve, & Love,
2003; Boone & Lu, 2003; Paniak, 2009). Slick et al.
Assessment of Malingering 149
noted that one of the most pressing questions is
whether it is possible to tease apart legitimate
from exaggerated impairment when both may be
present.
I have encountered a case, referred by the
attorneys for the defense, in which the plaintiff
suffered a severe CHI (admission Glasgow Coma
Scale of 3, with 1 month to follow commands and
3 months of post-traumatic amnesia). On direct
evaluation, the plaintiff failed the Rey 15-Item
Test with a score of 5, PDRT-27 correct total of
48%, and a Lees-Haley FBS of 28. On earlier test-
ing with another examiner, the plaintiff performed
poorly on the “Easy” items of the Category Test
and had an RDS score of 7. These poor scores on
measures of effort and malingering precluded
confident interpretation of the plaintiff ’s very
poor performance across a variety of tasks. He did
appear to have a potentially valid pattern of motor
impairment, with performance declining from
Grip Strength to FT, to the Purdue and Grooved
Pegboards (cf. Greiffenstein et al., 1996). Because
of his poor effort, other conclusions had to be
based on base rate expectations. Per the results
of Dikmen et al. (1994) regarding employment
following TBI, it was pointed out that only 8% of
patients with TBI who had time-to-follow-
commands of 29 days or more had returned to work
within 2 years, making it unlikely that the plaintiff
was going to return to gainful employment.
Thus, when poor effort and brain dysfunction
coexist, it is possible to reach conclusions based
on published outcome data in patient groups
sharing similar injury severity characteristics (see
Dikmen, Machamer, Winn, & Temkin, 1995;
Dikmen et al., 1994; Rohling, Meyers, & Millis,
2003). Similarly, in the presence of evidence for
poor effort, scores in the low end of the normal
range should be given greater weight because
these low normal scores themselves may well rep-
resent an underestimate of actual ability. Perhaps
another approach to evaluating the presence of
legitimate deficit co-occurring with poor motiva-
tion can be derived from future research on sub-
types of malingering, such that patterns of various
cognitive performances that are valid can be dis-
criminated from invalid patterns of performance
(i.e., legitimate memory impairment accompa-
nied by malingered motor function). Bianchini
et al. (2003) provide additional discussion of these
issues.
Finally, future research on malingering needs
to further analyze clinical and individual differ-
ence variables related to the occurrence of false
150 forensic neuropsychology
positive scores on SVTs; in other words, we need
to determine the features of the Slick et al. (1999)
D criteria. Boone’s (2007) edited volume contains
pertinent information in this regard. Features of
clinical patients with bona fide impairment who
produce positive scores on SVTs typically include
documented severe brain injury (prolonged coma;
structural lesions in the brain), and/or need
for 24-hour supervised care (Larrabee, 2003a;
Larrabee et al., 2007; Meyers & Volbrecht, 2003).
AC K N OW L E D G M E N T
I acknowledge the assistance of Matthew Miliano
in the preparation of this chapter.
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 6
Functional Neuroimaging in
Forensic Neuropsychology
JOSEPH RICKER
INTRODUCTION AND
C H A P T E R O V E RV I E W
Technological advances in neuroimaging have
had a significant and still growing impact on
how the functions of the human brain are studied
and understood. In addition to providing a useful
adjunct to the psychometric approaches to
understanding human brain-behavior function
(i.e., neuropsychology and cognitive neurosci-
ence), the techniques developed by physicists,
engineers, and radiologists have provided ways of
assessing brain-behavior relationships that often
cannot be realized through any other approaches.
In fact, the growth of studies of human cognition
that utilize functional brain imaging techniques
has been exponential (Müller, 2007). This enthu-
siasm for exciting uses for technology, however,
must be tempered by an appreciation for scientific
rigor and the need to establish diagnostic utility of
these techniques. Clinical neuropsychologists and
others are increasingly encountering functional
neuroimaging and electrophysiological tech-
niques (e.g., SPECT, PET, QEEG, MEG, fMRI) in
individual clinical and forensic cases. The clinical
application of these techniques remains, more
often than not, still investigational in the popula-
tions encountered in forensic neuropsychological
evaluations (Ricker & Arenth, 2008). All tests,
however, whether based in MRI physics, radioiso-
tope emission, electrophysiology, or paper-and-
pencil administration, must demonstrate adequate
sensitivity, specificity, and acceptability within
their relevant disciplines before being applied in
clinical or forensic cases in a reliable and valid
manner.
As is the case in all forms of clinical tests and
procedures, neuroimaging technologies have crit-
ical limitations. Many psychological and medical
tests are quite sensitive to a variety of situations
that statistically depart from “average.” In other
words, many tests will differentiate between a
clinical group as compared to a nonclinical con-
trol group. What is of much greater importance,
however, and what must be established before a
test has clinical validity, is whether the test has
specificity: Is this test result specific or unique to a
particular condition or clinical population but not
to others. Of particular concern in both forensic
and clinical settings is the application of func-
tional neuroimaging procedures to cases of ques-
tioned or questionable injury (e.g., mild head
trauma, exposure to known or putative toxins).
The present chapter provides an overview of
several functional neuroimaging procedures and
their applications in the context of populations
that are routinely encountered in the practice
of forensic neuropsychology. This chapter will
also address many clinical limitations of these
procedures that have implications for exercising
caution when they are utilized in any evaluation,
forensic or otherwise.
The clinical responsibility for interpreting the
content of neuroimaging data rests with radiolo-
gists, not neuropsychologists. It is important, how-
ever, for neuropsychologists, other clinicians, and
triers of fact to consider the multitude of factors
and conditions that may result in positive neu-
roimaging findings. It is not advisable to simply
accept the findings from investigative techniques
as evidence of neuropathology and subsequently,
whether intentionally or unintentionally, draw
forceful conclusions of causality based on other
findings or the patient’s self-report. This seems like
it should be obvious, but stepping back from the
striking visual impact that pictures generated from
functional imaging often have can be difficult.
 Functional Neuroimaging in Forensic Neuropsychology
REVIEW OF CLAS SES OF
EVIDENCE FOR
NEURODIAGNO STIC
PROCEDURES
The U.S. Department of Health and Human
Services holds medical tests and procedures to
standards of evidence. The fact that a medical test
or procedure exists, is available, or has validity
with certain populations under certain conditions
does not constitute evidence of its reliability or
validity under other circumstances. Instead,
experts in appropriate fields evaluate new and
existing tests and technologies with reference to
their technical reliability and validity, and, most
importantly, their utility in specific situations and
with specific populations.
Technologies are, of course, evaluated for
safety, but they are also rated in terms of their
utility (i.e., “established,” “promising,” “investiga-
tional,” “doubtful,” or “unacceptable”). In addition,
there are classes of evidence ratings. These include,
in descending order of support, the following:
Class I—Supporting evidence is provided by one
or more well-designed, randomized, controlled
clinical trials; Class II—Supporting evidence pro-
vided by one or more well-designed clinical stud-
ies, for example, case control, cohort studies; Class
III—Supporting evidence is provided by expert
opinion, nonrandomized historic controls, or at
least one case report. It is notable that the types of
functional neuroimaging that are encountered in
forensic cases—SPECT, PET, fMRI, QEEG—are
all rated as investigational in terms of their
application in potential forensic populations,
for example, mild brain injury, (Therapeutics and
Technology Subcommittee of the American
Academy of Neurology, 1996; American College
of Radiology 2008; Nuwer, 1994). Nonetheless, as
empirical support is gradually established, their
valid use is likely to become a future reality.
The American College of Radiology rates all
neuroimaging and radiographic assessment and
interventions in detail, using various criteria for
clinically appropriate use (i.e., the technique or
device has sufficient evidence to support its non-
investigational use for a specific clinical syndrome
[e.g., brain injury] or procedure [e.g., mammog-
raphy]). Under current nomenclature, neuroim-
aging technologies are rated on a scale of 1 to 9,
with 1 representing “least appropriate,” and
9 representing “most appropriate.” Detailed
descriptions and downloadable full committee
reports are available from the American College
of Radiology at www.acr.org/ac.
161
RESTING VERSUS
A C T I VAT E D I M A G I N G
In functional neuroimaging, one can conceptual-
ize techniques into two broad categories: “resting”
and “activated” (Ricker, 2005). Resting paradigms
are those that acquire images during nondynamic
(i.e., “static” or baseline) conditions. There have
been numerous studies using resting functional
neuroimaging in various populations, most of
which have examined chronic glucose uptake
(exclusively with PET), resting cerebral blood
flow (using PET or SPECT) or resting electro-
physiological activity (e.g., EEG, QEEG, or MEG).
Essentially, resting studies are those that occur
when a participant is ostensibly not engaged in
any specific task. Resting studies, by design, have
no explicit or systematic requirements of the par-
ticipant other than those required to successfully
acquire a technically valid image, such as having
the participant lie still, minimizing head move-
ment, eliminating extraneous light and noise, and
so forth (Raichle, 2001).
Unlike resting studies, activation studies
require participants to systematically receive sen-
sory input (e.g., a visual array) or engage in an
activity (either cognitive or motor) in order to
examine changes in some time- or stimulus-
linked aspect of brain physiology (Roland, 1993).
These tasks are usually administered in adherence
to a necessarily strict protocol, typically with some
form of overt response required in order to pro-
vide verification that the participant is actively
engaged in the requested task. Because of the
technologies related to, and physical properties of,
the dependent variables examined, activation
studies have much briefer time windows than
resting studies. Some technologies are able to
image changes across time in a relatively continu-
ous manner (e.g., MEG and event-related fMRI).
Given this degree of control, the experimenter is
able to make more reliable inferences about
cerebral activity underlying the cognitive process
in question (Small, 2006).
RADIOLIGAND-BASED
IMAGING
Single Photon Emission Computed
Tomography (SPECT)
SPECT is an alternative approach to functional
imaging with an emphasis on regional cerebral
blood flow (rCBF) imaging, but specific neurore-
ceptor imaging studies are also possible (Masdeu
& Arbizu, 2008). SPECT technology is based on
162 forensic neuropsychology
the concept that regional changes in brain activity
or chemistry can be indirectly measured via
externally placed gamma radiation detectors
(“cameras”), which detect the regional accumula-
tions of tracer flow or receptor-binding isotopes.
The dependent variable in SPECT derives
from the well-established principle of increased
cerebral activity correlating with increased blood
flow. That is, when neural activity in a region of
the brain increases, related glucose and oxygen
requirements also increase. Since the blood supply
carries glucose and oxygen to the brain, the flow
of blood to the active area increases (Ingvar &
Risberg, 1965). The radioisotopes themselves are
absorbed into the glial cells, but are not readily
excreted. Thus, the absorbed radioisotopes remain
in greater concentration in the more active areas.
Through normal radioactive decay, the isotope
emits annihilated radioactive particles (i.e., pho-
tons), which are then detected by the external
cameras. Computer-based reconstruction then
permits representations to be made of differences
in blood flow.
Relative to other functional imaging tech-
niques, there are several advantages of SPECT
(Wintermark et al., 2005). It is more widely avail-
able than PET or fMRI. Unlike with PET, the
radioisotopes that are typically used with SPECT
can be ordered and delivered in advance, thus
precluding the necessity of an onsite cyclotron
and chemist, as required for PET.
SPECT has limited use in imaging a change in
blood flow from one point in time to another, for
example from pre-ictal to ictal state (Habert &
Huberfeld, 2008). It is not appropriate, however,
for use in mapping blood flow changes that change
rapidly over time within a single scanning session,
such as those encountered in most states of cogni-
tive activity, or for making direct inferences about
brain metabolism (Roland 1993; Small, 2006).
SPECT has some potential for studying discrete
cognitive processes if multiple scanning sessions
are used and explicit experimental task conditions
and complex subtraction analyses are utilized
(Ludwig et al., 2008). Such experimental and sta-
tistical rigor is quite beyond most nonacademic
clinical settings, however.
The most commonly used radioactive isotopes
for SPECT are absorbed by the brain within 2 min-
utes, but may have half-lives of several hours. The
effect of this is that once the tracer has been admin-
istered, the resulting images that are acquired will
remain the same for the next several hours, thus
making SPECT a poor tool for measuring rapid or
fluctuating changes. SPECT is also not as diverse
as other imaging techniques, such as PET, but
novel ligands are under continuous development
(Ogawa et al., 2009). Recent technologic advances
have provided for multiple-headed scanners,
which offers improved resolution. The compound
123-I–para iodoamphetamine (IAMP) provides a
unique look at immediate and delayed perfusion.
In addition, IAMP has amphetamine-like quali-
ties, which allow for distinct presynaptic and post-
synaptic imaging. Although IAMP is no longer
available in the United States, a newer compound
(99m-Technetium–HMPAO) is being used for the
same purposes. Technetium is a primary blood
perfusion agent with the property of rapid cerebral
uptake. It is retained in brain structures for several
hours, allowing for image capture at various time
points following ligand administration.
Recent technologic advances have provided
for multiple-headed scanners, which have
improved resolution. SPECT does have several
sources of potential measurement error, however
(Zhang et al., 1994; Sohlberg, Watabe, & Iida,
2008). Unlike PET, SPECT imaging requires that
regional counts be normalized to an area that is
presumably free of injury, and its resolution does
not yet approach that of PET imaging, although
resolution has improved dramatically with the
increased availability of combined SPECT/CT
technology (Seo, Mari, & Hasagawa, 2008). Color
SPECT imaging software can produce visually
striking images, but reliable and valid interpreta-
tion is best accomplished through quantitative
pixel counts (Loutfi & Singh, 1995; Habert et al.,
2011). It must also be noted that although SPECT
can be used quantitatively, this is not the case in
most settings. Visual inspection of SPECT maps is
a qualitative process, and interpretation may vary
from clinician to clinician. In addition, image
reconstruction is typically based on presumptions
about which brain regions are “normal.” Relative
flow values in SPECT are often based upon a
region such as the thalamus or cerebellum. While
such assumptions might be valid for some popu-
lations with focal lesions (e.g., stroke), they might
not be valid for populations whose involvement
is more diffuse (e.g., TBI). Although SPECT is
very sensitive to detecting regional differences in
resting blood flow, there is little specificity to the
patterns that are obtained and the results depicted
in series of SPECT images can be affected by
many factors including mood disturbances, medi-
cations, or current substance use (Ricker &
Zafonte 2000; Granacher, 2008).
 Functional Neuroimaging in Forensic Neuropsychology
Positron Emission Tomography (PET)
Positron emission tomography (PET) is another
radioisotope-based approach to imaging. The
variable of interest is usually glucose absorption
(measured by uptake of fluorodeoxyglucose),
although oxygen-15 PET scanning is also used for
activated imaging studies (Buckner & Logan,
2001). In spite of the exponential growth in inves-
tigational fMRI publications (overwhelmingly
conducted with healthy individuals), PET remains
the “gold standard” for functional neuroimaging
(Chen et al., 2008). It is also remains quite expen-
sive, however, (approximately US $3,000 for a
series of resting PET images) and requires a cyclo-
tron to be present onsite for most radioisotopes.
PET has been widely used as a research tool since
the 1970s, but its application for persons with
traumatic brain injury has been minimally inves-
tigated. PET has the capability of demonstrating
specific biochemical or physiologic processes
associated with cerebral blood flow and metabo-
lism (Gulyas & Sjoholm, 2007). The resulting PET
image represents the spatial distribution of radio-
isotopes, which is usually portrayed on an actual
or standardized anatomic (MRI) template.
PET studies typically utilize tracers such as
[18F]-fluorodeoxyglucose (FDG) for the quantifi-
cation of “resting” (i.e., nonactivated) regional
brain metabolism. Studies of blood flow changes
associated with motor or cognitive activity can be
accomplished through the use of tracers such as
oxygen-15 labeled water. Radiolabeled ligands
that target dopaminergic, serotonergic, and other
receptor systems have been developed, as are
genetically mediated transport markers and
pathology-specific ligands (Herholz, Carter, &
Jones, 2007).
Functional Magnetic
Resonance-Based Imaging (fMRI)
All magnetic resonance-based imaging techniques
capitalize on the presence of hydrogen in all of the
body’s tissues. When the nuclei of hydrogen atoms
are placed in a strong magnetic field, they align in
parallel to the field’s direction. In MRI, radiofre-
quency (RF) pulses are presented at a 90° angle
relative to the magnetic field. When this occurs,
the hydrogen nuclei realign and begin spinning in
a different direction (“excitation”). The RF pulse is
then stopped and the nuclei return to their origi-
nal alignment and spin. This process of resuming
previous nuclei states results in the emission of an
electronic signal that can be detected by the scan-
ner. It should be noted that only about 1% of the
163
hydrogen atoms in the magnetic field emit a
response, but this results in enough signal to
permit the reconstruction of images. Since most
of the atoms that are excited in this process are
found within water molecules, water content and
tissue density dictate the signal that is detected by
the scanner and subsequently digitally recon-
structed into an image (Springer et al., 2000;
Huettel, Song, & McCarthy, 2009)
Functional magnetic resonance imaging
(fMRI) is a variant of conventional MRI. The crit-
ical difference, however, is that the dependent
variable of interest in fMRI is alteration in signal
intensity related to increases in blood flow result-
ing from changes in brain activity. Thus, fMRI is
more concerned with changes in brain activity
than anatomic structure per se. While the primary
goal of structural MRI is to generate high-resolu-
tion anatomic images of underlying brain struc-
ture, the goal of functional MRI is to allow the
investigator to make inferences about regional
changes in brain activity (Aguirre, 2006). As has
been discussed with other blood-flow-dependent
techniques, in fMRI, specific tasks or stimuli are
introduced to the individual in the scanner in
order to elicit increased cerebral activity. When
neural activity increases in a region, there is an
increase in blood flow to that region. When the
brain is at rest, there is a tight correlation between
regional cerebral blood flow (rCBF), regional
cerebral metabolic rate for glucose (rCMRglc)
and regional cerebral metabolic rate for oxygen
(rCMRO2). With activity, however, rCBF can
increase by over 50%, which is well beyond meta-
bolic demands. The physiologic basis for this is
not clear (Weisskoff 2000). With the excess of
blood flow to the region, particularly in light of
only minimal increase in oxygen extraction, there
is a resulting localized abundance of oxyhemoglo-
bin relative to deoxyhemoglobin in the venous
and capillary beds that perfuse the active regions
of cortex. Oxyhemoglobin is naturally diamag-
netic, while deoxyhemoglobin is paramagnetic
(i.e., becomes readily magnetized within a mag-
netic field). With increased neural activity and
concomitant increased blood flow, there is a net
increase in diamagnetic material (oxyhemoglo-
bin), and a net decrease in paramagnetic material
(deoxyhemoglobin). This results in an increase in
signal intensity that can be detected externally,
and is represented as higher signal intensity on
T2* (“T2-star”)-weighted scans. This change in
signal intensity is referred to as the blood oxygen
level dependent (or “BOLD”) effect (Chen &
164 forensic neuropsychology
Ogawa, 2000). In magnets of “average” strength
(e.g., 1.5 Tesla), the signal changes appear to ema-
nate from veins and large venules. In high-field
magnets (e.g., 3, 4, or even greater Tesla, an index
of magnitude in comparison to the magnetic field
strength of the earth’s gravity), signal is more
likely obtained from microvessels, small venules,
and capillaries. The signal changes obtained are
very small, on the order of 1% to 6%, and occur
over approximately a 2- to 6-second timeframe
(depending on brain region, age of the partici-
pant, and the task being performed).
Because fMRI utilizes the body’s natural physi-
cal responses to high-strength magnetism, no
exogenous tracers, radioisotopes, or contrast
agents are necessary. The anatomic resolution of
fMRI is superior to that of SPECT or PET. There
are numerous activation paradigms that can be
carried out in fMRI, and it allows for greater flex-
ibility in paradigm with reference to repeatability
and brevity of overall session (Huettel et al., 2009)
As with any imaging procedure, however,
fMRI can be impacted by numerous variables.
Although publications using fMRI in healthy
individuals have appeared since 1990, few FMRI
studies exist in clinical populations, and compara-
tively fewer in populations of primary interest in
forensic neuropsychology practice. Movement
can disrupt head alignment, and may also perturb
the magnetic field itself. Thus, head movement
must be eliminated, and other extraneous move-
ments must be reduced. Overt responses to tasks
must be minimal at most. Movements of the jaw
required for talking are often considered too
excessive during fMRI, but event-related para-
digms do allow for some degree of verbal respond-
ing (Ishikawa, 2002).
The normal high frequency noise within the
scanner must be considered when evaluating
individuals with possible acquired neuropathol-
ogy or neuropsychiatric disturbance. The exam-
iner or technician must also monitor for
idiosyncratic responses such as claustrophobia,
anxiety, boredom, disengagement, or actual onset
of sleep while in the scanner. Although virtually
any contemporary MRI scanner can be adapted to
functional imaging, fMRI is still investigational in
virtually all populations, including brain trauma,
and is not considered appropriate for routine clin-
ical use (American College of Radiology, 2008),
and is thus primarily a research tool at this time.
This also limits its availability to primarily aca-
demic medical centers. Even a single fMRI session
will generate a very large volume of data. Thus,
computer hardware requirements must be con-
sidered, along with data storage and data security.
Finally, fMRI protocols do not and cannot “auto-
matically” or “objectively” yield brain maps, nor
are there at present normative values for fMRI
scans or activity levels (Aguirre, 2006). The result-
ing images must be carefully processed and skill-
fully reconstructed, and this reconstruction
process should be considered to be as much art as
science. The approach that one takes in recon-
structing and displaying the data in the form of
brain images data will impact the portrayal, and
potentially the interpretation, of the end product.
ELECTROPHYSIOLOGICAL
TECHNIQUES
Quantitative
Electroencephalography (QEEG)
Electroencephalography (EEG) is a neuro-
physiological index of cerebral function that has
widespread use. In medical rehabilitation popula-
tions, it is used to assess seizure activity, coma,
and gross outcome. Data from traditional qualita-
tive EEG analysis does not, however, allow for
identification and quantification of the spectra of
wave frequencies that occur in the human brain.
Thus, conventional EEG is useful clinically only as
a very gross monitor, and has little utility in
advance prediction of outcome. When Fourier
transform analysis is applied to EEG, however, it
allows for continuous monitoring and quantifica-
tion across all cerebral wave frequencies. This
approach is more commonly referred to as quan-
titative electroencephalography
Quantitative electroencephalography (QEEG)
is the term applied to a group of inter-related
technologies that are centered on the mathemati-
cal concept of spectral analysis (Wallace et al.,
2001). In essence, the EEG signal is digitally pro-
cessed and the relative contributions of each fre-
quency are identified and quantified. When
digitized, the individual component frequencies
of a complex waveform (i.e., amount of alpha,
beta, delta, and theta contained within the signal)
can be discerned in a manner superior to that of
traditional visual analysis of EEG printed output
(Nuwer et al., 2005)
There are several approaches to displaying
QEEG spectral data. In the compressed spectral
array (CSA) format, the frequency components
from a series of epochs (e.g., 30 sec. blocks of
time) are quantified. The output is then repre-
sented sequentially either in print or graphically,
 Functional Neuroimaging in Forensic Neuropsychology
permitting interpretation of changes in the EEG
signal over time (Luccas et al., 1999). Another
approach is topographical mapping (Skrandies,
1995). In this format, each electrode in the EEG
montage is assigned a color value (or grayscale
shading level) for each frequency range. The color
or shading represents the frequency level underly-
ing the electrode. The color map (or shading
gradient) is then superimposed on an oval (repre-
senting the head). The resulting brain map resem-
bles what might be obtained from a resting SPECT
or PET. It is imperative, however, that one appre-
ciates the fact that the topographical map is
derived from a minimal number of data points,
reflects only cortical surface activity, and has
many interpolated color values (e.g., the colors or
shadings between electrodes are interpolated). A
third approach to data representation is that of
probability mapping (Nuwer et al., 2005). This
approach utilizes topographic mapping as a basis,
but compares the map to a normative database
(i.e., a composite map). An individual’s map may
then be statistically compared to the normative
map, and inferences based on the normal distri-
bution are made in interpretation.
Magnetoencephalography (MEG)
In addition to electrical activity, neurons also gen-
erate minute magnetic fields that can be measured
using an approach known as magnetoencepha-
lography (MEG). MEG involves the use of liquid
helium that cools conducting coils to almost abso-
lute zero. When cooled to such low temperatures,
the electrical resistance of the conductor is greatly
reduced, and very small changes in magnetic field
can be detected (King et al., 2000). The miniscule
nature of these fields requires significant ampli-
fication in order to be useful. Using devices known
as superconducting quantum-interference devices
(SQUIDs), the changes in magnetic fields pro-
duced by neuronal activity can be detected. An
array of conductors is situated around the head of
the participant, which allows for the placement of
multiple detectors (Bagic, 2007).
The physiological basis of MEG is that of
normal neuronal membrane signal conduction.
The flow of electrical current within an active
neuron generates a magnetic field. When a syn-
apse becomes active, there is a current flow across
the neuronal membrane. This current diffuses
intracellularly, and then emerges extracelluarly at
a fixed distance from where it began (i.e., from
dendrite to synapse). This results in the opportu-
nity for “sources” and “sinks” extracelluarly. In the
165
presence of an asymmetrically oriented neuron,
the sources and sinks create dipolar electromag-
netic fields that cancel one another out. The intra-
cellular current between the region of synaptic
activation and the point at which the current
returns to extracellular space does not cancel out
(Tang et al., 2002). This magnetic field can be
recorded.
Although intuitively similar to EEG, MEG has
some advantages. First, MEG frequencies are
technically easier to record than those from EEG,
given that the detectors are located in a helmet for
placement adjacent to the scalp, and thus do not
have to be individually applied (or intercon-
nected). Second, magnetic fields are not affected
by the variability in skull thickness over different
regions of cortex. Third, in general, the compo-
nent structure of the MEG response is actually
simpler than that derived through EEG. There are,
of course, disadvantages to MEG. MEG is very
expensive and thus not widely available. MEG
also does not detect deep (e.g., subcortical)
sources of activity. MEG, along with EEG, lacks
the anatomic precision of other neuroimaging
techniques (Stern & Silbersweig, 2001).
DIAGNO STIC GROUPS
ENCOUNTERED IN
FORENSIC CONTEXTS
Brain Injury
SPECT Studies of Brain Injury
In chronic moderate and severe TBI (i.e., at least
several months following acute injury), resting
PET and SPECT studies generally consistently
demonstrated either hypometabolism or decrea-
sed resting blood flow, predominantly within
prefrontal cortex (Bergsneider et al., 1997, 2001;
Fontaine et al., 1999; Gross et al., 1996; Jansen
et al 1996; Langfitt et al., 1986; Rao et al., 1984;
Ricker et al., 2001; Tenjin et al., 1990). In most of
these studies, decreased blood flow and metabo-
lism were generally in excess of what might be
expected based solely on findings from structural
scans (i.e., CT and MRI). The presence of
decreased resting blood flow or metabolism is
not, however, in and of itself evidence of compro-
mised or nonfunctional brain tissue (e.g., Duara
et al., 1992).
Numerous investigations have demonstrated
that SPECT is better than structural imaging (i.e.,
CT and MRI) in the detection of the presence
and extent of trauma-related lesions. SPECT
has been applied to acute brain injury and has
166 forensic neuropsychology
demonstrated regionally decreased blood flow in
the presence of normal acute CT scans, but there
is tremendous variability across individuals (i.e.,
no pathognomonic profile emerges) (Abdel-
Dayem et al., 1987). Positive SPECT findings have
also sometimes demonstrated in cases of below-
average neuropsychological test scores in cases of
mild brain trauma, but it should be noted that
SPECT findings are usually not predictive of test
performance (Umile et al., 1998).
In spite of advances in technology and
data analysis, the utility of SPECT’s characterizing
specific illness and injury states or predicting
outcome remains controversial (Granacher,
2008). SPECT has shown particular utility
when correlating neuropsychological parameters
with the chronic effects of severe brain injury
(Ichise et al., 1994), but caution must be exercised
given that systemic metabolic abnormalities,
substance use, and emotional disorders can
impact SPECT results and interpretations
(Wortzel et al., 2008). For example, the results of
SPECT (and PET) studies have been shown to be
abnormal in disorders such as depression
(Sackheim et al., 1990), manic-depressive disor-
der (Iidaka et al., 1995), obsessive-compulsive
disorders (Adams et al., 1993), generalized anxi-
ety disorders (Uchiyama et al., 1997), and schizo-
phrenia (Paulman et al., 1990). SPECT frequently
demonstrates abnormalities in dementia (Read
et al., 1995) and cerebrovascular disease (Masdeu
& Brass, 1995), and also suggests decreased tracer
uptake in normal aging (Mozley et al., 1996).
SPECT also demonstrates positive functional
neuroimaging findings in domains that frequently
covary with (or are attributed to) TBI, such as
learning disabilities (Wood et al., 1991) and som-
atization disorder (Lazarus et al., 1989). Finally,
SPECT often demonstrates abnormalities in
aggression (Amen et al., 1996), alcohol depen-
dence (Modell & Mountz, 1995), alcohol with-
drawal (Mampunza et al., 1995), opiate use
(Krystal et al., 1995), hallucinogenic drug use
(Hertzman et al., 1990), and cocaine abuse (Miller
et al., 1992). In addition, at least 6% of noninjured,
medically healthy individuals may demonstrate
focal abnormalities on SPECT imaging (Umile
et al., 1998). Some investigators have noted that
when used in a prospective design, a negative
SPECT scan is a good predictor of a favorable out-
come after brain injury, and that SPECT overall
correlates well with the severity of the initial
trauma (Jacobs et al., 1994). Still lacking are pro-
spective studies of SPECT (as well as PET and
fMRI) in differential diagnosis, prognosis, and
intervention.
SPECT has been shown to be of use in research
studies following brain injury, but there is no
particular SPECT profile that is pathognomonic
or reliable for brain injury (Herscovitch, 1996;
Granacher, 2008). Clinically, the literature does
not support the routine use of SPECT for the
evaluation of post-concussion syndrome in
specific, or actually for brain injury in general.
The Therapeutics and Technology Subcommittee
of the American Academy of Neurology (1996)
has rated SPECT as an investigational procedure
for the study of brain trauma. More recently, the
American College of Radiology (2008) continues
to rate SPECT as inappropriate (a rating of “1” on
a 1 to 9 scale, with “1” indicating “least appropri-
ate”) in the evaluation of mild head trauma, with
slightly increased appropriateness (a rating of “4”
on the same scale) “for selected cases” of closed
head trauma (across levels of injury severity) with
associated neurologic or cognitive signs. In spite
of the professional cautions and the present con-
clusions regarding the lack of scientific support
for the routine use of SPECT in brain injury,
SPECT appears to be used frequently in clinical
and forensic contexts as a means of supporting a
diagnosis of brain injury.
PET Studies of Brain Injury
Experimental studies of traumatic brain injury
have shown that cerebral hyperglycolysis is a
pathophysiological response that occurs in
response to injury-induced neurochemical cas-
cades. Bergsneider and colleagues (1997; 2001)
have shown, via FDG-PET, that hyperglycolysis
occurs in both regional and global settings after
severe brain injury in humans. Such abnormali-
ties may also exist transiently after milder injury.
Several studies have demonstrated PET’s abil-
ity to detect abnormalities not seen on static imag-
ing in cases of moderate and severe brain injury
(see review in Ricker, 2005). In addition, data exist
to suggest that functional imaging demonstrates
areas of physiological dysfunction beyond the
boundaries of static lesions seen on structural
imaging. Langfitt and colleagues (1986) presented
some of the earliest functional imaging data from
individuals who had sustained severe TBI. FDG-
PET was also compared with CT, MRI, and SPECT
studies. They were able to demonstrate with PET
that cerebral hypometabolism extended beyond
the morphometric boundaries of lesion as imaged
with the structural methods of CT and MRI.
 Functional Neuroimaging in Forensic Neuropsychology
Cobalt-55 PET can also demonstrate regional
abnormalities following severe TBI beyond those
shown by CT and MRI (Jansen et al., 1996). It has
been demonstrated that the intermediate meta-
bolic reduction phase begins to resolve approxi-
mately one month following injury, regardless of
injury severity (Bergsneider et al., 2001). The cor-
relation between the extent of change in neuro-
logic disability and the change in CMRglc from
the early to late period is modest, however.
In spite of the application of functional imag-
ing studies in forensic situations when there is a
question about the occurrence of, or disability
resulting from, traumatic brain injury, there are
surprisingly few studies that have actually
attempted to correlate functional imaging find-
ings with cognition. In most of the studies that
have attempted to correlate functional imaging
with testing, the findings from psychometric
assessment have been examined with those from
functional imaging conducted either prior to or
following memory evaluation. For example, Ruff
and colleagues described FDG-PET and neurop-
sychological test findings among a selected series
of nine individuals who had sustained mild brain
trauma whose static imagings (CT or MRI) were
negative (Ruff et al., 1994), but the findings have
minimal generalizability given that subjects were
specifically selected for inclusion based upon out-
come rather that a priori criteria. In addition,
scanning and the neuropsychological evaluation
were separated in time by an average of 11 months.
In a study of 20 persons with mild traumatic brain
injury it was noted that local abnormal cerebral
metabolic rates correlated with complaints and
neuropsychological test results obtained during
the chronic phase of recovery (Gross et al., 1996).
In moderate and severe TBI, resting PET studies
have demonstrated frontal hypometabolism, with
correlated poor performance on neuropsycho-
logical tests that are thought to be mediated by
frontal lobe functioning (Fontaine et al., 1999) as
well as widespread white matter disconnection
(Wu et al., 2004).
PET activation studies are likely to be far more
sensitive to the functional effects of brain injury
or disease, as such paradigms introduce in vivo
cognitive challenges (Baron, 1995). The first PET
study to apply a cognitive activation paradigm
with individuals who sustained severe TBI (Ricker
et al., 2001) demonstrated left frontal lobe rCBF
changes in individuals with TBI during free recall
when compared to controls, but rCBF increases
were noted in more posterior brain regions in TBI
167
subjects during both free and cued recall. The
change in allocation of neural resources during
tasks with greater cognitive load may suggest
greater frontal lobe involvement resulting from
increased cognitive effort. Of additional note is
the finding that during recognition tasks, both the
controls and the individuals with TBI performed
at comparable behavioral levels (and within
normal limits), yet the individuals with TBI still
demonstrated increased change in regional cere-
bral blood flow relative to the controls. This sug-
gests that after brain injury, individuals must exert
more cognitive effort than controls to attain the
same level of overt behavior. A subsequent O-15
PET study in TBI by a different group of investiga-
tors has also demonstrated similar findings on a
verbal list-learning task (Levine et al., 2002).
FMRI Studies of Brain Injury
In the first fMRI studies of individuals with TBI
(McAllister et al., 1999; 2001), the investigators
examined individuals with a very recent history of
mild brain injury (i.e., within the previous 30
days). As in the Ricker et al. (2001) PET study of
chronic severe TBI, the individuals with mild TBI
in the McAllister studies demonstrated intact
behavioral performance on a verbal working
memory task, but they did show right hemisphere
lateralized fMRI activation in response to
increased working memory load. In an fMRI
investigation of working memory following mod-
erate and severe TBI (Christodoulou et al., 2001),
increased blood flow and more widespread dis-
persion of cortical activation was noted during
working memory tasks. This again suggests that
increased cognitive effort is reflected in increased
brain activation on fMRI. A study by Perlstein
and colleagues (2004) represented a significant
advance in the study of TBI-related problems in
working memory. In the fMRI component of their
study, they used an event-related design, employed
parametric manipulation of task difficulty, and
examined not only the central executive but also
the phonological loop within verbal working
memory. As part of a larger behavioral study,
seven persons with TBI and seven controls were
examined using fMRI during the verbal N-Back.
They provided data that demonstrated a disrup-
tion in the dorsolateral prefrontal and parietal
network known to mediate verbal working
memory, with greater disruption occurring at
increasing levels of cognitive load. Although this
study was certainly a needed contribution to the
literature, there were several methodological
168 forensic neuropsychology
limitations. There was no examination of spatial
working memory, thus any generalizations must be
strictly limited to verbal working memory. The
authors point out that they did not have informa-
tion on acute injury status for most of the persons
with TBI, nor did they have prior neuroradiologic
data, loss of consciousness duration, or length of
post-traumatic amnesia for many patients. Finally,
of the seven patients examined, one had sustained a
severe initial TBI, and the remaining six were char-
acterized as having sustained moderate injuries.
In a recent study (Newsome et al., 2007), ten
persons with severe TBI were compared to six
persons with orthopedic injuries using an N-Back
task in a 1.5 Tesla MR scanner. The stimuli were
photographs of faces. The findings of this study
were generally comparable to those of previous
studies, with most group differences noted in the
1-Back condition. This study only examined per-
sons with severe TBI, however, and only up to a
2-Back level of cognitive load, thus application of
the results to other levels of TBI must be made
with caution. In addition, although the stimuli
used in this study were visual, faces are processed
differently by the brain than purely spatial infor-
mation. As such, this paradigm did not address
the specific cognitive or neural architecture of the
visuospatial sketchpad component of working
memory. Each of the published fMRI studies of
working memory after TBI has addressed rather
limited aspects of working memory processing
and examined rather limited ranges of injury
severity (e.g., mild only, severe only, or small
numbers of moderate and severe only).
Only very recently has episodic memory,
which is arguably the memory domain that is
most frequently assessed clinically (e.g., through
list-learning tests), been formally studied with
fMRI in persons with TBI. The first of these
studies (Strangman et al., 2008) involved the
teaching of a verbal learning strategy to a group of
54 individuals with documented memory impair-
ment after moderate or severe TBI and a matched
group of controls. FMRI scanning was conducted
only during the encoding phase of a verbal learn-
ing paradigm. Free recall and recognition were
assessed outside of the scanner. The aim of the
study was to assess the ability of fMRI results to
predict outcome after a subsequent 12-session
rehabilitation program focused on teaching of
internal strategies for memory improvement. The
findings suggested that left prefrontal areas were
related to strategic verbal learning. They also
observed that BOTH under- and over-activation
in the TBI group was associated with reduced
performance on memory tasks after rehabilita-
tion, creating an inverted-U quadratic relation-
ship between performance and activation, which
was therefore predictive of outcome. The authors
opined that underactivation may represent struc-
tural injury to the gray or white matter within the
region of interest or possibly injury to areas pro-
jecting to that region, while overactivation may
indicate intact and engaged cortical areas, which,
despite “effortful utilization,” failed to produce
improvement in functional memory as tested.
Strangman and colleagues (2009) subsequently
conducted an additional study of 20 participants
with moderate or severe TBI and 20 healthy con-
trols using the same behavioral and fMRI para-
digm from their 2008 study. This study evaluated
whether individuals with TBI and controls acti-
vated the same networks during verbal learning,
and whether TBI affected neural activity during
encoding when participants were instructed to
use semantic clustering. Despite baseline testing
indicating significant differences in behavioral
performance between groups, direct comparison
of group fMRI activation across all tasks, indicated
no significant differences, suggesting that indi-
viduals in the TBI group activated the same gen-
eral networks as healthy controls. Further
functional connectivity analyses suggested a func-
tional (but not anatomical) breakdown in connec-
tivity between the left DLPFC and other areas
normally associated with strategic control.
Most recently, Russell, Arenth, Scanlon,
Kessler, and Ricker (2011) examined both encod-
ing and recognition of verbal and visual stimuli
using fMRI. Twelve adults with chronic severe,
moderate, and complicated mild injuries were
compared with a matched group of 12 controls.
Behavioral task performance did not differentiate
the groups. During neuroimaging, however, the
group of individuals with TBI exhibited increased
activation, as well as increased bilaterality and
dispersion as compared to controls. These results
were generally consistent with previous imaging
and behavioral findings in TBI, but there was an
additional novel finding. Persons with TBI dem-
onstrated more subcortical activation, (i.e., cau-
date and thalamus), while activations for the
control group was mostly cortical. While the exact
nature of this finding is not known, there is evi-
dence that these subcortical structures are
involved in cognitive processes, and, even if not
typically injured after TBI, are highly intercon-
nected with frontal cortex through white matter
 Functional Neuroimaging in Forensic Neuropsychology
tracts that are known to be susceptible to compro-
mise after moderate and severe TBI.
Although PET and FMRI clearly represent
more advanced approaches to brain imaging when
compared to SPECT, neither has reached a suffi-
cient threshold of evidence for routine use in mild
brain trauma. PET is currently classified at the
same level of clinical appropriateness (or lack
thereof) as SPECT by the American College of
Radiology (2008). Although there are now more
fMRI studies of TBI, and many are currently per-
forming large-scale studies, the ACR has not fully
evaluated fMRI.
QEEG Studies after TBI
The literature regarding the utility of QEEG in
brain injury is growing. Much of the investiga-
tional work in the area of QEEG and brain injury
has been in the area of coma (Wallace, Wagner, &
Wagner, 2001). For example, previous work has
shown poor outcome among a population of per-
sons with severe TBI who continued to show slow
pattern responses (Bricolo et al., 1978). A poor
prognosis is more likely among individuals with
severe TBI that have silent or slow QEEG patterns,
while those that have active sleep-wake cycles and
variation of pattern tend to have much better out-
comes (Sironi, 1983). The amount of QEEG slow-
ing corresponds to reaction level scale scores in
comatose individuals (Matousek et al., 1996). The
prognostic efficacy of QEEG spectral analysis has
been compared to that of the Glasgow Coma Scale
(GCS; Teasdale & Jennett, 1974), brainstem audi-
tory evoked potentials, and CT in individuals in
coma within 3 weeks of TBI (Thatcher et al., 1991),
although generalizability is limited (Ricker &
Zafonte, 2000).
There has been less systematic evaluation of
the efficacy of QEEG in discriminating individu-
als with mild TBI from controls, and there remains
some question as to the clinical utility of this
brain-mapping approach in this type of differen-
tial diagnosis (Hagglund & Persson, 1990;
Thatcher et al., 1989). In fact, although QEEG can
demonstrate impressive statistical discriminant
functions in mild brain injury, it has been demon-
strated that it may actually have an inferior hit
rate relative to traditional clinical diagnosis
(Ricker & Zafonte, 2000; Nuwer et al., 2005).
While still certainly holding promise, it can be
concluded that, at present, QEEG remains more
of a research tool than a diagnostic instrument in
brain trauma. The Therapeutics and Technology
Assessment Subcommittee of the American
169
Academy of Neurology, along with the American
Clinical Neurophysiology Society (formerly the
American Electroencephalographic Society), have
published a practice guideline report on the use of
digital EEG which discusses the insufficiency of
evidence for the use of digital EEG in the diagno-
sis and assessment of post-concussion syndrome,
or minor or moderate brain injury (Nuwer, 1994).
Although certainly not everyone aggress with the
conclusions of the AAN (e.g., Hoffmann et al.,
1999), additional cross-validation with indepen-
dent groups and appropriate experimental design
will be needed to establish the utility of QEEG in
clinical and forensic differential diagnosis. A more
recent comprehensive review by Nuwer et al.
(2005) summarizes the state of the science quite
succinctly: “QEEG may be useful as a research
technique in the hands of highly expert users. But
its high rate of false positive findings and the lack
of diagnostic specificity preclude routine clinical
usefulness” (p. 2017).
TOX I C E X P O S U R E
Neuroanatomic imaging techniques such as CT
and MRI are often utilized in cases of known or
suspected toxic exposure. Given the nature of
possible neurotoxin effects, however, functional
neuroimaging procedures are likely to be of
greater validity in the detecting of neuro-
physiological dysfunction.
Measures of neurotoxins in blood, urine, or
occasionally hair may be more useful in confirm-
ing exposure if available within a period of recent
exposure such that they would still be present.
Examples of these are carboxyhemoglobin levels,
blood lead levels, and 24-hour urinary mercury
and arsenic (Armstrong, 2004). Advanced func-
tional brain imaging tests are generally non-
specific and are more useful in ruling out other
causes of cognitive dysfunction, for example, mass
lesions or vascular changes.
Some toxic exposures (e.g., those from sol-
vents) are associated with a nonspecific finding of
cortical atrophy on CT. CT alone may not be con-
sidered sensitive to early subclinical signs (Triebig
& Lang, 1993) and may be most useful to rule
out mass lesions. Structural MRI (i.e., T1- and
T2-weighted) may be useful to identify white-
matter changes, especially after solvent exposure.
MRI has been shown to be more sensitive to chronic
cortical effects of solvent exposure than CT (Filley,
1999; Myint, 1995; Rosenberg et al., 1988).
Regional cerebral blood flow studies using
SPECT or PET have been used to demonstrate
170 forensic neuropsychology
functional correlates of abnormal neuropsy-
chological test results in occupational exposure
cases with various etiologies. These approaches
may not be very helpful in distinguishing neuro-
toxic from other abnormalities at present, however
(Armstrong, 2004). PET or SPECT studies of recep-
tor binding may be of greater utility in demonstrat-
ing receptor system-specific effects of toxins (Edling
et al., 1997). Cognitive activation paradigms have
been applied to persons with solvent exposure.
Using O-15 PET, Haut and colleagues (2000) dem-
onstrated regional activation differences during a
working memory task in persons exposed to
solvents. Activation differences were suggestive of
impaired frontal lobe activity with increased
recruitment of other brain regions during task
performance, a finding consistent with other
clinical populations during working memory tasks,
but not specific to solvent exposure.
There is a growing utilization of event-related
potentials, especially in the experimental litera-
ture (Reinhardt et al., 1997). P300 and N250 laten-
cies and P200 amplitude indicated significant
differences between solvent-exposed painters and
controls (Morrow et al., 1992). Visual evoked
potentials have been suggested being susceptible
to alteration by exposure to solvents, metals, pes-
ticides, and other neurotoxins such as carbon
monoxide (Urban & Lukas, 1990).
CRIMINAL FORENSICS
In the same manner that neuropsychological test-
ing is used in the determination of mitigating
brain-based factors in violence or even murder,
functional neuroimaging is also increasingly used
to defend individuals that have been charged with
such criminal activity. Functional neuroimaging
is also used in cases where a defendant has been
convicted but mitigating factors might result in a
reduction in penalty (e.g., avoidance of the death
penalty). As has been pointed out by others
(Intrator et al., 1997; Mayberg, 1996; Raine et al.,
1998; Raine & Yang, 2006), and should be quite
obvious to any reader of this chapter, one must
use great caution before inferring positive brain
imaging findings as mitigating criminal behavior.
The overwhelming majority of individuals that
demonstrate a positive finding in a neuroimaging
study will have no history or crime or violence,
nor will they be at any increased probability of
ever engaging in such behaviors.
Structural and functional neuroimaging stud-
ies of aggressive and violent individuals have gen-
erally demonstrated frontal lobe abnormalities
(Batts, 2009; Brower & Price, 2001). The nature of
these findings is not specific, however. Such find-
ings may be neurodevelopmental, or they may be
acquired through brain injury or substance
abuse.
There have been several studies that have used
SPECT to examine aggressive and antisocial
behavior (e.g., Hirono et al., 2000; Kuruoglu et al.,
1996; Amen et al., 1996). Each study has demon-
strated some level of decreased blood flow in the
frontal and temporal lobes (although there is
variability of blood flow differences within lobes
across studies). As with TBI, however, such
a finding is not, in and of itself, pathognomonic
for a propensity toward violence, and may be the
result of a variety of other factors. Of course, one
must also consider the possibility that genuine
frontal lobe dysfunction may result in disinhibi-
tion, emotional disruption, and deficient judg-
ment, which may contribute to some aspects of
violent or criminal behavior.
PET studies have contrasted forensic psychiat-
ric patients with controls. Some studies have dem-
onstrated decreased frontal blood flow and
metabolism associated with violent behavior
(Volkow & Tancredi, 1987; Volkow et al., 1995).
A PET investigation of “impulsive aggression”
with patients with personality disorders (chiefly
antisocial, borderline, and narcissistic) showed
decreased anterior medial and left anterior orbito-
frontal metabolism, which correlated with higher
self-ratings of aggression (Goyer et al., 1994).
Raine and colleagues (1997) presented PET
data from 41 individuals charged with murder or
manslaughter. Compared with controls matched
for age, gender, and previous psychiatric diagno-
sis where applicable, individuals charged with
murder or manslaughter demonstrated (as a
group) statistically significant bifrontal hypome-
tabolism while performing a cognitive task known
to activate prefrontal cortex. A later examination
of these data (Raine et al., 1998b) involved sepa-
rating this sample into either a “predatory” (oper-
ationalized as controlled, purposeful aggression)
or “affective” (operationalized as impulsive, emo-
tionally charged aggression) category. “Affective”
murderers demonstrated lower prefrontal metab-
olism compared to controls. Predatory murderers
actually resembled controls in terms of frontal
metabolism.
Most imaging studies of violent or criminal
behavior seem to demonstrate an association
between aggression and prefrontal hypoactivity
(Bufkin & Luttrell, 2005). Most studies in this
 Functional Neuroimaging in Forensic Neuropsychology
arena focus on bifrontal (specifically prefrontal)
decreases in activity, but there are often other
regions of hypoactivity as well. Inconsistencies in
findings are likely attributable to variability in
experimental design and selection of participants.
The finding of prefrontal hypoactivity cannot be
interpreted as a chronic substrate for uncontrol-
lable violent behavior, however, as such a finding
can be experimentally induced. For example, in a
PET study of healthy volunteers, Pietrini and
colleagues asked participants to imagine a sce-
nario involving their own aggressive behavior.
Such imagery was associated with significant focal
reductions in ventromedial frontal blood flow,
compared to those elicited by neutral scenarios.
Thus, frontal lobe hypoactivity may be more
associated with affective changes that may be
associated with aggression, but these do not
necessarily represent an inability to avoid com-
mitting an act of violence (Mayberg, 1996).
With reference to competency, the contribu-
tion of functional imaging is less clear (in com-
parison to the examination of possible mitigating
factors), and might in fact be inappropriate.
Competency to stand trial, as one example, is
based upon a multitude of factors related more to
cognitive capacity and behavior rather than a yes/
no decision as to the presence or absence of a
change in the brain. A defendant might certainly
have a previous brain injury or chronic neurologic
illness (e.g., seizure disorder), but could still be
quite competent to participate in trial proceed-
ings and to ultimately be held accountable for his
or her actions. A very detailed and thoughtful
examination of these factors is presented in this
volume in the chapters by Denney. Finally, Patel,
Meltzer, Mayberg, and Levine (2007) have
discussed many methodological problems in this
literature, including an absence of prospective
data, small sample sizes, or inadequate controls.
In particular, there are factors than can certainly
impact functional imaging that are not taken
into account in many studies, including poverty,
abuse, violence, emotional disruption (either pre-
existing or in reaction to involvement with the
criminal justice system), and substance misuse.
Using Functional Neuroimaging
to Study Deception
In recent years, there has been increased emphasis
on the use of functional brain imaging to
detect the cerebral correlates of deception.
Although the search for a neurobiological “sub-
strate” of deception is not new (see event-related
171
potentials studies by Rosenfeld, e.g., Rosenfeld,
Ellwanger, & Sweet, 1995), this line of inquiry has
seen rapid growth in the cognitive and social
neuroscience literatures with advances in func-
tional neuroimaging, and has received a great deal
of attention in forensic circles (Moriarty, 2008)
and the popular media (Adler, 2008). In fact, at
least two private companies in the US offer com-
mercial “lie detection” services through the use of
fMRI (Greeley & Iles, 2007).
The first fMRI studies to experimentally
examine deception utilized tasks that required
“simple” deceptive responses (e.g., lying about
whether one has a particular playing card in one’s
possession). These studies have demonstrated
increased prefrontal and parietal activity when
participants are lying (Ganis et al., 2003; Kozel
et al., 2004; Langleben et al., 2002; Lee et al., 2002;
Nunez et al., 2005; Spence et al., 2001). This has
been interpreted as an “inhibition of truth” medi-
ated by prefrontal cortex, whereas true responses
are seen as being mediated by posterior brain
structures (Spence et al., 2004).
More recently, the focus of this literature has
expanded from simply looking at the neural
correlates of deception in group data toward using
fMRI to attempt to differentiate lies from truth in
individuals. Langleben and colleagues (2005) used
fast event-related fMRI in a forced-choice
paradigm and examined individual changes in
brain activation using receiver operator charac-
teristic (ROC) curves. They reported being able to
discriminate deception from true responding for
single events at an accuracy of 78%, while the
predictive ability expressed as the area under the
ROC curve was 85%. Critics of the use of fMRI as
a “lie detection” technology note that experimen-
tal tasks do not mimic real-world scenarios in
which persons might be motivated to lie, for
example, for financial gain or to avoid a negative
consequence (Greely & Illes, 2007).
Although not asked to determine if a state-
ment by a patient is an outright lie, forensic
neuropsychologists are routinely asked to use psy-
chometric tests to evaluate effort and the potential
for embellishment of cognitive impairment. Thus,
a potential topic of interest would be to examine
the neural correlates of performance on symptom
validity paradigms that are used to measure
effort. Allen et al. (2007) recently administered
the delayed recognition component of the Word
Memory Test (Green, 2003) and demonstrated
that performance on the WMT was associated
with changes in brain activation in regions of
172 forensic neuropsychology
dorsolateral prefrontal cortex and parietal lobes,
regions which are well known to be active during
even simple cognitive task performance. While
the authors conclude that their findings cast
doubt on the WMT as a symptom validity test, this
conclusion was premature. The study examined
four healthy men in their 20s. No patient popula-
tion was examined and, more importantly, there
was no dissimulation condition presented against
which one could contrast all participants’ error-
free performances. Such a dissimulation condition
is critical, as more recent fMRI studies have dem-
onstrated that cerebral activity elicited by honest
recall errors is different from activity associated
with intentionally feigned memory impairment.
For example, Lee et al. (2009) used fMRI to char-
acterize cerebral activity in ten men who were
examined using a forced-choice word list recogni-
tion paradigm. Participants were examined in a
truthful recognition condition (i.e., answer as
accurately as possible) and also in a condition in
which they were instructed: “You are required to
feign a memory problem and deliberately do badly
on the test. Imagine a scenario which envisages
that a poor result will lead to an attractive sum of
money as compensation for your memory prob-
lem. You should fake skillfully to avoid detection”
(Lee et al., 2009; p. 407). The findings demon-
strated that intentionally faked responses were
associated with significant activation in left vent-
rolateral prefrontal cortex, right posterior cingu-
late, and left precuneus. No significant activations
were observed for errors during the truthful
responding condition. The authors conclude that
faking memory impairment is actually a more
cognitively demanding process than responding
truthfully, and that it requires different cerebral
substrates, namely those associated with inhibited
a correct response. While compelling and well
designed, these findings will need replication by
other groups, and application with clinical popu-
lations with bona fide acquired brain injury.
FUTURE RESEARCH
The past decade has yielded tremendous advances
in functional neuroimaging technologies and
approaches to data analysis. In addition, there
have been exploratory studies in several clinical
populations, including populations that might
be encountered in the context of forensic neuro-
psychological practice. In spite of these techno-
logical advances, these techniques remain
investigational in most clinical populations,
and do not, from a scientific perspective, appear
ready for routine deployment in forensic
evaluations (Batts, 2009). This should not be mis-
interpreted as a negative statement, however.
In fact, it remains the opinion and expectation of
the author that functional neuroimaging will
eventually achieve the same level of applicability
in forensic contexts that neuropsychological
assessment has already achieved. As with neuro-
psychological assessment, this will not occur
overnight, nor will it occur solely from the publi-
cation of a handful of case studies or small inves-
tigations drawn only from pre-selected personal
injury or criminal forensic cases. It will occur after
years of additional systematic research, first
with many independent samples of clinical popu-
lations, and then in studies that directly compare
clinical populations with litigating populations.
This is the standard that has been successfully
followed in forensic neuropsychology, and there is
no reason to hold functional neuroimaging
techniques to a lower standard. In addition, this
standard is not solely restricted to forensic appli-
cations, as well-designed and controlled studies of
functional imaging can only serve to improve
diagnosis and treatment for all clinical popula-
tions, regardless of the context or setting in which
such studies are requested.
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 7
Perinatal Brain Injury
H . G E R RY TAY L O R
INTRODUCTION
The human brain is undergoing rapid matura-
tional changes during the last trimester of fetal
development, beginning at 28 weeks’ gestational
age (GA). Studies examining brain growth reveal
a four-fold increase in cortical gray matter (GM)
from 29–42 weeks’ GA and a five-fold increase in
myelinated white matter (WM) from 35–41 weeks’
GA (Ajayi-Obe, Saeed, Cowan, Rutherford, &
Edwards, 2000; Huppi & Inder, 2001; Huppi
et al., 1996). This period of development is also
characterized by an increase in GM-WM differ-
entiation, cellular metabolism, and cortical
infolding. Birth substantially prior to term GA
and at a very low birth weight interferes with this
growth process, as children born preterm show
reduced GM and WM volumes and less cortical
surface area and complexity at term equivalent
age than term-born children (Inder, Warfield,
Wang, Huppi, & Volpe, 2005). Other major causes
of disruption in early brain development are
perinatal hypoxic ischemic encephalopathy (HIE)
and ischemic or hemorrhagic strokes in term or
near-term children. The present chapter focuses
on these conditions as the three most common
causes of acquired brain insults during the perin-
atal period, which extends from 20 weeks’ GA and
28 days postnatal age (Raju et al., 2007). Other
forms of perinatal brain insult not considered
in this chapter include those caused by brain
infections (e.g., meningitis, herpes simplex
encephalitis), malnutrition, prenatal toxic expo-
sures, and genetic diseases or malformations
(e.g., fetal alcohol exposure, spina bifida, neurofi-
bromatosis).
In the first section of this chapter, I summarize
the neuropathological features of these condi-
tions, their developmental consequences, and
factors that place children at risk for poorer out-
comes. The second section describes procedures
and principles of forensic neuropsychological
assessments of children with potential perinatal
brain insults, as well as some of the challenges
involved in conducting these evaluations. The
concluding section provides an overview of cur-
rent knowledge, highlights important themes, and
emphasizes the need for further research.
COMMON FORMS OF
P E R I N ATA L B R A I N I N S U LT
Very Low Birth Weight/Very Preterm
Birth (VLBW/VPTB)
Definition and Epidemiology
Improvements in neonatal intensive care made
over the last few decades have resulted in increased
survival of children with low birth weight (<2500
g, 5 lbs. 8 oz.), comprising 8.2% of the population
of live births (Hamilton, Martin, & Ventura,
2006). Most of these increases have occurred in
the subset of children with very low birth weight
(VLBW, <1500 g, 3 lbs. 5 oz., 1.5% of births), with
even more dramatic changes in survival observed
in the smaller subset of children with extremely
low birth weight (<1000 g, 2 lbs. 3 oz., 0.5% of
births). Many studies use GA rather than birth
weight to index the extent of prematurity. Preterm
birth is defined as GA <37 weeks, very preterm
birth (VPTB) as GA <32 weeks, and extremely
preterm birth as GA <29 weeks. Although either
birth weight or GA criteria can be used to define
the degree of prematurity, birth weight may fall
below the level that is expected for GA (e.g., birth
weight <10% for GA). In these cases, the child is
said to be small for GA (SGA) or to have intra-
uterine growth retardation. Because developmen-
tal problems have been widely documented in the
children with VLBW or VPTB (Taylor, 2009),
referred to here collectively as children with
VLBW/VPTB, this subset of the broader popula-
tion of children born preterm or at a low birth
weight is the focus of the present section.
Most preterm births are spontaneous and of
unknown etiology, though risk factors include
180 forensic neuropsychology
previous preterm deliveries, fertility treatments
and multiple gestations (twins or other multiple
births), placental or uterine abnormalities, and
pre-eclampsia (Alexander & Slay, 2002;
Goldenberg & Rouse, 1998). In a minority of
cases, delivery is induced because of fetal growth
restriction or maternal risk factors. The vast
majority of infants born with birth weight <750 g
now survive with higher mortality among
those with birth weight <500 g or with GA
<25 weeks (Fanaroff et al., 2007; Hintz, Kendrick,
Vohr, Poole, & Higgins, 2005b; Wilson-Costello,
Friedman, Minich, Fanaroff, & Hack, 2005).
Neuropathology and Neonatal
Medical Complications
The four major types of neuropathology
associated with VLBW/VPTB are germinal
matrix-intraventricular hemorrhage (IVH), per-
iventricular hemorrhagic infarction (PHI),
periventricular leukomalacia (PVL), and post-
hemorrhagic ventricular dilatation (Volpe, 2008,
2009). Germinal matrix-IVH is graded from I-III.
Grade I IVH remains within the germinal matrix,
grade II IVH extends into the ventricular space,
and grade III IVH involves both hemorrhage into
and expansion of this space. PHI is often associ-
ated with germinal matrix-IVH but is a larger and
more asymmetric type of IVH frequently localized
in the caudothalamic grove (Inder & Volpe, 2000).
Formerly considered a grade IV germinal matrix
IVH, PHI is now recognized as a distinct form of
brain insult that results in extensive damage to
periventricular WM. PVL involves more diffuse
and bilateral damage to WM that can entail either
WM necrosis, referred to as cystic PVL, or damage
to oligodendroglial precursors of myelin manifest
as noncystic changes to WM on T2-weighted
magnetic resonance imaging (MRI). While only
5–15% of neonates with VLBW show evidence of
PVL on neonatal ultrasounds, this procedure is
less sensitive to smaller lesions than MRI and rates
of noncystic PVL are much higher (Inder, Wells,
Mogridge, Spencer, & Volpe, 2003). Counsell et al.
(2003), for example, found evidence for noncystic
WM abnormalities in 68% of a sample of neonates
with a mean birth weight 1086g and mean GA of
29 weeks. Finally, post-hemorrhagic ventricular
dilatation is a rarer form of insult involving hydro-
cephalus secondary to necrotic tissue surrounding
the ventricles or to malabsorption of cerebral
spinal fluid.
One important determinant of these brain
insults is the susceptibility of the preterm brain to
hypoxic ischemia, with associated deprivation of
oxygen and glucose (Volpe, 2008). Secondary
sources of insult include excitotoxicity related to
the release of glutamate, the presence of pro-
inflammatory cytokines associated with maternal
or fetal infection, and free radical production in
response to injury. Because of the presence of
arterial end zones in the periventricular and sub-
cortical WM and the special sensitivity of WM to
secondary damage, this brain region is selectively
affected. Damage to subplate neurons in this
region also adversely affects early neurogenesis.
WM is more involved than GM, though early
development of GM is also affected, with cortical
atrophy and ischemic/infarctive insults to GM in
the hippocampus, thalamus, basal ganglia, brain
stem, and cerebellum (Inder et al., 1999; Srinivasan
et al., 2007; Volpe, 2009). MRIs conducted later in
childhood and beyond show residual forms of
neuropathology as evident in reduced volumes of
WM and GM, ventricular dilatation, and intra-
parenchymal cysts and porencephaly (Allin et al.,
2004; Nosarti et al., 2002, 2004). Selective reduc-
tions in volume relative to total brain volume have
also been documented in the temporal, parietal,
and occipital lobes, basal ganglia, corpus callo-
sum, amygdala, hippocampus, thalamus, and
cerebellum (Nosarti et al., 2008; Srinivasan et al.,
2007). Neonatal medical factors associated with
volume reductions include more extreme VLBW/
VPTB and evidence of brain abnormality as man-
ifest by ventriculomegaly, IVH, PVL, or WM
injury (Inder, Warfield, Wang, Huppi, & Volpe,
2005; Kessler et al., 2004; Peterson et al., 2000,
2003). Other medical complications of VLBW/
VPTB that either contribute directly to neuropa-
thology or compromise subsequent brain devel-
opment include chronic lung disease (otherwise
known as bronchopulmonary dysplasia, or BPD),
lack of respiration (apnea), a collapsed lung
(pneumothorax), failure of normal closure of a
pathway between the aorta and pulmonary artery
(patent ductus arteriosis), jaundice (hyperbiliru-
binemia), infection (sepsis), inflammation/infec-
tion of the intestines (necrotizing enterocolitis),
abnormal formation of retinal blood vessels
(retinopathy), and nutritional problems.
Outcomes
Medical consequences of VLBW/VPTB include
neurological and sensory disorders, such as
cerebral palsy (CP), vision and hearing problems,
and shunt-dependent hypdrocephalus. CP most
typically entails spastic hemiplegia or diplegia,

with greater involvement of lower extremities.
These impairments are most common in children
with extremely low birth weight, with estimates in
this subset of the VLBW/VPTB population of
8–17% for CP, 1–2% for hearing impairment
requiring hearing aids, and 1–5% for vision
impairment as defined by a corrected acuity of
worse than 20/200 (Msall, 2006). Other medical
consequences for some children are respiratory
problems such as asthma, rehospitalizations for
surgeries or treatments for related medical condi-
tions such as lung disease, and reduced height,
weight, and head circumference relative to age
standards (Wilson-Costello, 2007).
Administration of neonatal and early child-
hood behavior scales reveals more abnormalities
in state control, orientation, and attention in
VLBW/VPTB survivors compared with term-
born normal birth weight (NBW, ≥37 weeks GA,
≤2500g birth weight) controls (Brown et al.,
2009; Rose, Feldman, Rose, Wallace, & McCarton,
1992; Wolf et al., 2002). Other early develop-
mental deficits in children with VLBW/VPTB
compared with NBW controls include less-well-
developed social and communicative interactions
with parents and lower scores on tests of executive
function and motor and language skills
(Woodward, Edgin, Thompson, & Inder, 2005;
Edgin et al., 2008; Grunau, Kearney, & Whitfield,
1990; Landry, Smith, Miller-Loncar, & Swank,
1997; Rose, Feldman, & Jankowski, 2005; Rose,
Feldman, Jankowski, & Van Rossem, 2005).
Children with VLBW/VPTB also obtain lower
scores than their NBW peers on the original or
revised versions of the Bayley Scales of Infant
Development (BSID) (Hack et al., 2000); rates of
impairment as defined by scores <70 ranging
from 22–37% in children with extremely low birth
weight (Msall, 2006). Cognitive impairments in
areas such as executive function are not fully
accounted for by global developmental delays and
can be found even in children with less extreme
low birth weight (Edgin et al., 2008; Espy et al.,
2002). Developmental delays in early childhood
are of questionable value in predicting future cog-
nitive competence. Although severe impairment
in early childhood is a valid predictor of future
deficits, many children with mild-to-moderate
delays function within the average range of intel-
ligence in later school-age testing (Hack et al.,
2005a). The poor predictive validity of mid-to-
moderate impairments may reflect neural plastic-
ity, limitations in testing methods, or difficulties
in engaging young children with weakness in
Perinatal Brain Injury 181
attention and psychomotor abilities in formal
testing.
By early school age (ages 5–6 years), children
with VLBW/VPBT begin to display problems in
academic learning and are more likely than NBW
children to receive special education services
(Resnick et al., 1999; Saigal, Szatmari, &
Rosenbaum, 1992; Schneider, Wolke, Schlagmuller,
& Meyer, 2004). Cognitive deficits and behavior
problems are also well documented in this age
group (Kilbride, Thorstad, & Daily, 2004; Marlow
et al., 2007; Mikkola et al., 2005; Taylor et al.,
2000). Adverse effects of VLBW/VPTB on cogni-
tion, behavior, and learning extend throughout
the school-age years and into adulthood (Hack,
2005; Saigal, 2000; Taylor, Minich, Klein, & Hack,
2004b). A small minority of children with VLBW/
VPTB are globally mentally deficient, while the
majority has scores on IQ or other tests of general
cognitive ability that range from borderline to
average levels (Taylor, 2009). Even children with
more extreme degrees of VLBW/VPTB have
mean scores on these tests in the low average to
average range (Anderson, Doyle et al., 2003;
Taylor et al., 2000), demonstrating considerable
variability in outcome.
Cognitive deficits are most pronounced in the
domains of executive function, visuomotor skills,
and memory (Taylor, 2008, 2009). Simple lan-
guage functions such as naming vocabulary are
relatively intact, though language processing skills
are more clearly affected and global language
delays may be more evident in younger children
(Luu et al., 2009; Luoma, Herrgard, Martikainen,
& Ahonen, 1998). Academic problems in VLBW/
VPTB samples relative to NBW control groups are
documented by lower scores on tests of reading,
spelling, math, and writing, and higher rates of
grade repetition and special education assistance
(Taylor, in press). Learning disabilities are also
more common in children with VLBW/VPTB
than in NBW controls, and mathematics skills are
more negatively affected than reading or global
cognitive abilities (Litt et al., 2005; Taylor, Espy, &
Anderson, 2009). Children with VLBW/VPTB
have more attention difficulties, social problems,
internalizing and externalizing symptoms, and
atypical behavior than NBW controls (Anderson
et al., 2003; Breslau et al., 1996a; Hoff, Hansen,
Munck, & Mortensen, 2004; Indredavik et al.,
2005; Saigal, Pinelli, Hoult, Kim, & Boyle, 2003).
Attention deficit hyperactivity disorder (ADHD)
is especially prevalent relative to base rates, with
one study reporting this disorder in 23% of a
182 forensic neuropsychology
VLBW/VLTB sample compared with 6% of NBW
controls (Botting, Powls, & Cooke, 1997).
Cognitive, achievement, and behavior deficits
in VLBW/VPTB cohorts remain relatively con-
stant throughout the school-age years relative to
similarly aged NBW children (Breslau, Paneth, &
Lucia, 2004; Breslau et al., 2001; Saigal, 2000;
Taylor, 2009, in press). In a longitudinal study that
compared the cognitive development of children
with birth weights <750 g and 750–1499g with
NBW controls, our research team found increas-
ingly pronounced deficits from mean ages 7–14
years in the <750 g group on measures of execu-
tive function and psychomotor skills (Taylor et al.,
2004b). We found increasing deficits in one or
both of the VLBW groups on other cognitive
measures only at higher levels of environmental
advantage. This pattern of results suggests either
that the negative effects of social disadvantage on
children with VLBW/VPTB wane over time or
that children with VLBW/VPTB are less respon-
sive to environmental advantage than NBW chil-
dren. For other measures, we found that the gap
between the 750–1499 g group and NBW group
narrowed with age, but only for children from
more disadvantaged families. This second pattern
of findings suggest some recovery or compensa-
tion over time in the latter subset of children,
perhaps because they were able to become more
independent learners or were less constrained by
their family environments with increasing age.
Changes over time were nevertheless evident for
only select measures, with the bulk of the assess-
ments suggesting relatively stable deficits across
the school-age years in the <750 g group and with
the 750–1499 g group exhibiting persisting
deficits only in motor skills and executive func-
tion. Similar deficits continued to be present at
mean age 17 years (Taylor, Minich, Bangert,
Filipek, & Hack, 2004a).
Compared with same-aged NBW controls,
young adults with VLBW/VPTB have persisting
weaknesses in IQ and executive function, lower
educational attainment, and more health and
behavior problems (Allin et al., 2006; Cooke,
2004; Hack, 2005; Saigal et al., 2007). Behavior
problems in the young adults with VLBW include
internalizing symptoms in women, inattention
problems in men, and thought problems in both
sexes (Hack, 2005). Moster, Lie, and Markestad
(2008) found that proportionally more adults
born at 23–27 weeks’ GA in Norway had disability
pensions compared with term-born adults. They
also found a higher rate of medical disabilities
that affected work capacity in the individuals with
preterm birth. However, rates of unemployment
in a U.S. sample did not differ between young
adults with VLBW and NBW controls (Hack et al.,
2004) and adult outcomes of VLBW/VPTB have
in some ways proved to be more positive than
anticipated based on the high rates of disabilities
present in this population during the school-age
years (Saigal & Rosenbaum, 2007; Wilson-
Costello, 2007). Differences in educational attain-
ment and health status are relatively small;
most adults with VLBW complete high school,
live independently, and exhibit less risk-taking
behaviors than their NBW peers.
Predictors
Several risk factors account for variability in
outcomes of VLBW/VPTB. Children with brain
abnormalities on neonatal cranial ultrasounds are
more likely than other survivors of VLBW/VPTB
to have neurodevelopmental impairments (Ansel
et al., 2006; Luu et al., 2009; Sherlock et al., 2005;
Vohr et al., 2003; Whitaker et al., 1996, 1997;
Woodward, Anderson, Austin, Howard, & Inder,
2006). The risk for these impairments is highest in
children with grade III germinal matrix-IVH or
PHI (Sherlock, Anderson & Doyle, 2005), whereas
children with grade I and II germinal matrix-IVH
are at some, though lesser, risk (Patra, Wilson-
Costello, Taylor, Minich, & Hack, 2006). Accom-
panying shunt-dependent hydrocephalus is an
additional risk factor (Adams-Chapman, Hansen,
Stoll, & Higgins, 2008). Early brain insults as
revealed on MRIs conducted at term equivalent
age or later in childhood also predict poorer devel-
opmental outcomes (Abernethy, Cooke, & Foulder-
Hughes, 2004; Edgin et al., 2008; Inder et al., 2005;
Indredavik et al., 2005; Nosarti et al., 2008; Peterson
et al., 2000). MRI findings related to poorer out-
comes are structural abnormalities such as PVL,
IVH, ventricular enlargement, and reduced WM
and GM volumes. However, severe deficits are not
inevitable, even in children with the most severe
neonatal brain insults. In their follow-up assess-
ments of 21 preterm children with PHI at 12 years
of age, Roze et al. (2009) found 5 children (24%)
without CP, 8 with IQ scores within the average
range (42%), and 9 (53%) with behavior ratings
within the normal range. Similarly, Bassan et al.
(2007) found that one-third of their sample of
preterm children with PHI had no detectable
motor or cognitive deficits at 30 months of age.
The degree of VLBW/VPTB is another
important risk factor. Children with more extreme

low birth weight or prematurity are more vulner-
able to neonatal brain insults and have more pro-
nounced deficits in cognition, achievement, and
behavior (Anderson et al., 2003; Klebanov et al.,
1994; Sherlock et al., 2005). To illustrate, our
research group found that 63% of children with
<750 g birth weight had a developmental impair-
ment at middle school age, compared with 38% of
the 750–1499 g birth weight group and 18% of the
NBW group (Taylor et al., 2000). Impairment was
defined broadly as a neurological or sensory dis-
order, low IQ or adaptive functioning, an aca-
demic problem, or behavior ratings suggestive of
ADHD. Adverse effects of VLBW/VPTB on devel-
opment are also observed in children with less
extreme VLBW/VPTB, such as the participants in
our study with 750–1499 g birth weight (Taylor
et al., 2004b), though deficits in these children
tend to be milder and more selective than those
observed in cases of more extreme VLBW/VPTB.
This gradient of sequelae, with milder deficits in
children with higher birth weight and GA, extends
throughout the range low birth weight and pre-
maturity (Breslau, Chilcoat, DelDotto, Andreski,
& Brown, 1996b; Linnet et al., 2006; van Baar,
Vermaas, Knots, de Kleine, & Soons, 2009).
Neonatal medical risks other than identifiable
brain injury are chronic lung disease, treatment
with postnatal steroids, necrotizing enterocolitis,
jaundice, sepsis, apnea, hypothyroxinemia, patent
ductus arteriosis, and retinopathy of prematurity
(Cooke, 2005; Hack et al., 2000; Hintz et al., 2005a;
Ishaik, Mirabella, Asztalos, Perlma, & Rovet,
2000). Longer neonatal hospital stays and greater
numbers of neonatal risks also predict poorer
outcomes (Laptook et al., 2005; Taylor, Klein,
Drotar, Schluchter, & Hack, 2006). Associations
of placental abnormalities with later cognitive
functioning suggest that risks include antenatal as
well as neonatal factors (Redline, Minich, Taylor,
& Hack, 2007).
Outcomes for children with VLBW/VPTB are
also associated with characteristics of the home
and family environment. Lower socioeconomic
status and nonoptimal parenting characteristics
are associated with poorer outcomes indepen-
dently of VLBW/VPTB (Aylward, 2005; Taylor
et al., 2004b; Vohr et al., 2003). While associations
of environmental factors with developmental out-
comes are generally similar in VLBW/VPTB and
NBW samples, these factors can also moderate
the effects of VLBW/VPTB. For example, some
studies have found more pronounced effects of
VLBW/VPTB on children from more socially
Perinatal Brain Injury 183
disadvantaged families (Breslau et al., 1996a;
Taylor et al., 1998; Landry, Smith, Miller-Loncar,
& Swank, 1998). Other studies have observed the
opposite pattern, with the effects of VLBW/VPTB
more evident in children from more advantaged
backgrounds (Taylor et al., 2006). Differences in
this regard may reflect variations in the type of
outcome assessed (e.g., behavioral adjustment vs.
cognitive abilities) or in sample characteristics
(Taylor et al., 1998).
HIE in Term Infants
Definition and Epidemiology
Hypoxic ischemia is the combination of dimin-
ished oxygen in the blood (hypoxia) with dimin-
ished blood perfusion (ischemia). These
conditions deplete glucose to the brain, adversely
affect metabolism, and result in accumulation of
the neurotransmitter glutamate and firing of glu-
tamate receptors (Perlman, 1997, 2006; Volpe,
2001, 2008). Causes of hypoxic ischemia include
impaired exchange of oxygen and carbon dioxide
(asphyxia), lack of respiration, heart failure/mal-
function, and loss of cerebrovascular autoregula-
tion. Hypoxic ischemia can occur in the
antepartum, intrapartum, or postpartum periods
(i.e., before, during, and after labor and delivery).
Antepartum factors contributing to hypoxic isch-
emia include conditions such as maternal
hypotension, maternal diabetes, placental abnor-
malities, coagulation disorders during the fetal
period, intrauterine growth retardation, uterine
hemorrhage or infection, hydrops fetalis (fetal
edema), and congenital malformations (Rolland
& Hill, 1995). Intrapartum factors are labor events
such as placental abruption, cord prolapse, meco-
nium, persistent late or variable heart rate decel-
erations, and mechanical injury. Postpartum
sources are complications such as respiratory dif-
ficulties and heart or lung malfunction. Infants at
risk for hypoxic ischemia due to events occurring
during labor and delivery frequently have histo-
ries of antepartum risks, making it difficult in
many cases to sort out the origins of perinatal
brain insult.
The term “HIE” has been inconsistently applied
and is at times referred to in the literature as “birth
asphyxia” or “neonatal encephalopathy.” The latter
term is sometimes used to refer to a wider range of
brain insults at term birth and to avoid the assump-
tion of asphyxia as the causal factor in all cases.
Nevertheless, there is reasonable consensus that
asphyxia is a meaningful clinical entity that can
cause encephalopathy in term-born infants and
184 forensic neuropsychology
that it can be identified by the occurrence of three
consecutive events (Dilenge, Majnemer, & Shevell,
2001; Perlman, 2006; Shaywitz & Fletcher, 1993;
Robertson & Finer, 1988; Volpe, 2008). The first
event is an indication of placental asphyxia as evi-
denced by placental abruption, a prolapsed cord,
in utero passage of meconium, or abnormal fetal
heart rate decelerations (as defined relative to end
of uterine contractions). The second event is phys-
iological stress immediately at or shortly after birth
as evidenced by low Apgar scores, acidosis (e.g.,
cord umbilical arterial pH < 7), lack of respiration,
and/or multi-organ failure (Shaywitz & Fletcher,
1993). The Apgar score is a clinical rating of the
infant’s appearance or skin color, pulse rate,
grimace or other signs of irritability, activity as an
indication of muscle tone, and respiration. Each
of the five items is rated from poor to good on a
0–2 scale, for a total of up to 10 points. The Apgar
rating is typically done at 1, 5, and 10 minutes after
birth, with persistently low scores (e.g., <6 at 1
and 5 minutes) indicating significant concern. The
risk for asphyxia-related brain insult is increased
with multiple signs of physiological stress (Dilenge
et al., 2001; Perlman, 2006). The third event is a
persistent clinical/behavioral symptom of brain
insult (i.e., encephalopathy), such as hypotonia or
reflex abnormalities, abnormal levels of arousal,
feeding or breathing difficulties, or seizures. Most
studies of children with HIE grade the severity of
encephalopathy from mild to severe based on a
system originally developed by Sarnat and Sarnat
(1976). Mild or Stage 1 HIE is typically defined by
a hyper-alert or hyper-excitable state in the absence
of other clinical signs; moderate or Stage 2 HIE by
lethargy, hypotonia, or diminished reflexes, with
or without seizures; and severe or Stage 3 HIE by
stupor, motor flaccidity, or absent reflexes.
The incidence of HIE is estimated at 2–4 per
1000 lives births, with estimates of neonatal mor-
tality rates of 15–20% (Huang & Castillo, 2008).
Although neonatal encephalopathy can be present
without evidence of perinatal stress, this form of
encephalopathy is more likely to be of antenatal
origin (Perlman, 2006). Indications of fetal distress
without accompanying encephalopathy are much
more common than HIE and usually associated
with normal outcomes (Dilenge et al., 2001).
Neuropathology and Risk Factors
Hypoxic-ischemia results in immediate cell
death (necrosis) due to swelling and rupturing of
cells, as well as secondary or reperfusion damage
in response to injury. This secondary damage
(apoptosis) has a delayed time course and reflects
responses to injury that lead to further brain insult
due to the production of glutamate and the related
build-up of calcium, free radicals such as nitric
oxide, and inflammatory cytokines, as well as
alternations in cerebral blood flow (Volpe, 2008).
In contrast to the greater effects of prematurity on
WM, HIE results in more damage to GM. Term-
born infants with HIE may have PVL, IVH, or
intraparenchymal hemorrhage (Cowan et al.,
2003; Ramaswamy, Miller, Barkovich, Partridge,
& Ferriero, 2004; Volpe, 2008). However, the two
major forms of neuropathology associated with
this condition are selective neuronal necrosis and
parasagittal cerebral injury (Chau et al., 2009;
Ferriero, 2004; Huang & Castillo, 2008; Lawrence
& Inder, 2008). Selective neuronal necrosis can be
diffuse or fall into one of three regional patterns
involving insult to the subcortical GM and paras-
agittal region of the perirolandic cortex, subcorti-
cal GM and brainstem, or ventral pons and
hippocampus. The cerebellum and spinal cord are
other vulnerable brain regions. Figure 7.1 illus-
trates that pattern of brain insult in an infant with
the combination of subcortical GM and parasag-
ittal insult. Parasagittal cerebral injury is more
confined to cortical GM, most commonly in the
parietal occipital region, but includes damage to
underlying subcortical WM. The latter form of
insult is often referred to as a “watershed injury”
due to its location in border zones between the
anterior, middle, and posterior cerebral circula-
tion. In addition to revealing lesions in these
areas, MRIs taken with the first several days of
birth indicate lost of GM-WM differentiation,
with decreased diffusion evident in diffusion-
weighted MRI.
A population-based study conducted in
Western Australia found that several antenatal
risk factors were associated with HIE in term
infants, including maternal thyroid disease,
maternal viral illness, relatively short or long GA,
infertility treatment, severe pre-eclampsia, mod-
erate to severe vaginal bleeding, placental abnor-
mality, intrauterine growth retardation, a family
history of seizures or other neurological disorder,
and socioeconomic status (Badawi et al., 1998a).
Intrapartum risk factors were also identified but
were present in only a minority of cases (Badawi
et al., 1998b). Although the high prevalence of
antenatal risk factors is well established (Ferriero,
2004; Perlman, 2006; Redline, 2008; Rolland &
Hill, 1995; Volpe, 2008), there is substantial evi-
dence that most brain insults associated with term
 Perinatal Brain Injury 185

FIGURE 7.1: Deep nuclear gray matter with cortical injury in a term infant who had a history of hypoxic
ischemic encephalopathy (HIE). (A) T1-weighted axial view from magnetic resonance imaging (MRI)
shows hyperintense injury throughout deep nuclear gray matter. (B) T1-weighted coronal view shows exten-
sion of hyperintense injury from the deep nuclear gray matter into the parasagittal area. (C) T2-weighted
axial image demonstrates low intensity extending from subcortical to parasagittal cortex bilaterally. Reprinted
from Clinics in Perinatology, Vol. 35, R. K. Lawrence & T. E. Inder, Anatomic changes and imaging in assess-
ing brain injury in the term infant, pp. 679–693, 2008, with permission from Elsevier.

HIE occur around the time of birth. Cowan et al.
(2003) found evidence on MRI of acute brain
insult in 80% of term infants with HIE and in 69%
of term infants presenting only with neonatal sei-
zures. The determination that brain insults
occurred prior to labor and delivery, rather than
acutely, was made on the basis of signs of gliosis,
mineralization, or cysts. The investigators sug-
gested that antenatal events may predispose some
infants to perinatal brain insults but that these
insults often occur in the intrapartum period.
Consistent with these findings and notwithstand-
ing the complexities of sorting out causation in
cases of term HIE, authorities on perinatal brain
insults regard events occurring in the intrapartum
period as playing a major role in at least a minor-
ity of cases of term HIE (Ferriero, 2004; Perlman,
1997; 2006; Volpe, 2008).
Outcomes
A population-based study by Badawi et al. (2005)
revealed a 13% prevalence of CP in children with
term newborn encephalopathy, whereas Vannuci
and Perlman (1997) found that about 25% of chil-
dren with term HIE had a permanent neurologic
deficit. Available estimates suggest that about
half of infants with severe HIE die and almost
all survivors have neurologic deficits, whereas
about 10–20% of those with moderate HIE die
and 30–40% have neurologic deficits (Bhat et al.,
2009). CP is most typically spastic quadriplegia,
often with a dyskinetic component and with
greater involvement in the upper than lower
extremities (Badawi et al., 2005; Himmelmann,
Hagberg, Wiklund, Eek, & Uvebrant, 2007;
Perlman, 2006; Rennie, Hagmann, & Robertson,
2007; Volpe, 2008). In some cases, children exhibit
extrapyramidal signs (i.e., dystonia and chore-
oathetosis) 6 months to several years later. This
“delayed onset” syndrome is considered second-
ary to damage to the thalamus and putamen.
Studies that have examined developmental
outcomes in children with term HIE have docu-
mented lower IQ and other cognitive weaknesses
relative to same-aged peers without HIE. In one of
the first formal investigations of developmental
outcomes in a well-defined cohort, Robertson and
Finer (1985) compared term-born children to
groups with mild, moderate, or severe HIE at 3½
years of age. The children with mild HIE had no
neurodevelopmental handicaps as defined by CP,
visual or hearing impairment, mental retardation,
or severe seizure disorder. Moreover, mean scores
on measures of IQ, language, and perceptual-
motor skills fell within the average range for this
group. In contrast, all of the children with severe
HIE and 21% of the moderate HIE group had at
least one handicap. The mild HIE group scored
better in testing than both other groups with HIE,
and the moderate group did better than the severe
group. In a subsequent follow-up at 5½ years of
age of children without major neurologic or
mental disability, Robertson and Finer (1988)
found that the group with moderate HIE had
186 forensic neuropsychology
lower scores on IQ perceptual-motor tests com-
pared with the mild HIE group, other term chil-
dren treated in a tertiary neonatal care center
without encephalopathy, and a group of term chil-
dren cared for in well-child nurseries. This
research team also documented delayed school
readiness skills in 40% of children with moderate
HIE without CP, sensory deficits, seizures, or
mental retardation (Robertson & Grace, 1992). In
a third follow-up of this sample at 8 years of age,
Robertson, Finer, and Grace (1989) again docu-
mented poorer performance by the moderate and
severe HIE groups relative to a representative
sample of peers on tests of IQ and perceptual-
motor ability, as well as on measures of vocabu-
lary, reading, spelling, and arithmetic. Even
children with moderate HIE who did not have
severe cognitive deficits or neurologic impair-
ment obtained lower IQs and had more learning
problems than the peer controls, while the mild
HIE group performed similarly to the controls.
More recent studies substantiate a high rate of
mental deficiency in children with severe HIE,
with evidence for less severe developmental
impairments in a number of skill areas in children
with moderate HIE (Gonzalez & Miller, 2006).
Shankaran, Woldt, Koepke, Bedard, and Nandyal
(1991) found that 15 of 24 term children with
moderate or severe HIE had either a neurologic
deficit or low IQ at 5 years of age, and that there
was a high level concordance between these out-
comes and outcomes measures at 1 year. In
another study of early childhood outcomes, Dixon
et al. (2002) found that scores on the Griffiths
Mental Development Scales at 16 months were
lower in their population-based cohort of term
children with neonatal encephalopathy than in a
community control group. These differences
remained even when they excluded children with-
out CP. Low total scores on this measure, defined
as scores more than two standard deviations
below the means for controls, were found in 36%
of the severe HIE group and 19% of the moderate
HIE group.
Rates of CP in a sample followed to 7 years of
age by Marlow, Rose, Rands, and Draper (2005)
were 6% in children with moderate HIE and 42%
in those with severe HIE, though the criteria for
severe HIE were less restrictive than in many
other studies. The major contribution of this study
is the evidence it offers for deficits in children
without CP. Compared with classroom controls,
the children with severe HIE but without CP
obtained lower scores on tests of global mental
ability, performed more poorly on a wide range of
specific neuropsychological skills, and had more
symptoms of hyperactivity and emotional prob-
lems and fewer pro-social behaviors on parent or
teacher ratings. The children with moderate HIE
without CP did not differ from their classmates in
overall cognitive ability but had weaknesses in
language, sensorimotor skills, narrative memory,
and sentence repetition. Teacher ratings indicated
that both HIE groups made less progress toward
educational goals than their classmates. Although
mean test scores for the severe HIE group that
fell within the average range indicate that some
of these children survived without generalized
cognitive impairment, the results also docu-
mented lower skill levels in this group compared
with peers.
Studies of older survivors of term HIE
reveal persisting developmental impairments.
Lindstrom, Lagerroos, Gillberg, and Fernell
(2006) examined 28 adolescents and young adults
aged 15–19 years with moderate HIE selected
from a larger population with 5-minute Apgar
scores <7. Eight of the participants (29%) had a
neurological diagnosis. Seven of the 11 persons
with intelligence testing scored in the borderline
range of IQ or below. Parent data revealed more
problems in short-term memory, time perception,
making friends, attention, and a measure of atypi-
cal behaviors in the HIE sample compared with
siblings. Maneru, Junque, Botet, Tallada, and
Guardia (2001) compared another small sample
of adolescents with mild or moderate HIE with a
matched group of healthy adolescents on a neu-
ropsychological test battery. Adolescents with IQ
<85, CP, sensory deficits, or mental retardation
were excluded from the sample. Results revealed
that the adolescents with moderate HIE had lower
scores on tests of memory, perceptual-motor
skills, and executive function, while scores for the
group with mild HIE did not differ from controls.
Other case studies of children meeting criteria for
HIE demonstrate that effects on adolescents can
be specific to episodic memory, with relative pres-
ervation of immediate recall and acquired seman-
tic knowledge (de Haan et al., 2006; Gadian et al.,
2000). Asphyxia-related damage to the hippocam-
pus has been implicated in these cases.
Predictors
As evident from these findings, more severe HIE
is a major predictor of developmental outcomes
and outcomes are worst for children with severe
HIE. Less pervasive deficits are found in children

with moderate HIE, though as a group these chil-
dren are a higher risk for cognitive, learning, and
behavior impairment compared with children
with mild HIE or control groups without HIE.
Additional clinical predictors of poorer outcome
include more persistent neonatal neurological
symptoms, CP or sensory disorders, seizures, and
placements on multiple anticonvulsant medica-
tions (Dixon et al., 2002; Himmelmann et al.,
2007; Rennie et al., 2007; Robertson & Finer, 1988;
Shankaran et al., 1991; Volpe, 2008). Children
with delayed-onset extrapyramidal syndrome
may do well relative to others with CP.
Neonatal encephalopathy appears to be criti-
cal component of risk for neurodevelopmental
impairment in infants with HIE (Amiel-Tison &
Ellison, 1986; Badawi et al., 2005; Dilenge et al.,
2001; Perlman, 2006; Volpe, 2008). To illustrate,
Moster, Lie, and Markestad (2002) assessed out-
comes in a sample of children 8 to 13 years of age
with 5-minute Apgar scores <4 and in a control
group without neonatal problems. Compared
with the controls, children in the low-Apgar
sample with neonatal encephalopathy had more
motor impairments; more developmental, learn-
ing, attention, and other behavior problems by
parent report; and higher rates of epilepsy, whereas
children in the low-Apgar sample without enceph-
alopathy were at much lower risk for negative out-
comes. Consistent with these results, Thomson,
Searle, and Russell (1977) found that a sample of
5- to 10-year-old children with low Apgar scores,
most of whom did not show signs of neonatal
encephalopathy, performed similarly to children
with normal Apgar scores on a measure of psy-
cholinguistic abilities. Other studies have also
found that low Apgar scores lack utility in pre-
dicting outcomes when considered in isolation
(Blackman, 1988; Viggedal, Lundalv, Carlsson, &
Kjellmer, 2002), and one investigation demon-
strated normal development in a majority of chil-
dren requiring resuscitation at birth so long as
Apgar scores rebounded within the first several
minutes of birth (Jain, Ferre, Vidyasagar, Nath, &
Sheftel, 1991).
Recent evidence, however, suggests that even
brief depressions in Apgar scores may have some
effect on long-term cognitive development (Odd,
Lewis, Whitelaw, & Gunnell, 2009; Odd,
Rasmussen, Gunnell, Lewis, & Whitelaw, 2008).
Odd et al. (2008) examined IQ in 18-year-old
term-born individuals from the Swedish Birth
Registry in two low-Apgar groups, one with scores
<7 for only 0–5 minutes after birth and the other
Perinatal Brain Injury 187
with scores <7 for more than 5 minutes. Persons
with histories of encephalopathy, asphyxia, or
congenital disorders were excluded and the two
low-Apgar groups were compared with a refer-
ence group of persons who met these same crite-
ria but had 1-minute Apgar scores >6. Adjusting
for antenatal, neonatal, and social factors, both
low-Apgar groups had slightly higher rates of low
IQ than the group with Apgar scores >6. The
group with prolonged low scores also had lower
school grades at ages 15–16 years. In a subsequent
study, Odd et al. (2009) assessed the effect of
resuscitation with or without encephalopathy on
the IQs of 8-year-old term-born children partici-
pating in a longitudinal study. Findings revealed
higher rates of low IQ (<80) in both resuscitation
groups compared with controls, though the
increased risk associated with low Apgar scores
was low and rates were higher among the children
with encephalopathy. The results of both studies
were interpreted as evidence that even mild, tran-
sient hypoxia has the potential to lead to neuronal
damage with associated decrements in IQ.
The type of abnormalities found on MRI is
one of the best predictors of neurodevelopmental
outcome. CP, visual impairment, and generalized
cognitive deficits or developmental delays are
most common in children with insult to the basal
ganglia, thalamus, posterior limb of the internal
capsule, and perirolandic cortex (Barnette et al.,
2002; Mercuri et al., 2004; Miller et al., 2005;
Rutherford et al., 1998). More widespread cortical
involvement accompanies more severe insults to
these regions. A second pattern of brain insult
detected on MRI involves damage to cortical WM
in the arterial borderline or watershed zones that
extends in more severe cases to cortical GM. In
examining neonatal MRIs in 173 term infants
with neonatal encephalopathy, Miller et al. (2005)
found that 30% of their sample had normal scans,
25% displayed the basal ganglia/thalamus pattern
of insult, and 45% had insult primarily to water-
shed regions. Infants with the basal ganglia/thala-
mus pattern had more severe degrees of
encephalopathy and more seizures and they
received more intensive resuscitation compared
with infants with the watershed pattern. None of
the infants with normal MRIs had CP or impair-
ment on developmental testing at 30 months,
compared with rates of CP and developmental
impairment, respectively, of 50% and 56% for
infants with the basal ganglia/thalamus pattern
and 11% and 18% for infants with the watershed
pattern. Findings from Rutherford, Pennock,
188 forensic neuropsychology
Schwieso, Cowan, and Dubowitz (1996) further
reinforce associations of more severe insults in
the basal ganglia or more extensive WM abnor-
malities with poorer neurodevelopmental out-
comes at 2 years of age. The effects of these insults
likely vary with the extent of injury, as one study
reports good cognitive outcomes in some children
with moderate encephalopathy for whom MRIs
indicated more isolated insults to the basal gan-
glia (Pasternak & Gorey, 1998).
Abnormalities on MRI are found even in chil-
dren without CP and are related to impairments
on tests of IQ and perceptual-motor ability and
minor neurological dysfunction. Barnette et al.
(2002) found WM abnormalities or mild to mod-
erate lesions in the basal ganglia in 80% of a
sample of 5- to 6-year-old children without CP
who had neonatal encephalopathy. In another
study of young children born at term who met
criteria for HIE but did not have CP, Steinman
et al. (2009) found that the severity of brain insults
conforming to the watershed-type pattern pre-
dicted Verbal IQ scores at 4 years of age. The
extent of watershed injury was related to Verbal
IQ only (i.e., not to Performance IQ) and was
evident even in analysis that controlled for the
severity of insult in the basal ganglia distribution.
Further support for the utility of MRI in predict-
ing outcomes is provided by van Kooij et al.
(2007), who examined the cross-sectional area of
the corpus callosum at school age in term-born
children with mild and moderate HIE and in
age-matched schoolmate controls. They found
that this structure was smaller in the group with
moderate HIE than in controls and that its size
correlated with performance on a test of motor
ability. These relationships remained even after
excluding children with CP. WM abnormalities
on MRI have been detected even in children with
mild HIE who are developing normally at 2 years
of age, though the implications of these abnor-
malities for longer-term outcomes are uncertain
(Rutherford et al., 1996). These several findings
suggest that the extent of watershed insults and
WM injury are related to cognitive deficits in chil-
dren without CP or generalized mental deficiency
(Gonzalez & Miller, 2006).
Stroke in Term Infants
A stroke is a neurological dysfunction due to a
disruption in the brain’s blood supply. The pri-
mary sources of this disruption in the term infant
without HIE are perinatal arterial ischemic stroke,
intracranial hemorrhage, and cerebral sinovenous
thrombosis (Barnette & Inder, 2009; Perlman,
2004; Raju et al., 2007; Volpe, 2008). Existing
research literature related to these conditions,
their developmental consequences, and predic-
tors of outcome is summarized below.
Perinatal Arterial Ischemic Stroke,
Referred to Commonly as Ischemic
Perinatal Stroke (IPS)
If IPS occurs in conjunction with neonatal enceph-
alopathy, clinical signs are similar to those seen
with HIE (e.g., seizures, hypotonia, lethargy, poor
feeding), though motor tone or movements may be
asymmetrically abnormal (Barnette & Inder, 2009;
Volpe, 2008). Often, however, IPS is not accompa-
nied by neonatal encephalopathy and is identified
by isolated focal seizures that appear either in the
neonatal or postnatal period or by post-natal
presentation of CP or motor asymmetries (Nelson
& Lynch, 2004). The majority of children with
CP related to perinatal stroke are not encephalo-
pathic at birth (Wu et al., 2004). Cases of delayed
diagnosis of IPS are referred to as presumed peri-
natal ischemic stroke and are defined as neuro-
logical deficits or seizures in infants with normal
neonatal neurological histories that become mani-
fest after the perinatal period and are accompanied
by neuroimaging findings consistent with perina-
tal stroke (Kirton et al., 2008; Raju et al., 2007).
Such evidence, however, is presumptive and in
some cases it may be difficult to be certain as to
whether insult occurred prior to the end of the
perinatal period. The incidence of IPS is estimated
at between 1 in 2,300–5,000 births.
The most common neuromotor disorder in
children with IPS is hemiplegic CP, although some
children have subtle motor asymmetries or
impaired motor abilities without CP (Cioni et al.,
1999; Mercuri et al., 2004; Volpe, 2008). Lesions
can also be bilateral and a small minority of chil-
dren present with quadriparesis or monoparesis
(Lee et al., 2005b). Infarction is most often found
in the distribution of the left middle cerebral
artery, with greater involvement of the arms than
the legs. The reasons for greater vulnerability of
the left hemisphere are not well understood, but
may reflect the more direct pathway for clots
from the heart through the left carotid artery or to
differences in blood flow in the left versus right
carotids related to early patent ductus arteriosus
(Trauner, Chase, Walker, & Wulfeck, 1993).
Hemiplegia is more likely when insults are large
and affect major portions of the middle cerebral
artery distribution, including the cerebral cortex,

WM, basal ganglia, posterior limb of the internal
capsule, and cerebral peduncles (De Vries, Van der
Grond, Van Haastert, & Groenendaal, 2005; Lee
et al., 2005b; Raju et al., 2007; Trauner et al., 1993).
Insult to the non-stroke hemisphere also increases
the likelihood of hemiplegic CP (Volpe, 2008).
Fortunately, many young children function well
motorically despite having hemiplegic CP, and
hemiplegia may resolve during early childhood
(Wulfeck Trauner, & Tallal, 1991). Possibly related
to the manner in which cases without neonatal
encephalopathy are ascertained (i.e., based on
asymmetric motor impairment), children diag-
nosed with presumed perinatal ischemic stroke
have higher rates of hemiplegia than those with
neonatal diagnoses of IPS (Lee et al., 2005b).
Distinctive features of presumed perinatal ischemic
stroke include a tendency for greater impairment
in the legs than arms and evidence of PHI in some
children (Kirton et al., 2008; Rennie et al., 2007).
Numerous maternal, fetal, and neonatal
factors place infants at increased risk for IPS
(Barnette & Inder, 2009; Nelson & Lynch, 2004;
Raju et al., 2007). Risks for IPS include both intra-
partum factors and maternal-fetal factors, such as
thrombocytopenia or infection, maternal autoim-
mune disorder, preeclampsia, congenital heart
disease, polycythemia (excess red blood cells),
persistent pulmonary hypertension, and twin-to-
twin transfusion syndrome. Lee et al. (2005a)
examined risk factors associated with IPS in
infants enrolled in a large health care system.
Eighty-five percent of the 40 cases they identified
with IPS were term-born. Results revealed that
several intrapartum factors were more common
among the cases than among matched controls,
including chorioamnionitis (a vaginal infection),
prolonged rupture of membranes, prolonged
second stage of labor, fetal heart rate abnormality,
cord abnormality, vacuum-assisted delivery, and
emergency cesarean delivery. Maternal factors
associated with IPS were preeclampsia, oligohy-
dramnios (excessive amniotic fluid), and decreased
fetal movement. The children with IPS were also
more likely to be diagnosed with asphyxia or HIE.
Adverse consequences of IPS other than CP
and motor impairments include epilepsy in
25–50% of children, deficits in vision and sensory
perception, and problems relative to normative
standards or control groups in cognition, lan-
guage, learning, and behavior (Barnette & Inder,
2009; Golomb et al., 2001; Golomb, Saha, Garg,
Azzouz, & Williams, 2007; Mercuri et al., 2003;
Trauner, 2003). Talib et al. (2008) found that
Perinatal Brain Injury 189
scores on measures of IQ, immediate verbal
memory, receptive vocabulary, and verbal fluency
were lower in term-born 5- to 8-year-old children
with IPS from twin gestations than in the co-twin
without IPS. Other studies have found that,
while children with IPS score below expectations
on developmental, IQ, and neuropsychological
measures, mean scores generally fall within the
average range (Hogan, Kirkham, & Isaacs, 2000;
Jan & Camfield, 1998). Variations in outcome are
nevertheless evident in the literature, with some
studies indicating significant deficits in children
with IPS (Koelfen et al., 1993; Raju et al., 2007).
These inconsistencies may relate to different crite-
ria for sample selection. Some studies select only
children with strictly focal or unilateral lesions
and exclude children with symptoms of HIE,
while other studies recruit children without regard
to these features or fail to specify ascertainment
methods.
Trauner and colleagues at the University of
California, San Diego followed well-specified
cohorts of children with unilateral perinatal focal
stroke and compared these children with controls
(Ballantyne, Scarvie, & Trauner, 1994; Ballantyne,
Spilkin, Hesselink, & Trauner, 2008; Ballantyne,
Spilkin & Trauner, 2007; Bates & Roe, 2001; Stiles,
Nass, Levine, Moses, & Reilly, 2009; Trauner et al.,
1993; Trauner, Nass, & Ballantyne, 2001; Wulfeck
et al., 1991). The samples recruited by this research
group were restricted to children with either IPS
or hemorrhagic strokes within the perinatal
period and excluded cases with bilateral, progres-
sive, or multifocal lesions. Wulfeck et al. (1991)
found seizures in about half of a sample of 14 chil-
dren selected in this manner and followed to 6–24
months of age. Delays in language and motor
development were also observed in about half of
this cohort. However, global cognitive function-
ing on the Bayley Scales of Infant Development
was within the normal range for most of the
children. Trauner et al. (1993) documented
normal IQ scores in all 21 children followed to
between 2 and 9 years of age. A later study revealed
higher parent ratings of behavior problems on
several scales of the Child Behavior Checklist
in 4- to 15-year-old children with unilateral
perinatal strokes compared with a control group
(Trauner et al., 2001). However, none of the group
differences was significant when IQ was con-
trolled and mean behavior problem ratings for the
stroke group fell within the average range.
For the most part, studies by the San Diego
group have failed to reveal differential effects of
190 forensic neuropsychology
left-versus right-sided lesions on language and
visual-spatial skills, as is typical of later-occurring
strokes (Ballantyne et al., 2008; Bates & Roe, 2001;
Bates et al., 2001; Stiles et al., 2009). These investi-
gators have observed early language delays with
lesions to either hemisphere, with the type of
delay varying somewhat according to the side of
lesion (left-hemisphere lesions more strongly
associated with delays in speech production and
right-hemisphere lesions with poor comprehen-
sion). Although the early language delays resolved
with advancing age, residual deficits in language-
processing skills were observed at older ages
(Ballatyne et al., 2007). Unilateral lesions to either
hemisphere also resulted in impairments in
visual-spatial abilities. Like language impair-
ments, these deficits changed with age but per-
sisted into childhood and were to some extent
lesion-specific. Children with left-hemisphere
insult had more problems in processing the
component parts of figures than the overall
spatial configuration, whereas those with right-
hemisphere stroke showed the reverse pattern
(Stiles et al., 2008). Face and affect processing may
also be compromised in children with unilateral
perinatal stroke, at least early in development
(Stiles et al., 2009).
Similarly, Ballantyne et al. (1994) found that
perinatal strokes in either hemisphere had adverse
effects on IQ. In this study, a post-stroke group of
persons tested at 4–20 years of age was compared
with controls on Wechsler Verbal, Performance,
and Full-Scale IQs. Although all three IQ scores
for the stroke group were within the broadly aver-
age range, they were lower than the IQ scores of
the controls. Verbal and Performance IQs were
comparable for the left-hemisphere lesion group,
while Verbal IQ was higher than Performance IQ
for the group with right-hemisphere lesions.
Replication of this finding is needed but the
pattern of results is consistent with the right-
hemisphere “crowding hypothesis,” wherein reor-
ganization of a damaged right hemisphere in
support of language functions occurs at the
expense of nonlanguage functions (Lidzba, Staudt,
Wilke, & Krageloh-Mann, 2006). A more general
theme that emerges from review of this literature
is the capacity for neural reorganization following
early focal stroke (Bates & Roe, 2001; Bava,
Ballantye, & Trauner, 2005; Staudt, Krageloh-
Mann, Holthausen, Gerloff, & Grodd, 2004; Staudt
et al., 2002; Stiles et al., 2009; Talib et al., 2008).
Risks for worse developmental and cognitive
outcomes following IPS include CP, seizures and
electroencephalographic (EEG) abnormalities,
large or bilateral lesions, multiple lesion types,
and coagulation disorders (Ballantyne et al., 2007;
Ballantye et al., 2008; Bava, Archibald, & Trauner,
2007; Bava et al., 2005; Golomb et al., 2007;
Koelfen et al., 1993; Mercuri et al., 2003; Stiles
et al., 2009). CP accompanied by neonatal enceph-
alopathy is associated with worse developmental
outcomes than either condition in isolation
(Badawi et al., 2005; Golomb et al., 2007; Jan &
Camfield, 1998; Ramaswamy et al., 2004). Poor
outcomes are also more common with presumed
perinatal ischemic stroke than with non-delayed
(i.e., neonatal or early postnatal) presentations of
IPS (Kirton et al., 2008). Golomb et al. (2001)
found that all 22 of the children they followed
with this diagnosis into early childhood had
persistent hemiparesis and that nearly half of
the sample had speech, behavior, or learning
problems. In examining a sample of 59 children
with presumed perinatal ischemic stroke to a
median age of 4 years, Kirton et al. (2008) found
cognitive or behavioral problems in 29%,
language disorders in 22%, visual deficits in 18%,
and epilepsy in 42%. Cortical insults were associ-
ated with cognitive-behavioral problems, visual
impairment, or epilepsy, while involvement of the
basal ganglia predicted motor deficits.
Intracranial Hemorrhage
Intracranial hemorrhage in term newborns can
be classified as epidural, subdural, subarachnoid,
intracerebral (intraparenchymal or intraventricu-
lar), or intracerebellar (Volpe, 2008). Estimates of
the annual incidence of all types of intracranial
hemorrhages are about 1 per 4,000 births (Gupta,
Kechli, & Kanamalla, 2009; Perlman, 2004).
Subarachnoid and subdural hemorrhages are the
most frequent types among term neonates,
whereas intracerebral and intracerebellar hemor-
rhages are more common in preterm children.
Intracranial hemorrhage in term neonates often
occurs in association with birth trauma and
asphyxia, though some hemorrhages occur with-
out a recognizable precipitating event and smaller
hemorrhages are found even in term infants with
normal outcomes (Bergman et al., 1985; Gupta
et al., 2009; Jhawar, Ranger, Steven, and Del
Maestro, 2005; Volpe, 2008). Some neonates with
significant intracranial hemorrhage present
with seizures, generalized hypotonia, or signs of
increased intracranial pressure such as a decreased
level of consciousness, but others are asymptom-
atic. Risk factors include maternal-placental

problems, such as pregnancy-induced hyper-
tension and placental abruption, and perinatal
complications, such as birth trauma, asphyxia,
thrombocytopenia, inherited coagulopathy (pre-
disposition to hemorrhage), and sinovenous
thrombosis. More rarely, intracranial hemorrhage
can stem from a ruptured aneurysm or arterio-
venous malformation (Perlman, 2004).
Jhawar, Ranger, Steven, and Del Maestro
(2003) found that rates of forceps use, thrombo-
cytopenia, and signs of hypoxia (low Apgar scores
and need for resuscitation) were higher in a cohort
of 66 full-term infants with intracranial hemor-
rhage than in a group of 104 controls. They also
found that forceps use was more closely associ-
ated with subarachnoid or subdural hemorrhage,
whereas thrombocytopenia was more closely
related to intraparenchymal hemorrhage. This
finding is consistent with other reports indicating
an association of intrapartum trauma with sub-
dural and subarachnoid hemorrhages (Perlman,
2004; Volpe, 2008). Jhawar et al. (2003) emphasize
that their data do not imply a causal relationship
of forceps use or hypoxia with intracranial
hemorrhage, as pregnancy complications may
result in both forceps use and intracranial hemor-
rhage, and intracranial hemorrhage may itself
precipitate respiratory distress.
Although the above-cited studies by the
San Diego group included participants with
focal intraparenchymal hemorrhage, few studies
have examined the developmental consequences
of more diverse types of perinatal intracranial
hemorrhage. One exception is an investigation
that followed 18 full-term survivors with neonatal
supratentorial (i.e., intraparenchymal or intra-
ventricular) hemorrhage at 1–7 years of age
(Bergman et al., 1985). Outcomes included
nine children with no evidence of neurodevelop-
mental abnormality, three with severe cognitive
deficits, spastic quadriplegia, and frequent
seizures, two with IQ <50 and hemiplegia, three
without CP who had cognitive deficits, and one
child with a history of neurological disorder
who died in infancy. Discovery of abnormal
outcomes in about half of this small sample is
consistent with results from studies that followed
children with neonatal intracranial hemorrhage
over only the first year of life (Bergman
et al., 1985). The children in this study whose
histories were suggestive of hypoxic ischemia or
traumatic injury at birth had a much higher rate
of disability than children for whom the hemor-
rhage was of unknown etiology. Findings from a
Perinatal Brain Injury 191
study of full-term children with more diverse
types of intracranial hemorrhage also suggested
an association of neonatal asphyxia with poorer
developmental outcomes (Hanigan, Powell,
Miller, & Wright, 1995). More recently, Jhawar
et al. (2005) contacted parents by phone or during
clinic visits to obtain outcome information in a
sample of 1- to 10-year-old full-term children
with different types of intracranial hemorrhage.
Of the 49 children assessed, about one quarter
had motor problems and one quarter had either
sensory impairments or indications of learning
difficulties. Factors related to worse outcomes
were thrombocytopenia and a frontal location of
hemorrhage. Poorer outcomes are also associated
with IVH and early and recurrent seizures,
whereas outcomes are frequently good for chil-
dren with uncomplicated subdural hemorrhage
or subarachnoid hemorrhage over the cerebral
convexities (Gupta et al., 2009; Perlman, 2004;
Volpe, 2008).
Cerebral Sinovenous Thrombosis
Cerebral sinovenous thrombosis involves block-
age of the system of veins outside the parenchyma
that drain blood from the brain. With an esti-
mated annual incidence of <1 per 100,000 chil-
dren (deVerber et al., 2001), this form of stroke is
rare and occurs most frequently in neonates. The
veins most often involved are the superior sagittal
sinus and lateral sinuses, but thrombosis may also
occur in the cortical veins, straight sinus, vein of
Galen, internal cerebral vein, or jugular vein.
Brain edema is most commonly observed on neu-
roimaging, though IVH or intraparenchymal
hemorrhagic infarction may also be present
(Fitzgerald, Williams, Garg, Carvalho, & Golomb,
2006; Volpe, 2008). Presenting symptoms fre-
quently include seizures and a decreased level of
consciousness. Risks factors include maternal-
placental problems, such as infection, maternal
hypertension/preeclampsia, premature rupture of
membranes, placental abruption, and gestational
diabetes (deVerber et al., 2001; Fitzgerald et al.,
2006). Neonatal illnesses or complications, such
as hypoxia, infection, dehydration, and heart
disease, are additional risk factors. Although
long-term outcome studies are lacking, 23 of the
29 neonates (79%) with cerebral sinovenous
thrombosis followed by Fitzgerald et al. (2006) to
a median of 2 years had seizures, developmental
problems, or CP. Worse outcomes are associated
with infarction (Fitzgerald et al., 2006; deVerber
et al., 2001).
192 forensic neuropsychology
FORENSIC AS SES SMENTS OF
C H I L D R E N W I T H P E R I N ATA L
B R A I N I N S U LT S
Procedures for Conducting Forensic
Child Neuropsychological Assessment
Forensic neuropsychological assessments of
children with perinatal brain insults are typically
conducted because of an alleged personal injury
resulting from the medical care received during
the perinatal period. As in other personal injury
cases, the purposes of these assessments are to
identify impairment, determine the likely cause of
impairment, and make projections regarding
the child’s future outcomes and needs (Dennis,
1989; Donders, 2005; Goldberg, 2006; Wills &
Sweet, 2006). As in all forensic neuropsycho-
logical assessments, the overarching goal is to
provide triers of fact, including the judge and jury,
with assessment findings and research informa-
tion that pertain to legal questions about a case
(Giuliano, Barth, Hawk, & Ryan, 1997). Neuro-
psychologists are unable to address questions
about standards of care of other professionals or
render opinions that require training and exper-
tise outside their own (e.g., medicine, neurophysi-
ology, neurochemistry). Their role is to review
medical records to obtain information about the
child’s neurological, developmental, family, and
educational history of potential relevance to any
current problems in cognition, learning, or behav-
ior. They then assess the child and interpret find-
ings in light of this information.
A unique feature of forensic assessments, as
opposed to nonforensic ones, is the need for the
neuropsychologist to be able to explicitly defend
methods and conclusions and make judgments
regarding cause and prognosis based on “reason-
able certainty.” These evaluations also involve
more limited relationships with the child and
family and a willingness to subject one’s methods,
findings, and interpretations to scrutiny from
attorneys and other neuropsychologists working
with them. Familiarity with the disorder or condi-
tion for which the child has been referred, a com-
prehensive and organized approach to assessment,
circumspection in drawing conclusions, and a
willingness to communicate with attorneys and
work within the time constraints often imposed
by these cases are also important in undertaking
evidence-based forensic assessments.
The assessment procedures I employ in these
cases are in most ways identical to procedures I
follow in conducting nonforensic assessments
and follow the guidelines as set forth by the Board
of Directors, American Academy of Clinical
Neuropsychology (2007). One of the differences is
the need for families to understand that a forensic
assessment is done for purposes of litigation and
on referral from an attorney, and that this implies
that the family will not be billed for the evaluation
and will not receive direct feedback regarding
findings and recommendations or be followed for
clinical care. As in other assessments, my personal
preference is to begin by asking about current
concerns about the child. I then review the child’s
medical, developmental, educational, and family
history with the parent. I typically review medical,
therapy, and educational records prior to seeing
the child and family and thus already have infor-
mation about the child’s medical history. This
information is critical in interpreting findings and
drawing conclusions as it is more objective than
parent report and may provide information not
obtained from parent interview. However, asking
parents to review the child’s birth and other med-
ical history can sometimes provide information
that may not be included in the medical record,
such as the sequence of interventions undertaken
following neonatal hospital discharge. One of the
objectives of parent interviews and record reviews
is to obtain information about the child’s past
and current medical status and abilities. Perinatal
events are of special interest in cases of alleged
perinatal brain insult, though subsequent medical
history is relevant in evaluating the outcomes of
these events and in exploring other potential
influences on development, such as postnatal
illnesses or injuries. Additional aims are to con-
sider other factors that may contribute to neu-
robehavioral or learning problems, such as
disadvantages related to schooling or the family
environment or a family history of learning, atten-
tion, or psychiatric disorder.
My practice is to employ the same basic
approach to child assessment that I would in non-
forensic cases, including comprehensive assess-
ments of a wide range of cognitive abilities and
academic skills, a child interview, and parent
and teacher behavior checklists. To enhance the
interpretability of findings, I am careful to restrict
assessment as much as is feasible to measures
that are in reasonably common use by child neu-
ropsychologists and that have well-established
norms and reliability. When possible, I also avoid
tests that have been administered recently
and that may be susceptible to practice effects.
For example, if one intelligence test has been

administered within the previous year, preference
is given to an alternative test. Finally, I give special
consideration to issues of effort and potential
malingering. I have seldom encountered what
I would consider intentional distortion or mis-
representation of test performance by a child or
adolescent involved in a forensic evaluation.
But the possibility of malingering exists even in
young children (Henry, 2005; Lu & Boone, 2002;
Seidel, 1998). Documentation of effort is also
justified by the fact that children and adolescents
vary substantially in motivation level and that
poor effort can limit the interpretability of test
results in the absence of outright malingering.
I have found the Test of Memory Malingering
(TOMM, Constantinou & McCaffrey, 2003) useful
for this purpose. Alternative effort testing is
available for children (Courtney, Dinkins, Allen,
& Kuroski, 2003; Green & Flaro, 2003), but the
TOMM is applicable to a wide age range and
involves only picture stimuli. More comprehen-
sive evaluation of effort requires awareness of
worse-than-expected performances, unexpected
or inconsistent patterns of findings, and lack
of congruity of test results with performance of
activities of daily living, as well as monitoring
of the child’s affect, verbalizations, and attempts to
maintain motivation (Heilbronner et al., 2009).
Child testing typically entails administration
of a broad range of standardized measures of cog-
nitive and academic competencies. Cognitive
assessments include developmental or intelligence
test batteries combined with measures of language
abilities, visual-spatial and perceptual-motor
skills, memory, and attention and executive func-
tion. Tests of academic readiness skills or of read-
ing, mathematics, and other academic skills serve
a dual purpose. Results help both in evaluating the
impact of a potential perinatal brain insult on an
important area of functioning and in establishing
needs for special interventions. To illustrate, dis-
covery of disorders in reading or mathematics that
are not accompanied by the types of cognitive
deficits typically associated with these disorders
raise the possibility that poor motivation or sub-
standard instruction may be in part responsible
for the child’s poor academic performance. Con-
versely, significant cognitive impairments not
accompanied by academic problems suggest either
poor effort on the cognitive tasks or provision of
special academic assistance that has helped the
child to compensate for cognitive weaknesses.
Assessment of emotional adjustment, behavior
problems, and adaptive behavior skills is another
Perinatal Brain Injury 193
key aspect of a comprehensive neuropsychological
evaluation. Well standardized behavior rating
scales provide measures of a range of behavior
problems and are useful in determining if the
child meets criteria for a behavior disorder.
Administration of parent and teacher question-
naires and of child self-report ratings provides
multiple perspectives on the nature and severity of
behavior problems across different contexts. The
validity scales contained in several of the currently
available behavior questionnaires permit formal
assessment of response bias. Measures of adaptive
behavior skills are likewise important in determin-
ing the child’s level of functioning, or disability, in
everyday settings in areas such as communication,
self care, and socialization. Results suggestive of
problems in behavior, adjustment, or adaptive
functioning also help justify recommendations for
interventions in these areas.
Considerations in Rendering
Judgments in Forensic Cases
In formulating impressions regarding children
with alleged perinatal brain insults, the neuro-
psychologist summarizes the child’s strengths and
weaknesses and the nature of any developmental
deficits, describes factors that are likely to have
contributed to deficits, and utilizes information
from the assessment to recommend appropriate
clinical, educational, or family interventions.
What most clearly distinguishes forensic neurop-
sychological assessments of children from nonfo-
rensic evaluations is the need to render formal
judgments with regard to the cause of the child’s
impairments and the child’s future problems
and service needs. As in forensic assessments of
adults, these judgments are made with “reason-
able neuropsychological certainty” and are based
on several considerations (Arkes, 1989; Hartman,
1999; Lewin, 1998).
One consideration in rendering a judgment
about causality is the plausibility of perinatal brain
insult as a potential explanation for the child’s
impairment. Past or present abnormalities on
neuroimaging or neurological examinations help
establish brain insult as a credible cause of impair-
ment. The severity of neonatal encephalopathy is
another consideration, even when neuroimaging
is unavailable or fails to reveal abnormality.
A developmental history consistent with perinatal
injury is also relevant in evaluating the causal
basis for impairment. To illustrate, a neurological
basis for impaired attention and executive func-
tion in a school-age child with VLBW/VPTB
194 forensic neuropsychology
would be implausible in the face of evidence for
fully normal development during the first year of
life. Similarly, with the exception of the postnatal
emergence of CP in presumed perinatal ischemic
stroke and in some cases of HIE involving dela-
yed-onset extrapyramidal syndrome, children
diagnosed with HIE or perinatal strokes typically
display developmental problems early in life.
Deficits first detected during the preschool or
school-age years and preceded by normal early
postnatal development suggest that perinatal
brain insult, if it occurred at all, may have been
too minimal to yield enduring deficits.
Another consideration in evaluating causality
is the consistency of assessment findings. Parent
and teacher ratings can differ in relation to the
different demands placed on children at home
and at school and the different expectations of
parents and teachers. Nevertheless, gross discrep-
ancies between parent and teacher ratings or
between questionnaire data and descriptions of
the child contained in medical or educational
records or child observations during the assess-
ment suggest caution in interpreting findings. The
consistency of results across different measures of
child outcome is also relevant. For example,
evidence for a level of daily functioning that is
higher than expected based on assessment
findings suggests that the child did not perform
optimally in testing, whereas lower-than-expected
daily functioning raises the possibility that adverse
environmental circumstances may be interfering
with the child’s development.
A further consideration is the possibility of
other explanations for the child’s impairment.
Children from families with lower socioeconomic
status, fewer resources, and greater stress or insta-
bility are at increased risk for lower cognitive abil-
ities and more behavior problems (Bradley &
Corwyn, 2002; Burchinal, Roberts, Hooper, &
Zeisel, 2000; McLoyd, 1998). For this reason,
environmental factors need to be taken into
account in interpreting assessment findings. One
way to do so is to revise developmental expecta-
tions for children growing up under disadvan-
taged circumstances. In weighing the influence of
environmental factors, it is also important to
entertain the possibility that the child’s disability
may itself have contributed to family adversity
and to examine the child’s history of develop-
mental problems. Children whose problems are
primarily due to environmental disadvantage
may have less severe or selective deficits and his-
tories that are relatively free of the early postnatal
developmental impairments that are characteris-
tic of perinatal brain insults. Other possible
origins of impairment are suggested by medical
histories of significant illnesses or trauma and by
family histories of learning, attention, develop-
mental, or behavior disorders. Postnatal illnesses
or injuries are relevant to the extent that they could
plausibly account for any impairment identified by
the assessment. Family histories of neurodevelop-
mental or psychiatric conditions raise the possibil-
ity that the child’s impairments would have been
present even in the absence of an alleged perinatal
brain insult. The case for perinatal brain insult as a
primary cause is weakened if there is a clear family
history of developmental disorder and the child’s
deficits and developmental history conform to
that disorder, especially in the absence of evidence
for an earlier neurological or developmental
impairment linked to perinatal brain insult.
The neuropsychologist can render one of three
opinions with regard to the causation of impair-
ments identified in the assessment. The first
option is to conclude, with reasonable neuropsy-
chological certainty, that the perinatal event
alleged to have resulted in brain insult is a proxi-
mal cause of the deficits, indicating a judgment
that impairment would not have occurred had it
not been for the event. The second option is to
determine that the alleged event is not, to a rea-
sonable degree of certainty, the proximal cause of
the impairments, suggesting that the impairments
were likely caused by factors other than perinatal
event. The third option is to indicate that the
perinatal event may have contributed to the
impairments but that it is not possible with
reasonable certainty to conclude that the event
was a proximal cause.
Because opinions about prognosis and service
needs, like those regarding causation, are made
with reasonable neuropsychological certainty, the
neuropsychologist may also be called upon to
defend these judgments. While calling up one’s
own clinical experience is relevant in justifying
these opinions, reference to relevant research find-
ings is essential in formulating evidence-based
opinions. As summarized above, research on the
long-term effects of VLBW/VPTB documents
residual problems in cognition, achievement, and
behavior. Similarly, longer-term follow-up studies
of children with perinatal HIE or stroke, as well as
with other pediatric neurological conditions affect-
ing infants and young children, offers convincing
evidence that deficits persist throughout develop-
ment and into adulthood (Ballantyne et al., 2008;

Grimwood, Anderson, Anderson, Tan, & Nolan,
2000; Hack, 2005; Haupt et al., 1994; Kerns, Don,
Mateer, & Streissguth, 1997; Klapper & Birch,
1966; Klonoff, Clark, & Klonoff, 1993; Lindstrom
et al., 2006; Maneru et al., 2001; Muter, Taylor, &
Vargha-Khadem, 1997; Taylor & Alden, 1997;
Taylor et al., 2000; Taylor et al., 2004a). Exceptions
to this generalization include a tendency toward
less pronounced language impairments and devel-
opmental delays across the first few years of life in
children with VLBW/VPTB (Hack et al., 2005a;
Luoma et al., 1998) and improvements relative to
age standards in early language delays and in some
later-developing language abilities following focal
unilateral stroke (Ballantyne et al., 2008; Stiles et al.,
2009). Other research suggests that some of the
cognitive consequences of VLBW/VPTB become
more pronounced with age relative to normative
expectations, but only among children at highest
neonatal risk (Ment et al., 2003; Taylor et al., 2004b).
The possibility the deficits become more pro-
nounced with age is reasonable in view of the
increasing cognitive and social demands imposed
by higher levels of education, independent living,
and entry into the work force. However, few studies
have followed children with perinatal brain insults
longitudinally and there is little basis for projecting
overall declines in functioning relative to age
expectations in a majority of this population.
Based on developmental research and studies
of children with various types of early brain insult,
predictors of worse long-term outcomes include
educational or behavioral problems during the
school-age years, low IQ, and physical handicaps
(Cooke, 2004; Hack, 2005; Hack et al., 2005a;
Hack et al., 2005b; Haupt et al., 1994; Klapper &
Birch, 1966; Klebanov et al., 1994). One or more
of these factors has been associated with more
limited educational attainments, more behavior
problems, and lower rates of employment and
independent living during adulthood. Risks for
unemployment and lack of independence may be
greatest in children with mental retardation,
CP, or sensory disorders (Hack, 2005; Klapper
& Birch, 1966; Richardson & Koller, 1996). I am
nevertheless circumspect in rendering judgments
about long-term outcomes based on findings from
evaluations conducted in childhood, as outcomes
will depend on subsequent experiences and inter-
ventions. While limitations in independent func-
tioning during adulthood are likely for children
with severe neurodevelopmental disabilities, long-
term outcomes may be less predictable for chil-
dren with less profound or pervasive impairments.
Perinatal Brain Injury 195
On the other hand, the tendency for deficits to
persist over time suggests some ongoing impact
on functioning even for children with less perva-
sive impairments.
Few controlled studies have been conducted to
test the efficacy of rehabilitation programs, special
education services, or behavioral treatments
designed for children with perinatal brain insults
(Taylor, 2009). Recommended interventions are
thus based on clinical needs and typically include
occupational, physical, and speech-language thera-
pies, psychological counseling, and educational
programs. Other options include full-time care
facilities for children or adults with the most severe
disabilities and assisted living or group home
arrangements for adults requiring daily supervi-
sion. Each of these services can be justified by evi-
dence that the individual would be unable to
function adequately without assistance and by
research support for the effectiveness of rehabi-
litation, education, and behavioral programs for
individuals with brain injuries (Beaulieu, 2002;
Cicerone et al., 2005; Ylvisaker et al., 2001; Ylvisaker
et al., 2005; Ylvisaker et al., 2007). Based on clinical
experience with patients with neurodevelopmental
disorders and the advice of educational experts
(e.g., Goldstein, Sprafkin, Gershaw, & Klein, 1980;
Shapiro, 1996; Thompson, 1999), I typically
recommend the types of strategies outlined in
Table 7.1. Considerations in making recommenda-
tions are the correspondence of treatment strate-
gies and regimens with the individual’s present or
projected strengths and weaknesses, their consis-
tency with current standards of practice, and their
viability for the individual or family.
Communicating Findings and
Providing Expert Testimony
Discussions of the assessment findings with attor-
neys and preparation of the written report take
place after the neuropsychologist has drawn con-
clusions about the child’s strengths and weak-
nesses and made judgments about causation,
future outcomes, and treatment needs. Professio-
nal integrity and the utility of the findings for
triers of fact demand that the neuropsychologist
maintain objectivity in interpreting results and
forming opinions. Steps that the neuropsycho-
logists can take to protect against bias are to:
(1) accept referrals with the explicit understand-
ing that the evaluation will be objective and
impartial; (2) include multiple sources of
information in drawing conclusions (e.g., test
results, observations, background information,
TABLE 7.1. RECOMMENDATIONS FOR CHILDREN WITH PERINATAL BRAIN INSULTS

1. A predictable environment. Provide a predictable and consistent environment with clear and specific rules
and daily routines. Target particular behaviors for reward or correction, determine specific consequences
beforehand, and carry through on consequences as consistently as possible. Consequences should be
reasonable and appropriate (e.g., not letting the child go on to a second activity before cleaning up after the
first activity) and should not prevent the child from taking advantage of opportunities for positive interactions
with others.
2. Positive feedback. Provide frequent positive attention consisting of praise, or demonstrations of interest in how
the child is doing on an assigned task or about an area of special interest. Verbalize and then model behaviors
the child is expected to use when upset or frustrated. Avoid lecturing or threatening.
3. Structure. Structure tasks as much as possible, breaking complex assignments into simple steps and offering
guidance through each step to insure successful completion. If the child confuses multistep instructions,
present directions one step at a time, and limit the amount of new information given at one time. Set work
priorities so that the child does not become overwhelmed with too many demands at once. Allow for sufficient
practice to master the information or skill. Monitor learning to determine when supplemental instruction is
needed, and consider providing outside tutoring to reinforce classroom learning. Shorten periods of direct
instruction and intersperse these with high interest activities to aid sustained attention. Teach study and test
taking skills by incorporating these activities into the child’s daily lesson plans.
4. Engagement. Use “advanced organizers” (e.g., pre-exposure to vocabulary words in a new reading assignment,
or questions to answer in reading a textbook passage), focus on specific and explicit learning goals, and use
concrete methods and examples for tying concepts together or organizing information. Directly engage the
child in learning through active recitation, retelling, demonstrations, visual aids, and manipulatives. Provide
assistance with perceptual-motor and spatial tasks (e.g., charts, graphs, maps) through step-by-step approach,
modeling, and verbal guidance. Encourage the family to reinforce concepts at home by taking advantage
of activities of daily living. For example, teach number concepts by counting and grouping (adding and
subtracting) silverware when helping to set or clear the table or doing laundry.
5. Problem-solving. Use problem-solving approach in tackling larger projects. This approach includes
(1) identifying the goals, (2) brainstorming to consider possible plans of action and to select the best one,
(3) specifying steps to accomplish the plan, (4) getting together required materials, (5) carrying out the plan,
and (6) monitoring the product for accuracy and revising until goals reached. If original goals are not realistic,
reset goals and repeat above steps.
6. Social skills. Make rules for social interactions and communication with peers explicit and practice these skills.
To foster pragmatic language and social skills, place the child in smaller groups of children who are accepting,
who model positive social interactions, and who are responsive and patient (e.g., study buddies or project team
members).
7. Classroom routines. Have the child follow the same routine from the beginning to the end of class. For
example, at the beginning of each class have the child copy the assignment from the board or begin work
on a prearranged assignment. Consider seating the child next to a student who can help the child prepare
for classwork. Assemble a work folder that follows the child from class to class to encourage completion
of assignments during “down times” when the teacher cannot work with the child individually, or when
the regular class material may be inappropriate for the child. Also follow a set routine in doing homework.
Structure and anticipatory guidance may be especially important in transitioning to new settings or procedures
and in peer social interactions.
8. Appropriate goals. Assess the appropriateness of the level of work to be completed and the child’s
understanding of the assignment. Expectations should be within the child’s capabilities. Allow extra time to
complete assignments or for more direct engagement with materials. Encourage self correction of errors on
homework and tests. Go over these expectations with the child and provide cues regarding differing classroom
demands (e.g., log book of rules and assignments, list of rules posted to desk). Explain to the child how to ask
for help, when it is allowed to leave the room and for what reasons, what to do when there are interruptions in
the classroom, and when talking is permitted. Allow the child extra time to respond to requests or directions
and, whenever possible, help the child prepare ahead for question sessions or discussions.

196
 Perinatal Brain Injury 197

TABLE 7.1. Continued

9. Test modifications. Modify classroom tests by: (1) arranging for individual review of test materials prior to test,
(2) telling the child how many answers will be true and how many answers will be false in a true/false test,
(3) reducing the number of foils in multiple-choice tests, (4) prearranging before the test, but unannounced to
the rest of the class, to have the child only attempt every other problem with double credit for each problem, or
(5) allowing the child to use class notes along with a study guide or any other essential aids (e.g., dictionary).
10. Support services. Make use of available resources to treat identified developmental, learning, and behavior
disorders, including special education, rehabilitation therapies (occupation, physical, speech-language),
accommodation plans, medical management as appropriate for the child’s condition, and counseling services.
11. Monitoring of progress and needs. Periodically reevaluate progress and school performance as the child
advances through the grades so that interventions can be adjusted as needs change. Assist in developing
learning skills, independence, and interests. Work toward higher educational and vocational attainments of
persons with special needs by suggesting enrollment in colleges or universities that have programs to meet
these needs or by recommending involvement in vocational rehabilitation programs. Re-evaluate levels of
functioning in young adulthood to determine capabilities for independent living and to arrange for appropriate
rehabilitation and support services. Some individuals may not need ongoing support or may require only
periodic counseling to assist in decision-making, coping with interpersonal problems, or management of
finances, while others may have to remain in the care of their family or be placed in group homes or assisted
living settings.

interviews, ratings); (3) consider multiple factors
that may affect test findings and alternative expla-
nations for the results; and (4) render only those
opinions that can be defended based on the facts
of the case and relevant research literature (Borum,
Otto, & Golding, 1993; Meyer et al., 2001; Sweet,
1999). The utility of written reports is enhanced
by statements explaining the basis for the opin-
ions offered and by inclusion of relevant historical
information. In appearing at depositions and in
court to present and defend assessment methods
and findings, it is useful to be well acquainted
with the details of the case and to discuss the logic
of assessment and the basis of test interpretations
and other judgments in layman’s terms. The neu-
ropsychologist is also well advised to ask for rep-
etition and clarification to insure full understanding
of questions posed, resist making unsupported
speculations, qualify responses to avoid overgen-
eralizations, and confine testimony to one’s area of
competence (Adams & Rankin, 1996; Barsky &
Gould, 2002; Greiffenstein & Kaufmann, present
volume; Guilmette & Giuliano, 1991; Hess, 1999;
Larrabee, 2005).
Challenges in Conducting Forensic
Assessments of Children with
Perinatal Conditions
A child with a perinatal condition is typically
referred for neuropsychological assessment
after suit has been brought against medical
professionals or hospitals for care alleged to have
caused the condition. These suits may also claim
that improper acute medical management led to a
worsening of the condition and more adverse
outcomes. In my experience, the most common
claim is that the perinatal condition would
not have occurred had pregnancy, fetal, or labor
status been properly monitored and actions
been taken to prevent its occurrence. Examples
of such actions include earlier treatments to
prevent or forestall preterm birth or, more
commonly, efforts to deliver full-term children
sooner or via a cesarean section rather than vagi-
nally. Another type of claim is that skull fractures
or intracranial hemorrhages occurring at the time
of delivery were caused by delivery procedures,
such as inappropriate or improper use of forceps
or vacuum extraction. Medical malpractice suits
involving a child with a perinatal condition fur-
ther allege that the condition resulted in brain
damage and that this damage is the primary
reason for the child’s subsequent cognitive, learn-
ing, or behavior problems. My experience sug-
gests that personal injury claims are rarely made
in cases of preterm birth, perhaps because most
of these births are spontaneous, induced deliver-
ies are performed out of medical necessity, and
care is typically provided in neonatal intensive
care units. Neuropsychological assessments are
most often requested in cases involving HIE or
stroke in full-term or near-term infants and entail
198 forensic neuropsychology
alleged intrapartum mismanagement of labor and
delivery.
Offering evidence-based opinion in these
cases places several demands on the neuropsy-
chologist. One of these demands is to be aware of
evidence for and against the claim that the perina-
tal condition was related to an intrapartum event.
The neuropsychologist is not qualified to assess
standards of care or make medical judgments.
However, knowledge with regard to both intra-
partum and prepartum risk factors may be useful
in reviewing the medical record and in under-
standing the basis of a suit. If the medical record
suggests that prepartum risks were present
(e.g., pregnancy complications, thrombocytope-
nia), the neuropsychologist may be able to form
an opinion as to whether HIE or stroke was the
cause of a neuropsychological impairment, but
may wish to avoid reference to intrapartum events
as the ultimate source of HIE or stroke. In these
instances, opinion with regard to the causal mech-
anism responsible for HIE or stroke may be best
to deferred to the appropriate medical specialist.
It is also important that the neuropsychologist
critically review evidence for the presence and
severity of perinatal complications and search
for information in the medical record that may
help predict developmental outcomes. Although
neuropsychologists rely on medical experts for
their opinions in this regard, definitions of HIE
and asphyxia may vary across practitioners.
Knowledge of the broader professional literature
and standard definitions of this condition helps
to maintain an evidence-based orientation. Depe-
nding on their backgrounds and areas of speci-
alization, medical experts also vary in their
knowledge of the factors that predict worse out-
comes in children with the perinatal conditions
discussed in this chapter. Awareness of medical
risk factors, such as the degree of low birth weight/
preterm birth and accompanying medical prob-
lems, the presence and severity of seizures and
neurological disturbance, and abnormalities on
neonatal ultrasounds or postnatal neuroimaging,
is useful in making and defending judgments
about causation and prognosis.
A further challenge is to consider the possibil-
ity of alternative explanations for children’s
impairments. While no uniform or “signature”
deficits are associated with perinatal brain insults,
impairment in children with VLBW/VPTB is
more likely on tests of perceptual-motor skill,
memory, and executive function than on tests of
more “crystallized” abilities such as naming
vocabulary or word knowledge. Problems in
mathematics are also common. Questions about
etiology would thus be raised if a school-age child
presented with a specific language-based learning
disability with intact nonverbal and mathematics
skills. As evident from the above review, less is
known about cognitive profiles associated with
HIE, although problems have been identified in
both language and nonverbal skills. The existing
literature suggests more age-dependent and subtle
cognitive deficits in children with focal unilateral
strokes. A related issue is the extent to which the
severity of a perinatal brain insult corresponds
with the severity of the child’s impairment.
A child with less extreme VLBW/VPTB who did
not have significant neonatal complications is
not likely to be diagnosed with moderate to
severe mental retardation, while global develop-
mental deficits are common in survivors with
PHI (Sherlock et al., 2005). Likewise, global
mental deficiency would be more consistent with
severe HIE or large bilateral strokes than with
moderate HIE or unilateral strokes.
Additional challenges relate to the young age
at which children with perinatal conditions are
often referred and the significant numbers of these
children with neurological disorders. Tests appro-
priate for infants and young children (birth
through the preschool years) provide useful mea-
sures of cognitive skills and allow for some dif-
ferentiation of abilities. Measures of early motor
skills, language, adaptive functioning, and behav-
ior problems shed further light on early develop-
mental progress across multiple domains.
However, owing to the early stage of the child’s
development and to difficulties in testing young
children, these assessments may provide limited
information about learning and memory, execu-
tive functions, and higher-order reasoning. Except
in cases of more severe neurodevelopmental dis-
ability, the eventual effects of brain insult on child
behavior, socialization, and academic competence
may also be difficult to gauge from these evalua-
tions. Although assessments of early development
are useful in determining needs for interventions,
more definitive judgments with respect to the
effects of a perinatal brain insult on development
may need to be deferred until the child is older
(Baron, 2008).
Determining the nature and extent of impair-
ment can also be problematic in children who
have epilepsy, CP, or a sensory disorder. In these
cases, the consequences of perinatal brain insult
on test performance or behavior are confounded

by problems that the child has in manipulating or
seeing test materials, hearing instructions, or
speaking intelligibly; or by active seizure activity
or side effects of anticonvulsant medications on
alertness or cognition. Tests that reduce depen-
dence on motor skills or speech may be useful in
assessing children with CP or sensory disorders.
Examples include forced-choice tests of memory,
spatial skills, or problem solving that minimize
demands on manipulative or oral-motor skills.
Efforts to become familiar with a child’s speech
patterns and testing limits by allowing extra time
for motor or oral responses can also be helpful in
discerning the nature of the child’s abilities.
Testing of children with poorly controlled seizures
may need to be put off until seizures are under
better control or spread across multiple sessions
to allow for assessment during seizure-free
periods. The potential effects of anticonvulsant
medications on test performance and behavior
also need to be taken into account in interpreting
assessment findings.
CONCLUSIONS
Survey of the existing literature reveals a good
deal of information that is relevant in conducting
neuropsychological assessments of children with
perinatal brain insults, whether for forensic or
nonforensic purposes. One conclusion from this
review is that the conditions that lead to most of
these insults—VLBW/VPTB, HIE, and stroke—
cannot be considered unitary disorders with
singular causes and outcomes. Each condition is
highly variable with respect to severity and acute
complications, precipitating factors, and deve-
lopmental outcomes. For example, while some
children with VLBW/VPTB fail to exhibit demon-
strable developmental problems, other children
have selective neuropsychological, academic, or
behavior problems despite normal IQ, and still
others have severe and pervasive impairments.
Children with HIE and stroke also have variable
outcomes ranging from normal development to
selective neurobehavioral problems and more
profound neurodevelopmental disorders.
A second conclusion is that outcomes are
shaped in part by perinatal disease factors that are
unique to each condition. For children with
VLBW/VPTB, these factors include the degree of
prematurity, brain abnormalities evident in the
perinatal period or later in development, and
neonatal medical complications, such as necrotiz-
ing enterocolitis and chronic lung disease.
Brain insults in infants with VLBW/VPTB occur
Perinatal Brain Injury 199
primarily in white matter and in subcortical and
periventricular structures but vary with the degree
of neonatal risk (Inder et al., 2005; Kesler et al.,
2004; Volpe, 2008, 2009). The sequelae of HIE
differ according to the severity of neonatal ence-
phalopathy and the pattern of associated brain
lesions, with generally worse outcomes for chil-
dren with the basal ganglia/thalamus pattern of
selective neuronal necrosis than for those with
watershed-type lesions. Strokes may result in
more focal damage and less developmental
impairment than either VLBW/VPTB or HIE, but
poorer outcomes are found in children with larger
or bilateral lesions, neonatal encephalopathy, CP,
and seizures. The three perinatal conditions also
have distinct neuromotor sequelae. CP in children
with VLBW/VPTB is more likely to involve the
lower limbs than the upper limbs, while children
with HIE may manifest dyskinetic CP and
hemiplegia is more characteristic of children with
perinatal stroke.
A third conclusion is that the developmental
consequences of perinatal brain insults differ from
the effects of lesions sustained at later ages and
from common heritable conditions, such as learn-
ing disabilities, speech-language impairment, and
ADHD. A recent comparison by Anderson et al.
(2009) of children with brain damage originating
at different stages of development revealed poorer
cognitive outcomes in children with congenital
and perinatal insults than in those with later-
occurring lesions. Their results are consistent with
other findings indicating more adverse develop-
mental consequences of perinatal or early postna-
tal injuries (Max et al., 2004; Pavlovic et al., 2006).
At the same time, the research reviewed in this
chapter suggests considerable potential for plastic-
ity of function and neural reorganization following
perinatal brain insults. Studies of focal perinatal
stroke suggest that early-appearing deficits in lan-
guage and visual-spatial abilities can even resolve
over time, albeit with subtle residual deficits
(Akshoomoff, Feroleto, Doyle, & Stiles, 2002; Stiles
et al., 2009). A limited form of neural plasticity is
also implied by findings indicating that, despite
persisting deficits, children with VLBW/VPTB
acquire many skills at rates similar to those of their
term-born peers (Taylor et al., 2004b).
In contrast to heritable disabilities, perinatal
brain insults are frequently associated with early
postnatal neurological or developmental deficits.
Other distinctions are specific to the type of
perinatal insult. Children with focal perinatal
stroke have less extensive language impairments
200 forensic neuropsychology
and exhibit a different course of language devel-
opment than children with specific language
impairment (Reilly & Wulfeck, 2004). Children
with VLBW/VPTB are more prone to generalized
impairments in academic skills and pronounced
problems in mathematics than children with con-
genital (nonacquired) forms of learning disabili-
ties; and ADHD in this population may be
characterized more by inattentiveness than by
hyperactivity (Litt et al., 2005; Taylor, Espy, &
Anderson, 2009; Taylor, 2009; Taylor, in press).
The learning and behavior problems associated
with HIE have not been well specified but include
deficits in executive function and new learning.
Discovery of prominent problems in these areas
may thus be useful in distinguishing the develop-
mental “footprint” of these conditions from pat-
terns of impairment that are more typical of
children with heritable disabilities.
Further research is needed to enhance the
value of neuropsychological assessments of chil-
dren with perinatal brain insults. One important
research direction will be to follow children with
these insults from an early age using measures
that can evaluate specific cognitive abilities.
Evaluations of outcomes have often been limited
to neurological diagnoses or global measures of
development, especially in assessing the effects of
HIE (de Haan et al., 2006). As demonstrated by
the extensive research literature on neuropsycho-
logical outcomes of VLBW/VPTB, measures of
more subtle or selective deficits in language, per-
ceptual-motor and spatial skills, memory, and
executive function are fundamental to compre-
hensive assessment of the sequelae of perinatal
brain insults (Aylward, 2002). These measures
also provide more precise endpoints for assessing
the effects of variations in disease severity, perina-
tal complications, and findings from brain imag-
ing. Research involving longer-term follow-up
and comprehensive neuropsychological testing
may uncover previously undetected consequences.
To illustrate, this approach may reveal subtle
effects of mild HIE or of symptoms of asphyxia
even when not accompanied by neonatal enceph-
alopathy. More objective and uniformly applied
measures of asphyxia, encephalopathy, and stroke
will further advance research on risks for poor
outcomes of HIE (Ferriero, 2004; Raju et al., 2007;
Rolland & Hill, 1995). Forensic evaluations of
children with HIE will also be better informed by
research on the specific contributions of intrapar-
tum events to HIE and by studies of outcomes fol-
lowing different types of intracranial hemorrhage.
Few studies, for example, have examined develop-
mental outcomes in children with uncomplicated
forms of extraparenchymal hemorrhage. Finally,
to better appraise the “real life” consequences of
perinatal brain injury we need to know more
about effects of perinatal brain insults on chil-
dren’s behavior and learning, to examine how
these effects change with advancing age, and to
evaluate adult outcomes. A related need is to iden-
tify environmental and genetic factors that buffer
or exacerbate injury consequences, examine
favorable outcomes in high risk children to
explore compensatory processes, and test treat-
ments to promote children’s development
(Aylward, 2005; de Haan et al., 2006; Luciana,
2003; Taylor, 2009). Neural reorganization is pos-
sible but may be optimized by early and continu-
ing efforts to foster new learning (Nelson, 2000).
The utility of neuropsychological assessment
stems from the sensitivity of tests of specific cog-
nitive abilities to different types of insult and the
potential of these tests to further knowledge of
brain-behavior relationships. Results from these
evaluations are also useful in determining
the cognitive basis of behavior and learning prob-
lems and in recommending interventions. An
evidence-based approach requires that findings
be interpreted in light of existing research on test
validity, disease manifestations, and predictors of
outcome, as well as an appreciation of the multiple
influences on children’s development.
AC K N OW L E D G M E N T S
Past studies by our research team sited in the
chapter were funded by NIH grants HD39756,
HD26554, and HD34177. The author is indebted
to Maureen Hack, M.B.Ch.B. for her collaboration
and leadership in the area of neonatal follow-up.
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 8
Forensic Aspects of Pediatric Traumatic
Brain Injury
J AC O B U S D O N D E R S
Traumatic brain injury (TBI) is an acquired
condition where the head is subjected to acute
external mechanical forces that cause at least tem-
porary alteration in the physiological functioning
of the brain. This is a significant public health
problem because about 30% of all childhood
injury deaths result from TBI and there is consid-
erable neurobehavioral morbidity in the survivors
of pediatric TBI. The purpose of this chapter is to
provide an update of the most recent neurobehav-
ioral research and evidence-based practice guide-
lines regarding TBI in children and adolescents,
with a specific focus on legal and forensic aspects.
EPIDEMIOLOGY
Incidence statistics vary considerably across
studies because of differences in definition and
inclusion criteria. In a comprehensive review,
Kraus (1995) estimated an average incidence of
180 per 100,000 children per year, but a recent
prospective birth cohort study that also included
nonhospitalized cases yielded considerably higher
estimates, ranging from 1,100 to 1,850 per 100,000
across the 0–15-year age span (McKinlay et al.,
2008). It should be realized that, in the latter
investigation, about 90% of the injuries were fairly
mild in nature and that only 30% warranted
hospital admission. In the US, rates of hospitaliza-
tion for TBI range from 80 per 100,000 in toddlers
to 129 per 100,000 in older adolescents, whereas
death rates range from 6 to 24 per 100,000, respec-
tively (Keenan & Bratton, 2006).
Rates of TBI are about 1.3 to 2.0 times greater
for boys than those for girls (Rivara, 1994),
and there are indications for higher death and
hospitalization rates among African-American
compared to Caucasian children (Langlois,
Rutland-Brown, & Thomas, 2005). Falls are a
common cause in young children but with
increasing age, motor vehicle accidents account
for the majority of the more severe injuries
(DiScala, Osberg, Gans, Chin, & Grant, 1991).
It must be appreciated that many cases of
childhood TBI are preventable. For example,
alcohol abuse and perception of injury risk by
parents are much more meaningful predictors
of accidental injury in children than a develop-
mental personality characteristic of being “acci-
dent-prone” (Rivara, 1995). Furthermore, the
presence of pre-injury risk-taking behaviors
is not necessarily associated with risk for greater
severity of TBI (Olsson, Le Brocque, Kenardy,
Anderson, & Spence, 2008). Unfortunately, avail-
able protective measures such as infant car seats,
belt restraints, and bicycle helmets are not always
used consistently or most effectively (for a review,
see Gregg & Appleton, 2006). Improvements are
still needed with regard to the ability of health
care professionals to recognize risks of serious
child abuse TBI before it takes place (Hicks &
Gaughan, 1995; Miller, 1999). There is also evi-
dence that a very brief hospital-based education
program, aimed at parents and provided at the
time of all infants’ births, can be effective in reduc-
ing the incidence of child abuse-related TBI (Dias,
Smith, DeGuehery, Mazur, & Shaffer, 2005).
I N J U RY S E V E R I T Y
The vast majority of cases of pediatric TBI can
likely be considered “mild” in nature in the sense
that they are not associated with prolonged coma
or intracranial lesions on neuroimaging. However,
most of the classifications of severity of TBI were
initially developed for use with adults, so caution
is necessary when applying them to children. For
example, estimates of posttraumatic amnesia may
be difficult to obtain with young children who
have limited verbal skills, and such estimates are
212 forensic neuropsychology
notoriously unreliable when they are obtained
retrospectively. The Glasgow Coma Scale (GCS,
Teasdale & Jennett, 1974) is an ordinal rating scale
that classifies TBI as mild (scores 13–15), moder-
ate (9–12), or severe (3–8). However, reliability of
this scale may be compromised when children are
sedated or when they have compromise of other
parts of the body such as intubation or spinal cord
injury. Furthermore, it is customary to classify an
injury as “complicated mild” when the GCS com-
posite score exceeds 12 but is accompanied by an
intracranial lesion on neuroimaging (Williams,
Levin, & Eisenberg, 1990). In addition, focal neu-
rological signs such as pupil reflex abnormalities
may also signify more serious injury (Capruso &
Levin, 1992; Prasad, Ewing-Cobbs, Swank, &
Kramer, 2002). For all of these reasons, exclusive
reliance on the total score of the GCS is not
advised with pediatric TBI. However, the time to
which children follow verbal commands (equiva-
lent to a score of 6 on the Motor subscale on the
GCS) appears to be a fairly reliable and commonly
used indicator of length of coma, with the latter
being negatively correlated with neurobehavioral
outcomes (Massagli, Michaud, & Rivara, 1996).
Posttraumatic epilepsy, defined as repeated sei-
zures that persist for more than 1 week post injury,
can also occur in about 10–20% of (especially
young) children with severe TBI, and is also asso-
ciated with worse outcomes (Statler, 2006).
CT scan is still the most appropriate technique
to evaluate acute lesions on the day of impact but
some chronic neurodegenerative changes may not
become fully stable until evaluated with MRI
months or years later (Adelson et al., 2003). There
have been considerable developments in recent
years in the area of more advanced MRI tech-
niques, including diffusion weighted and diffu-
sion tensor imaging with associated fractional
anisotropy and tractography, that show consider-
able promise in the evaluation of children with
TBI (Ashwal, Holshouser, & Tong, 2006; Ewing-
Cobbs et al., 2008; Galloway, Tong, Ashwal,
Oyoyo, & Obenaus, 2008; Hanten et al., 2008,
Wozniak et al., 2007).
PAT H O P H Y S I O L O G Y
The mechanisms by which TBI causes brain
impairment are multifactorial, and involve both
primary and secondary injuries (for a review, see:
Bauer & Fritz, 2004). Most often, there is an accel-
erating or decelerating force to the skull that can
cause primary disruption of the underlying brain
matter at the time of trauma. These forces include
linear displacement that causes focal lesions such
as cortical contusions and subdural hemorrhage,
and intracranial rotation that may result in diffuse
lesions such as axonal shearing.
Focal involvement of the prefrontal areas
tends to be associated with an increased risk for
long-term neurobehavioral sequelae of TBI
(Levin, Zhang et al., 2004; Max et al., 2006)
although an increasing number of studies have
suggested that it may be more the total number
and volume rather than the location of the cere-
bral lesions that is predictive of such outcome
(Power, Catroppa, Coleman, Ditchfield, &
Anderson, 2007; Salorio et al., 2005; Slomine
et al., 2002). In addition, diffuse white matter
involvement and thinning of the corpus callosum,
as well as reduction of the cortical gray mantle,
have been associated with detrimental neurobe-
havioral effects (Catroppa, Anderson, Ditchfield,
& Coleman, 2008; Fearing et al., 2008; Merkley
et al., 2008; Serra-Grabulosa et al., 2005; Verger
et al., 2001). Recent research has also highlighted
the vulnerability of subcortical structures such as
the hippocampus and cerebellum (Braga, Souza,
Najjar, & Dellatolas, 2007; Wilde et al., 2007).
Secondary injuries are those that arise indi-
rectly from trauma, and may continue to develop
for several days after injury. In children, they are
most often the result of disrupted cerebral circula-
tion and an associated cascade of neurochemical
events, leading to hypoxic-ischemic injury, diffuse
edema, and neuronal excitotoxicity. There is grow-
ing evidence that prevention of such secondary
insults, aimed at adequate management of cere-
bral homeostasis through limiting intracranial
hypertension and optimizing cerebral perfusion
pressure, is critical with regard to survival after
pediatric TBI (Adelson et al., 2003, Kochanek,
2005; Udomphorn, Armstead, & Vavilala, 2008).
There is some controversy about the potential
benefit of other specific acute care interventions,
such as hypothermia (Giza, Mink, & Madikians,
2007; Hutchison et al., 2008). There are promising
developments in the area of utilization of serum
biomarkers in the prediction of outcome of pedi-
atric TBI, but much of this research is in the early
stages and will require further replication (Berger,
2006; Berger, Beers, Richichi, Wiesman, &
Adelson, 2007). In addition, there is some recent
research identifying the presence of the apolipo-
protein E epsilon 4 genotype as being associated
with an increased risk for unfavorable outcomes
after pediatric TBI (Brichtová & Kozák, 2008), but
this has not yet seen extensive replication.
 Forensic Aspects of Pediatric Traumatic Brain Injury
COMMON
N E U R O B E H AV I O R A L
SEQUELAE
There is a growing consensus that the vast
majority of children who sustain uncomplicated
mild TBI have an essentially unremarkable long-
term recovery, especially when compared to chil-
dren with orthopedic injuries, even though they
may be symptomatic within the first few weeks to
months after injury (for reviews, see: Carroll et al.,
2004; Kirkwood et al., 2008; Satz et al., 1997).
Persistent symptomatology may be more common
in those children with uncomplicated mild TBI
who have premorbid complications such as spe-
cial education histories or family dysfunction
(Ponsford et al., 1999). However, these symptoms
do not appear to be specific in any way to the
experience of a concussion (Nacajauskaite,
Endziniene, Jureniene, & Schrader, 2006). The
inclusion of a control group with orthopedic inju-
ries has proven to be of crucial importance in
evaluating the sequelae of mild TBI. Otherwise,
such children may appear to have neurobehav-
ioral impairments when compared to healthy
children, whereas they tend to be indistinguish-
able from children with injuries that were
restricted to other parts of the body (Bijur &
Haslum, 1995; Bijur, Haslum, & Golding, 1996).
It has been well established that more severe
forms of pediatric TBI (i.e., when there are objec-
tive intracranial lesions on neuroimaging and/or
prolonged coma) are associated with an increased
likelihood of persistent neurobehavioral sequelae
(for detailed reviews, see Donders, 2007, 2008). It
is also abundantly clear that there is no such thing
as a unitary profile of cognitive and psychosocial
strengths and weaknesses after pediatric TBI. In
fact, various distinct subtypes of recovery have
been identified in both domains, and have been
related to injury severity characteristics (Butler,
Rourke, Fuerst, & Fisk, 1997; Campbell, Kuehn,
Richards, Ventureyra, & Hutchison, 2004;
Donders & Warschausky, 1997; Mottram &
Donders, 2006). With those reservations in mind,
a few general trends can be identified.
Taylor and Yeates and their colleagues (Taylor
et al., 2002; Yeates et al., 2002a, 2004) have com-
pleted a series of studies of children with pediatric
TBI that included baseline measures of premor-
bid status as well as a control group with orthope-
dic injuries. Moreover, the children received
comprehensive, multimodal follow-up for several
years and the authors employed multivariate
statistical procedures to consider the additive and
213
interactive effects of multiple potential predictor
variables. Results from these studies indicated
that children with severe TBI continue to demon-
strate considerable behavioral adjustment diffi-
culties as well as cognitive deficits for several years
after injury; the latter most notably in speed of
information processing and delayed recall of new
information. Those cognitive skills have been
identified in various independent studies as
vulnerable to severe pediatric TBI (Calhoun &
Dickerson-Mayes, 2005; Hanten et al., 2004;
Prigatano, Gray, & Gale, 2008; Van Heugten et al.,
2006). Other comprehensive investigations have
also identified deficits in complex attention as well
as various aspects of executive functioning, such
as working memory, prospective memory, and
novel problem solving, as fairly common after
severe pediatric TBI (Catroppa, Anderson, Morse,
Haritou, & Rosenfeld, 2007; Slomine et al., 2002;
Mandalis, Kinsella, Ong, & Anderson, 2007;
Nadebaum, Anderson, & Catroppa, 2007; Ward,
Shum, McKinlay, Baker, & Wallace, 2007).
Severe TBI is a direct risk factor for novel
psychiatric disorders in children, ranging from
affective instability to impaired social judgment
(Max, Robertson & Lansing, 2001), although
worsening of premorbid aggressive behaviors is
also possible (Cole et al., 2008). Furthermore,
children with severe TBI tend to have significant
difficulties with the pragmatic and interpretive
aspects of language and social cognition/problem
solving (Chapman et al., 2004; Dennis & Barnes,
2001; Ganesalingam, Yeates, Sanson, & Anderson,
2007; Yeates et al., 2004, 2007), all of which can
affect behavioral and interpersonal adjustment.
It is important to keep in mind that some of
the symptoms that are common after severe pedi-
atric TBI are not specific to that condition. For
example, problems with complex attention are
also commonly seen in children with attention
deficit/hyperactivity disorder (ADHD) in the
absence of any history of TBI (Barkley, 2003,
2006). There is at this time no “signature” profile
of neuropsychological or other test results that
can be used unequivocally in isolation to distin-
guish TBI from other common pediatric condi-
tions.
As much as the research has advanced in
recent years in describing the impact of pediatric
TBI, there have been relatively fewer studies that
have provided evidence-based support for specific
interventions. In order to prevent the potentially
cumulative effect of repetitive mild injuries within
a short time period, the general consensus about
214 forensic neuropsychology
sports-related concussion in children and adoles-
cents is that return to play should be based on
resolution of symptoms and that “when in doubt,
sit them out” (Kirkwood, Yeates, & Wilson, 2006;
Lovell & Fazio, 2008) but there is not yet a firm
scientific base for determining the exact duration
of suspension of sports activities in these cases.
There is modest support for the effect of stimulant
medication for the management of attention
problems in children with TBI (Bates, 2006; Jin &
Schachar, 2004), but ADHD symptoms tend to
get treated more frequently when there is a pre-
injury history of that diagnosis (Levin et al., 2007).
Despite the evidence for an increased risk for
sleep problems for several years after severe pedi-
atric TBI, there are essentially no clinical guide-
lines or efficacy data for treatment of these
problems (Beebe et al., 2007). The empirical sup-
port for specific forms of cognitive and behavioral
rehabilitation interventions after pediatric TBI is
mixed, with one review paper endorsing recom-
mendations for family involvement and cognitive
rehabilitation of attention and memory (Laatsch
et al., 2007) and another one concluding that there
was insufficient evidence for specific recommen-
dations for interventions for executive dysfunc-
tion (Kennedy et al., 2008).
S P E C I A L E D U C AT I O N
S E RV I C E S
In light of the significant neurobehavioral seque-
lae that have been described with severe pediatric
TBI, it is no surprise that children who incur
such injuries at an early age are at risk for under-
developed school readiness skills (Taylor et al.,
2008). Furthermore, considerable proportions
of these children need special education services
for extended periods of time (Clark, Russman,
& Orme, 1999; Ewing-Cobbs, Fletcher, Levin,
Iovino, & Miner, 1998; Kinsella et al. 1997).
Neuropsychological assessment can be helpful in
identifying children who need such services.
Miller and Donders (2003) demonstrated that
scores on the California Verbal Learning Test—
Children’s Version (CVLT–C; Delis, Kramer,
Kaplan, & Ober, 1994), obtained at an average of
three months after injury, were more accurate in
the prediction of special education placement two
years later than a host of demographic (age,
gender, parental occupational status) and injury
(length of coma and lesions on neuroimaging)
variables. This reinforces the criterion validity and
incremental value of neuropsychological assess-
ment in children with TBI.
Longitudinal research has also demonstrated
that a considerable minority of children with
residual neurobehavioral sequelae of TBI who
could profit from special education support are
not receiving adequate services (Taylor et al.,
2003). Thus, even when neuropsychological
assessment is helpful in establishing risks and
characterizing the problems that contribute to
academic difficulties in children with TBI, this
does not automatically guarantee efficient or ade-
quate service delivery. For this reason, knowledge
of federal and state guidelines regarding eligibility
for special education services is important.
Under U.S. public law enacted as part of the
Individuals with Disabilities Education Act, TBI
was defined as a separate category of special educa-
tion in 1991, which was reauthorized as the
Individuals with Disabilities Education Improve-
ment Act in 2004. The following definition of TBI
was included in this federal legislation:
Traumatic brain injury means an acquired
injury to the brain caused by an external physi-
cal force, resulting in total or partial functional
disability or psychosocial impairment, or both,
that adversely affects a child’s educational per-
formance. The term applies to open or closed
head injuries resulting in impairments in one
or more areas, such as cognition; language;
memory; attention; reasoning; abstract think-
ing; judgment; problem solving; sensory, per-
ceptual, and motor abilities; psychosocial
behavior; physical functions; information pro-
cessing; and speech. The term does not apply to
brain injuries that are congenital or degenera-
tive or brain injuries induced by birth.
It is important to realize that states differ
widely in their level of embracement or expansion
of this federal definition. States cannot use a defi-
nition of TBI that is more restrictive than the fed-
eral one, but they are at liberty to adopt a more
inclusive definition. For example, some states have
added provisions to include children under the
definition of TBI who acquired their brain injury
as the result of vascular (e.g., stroke) or hypoxic
(e.g., near-drowning) conditions (Katsiyannis &
Conderman, 1994). Therefore, it is crucial that
both families and providers be aware of their local
state laws in this regard. This kind of information
can typically be obtained from the state’s
Department of Education.
Regardless of the state or local jurisdiction,
there are federal guidelines and requirements
 Forensic Aspects of Pediatric Traumatic Brain Injury
under the Individuals with Disabilities Education
Improvement Act with regard to the special educa-
tion process (for detailed reviews, see Hibbard,
Martin, Cantor, & Moran, 2006; Madigan, Hall, &
Glang, 1997). These principles govern that any
student with TBI should be able to receive a free
and appropriate public education, based on a non-
discriminatory evaluation, and that this education
take place in the environment that is the least
restrictive for the child. Parents should be active
participants in this process and there should be a
set of procedures regarding accountability, gener-
ally known as due process. It is important to under-
stand that simply providing a diagnosis of TBI
does not automatically qualify the child for special
education services, and that there are often differ-
ences between what may be medically desirable
and what can is truly educationally necessary.
In order to be considered for any kind of spe-
cial education placement, the child must be
referred to the school system’s special education
services committee. For many children with TBI
who receive hospital-based rehabilitation services,
such a referral can often be made (with parental
consent) by treating professionals. In other
instances, the parents may need to request an
evaluation or meeting on their own. Schools
cannot ignore such a request and must provide a
meaningful response.
The most appropriate services for a child with
TBI will be determined by an Individualized
Educational Planning Committee (IEPC), which
should include an individual with some special-
ized training in the area of the suspected disability
(i.e., sequelae of TBI). Parents have the right to be
members of this team and they are also allowed to
have assistance in this regard. For example, many
states have “parent advocacy” programs.
The IEPC should result in a statement regard-
ing eligibility for services, specific goals, a delinea-
tion of the accommodations and adaptations for
the child, as well as a recommendation for specific
placement. If parents do not agree with the deci-
sion of the IEPC, they have the right to request an
arbitration or mediation hearing. State laws differ
widely on timeframes in this regard. However, the
mediation process cannot be used to deny or
delay a due process hearing, and the results of the
mediation are not binding (Lorber & Yurk, 1999).
A due process hearing is administered by an
impartial hearing officer of the court, and pediat-
ric neuropsychologists may be called upon as
expert witnesses in this context. Rulings from due
process hearings are binding to all parties involved.
215
It is important to realize that if parents do not agree
with the IEPC findings and do not want to go
through mediation, they have the right to argue
their case directly through the courts, and they can
seek a second opinion from an independent
expert. However, they are required to pay for all
the associated legal and professional fees privately.
Especially with children with TBI, who tend to
change in their performance and needs over time,
IEPC plans may need to be reviewed more fre-
quently than the yearly (or sometimes once every
three years) customary standard. More detailed
reviews about special education procedures that
have been written in language that is intelligible to
parents include Schoenbrodt (2001) and Semrud-
Clikeman (2001).
A final important thing to consider for neu-
ropsychologists in interaction with the education
system is that school professionals are typically
working under rules regarding privacy of infor-
mation that are different from those that apply in
health care. Although neuropsychologists are
used to medical records that are governed by the
Health Insurance Portability and Accountability
Act, educational records fall instead under the
relatively less restrictive Family Educational
Rights and Privacy Act. Ernst, Pelletier, and
Simpson (2008) provide a helpful discussion of
administrative, legislative, and practical aspects of
providing neuropsychological consultation to
schools.
M O D E R AT I N G A N D
M E D I AT I N G VA R I A B L E S
There is no doubt that the likelihood of long-
term neurobehavioral sequelae of pediatric TBI
increases with greater injury severity. However,
even among children with severe TBI, outcomes
tend to vary considerably. There are several demo-
graphic variables that may play a moderating or
mediating role in this regard (see Holmbeck, 2002
for a general review of moderating and mediating
effects). A moderator is a variable that specifies
the circumstances under which a condition results
in a particular outcome. In this case, the nature of
the relationship between severity of TBI and neu-
robehavioral outcome may vary as a function of
one or more characteristics of the child and family,
such as demographic background or premorbid
developmental history. A mediator, on the other
hand, is a variable that explains how a predictor
variable results in a particular outcome. In this
case, the effect of pediatric TBI on a specific neu-
robehavioral outcome is essentially transmitted
216 forensic neuropsychology
via another variable, such that TBI is associated
with the mediator, which in turn affects the
outcome measure.
One of the most significant moderating
influences on recovery after TBI is age. There
are three distinct but inter-related dimensions
of age that need to be considered in this
regard (Taylor & Alden, 1997): age at injury, time
since injury, and age at assessment of outcome.
Until the early 1990s, there was a common
lore that the earlier in life the TBI occurred,
the better, because of a presumed great degree
of plasticity in children’s brains. This myth has
clearly been debunked. There is strong evidence
that TBI that is acquired early in life interferes
with skills that are still in a phase of rapid devel-
opment, which puts young children at increased
risk for long-term deficits (Anderson, Catroppa,
Haritou, Morse, & Rosenfeld, 2005; Catroppa,
Anderson, Morse, Haritou, & Rosenfeld, 2008;
Ewing-Cobbs, Prasad, Landry, Kramer, & DeLeon,
2004). Longitudinal research has suggested that
children with severe TBI tend to show partial
recovery during the first year after injury but that
this recovery reaches a plateau after that time and
that there remain considerable residual neurobe-
havioral deficits at extended follow-up (Yeates
et al., 2002a). It is important to realize that this
recovery trend is typically much more apparent
for cognitive than for behavioral adjustment char-
acteristics (Taylor et al., 2002). Other researchers
have demonstrated that some neurobehavioral
deficits may not become fully manifest until the
child gets older (Anderson, Catroppa, Rosenfeld,
Haritou, & Morse, 2000; Fay et al., 1994; Levin,
Hanten et al., 2004). This may reflect an interac-
tion of delayed maturation of specific (especially
prefrontal) brain regions with an increase in the
complexity of environmental demands on the
child.
Related to the issue of age is the adult outcome
of children with TBI. Several studies have reported
poor vocational outcomes after severe pediatric
TBI (Kieslich, Marquardt, Galow, Lorenz, &
Jacobi, 2001; Nybo, Sainio, & Müller, 2004). When
such injuries are sustained early in childhood,
they are associated with worse cognitive and psy-
chosocial outcomes in early adulthood than when
sustained during adolescence (Donders &
Warschausky, 2007). However, it needs to be
understood that these are group data, and that
prediction of adult outcome in individual cases is
fraught with many uncertainties and a high risk of
misclassification.
Another moderator variable that has been
studied extensively is pre-injury family back-
ground. Taylor and colleagues (2002) found that
this tends to have a greater effect on behavioral
and psychosocial outcomes than on cognitive
outcomes, with the effects of severe TBI being
particularly detrimental in cases where there was
greater family stress and/or low socioeconomic
status. However, even with cognitive outcomes
such as calculation skills, children with severe
TBI caught up with orthopedic controls over a
12-month period only when family stressors were
low. Anderson and colleagues (2006) also sug-
gested the possibility of a “double hazard” in that
children with severe injuries from socially disad-
vantaged families are at greatest risk for poor
functional outcome at 30 months post injury.
Findings with regard to other potential
moderators of the impact of pediatric TBI have
been mixed, with some but not widely replicated
evidence for relatively greater risk for complicated
outcome with ethnic minority status (Yeates et al.,
2002b). However, these findings need to be inter-
preted in the context of the fact that attrition rates
tend to be higher among ethnic minority groups
in longitudinal studies. In addition, findings have
been somewhat inconsistent with regard to
a possible moderating effect of gender, with some
studies suggesting worse memory outcomes in
boys (Donders & Woodward, 2003) and others
identifying more frequent obsessive-compulsive
symptoms in girls (Grados et al., 2008). Thus,
the possible moderating impact of factors
other than age and psychosocial adversity remains
unresolved.
There is also increasing research with regard
to factors that mediate the effect of pediatric
TBI on neurobehavioral outcome variables. In the
cognitive domain, there is evidence that the
effect of severity of TBI on verbal learning is
mediated by speed of information processing
(Donders & Minnema, 2004; Donders & Nesbit-
Greene, 2004). Specifically, length of coma nega-
tively impacted processing speed, which was in
turn associated with worse performance on the
CVLT–C, a task where successive stimuli are pre-
sented to the child at a fairly rapid pace. Another
example of a mediator is the recent finding that
deficits in self-regulation mediated the effect of
pediatric TBI on some social and behavioral out-
comes (Ganesalingam, Sanson, Anderson, &
Yeates, 2007). Specifically, the presence of severe
TBI predicted poorer scores on measures of
behavioral inhibition, which were in turn related
 Forensic Aspects of Pediatric Traumatic Brain Injury
to worse parental ratings of assertion and worse
teacher ratings of self-control. The exploration of
mediating effects typically requires large samples
and advanced statistical analyses, but this is an
area of potential growth in the understanding of
the consequences of pediatric TBI.
FA M I LY F U N C T I O N I N G
When children sustain severe TBI, family life gets
interrupted and yet parents often need to be the
most important long-term advocates for their
children, particularly within the educational and
rehabilitation systems. As was mentioned above,
family factors account for variability in children’s
neurobehavioral outcomes, over and above that
explained by injury-related variables, and a more
adaptive pre-injury family environment may act
as a buffer regarding the impact of TBI (Anderson
et al., 2005; Schwartz et al., 2003). Examples of
more adaptive family coping include open com-
munication, lack of rigidity, equitable and efficient
role distributions, and acceptance. Chronic life
stressors and lack of interpersonal resources may
exacerbate the degree of TBI-related burden on
families (Stancin, Wade, Walz, Yeates, & Taylor,
2008). There are also indications that psychoso-
cial adversity, such as the presence of family
stressors, tends to remain more predictive of
cognitive outcomes than injury severity or lesion
location (Max et al., 2005).
Longitudinal research has confirmed that
substantial proportions of families of children
who have experienced a severe TBI continue to
report high levels of injury-related stress associ-
ated with some aspect of the child’s recovery or
the family’s reactions many years later (Wade
et al., 2002). This may actually worsen over time if
parents do not receive adequate social support
(Wade et al., 2006). Behavioral changes in the
child as the result of TBI may negatively affect
reciprocal interactions between child and parent
(Wade et al., 2008). It has also been shown that the
influences between child behavioral problems and
family adjustment are bidirectional in nature
(Taylor et al., 2001). This suggests that attempts at
intervention should target both children and par-
ents. A recent randomized clinical trial has sug-
gested that online cognitive-behavioral family
problem solving therapy can improve both paren-
tal level of distress and child behavioral outcomes
(Wade, Carey, & Wolfe, 2006a, 2006b). Although
effect sizes were somewhat small, this is an exam-
ple of empirical support for a specific clinical
intervention.
217
C O M P L I C AT I N G P R E M O R B I D
H I S TO R I E S
Most studies of pediatric TBI have excluded
children with premorbid complicating histories in
order to avoid potential confounding of results.
However, neuropsychologists are often asked
to determine whether persistent postinjury
neurobehavioral complaints or symptoms are due
to TBI or to pre-existing conditions such as
ADHD, learning disability, or both.
Several studies have documented that lower
levels of pre-injury functioning increase the risks
for less favorable outcome after severe pediatric
TBI, both for the child and the family (Anderson
et al., 2005; Rivara et al., 1996; Woodward et al.,
1999). However, such group studies do not
allow easy determination of which children with
prior complicating histories do or do not have
additional problems after severe TBI. Thus, the
presence of premorbid complicating factors is a
relative but not an absolute risk factor for poor
outcome.
Another interpretive problem is due to the
fact that some of the neurobehavioral symptoms
that children may demonstrate after TBI (e.g.,
inattention) are not specific to that condition.
Thus, one cannot assume on the basis of the pres-
ence of symptoms that are known to be common
after TBI that the associated cause must be TBI.
This kind of reverse reasoning would amount to a
logical fallacy with a high likelihood of misattri-
bution, particularly when dealing with children
with uncomplicated mild TBI, where the prepon-
derance of the studies does not suggest persistent
injury-related sequelae (Satz et al., 1997).
Although things may appear to be less compli-
cated with moderate to severe TBI, diagnostic
inferences are not a panacea with increasing
injury severity either. Specifically, it has been sug-
gested that moderate to severe TBI with subcorti-
cal involvement may result in “secondary” ADHD
(Gerring et al., 1998; Max et al., 2004; Slomine
et al., 2005). At the same time, level of pre-existing
problems with attention has been shown to
moderate post-injury attention deficits in chil-
dren with TBI (Yeates et al., 2005). For all of these
reasons, it is imperative that clinicians obtain
premorbid academic and health records on
children with TBI.
The fact that both injury severity and premor-
bid history affect outcome after pediatric TBI may
be illustrated by the findings from a consecutive
sample of 100 children with TBI (66% from
motor vehicle accidents) between the ages of
218 forensic neuropsychology

6 and 16½ years (median = 12½) who were T score. As can be seen in Table 8.1, variables
referred to a regional rehabilitation hospital. There associated with injury severity as well as variables
were no a priori exclusion criteria, other than reflecting premorbid history were statistically
that the child should have English as the primary significant predictors in this model. There were
language and not have any kind of hearing no problems with collinearity (e.g., all variance
problem. All children were evaluated with the inflation factors <1.72). The composite model
CVLT–C within 1 year after injury (median = 3 was statistically significant, F (10, 87) = 4.66,
months) as part of a more comprehensive neuro- p < 0.0001, R2 = 0.35, with longer length of
psychological evaluation. Data from two children coma explaining approximately 24% of unique
were excluded because they failed validity criteria variance and presence of a special education
on the Test of Memory Malingering (TOMM; history about 6%.
Tombaugh, 1996–see below). Characteristics of The independent contributions of injury
the remaining sample were as follows: 79% was severity and premorbid history can also be dem-
Caucasian, 60% was male, 53% had an acute onstrated by considering the respective CVLT–C
intracranial lesion on neuroimaging, 34% had T scores of the groups with (M = 41. 26, SD =
a length of coma ≥24 hrs (range = 0–47), and 11.25) and without (M = 49.33, SD = 10.88) prior
median parental education was 12 years (range = special education placement. First of all, children
8–20). Children with prior complicating histories in the former group were no more likely than chil-
were not excluded; most notably, 23% had received dren in the latter group to have coma ≥24 hrs, χ2
prior treatment for ADHD, 19% had received spe- (N = 98) = 0.05, p > 0.80. Second, in both groups,
cial education services (most often because of performance on the CVLT–C correlated strongly,
learning disability), and 19% had received some negatively with length of coma, ranging from
kind of psychopharmacological and/or psycho- –0.58 (p < 0.009) in the group with prior special
therapeutic treatment (note: categories were not education history to –0.46 (p < 0.0001) in the
mutually exclusive, as some children had multiple group without it. These findings confirm that
prior risk factors). This sample is completely inde- prior characteristics of the child as well as severity
pendent of those reported previously in Donders of injury are, largely independent of each other,
(2005) or Donders & Nesbit-Greene (2004). predictive of cognitive outcome after pediatric
The mean composite CVLT–C T score of the TBI. This is consistent with the results from other
final sample was 47.65 (SD = 11.36). Table 8.1 recent investigations pertaining to academic
presents the result from a linear multiple regres- (Catroppa & Anderson, 2007) as well as adaptive
sion analysis, considering the impact of various behavioral outcomes (Catroppa et al., 2008).
demographic and injury-related variables on this
CHILD ABUSE TBI
Child abuse TBI, also known as inflicted or
nonaccidental TBI, affects primarily children
TABLE 8.1 PREDICTORS OF CVLTC
under three years of age (Brown & Minns, 1993).
PERFORMANCE IN CHILDREN WITH In fact, 25% of all TBI and up to 90% of severe
TBI N = 98 cases of TBI in this age group are the result of
Variable SRC t p abuse (Carty & Pierce, 2002; King, MacKay, &
Sirnick, 2003). It has been suggested that the less
Prior psychiatric history –0.14 –1.24 .22 favorable neurobehavioral outcome after infant or
Prior special education 0.25 2.65 .01 preschool TBI compared to other age groups in
Prior treatment of ADHD 0.19 1.66 .10 epidemiological studies may be due at least in part
Age at assessment –0.04 –0.38 .71 to the high rate of inflicted injury in the youngest
Ethnicity 0.08 0.87 .39 children (Ewing-Cobbs, Duhaime, & Fletcher,
Gender –0.01 –0.04 .97 1995). Of these, the shaken-baby condition, in
Parental education –0.05 –0.60 .55 which the child is subjected to rapid angular
Diffuse neuroimaging lesion 0.11 1.00 .32 acceleration-deceleration forces that are often
Focal neuroimaging lesion 0.10 1.03 .31 compounded by actual impact, has the greatest
Length of coma –0.42 –3.73 .004 mortality and morbidity (Duhaime, Christian,
Moss, & Seidl, 1996). However, the extent and
Note. CVLT–C = California Verbal Learning Test—Children’s
Version. TBI = traumatic brain injury. SRC = standardized regres- implications of child abuse TBI are uncertain, for
sion coefficient. ADHD = attention-deficit/hyperactivity disorder. various reasons.
 Forensic Aspects of Pediatric Traumatic Brain Injury
First of all, it is difficult to get exact estimates
of the prevalence of the problem. Some available
statistics suggest that child abuse occurs in at least
13–15 per 1,000 children, but this may be a
gross underestimation due to inconsistencies in
definition and underreporting by perpetrators
(Ammerman & Galvin, 1998; Knutson & DeVet,
1995). A second problem is that family instability
and confidentiality restrictions make it difficult to
follow many abused children longitudinally
(Duhaime et al., 1996). Furthermore, nonabusive
experiences such as parental neglect, poverty,
and a highly stressed family environment are
common comorbid factors that can confound mea-
surement of the incremental significance of the
physical trauma (Brown, 2002). Child abuse TBI
often involves repetitive trauma, for which care is
often not sought for hours or days after injury,
leading to worse outcomes (Keenan, Runyan, &
Nocera, 2006; Makaroff & Putnam, 2003).
Despite all of these difficulties, there have been
important new developments in the field of child
abuse brain injury over the past several years.
Several studies have identified hypoxic-ischemic
injury as one of the most damaging factors affect-
ing mortality and neurobehavioral morbidity after
inflicted childhood TBI, with a possible secondary
augmenting effect of neurotoxicity due to a sharp
increase in excitatory amino acids (Geddes et al.,
2001; Ruppel et al., 2001; Stoodley, 2002). Recent
research suggests that specific serum biomarker
concentrations show a distinctly different tempo-
ral development after child abuse as compared to
accidental TBI, contributing to more prolonged
neuronal, astroglial, and axonal compromise
(Berger, Adelson, Richichi, & Kochanek, 2006).
The specific anatomical and radiological find-
ings associated with inflicted TBI in childhood
have also become clearer. It is important to realize
that children who have been physically and/or
sexually abused have been reported to have
smaller cerebellar volume, reduced mid-sagittal
callosal size, and increased lateral ventricles, com-
pared to demographically matched controls, even
in the absence of known trauma to the head (De
Bellis et al., 1999; De Bellis & Kuchibhatia, 2006).
This may be due to stress-induced hormonal
influences that adversely affect brain structure
and function (Bremmer, 2002). However, the
work by Ewing-Cobbs and her colleagues has
clarified neuroimaging and other physical find-
ings that appear to be unique to inflicted brain
injury. Most specifically, in addition to nonspe-
cific brain atrophy, the hallmarks of inflicted TBI
219
include subdural hemorrhages, seizures, and reti-
nal hemorrhages (Ewing-Cobbs, Kramer, et al.,
1998; Ewing-Cobbs et al., 2000). In a separate
recent investigation, children with inflicted TBI
were almost 7 times more likely than children with
accidental TBI to have subdural hemorrhage in
the absence of a skull fracture, and more than 9
times more likely to experience posttraumatic sei-
zures (Myhre, Grogaard, Dyb, Sandvik, & Nordhov,
2007). All these factors are associated with greater
overall injury severity, resulting poorer outcome
in motor, cognitive, and behavioral domains
(Ewing-Cobbs, Prasad, Kramer, & Landry, 1999).
Several other studies have reported that, after con-
trolling for demographic variables and severity of
injury, children with accidental TBI had better
neurobehavioral outcomes than children who sus-
tained their TBI as the result of child abuse (Beers,
Berger, & Adelson, 2007; Keenan et al., 2006).
Specific deficits in working memory, inhibition,
and other forms of executive functions have also
been reported after inflicted TBI in children, com-
pared to demographically matched controls
(Stipanicic, Nolin, Fortin, & Gobeil, 2008).
The role for the neuropsychologist in the
evaluation of child abuse TBI may be twofold.
First, whenever child abuse is suspected, medical
and health care professionals in virtually all states
are subject to mandatory reporting laws
(Kalichman, 1999). Second, a long-term develop-
mental perspective is needed regarding these
children (Finkelhor & Dziuba-Leatherman, 1994;
Miller, 1999). There is currently no evidence for a
unique neuropsychological profile that is selec-
tively associated with child abuse TBI. However,
since these children typically get injured at an
early age (when many skills are still emerging or
in a stage of rapid development) and are also more
likely to grow up in a stressful or unstable family
environment, they are at increased risk for long-
term neurobehavioral deficits. Consequently,
many of these children may need to be followed
for a considerable number of years post injury.
NEUROPSYCHOLOGICAL
E VA L UAT I O N
There is no single battery or assessment style
that is uniquely appropriate for the evaluation of
children with TBI but a few general guidelines
can be provided. First of all, a careful review of
medical and school records is important. For
example, parental retrospective estimates of their
child’s duration of coma or premorbid academic
achievement are not always accurate, and datings
220 forensic neuropsychology
of onset of psychopathological symptoms are
particularly unreliable (Angold, Erkanli, Costello,
& Rutter, 1996). Several studies have indicated
that the post-injury neuropsychological test
scores of children with learning disabilities or
psychiatric disorders and who subsequently
sustained a moderate to severe TBI were virtually
undistinguishable from those of demographically
matched children who sustained TBI of similar
severity but who did not have complicating
premorbid histories (Donders & Strom, 1997,
2000). It was only through formal comparison
with premorbid test results that a further deterio-
ration in functioning as the result of TBI could be
demonstrated in the children with pre-existing
conditions.
A careful interview and history are also essen-
tial. This should address in particular any factors
that might augment or interact with the direct
organic influence of TBI, such as pre-existing
problems or the post-injury family environment.
In addition, other stressors should be reviewed
that may have occurred at the time of injury (e.g.,
witnessing the accidental fatal injuries to a family
member) or that are unrelated but still potentially
relevant for the outcome of the child (e.g., range
of resources of the local school district). For
example, subjective anxiety may contribute to the
maintenance of nonspecific somatic, cognitive,
and behavioral symptoms after mild TBI
(Mittenberg, Wittner, & Miller, 1997).
As to specific tests, it is important to include in
the evaluation measures that tap into the abilities
most commonly affected by severe TBI. For exam-
ple, an evaluation that includes no or few tasks
with a speeded component may miss the difficul-
ties with processing speed that many of these
children have, and the associated potentially
helpful adaptations and accommodations that
could be considered in the classroom (Ylvisaker
et al., 2001). In addition, it is crucial to avoid over-
reliance on measures of academic achievement
and psychometric intelligence because those tests
rely heavily on overlearned skills that are often
relatively preserved after TBI. Rather, the evalua-
tion should incorporate reliable measures that tap
into new learning and that have established valid-
ity. A good example is the CVLT–C, a task that is
not only sensitive to severity of TBI (Levin et al.,
2000; Roman et al., 1998) but also has consider-
able predictive accuracy with regard to long-term
educational placement (Miller & Donders,
2003). In addition, this is one of the few tests
for which the multifactorial construct basis for
interpretation has been specifically validated in
children with TBI (Mottram & Donders, 2005).
Clinicians should also be cognizant of the psy-
chometric strengths and weaknesses of the instru-
ments that they use. It has been well established
that age is of considerable importance when con-
sidering neuropsychological test scores (Forster &
Leckliter, 1994). Yet, norms for a variety of com-
monly used instruments are often based on sam-
ples that are either too small or insufficiently
stratified to adequately capture these age effects
(Baron, 2004; Kizilbash, Warschausky, & Donders,
2001). In addition, clinicians should be knowledge-
able about the clinical validation of psychometric
tests for the specific populations with which they
intend to use them (American Educational
Research Association, American Psychological
Association, & National Council on Measurement
in Education, 1999). For example, the fact that a
certain test has a specific factor structure in the
standardization sample is no guarantee that it is
able to differentiate the same constructs in children
with TBI (Woodward & Donders, 1998). Even
when two tests are normed on the same, compre-
hensive sample it does not necessarily mean that
they are equally sensitive to injury severity (Donders
& Giroux, 2005; Donders & Nesbit-Greene, 2004).
Awareness of the differences in versions of
specific tests is also important. For example, sev-
eral studies have reported sensitivity of the Tower
of London, a measure of executive functioning, to
severity and lesion characteristics in children with
TBI (Levin et al., 1997; Shum et al., 2000).
However, very different versions of the task and
different scoring methods were used across inves-
tigations, which is potentially problematic (Baker,
Segalowitz, & Ferlisi, 2001; Berg & Byrd, 2002).
There are currently available at least two very dif-
ferent versions of this task that have been stan-
dardized and normed for use with children as
young as 7 years (Culbertson & Zillmer, 2001)
and 8 years (Delis, Kaplan, & Kramer, 2001) of
age. Research is still needed to determine the
degree to which they are interchangeable, or
which version has better criterion validity with
regard to the sequelae of pediatric TBI.
Neuropsychologists also need to be cognizant
of what happens to widely used tests when these
get revised, and how that impacts the sensitivity
of those tests to pediatric TBI. For example, the
recent revision of a commonly used test of psy-
chometric intelligence, the Wechsler Intelligence
Scale for Children—Fourth Edition (Wechsler,
2003), appears to have resulted in an instrument
 Forensic Aspects of Pediatric Traumatic Brain Injury
that is less sensitive to severity of TBI than its
predecessor; likely because of the reduced
emphasis on speed of performance (Donders &
Janke, 2008).
Particularly with regard to higher-level execu-
tive abilities, it is also important to avoid exclusive
reliance on psychometric instruments that have
been administered in the type of structured, dis-
tractor-free environment that is typical of most
neuropsychological evaluations. In fact, the eco-
logical validity of that practice has been chal-
lenged, specifically in reference to the evaluation
of children with TBI (Silver, 2000). In this context,
a potentially useful addition to the assessment
arsenal for the pediatric neuropsychologist may
be the Behavior Rating Inventory of Executive
Function (BRIEF; Gioia, Isquith, Guy, &
Kenworthy, 2000). This rating scale, which can be
completed by parents or teachers and for which a
self-report form is also available for older chil-
dren, appears to offer incremental information
about the daily functioning of children with TBI
that cannot be accounted for by laboratory tests
alone (Mangeot, Armstrong, Colvin, Yeates, &
Taylor, 2002; Nadebaum et al., 2007; Vriezen &
Pigott, 2002). In addition, it includes formal valid-
ity checks for possible inconsistent or overly nega-
tive responding. Recent research has also suggested
that this instrument can be used effectively for
prospective and longitudinal tracking of executive
functioning over the first year after pediatric TBI
(Sesma, Slomine, & McCarthy, 2008).
Finally, it is important to include formal mea-
sures of emotional and psychosocial adjustment
in the evaluation, instead of focusing on cognitive
variables only. In light of the research on behav-
ioral and interpersonal sequelae of pediatric TBI
(Bloom et al., 2001; Max et al., 2006; Taylor et al.,
2002), it is essential to address these areas of func-
tioning. Several rating scales offer global screen-
ing of adjustment from the perspective of the
child, the parent, or the teacher (Achenbach &
Rescorla, 2001; Reynolds & Kamphaus, 2004).
More in-depth measures of coping style and per-
sonality that offer both parent and child versions
are available in the Personality Inventory for
Children—Second Edition (Lachar & Gruber,
1999) and the Personality Inventory for Youth
(Lachar & Gruber, 1995).
S Y M P T O M VA L I D I T Y
TESTING
There has been an explosion in recent years of
investigations of effort and motivation affecting
221
the performance of adults with TBI, and formal
assessment of the validity of neuropsychological
symptoms and test results has pretty much
become the standard of care in that field (for
reviews, see Boone, 2007; Larrabee, 2007). Until
recently, relatively little attention was paid to this
issue in the evaluation of children with TBI.
However, even young children have the capability
to use deception (Polak & Harris, 1999) and they
are not always willing to do their best on neuropsy-
chological tests (Mäntynen, Poikkeus, Ahonen,
Aro, & Korkman, 2001).
There are several recent studies that have
explored the feasibility of using forced-choice
measures of effort and motivation in the clinical
assessment of children. Constantinou and
McCaffrey (2003) were the first to evaluate this
formally by examining the performance of 5- to
12-year old children on the Test of Memory
Malingering (TOMM), a task that had originally
been developed for use with adults (Tombaugh,
1996; Rees, Tombaugh, Gansler, & Moczynski,
1998). The results indicated that almost all
children were more than 90% accurate on the
second trial of this instrument; clearly “passing”
the cut-off point for invalid performance. Similar
findings were obtained in a mixed pediatric
sample (Donders, 2005) as well as in various
studies with healthy children (Blaskewitz, Merten,
& Kathmann, 2008; Nagle, Everhart, Durham,
McCammon, & Walker, 2006). Others have cau-
tioned, however, that some measures of effort that
were designed for adults need to be interpreted
with caution when used with children under the
age of 11 years (Courtney, Dinkins, Allen, &
Kuroski, 2003) or with children who do not have
at least a third-grade reading level (Green & Flaro,
2003).
To illustrate the fact that the TOMM really
measures effort and is not affected by the acquired
cognitive impairment that is so common after
pediatric TBI, it may be helpful to revisit the data
from the above-described consecutive sample of
100 6–16½ year-old children who were all evalu-
ated with the TOMM as well as the CVLT–C
within 1 year after injury. Only two of these chil-
dren failed conventional “adult” validity criteria
on the TOMM (i.e., 98% pass rate). In fact, slightly
more than half (n = 57) of the children had a score
of 100% correct on the first trial of the TOMM,
and the vast majority of them (n = 85) obtained a
perfect score on the second trial.
One of the two children who failed validity
criteria on the TOMM was a six-year-old girl
222 forensic neuropsychology
with an unremarkable premorbid history who
had sustained a right frontal skull fracture
with underlying contusion, with <30 min loss of
consciousness, when she was struck as a pedes-
trian by a motor vehicle. The other was a 13-year-
old boy who had sustained a mild concussion,
with negative neuroimaging findings, during a
sports activity, but his case was complicated by a
premorbid history of pharmacological treatment
for depression. Both children obtained scores on
the second trial of the TOMM that were not
statistically significantly different from chance.
Importantly, both children readily admitted to
having provided poor effort when they were
gently confronted about their behavior, and both
were able to modify this behavior. For example,
they obtained scores that were well within normal
limits on several other tests that were adminis-
tered after this conversation.
To formally evaluate the respective relation-
ships between injury severity and performances
on the psychometric tests, product-moment cor-
relations were computed in the complete sample
between length of coma, and respective perfor-
mances on the TOMM and CVLT–C. These data
are presented in Table 8.2. Inspection of this table
suggests that neither of the TOMM variables
covaried meaningfully with injury severity,
whereas performance on the CVLT–C was
strongly inversely related to duration of coma.
Thus, it is clear that poor performance on a symp-
tom validity test like the TOMM cannot be
explained away by acquired cerebral or cognitive
dysfunction in children with TBI.
CONCLUSION
Children with TBI can present in a variety of
forensic contexts, ranging from consideration of
TABLE 8.2 CORRELATIONS BET WEEN
INJURY AND PSYCHOMETRIC
VARIABLES IN CHILDREN WITH TBI
N = 100
1. 2. 3. 4.
1. TOMM Trial 1 — 0.82* 0.18 0.01
2. TOMM Trial 2 — 0.04 0.02
3. CVLT–C Total — –0.49*
4. Length of coma — VT: University of Vermont, Research Center for
Note. TOMM = Test of Memory Malingering. CVLT–C =
California Verbal Learning Test—Children’s Version.
* p < 0.0001
eligibility for special education services to evalua-
tion of possible sequelae of child abuse. Clinical
practitioners need to have a working knowledge
of federal and state guidelines and regulations
about special education criteria as well as manda-
tory reporting guidelines. It is clear that prior
child history, family characteristics, and psycho-
social adversity factors need to be considered
in the evaluation of the sequelae of pediatric TBI.
In addition, potential moderating (e.g., age) and
mediating (e.g., processing speed) variables must
be considered when evaluating outcomes.
Pediatric neuropsychologists must have a basic
appreciation of the pathophysiology of pediatric
TBI, especially the various risk factors contribut-
ing to hypoxic-ischemic injury, as well as a rea-
sonable degree of familiarity with recent advances
in neuroimaging, such as diffusion tensor MRI.
In addition, they need to have a more advanced
understanding of the construct, criterion, and
ecological validities of the psychometric tests that
they employ with these children. Development of
solid and properly stratified norms for more
pediatric neuropsychological tests is still needed.
Incorporation of formal measures of symptom
validity in the assessment of children with TBI in
a forensic context is desirable.
Mild, uncomplicated pediatric TBI is typically
not associated with significant permanent neu-
robehavioral sequelae. At the same time, there is
no doubt that a long-term developmental per-
spective is necessary with regard to the evaluation
of moderate to severe TBI in children. Particularly
with regard to TBI that is sustained early in life,
additional prospective studies are needed to delin-
eate recovery into adolescence and adulthood, as
well as the various influences on variability in
outcome. Future research should explore novel
opportunities for primary, secondary, and tertiary
prevention. Finally, additional randomized con-
trolled clinical trials are needed to provide an evi-
dence base for the best practices in the care of
children with TBI, all the way from acute care
medical management through rehabilitation to
long-term educational/vocational training and
independent community integration.
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Wade, S., Stancin, T., et al. (2005). Long-term atten-
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and Adolescent Psychiatry, 44, 574–84.
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Rubin, K. H., Stancin, T., et al. (2007). Social out-
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Drotar, D., Stancin, T., et al. (2004). Short- and
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Journal of Head Trauma Rehabilitation, 16, 76–93.
 9
Mild Traumatic Brain Injury
G L E N N J. L A R R A B E E
Mild traumatic brain injury (MTBI) accounts
for 85% of all traumatic brain injury, with an
average incidence of 503 per 100,000, placing the
annual incidence of MTBI at over 1 million cases
in the United States (Bazarian et al., 2005; National
Center for Injury Prevention and Control, 2003).
Not surprisingly, MTBI is the most frequent
type of case seen by neuropsychologists doing
forensic work in personal injury settings (Ruff &
Richardson, 1999).
Despite the frequency with which MTBI
occurs, and despite the significant research that
has occurred on sequelae of MTBI over the past
25 years, the issue of the incidence, cause, and
persistence of deficits following MTBI remains
controversial (Bigler, 2008; Mittenberg &
Strauman, 2000; Ruff & Jamora, 2009). Zasler
(2000) wrote of two “extreme camps”: one that
generally believes that mild brain injury or post-
concussive disorders do not occur or do not cause
long-term impairment or disability, and the other
that tends to overdiagnose or “overtreat” MTBI
and post-concussive disorders, with inadequate
consideration of alternative causes. There has
been a spirited exchange between Bigler and
Lees-Haley and colleagues regarding the issue of
persistent deficits and persistent neurological
damage in MTBI (Bigler, 2001, 2003; Fox & Allen,
2003; Green, 2003; Lees-Haley, Green, Rohling,
Fox, & Allen, 2003).
The continuing debate over the incidence,
cause, and persistence of deficits in MTBI likely
results from several factors. One factor involves
the criteria used to diagnose MTBI. Another
factor is the sophistication of research design for
evaluation of the consequences of MTBI. A third
factor is the confusion of symptomatic complaint
with neurological dysfunction. A fourth factor,
related to the first factor, is the lack of proper
differential diagnosis. In the following sections of
this chapter, I review the diagnosis of MTBI, the
outcome of MTBI, the role of symptomatic
complaint in MTBI, and last, the workup of the
individual MTBI case.
DIAGNO STIC CRITERIA
Diagnostic criteria for MTBI have evolved from
research criteria, as well as from the recommen-
dations of committees of learned clinicians.
Mittenberg and Strauman (2000) observed that
inconsistencies in the definition of MTBI compli-
cate comparison and generalization across stud-
ies. These authors did observe that there is a
general consensus across studies that MTBI is
defined by an admission Glasgow Coma Scale
(GCS) of 13 to 15. Yet, one of the largest outcome
studies of the full range of TBI severity identified
the MTBI group by the measure of less than
1 hour for time to follow commands (Dikmen,
Machamer, Winn, & Temkin, 1995). Levin, Mattis,
et al. (1987) specified MTBI by criteria that
included loss of consciousness for less than 20
minutes, post-resuscitation GCS of 13–15, absence
of focal neurological abnormalities, and no evi-
dence of intracranial mass lesion. In the Levin,
Mattis, et al. (1987) investigation, there was no
evidence of persistent neuropsychological deficit
on 3-month follow-up for patients meeting their
MTBI diagnostic criteria. In a subsequent investi-
gation, Williams, Levin, and Eisenberg (1990)
found that those TBI patients with admission
GCS values of 13–15 who had evidence of intrac-
ranial lesion, characterized as “complicated”
MTBI, had poorer 6-month outcomes than did
those subjects who had GCS values of 13–15
without evidence of intracranial pathology. The
Williams et al. complicated MTBI patients had
outcomes more similar to the moderate TBI (GCS
9–12) than the MTBI patients. In contrast,
Dikmen et al.’s (1995) MTBI group was classified
by time to follow commands less than 1 hour,
including patients with potential structural lesions
232 forensic neuropsychology
or secondary complications, and showed no evi-
dence of persistent neuropsychological deficits at
1-year post-trauma in comparison to an orthope-
dic trauma control group. These data suggest that
restricting of loss of consciousness to less than 20
minutes as a criterion for MTBI is too conserva-
tive; rather, the criterion for loss of consciousness
could be extended to just under 1 hour on the
basis of Dikmen et al.’s (1995) results.
The Mild Traumatic Brain Injury Committee
of the Head Injury Interdisciplinary Special
Interest Group of the American Congress of
Rehabilitation has proposed a definition of MTBI
(American Congress of Rehabilitation Medicine
[ACRM], 1993). These criteria define MTBI by
traumatically induced physiological disruption of
brain function, as manifested by at least one of the
following: (a) any period of loss of consciousness;
(b) any loss of memory for events immediately
before or after the accident; (c) any alteration in
mental state at the time of the accident (e.g., feel-
ing dazed, disoriented, or confused); (d) focal
neurological deficit(s) that may or may not be
transient, but for which the severity of the injury
does not exceed the following: (e) loss of con-
sciousness of approximately 30 minutes or less;
(f) after 30 minutes, an initial GCS of 13–15; and
(g) post-traumatic amnesia (PTA) not greater
than 24 hours.
The ACRM definition includes the head being
struck, the head striking an object, and the brain
undergoing an acceleration–deceleration move-
ment (i.e., whiplash) without direct external
trauma to the head. The ACRM does not include
specific symptoms as part of the primary criteria
for MTBI, but does state that physical symptoms
(e.g., dizziness, headache), cognitive deficits (e.g.,
attention, memory), and behavioral changes or
alterations in degree of emotional responsivity
(e.g., irritability, emotional lability) are additional
evidence that an MTBI has occurred.
A potential problem with the ACRM criteria
is that they allow for determination of criteria
beyond the acute (i.e., day of injury) status of
the patient. For example, I have seen several cases
of alleged MTBI with no evidence of loss of
consciousness, disorientation, or PTA based on
emergency medical service (EMS) or emergency
room (ER) records or based on detailed interview
(e.g., the patient accurately recalls the events of
the accident and post-accident treatment, verified
against Department of Motor Vehicles, EMS, and
ER records), but on examination 1 to 2 months
later are diagnosed as having MTBI based on their
report to a physician that they were “dazed” and
because they endorsed symptoms of headache,
irritability, and forgetfulness, typically on a history/
record form completed in the physician’s office.
This goes counter to the recommended practice of
defining MTBI by acute injury characteristics
rather than by severity of symptoms at random
points after trauma (see Alexander, 1995).
Indeed, Lees-Haley, Fox, and Courtney
(2001), studying groups of litigating individuals
with MTBI and other injury (nonbrain injury)
trauma, found, during retrospective questioning,
that although 67% of those with MTBI reported
confusion and 71% reported feeling dazed imme-
diately after trauma, high proportions of the non-
TBI group also reported being dazed (51%) and
confused (65%). These data highlight the limited
utility of self-reported feelings of being dazed and
confused as a marker of the occurrence of MTBI.
By contrast, EMS or ER records documenting
independently observed confusion or disorienta-
tion can provide evidence consistent with MTBI.
Influenced by the ACRM criteria and by the
report of the National Center for Injury Prevention
and Control to the Centers for Disease Control
(CDC; 2003), the World Health Organization
(WHO; Carroll, Cassidy, Holm, Kraus, &
Coronado, 2004) also proposed a definition of
MTBI. MTBI is defined by WHO as:
an acute brain injury resulting from mechani-
cal energy to the head from external physical
forces. Operational criteria for clinical identifi-
cation include: (i) one or more of the following:
confusion or disorientation, loss of conscious-
ness for 30 minutes or less, post-traumatic
amnesia for less than 24 hours, and/or other
transient neurological abnormalities such as
focal signs, seizure, and intracranial lesion not
requiring surgery; (ii) Glasgow Coma Scale
score of 13–15 after 30 minutes post-injury or
later upon presentation for healthcare. These
manifestations of MTBI must not be due to
drugs, alcohol, medications, caused by other
injuries or treatment for other injuries (e.g.
systemic injuries, facial injuries or intubation),
caused by other problems (e.g. psychological
trauma, language barrier or coexisting medical
conditions) or caused by penetrating cranio-
cerebral injury (p. 115).
Ruff et al. (2009) observed that there were
more similarities than differences between the
ACRM and WHO criteria for MTBI. Importantly,

the WHO criteria for alteration of mental state at
time of injury removed the term “dazed” from the
diagnosis, reducing the chance of false positive
diagnosis in non-TBI groups endorsing this
symptomatic complaint (see above earlier discus-
sion of problems caused by use of the term “dazed,”
and Lees-Haley et al., 2001). Second, the WHO
criteria emphasize that focal neurologic signs
must be transient, contrasted with the ACRM cri-
teria which allow focal signs to be persisting. This
modification may result in a lesser chance of
including cases of “complicated MTBI” (Williams
et al., 1990) in the MTBI diagnostic category. On
the other hand, allowing cases to be identified as
MTBI who have intracranial lesions not requiring
surgery could include cases considered to be
“complicated” by other investigators.
Another problem posed by various diagnostic
criteria for MTBI is that the criteria themselves do
not provide much information for assessing gra-
dations in severity of MTBI. This is particularly
important when attempting to assess or conduct
research on the group of patients with MTBI who
do not show the characteristic pattern of full
recovery, a group characterized by Ruff and
Richardson (1999) as the “miserable minority.”
Subdividing MTBI by severity was supported
by Culotta, Sementelli, Gerold, and Watts (1996),
who found greater need for neurosurgical inter-
vention, more computed tomography (CT) scan
abnormalities, and increased incidence of skull
fractures in patients with GCS of 13 compared to
GCS of 14. Patients with GCS of 14 had greater
morbidity than patients with GCS of 15. Culotta
et al. recommended segregating MTBI patients
with GCS of 15 from those with scores of 14 and
13. Although these data showed the benefits of
grading severity of MTBI relative to acute injury
characteristics, Culotta et al. did not study long-
term neuropsychological outcome for these dif-
ferent levels of GCS.
Ruff and Richardson (1999) proposed subdi-
viding MTBI by three categories of severity, pro-
ceeding from less to more severe: Type I, altered
state or transient loss of consciousness, PTA of 1
to 60 seconds, and one or more neurological
symptom; Type II, definite loss of consciousness,
with time either unknown or less than 5 minutes,
PTA of 60 seconds to 12 hours, and one or more
neurological symptom; and Type III, loss of con-
sciousness of 5 to 30 minutes, PTA greater than 12
hours, and one or more neurological symptom.
Published standards for gradation of concus-
sion in sports also allow for assessment of the
Mild Traumatic Brain Injury 233
severity of MTBI (American Academy of
Neurology, 1997). Concussion is defined as a
trauma-induced alteration in mental status that
may or may not involve loss of consciousness,
with confusion and amnesia identified as the hall-
marks of concussion. The American Academy of
Neurology (1997) proposed three different grades
of concussion: Grade I, characterized by transient
confusion, no loss of consciousness, and concus-
sion symptoms or mental status abnormalities on
examination that resolve in less than 15 minutes;
Grade II, characterized by transient confusion, no
loss of consciousness, and concussion symptoms
or mental status abnormalities on examination
that last more than 15 minutes; and Grade III,
characterized by any loss of consciousness, either
brief (seconds) or prolonged (minutes).
Hinton-Bayre and Geffen (2002) investigated
concussion severity grades in 21 professional
rugby league players who suffered concussion.
Testing concussed athletes at 2 and 10 days post-
trauma, Hinton-Bayre and Geffen found no rela-
tionship between concussion severity, using the
American Academy of Neurology (AAN) criteria,
and two other sets of criteria (Colorado Medical
Society, 1990; Cantu, 1986) and performance on
Speed of Comprehension, Digit Symbol, and the
Symbol Digit Test. Similarly, Lovell, Iverson,
Collins, McKeag, and Maroon (1999) found no
differences in neuropsychological test perfor-
mance as a function of positive loss of conscious-
ness, no loss of consciousness, or uncertain loss of
consciousness in persons admitted to the ER for
evaluation of uncomplicated MTBI.
In contrast, McCrea, Kelly, Randolph, Cisler,
and Berger (2002), in an investigation of immedi-
ate neurocognitive effects of sports concussion,
found that subjects with loss of consciousness
were most severely impaired immediately after
injury, whereas those without loss of conscious-
ness or PTA were least impaired. All of the McCrea
et al. subjects returned to preinjury baseline levels
of performance within 48 hours of injury.
The investigations of Culotta et al. (1996),
Hinton-Bayre and Geffen (2002), and Lovell et al.
(1999) did not provide consistent evidence either
supporting or contradicting the value of grading
severity of MTBI. In contrast, the study by McCrea
et al. (2002) demonstrated differences between
MTBI subjects as a function of presence/absence
of loss of consciousness both immediately follow-
ing and 15 minutes after trauma. The McCrea
et al. (2002) data clearly support the value of grad-
ing severity of MTBI in the first hour post-trauma,
234 forensic neuropsychology
providing support for the utility of these criteria
regarding return-to-play decisions (American
Academy of Neurology, 1997). Sports concussion
guidelines are in general agreement that athletes
should be symptom-free before returning to play
(Moser et al., 2007; Randolph, McCrea, & Barr,
2005). Additional research is needed to establish
the value of grading severity of MTBI relative to
long-term outcome of MTBI, although current data
showing acute, day-of-injury differences as a func-
tion of MTBI severity do not support persisting dif-
ferences beyond two days (McCrea et al., 2002).
A P P R O P R I AT E
RESEARCH DESIGNS
One significant factor that has contributed to the
apparent contradictory findings in the MTBI lit-
erature is the use of samples of convenience as
opposed to prospective outcome research or
sports concussion research utilizing pre-injury
baseline testing followed by repeated measures
examination subsequent to MTBI (McCrea, 2008).
Certainly, subject-as-own-control designs, includ-
ing pre-injury testing, with repeated measures
studies of nonconcussed persons to control for
practice effects, are the strongest designs for inves-
tigation of the outcome of MTBI. The weakest
designs are those employing clinical samples of
convenience, such as might be aggregated from a
clinic specializing in treatment of persons with
persisting symptoms 1 to 2 years post-MTBI.
Differences in study outcome as a function of
research design can be very significant. Dikmen
et al. (1995) conducted what is arguably the best
prospective outcome study of the complete range
of TBI severity. These investigators compared
patients with TBI with six different levels of sever-
ity, defined by time to follow commands (the
highest level of function on the motor component
of the GCS; this score is not affected by the pres-
ence of intubation, which can affect the verbal
component of the GCS and consequently have an
impact on the total GCS score). The mildest level
of injury was represented by the group that took
less than 1 hour to follow commands, whereas the
most severely injured group took 29 days or more
to follow commands.
In addition, Dikmen et al. (1995) collected a
large trauma control sample that had been
admitted to the hospital because of traumatic
injuries not involving the head. By using such a
control group, Dikmen et al. controlled for socio-
economic status as well as for psychosocial factors
associated with suffering traumatic injury, the
experience of being injured sufficiently to be
transported to the hospital, and the potentially
confounding effects of pain. The trauma control
and TBI patients did not differ on age, education,
or gender. Also, by using a trauma control group,
Dikmen et al. indirectly controlled for effects
related to litigation. Although Dikmen et al. did
not report percentage involved in litigation for the
trauma control group, there is no reason to expect
a significant difference in litigation for the trauma
control and the more mildly injured patients with
TBI, particularly those who followed commands
within less than 1 hour. Both the TBI and trauma
control subjects were examined at 1 month and
1 year post-trauma. At 1 year post-trauma, the
MTBI group (those taking less than 1 hour to
follow commands) did not differ significantly
from the trauma control group in performance on
a comprehensive neuropsychological test battery.
The importance of using orthopedic trauma
controls is underscored by the work of Bijur,
Haslam, and Golding (1996), who found that an
apparent cumulative effect of one versus two
versus three MTBIs in children disappeared when
these children were compared with children who
had suffered one, two, or three orthopedic inju-
ries. When Dikmen et al.’s (1995) orthopedic con-
trol group data mean data are scored using the
Heaton, Grant, and Matthews (1991) demograph-
ically corrected normative data, the T scores for
the two most brain-injury-sensitive measures on
the Halstead-Reitan, the Category Test and the
Impairment Index, are 43 and 45, respectively.
The orthopedic control Impairment Index itself
matches precisely the Impairment Index for
Dikmen et al.’s MTBI subjects, as well as closely
matches the T score for the Overall Test Battery
Mean, T = 44.54, for the MTBI sample reported
by Meyers and Rohling (2004). These data strongly
support the practice of using orthopedic trauma
controls to account for possible pre-injury neu-
ropsychological differences as well as for general
injury effects (i.e., effects due to injury but not
specifically related to brain injury).
Results from studies using samples of conve-
nience that did not control for effects of nonhead
traumatic injury can be quite different. For exam-
ple, Leininger, Gramling, Farrell, Kreutzer, and
Peck (1990) found significant neuropsychological
performance differences comparing 31 patients
with MTBI and brief loss of consciousness and
22 MTBI patients experiencing “dazing” injuries
without loss of consciousness to the performance
of a group of 23 control subjects who were friends

and family of inpatients with head injury at the
Medical College of Virginia. The MTBI patients
were tested, on average, 7 months post-trauma.
In another study, Guilmette and Rasile (1995)
compared the verbal memory performance of
16 patients with MTBI to the performance of
16 controls who were community volunteers
matched on age, education, and gender to the
MTBI patients. On testing done a mean of 16.4
months post-trauma, the MTBI patients per-
formed significantly less well than the control
subjects on all three memory tests.
The differences in outcome between the pro-
spective investigation using trauma controls con-
ducted by Dikmen et al. (1995) and the
nonprospective investigations of Leininger et al.
(1990) and Guilmette and Rasile (1995) that did
not use trauma control subjects, are more obvious
when the study results are examined for effect
sizes. These effect sizes, represented in terms of d,
the difference between the MTBI and control
group mean, in pooled standard deviation units
(i.e., the pooled MTBI/control group standard
deviation) are shown in Table 9.1.
As can be seen in Table 9.1, the effect size for
the Dikmen et al. MTBI group, tested 1 year post-
trauma, is essentially zero, consistent with com-
plete overlap of the MTBI and trauma control
group score distributions. In contrast, the 0.57
effect size for the Leininger et al. (1990) MTBI
group is most similar to the effect size for the
Dikmen et al. (1995) group who took between 6
and 13 days to follow commands. Even more sig-
nificant is the 1.10 effect size for the Guilmette and
Rasile (1995) MTBI group, which is most similar
to the effect size for the Dikmen et al. (1995)
group who took between 14 and 28 days to follow
commands. Clearly, the neuropsychological data
TABLE 9.1 EFFECT SIZE AS A FUNCTION OF SEVERIT Y
OF BRAIN INJURY
Severity of Injurya
Study Minor Brain
Injury
Dikmen et al., 1995 .02
Leininger et al., 1990 .57
Guilmette & Rasile, 1995 1.10
a
severity of injury is GCS of 13–15 and/or time–to–follow commands less than one hour for Minor Brain Injury; other values are
time–to–follow commands.
Mild Traumatic Brain Injury 235
reported by Leininger et al. (1990) and Guilmette
and Rasile (1995) cannot be accepted as represen-
tative of outcome from MTBI when considered in
terms of a dose–response analysis of TBI (Dikmen
et al., 1995; Rohling, Meyers, & Millis, 2003).
The above differences in study outcome may
be partly a consequence of motivational factors
secondary to litigation. In the Leininger et al.
(1990) study, 39 patients were pursuing litigation,
and 14 were not pursuing litigation. Leininger
et al. did compare the two groups and found that
the litigating group performed significantly less
well on the copy portion of the Complex Figure
Test, but this difference did not remain significant
when the Bonferroni correction procedure was
applied. However, the litigating/nonlitigating
contrasts suffered from both an imbalance of
subjects (over twice as many litigant as nonlitigant
subjects) and low power, given the sample size of
the nonlitigating group. Leininger et al. did
not report the mean performances and standard
deviations for the litigating and nonlitigating
subjects, so the reader is unable to see whether
there is a consistent pattern of lower mean
scores for the litigants. Guilmette and Rasile
(1995) did not specify the proportion of their
MTBI sample who had a potentially compensable
injury, but did note that they screened subjects
who had ongoing worker’s compensation or
personal injury litigation with forced-choice
symptom validity testing. They did not, however,
match their MTBI and control group subjects on
symptom validity test performance or use analysis
of covariance with symptom validity performance
as the covariate.
Litigation effects are significant. Binder
and Rohling (1996) found an effect size of 0.47
between litigating and nonlitigating TBI patients,
1–24 2–5 days 6–13 days 14–28 days 29+ days
hours
.23 .45 .69 1.33 2.30
— — — — —
— — — — —
236 forensic neuropsychology
with the effect particularly strong for those with
MTBI. Moreover, Binder and Kelly (1996) found
that, on the Portland Digit Recognition Test (a
measure of symptom validity and malingering), up
to 47% of a series of individuals with MTBI per-
formed at the level of the bottom 2% of a sample of
nonlitigating patients with severe TBI. Green,
Rohling, Lees-Haley, and Allen (2001) found that
measures of effort sensitive to malingering
accounted for 50% of the variance in neuropsycho-
logical test performance, in contrast to 10%
accounted for by TBI severity. Last, Mittenberg,
Patton, Canyock, and Condit (2002), in a survey of
American Board of Clinical Neuropsychology
(ABCN) board-certified neuropsychologists who
did forensic work, found a base rate of malingering
of approximately 40% in litigating MTBI subjects.
Thus, future outcome research on MTBI
optimally should be based on prospective investi-
gations using trauma control subjects (Dikmen
et al., 1995; Satz et al., 1999), and symptom valid-
ity testing (Green et al., 2001). Satz et al. also
advocated using a noninjury reference group as a
third group, so that MTBI versus other injury and
MTBI versus no injury comparisons can be made.
Per their Table 1, Satz et al.’s design with three
subject groups allows evaluation of four separate
conclusions: (a) no effect, head injury or other
injury; (b) general injury effect, body and head;
(c) specific head injury effect; and (d) other injury,
not head injury, must be the causal factor.
Studies involving MTBI clinical samples of
convenience can still yield potentially useful
information if they employ an orthopedic trauma
control group matched on age, education, and
gender and screened and matched for perfor-
mance on sensitive symptom validity tests such as
the Word Memory Test (Green, Iverson, & Allen,
1999) or the Portland Digit Recognition Test
(Binder & Kelly, 1996). Alternatively, studies that
have a primary focus other than MTBI, such as
Bornstein et al.’s (1993) study of HIV-positive
patients with and without history of MTBI or
Alterman, Goldstein, Shelly, and Bober’s (1985)
investigation of alcoholic subjects with and with-
out history of MTBI, can be considered “pseudo-
prospective” (cf. Binder, Rohling, & Larrabee,
1997) because the primary focus is the clinical
condition (HIV status or alcohol abuse) with the
presence or absence of MTBI on a historic basis.
THE TYPICAL OUTCOME
Cumulative research on the outcome of a single,
uncomplicated MTBI shows that neuropsycho-
logical deficits may persist for up to 3 months, but
the norm is full recovery, with no long-term
residual deficits (Belanger, Curtiss, Demery,
Lebowitz, & Vanderploeg, 2005; Belanger &
Vanderploeg, 2005; Binder, 1997; Binder et al.,
1997; Dikmen et al., 1995; Frencham, Fox, &
Mayberry, 2005; Levin, Mattis, et al., 1987; Ruff
et al., 1989; Schretlen & Shapiro, 2003). Binder
et al. (1997) conducted a meta-analysis of eight
published studies of adult MTBI, with 11 total
samples studied at least 3 months post-trauma and
selected on the basis of a history of MTBI rather
than because they were symptomatic; the study
had a subject attrition rate on follow-up of less
than 50%. The total aggregated sample included
314 patients with MTBI and 308 control subjects.
Using the g statistic (MTBI and control pooled
standard deviation), the overall effect size of
0.07 was nonsignificant, but the d statistic (control
group standard deviation) of 0.12 was significant
at p < .03. Measures of attention had the
largest effect sizes, with g = 0.17, p < .02, and d =
0.20, p < .006. Binder et al. (1997) observed that
these small effect sizes were equivalent to 2
points for the WAIS-R (Wechsler Adult Intelligence
Scale–Revised) IQ or WMS-R (Wechsler Memory
Scale–Revised) General Memory score (for d =
0.12) and 3 points on the Attention/Concentration
Index of the WMS-R (for d = 0.20). These values
are smaller than the measurement errors for
these WAIS-R and WMS-R scores (Wechsler,
1981, 1987).
Binder et al. (1997) computed an estimated
prevalence of persistent neuropsychological
impairment of 5% based on their effect-size anal-
ysis. At such a low base rate of impairment, the
positive predictive value of neuropsychological
test scores (true positives divided by true positives
plus false positives) was 0.32 at a sensitivity of
0.90 and specificity of 0.90 (note that lower sensi-
tivity of 0.80 and specificity of 0.88, values based
on the Heaton, Grant, and Matthews, 1991, data,
yield a positive predictive value of only 0.26). In
contrast, negative predictive values (true nega-
tives divided by true negatives plus false nega-
tives) were 0.98 to 0.99. Binder et al. (1997)
concluded that at these low positive but high neg-
ative predictive values, the clinician would more
likely be correct when not diagnosing rather than
diagnosing brain injury in patients reporting
chronic disability after MTBI.
The likelihood of full recovery from single,
uncomplicated MTBI is further supported by data
from sports concussion research. Macciocchi,
Barth, Alves, Rimel, and Jane (1996) followed
collegiate athletes who were tested preseason and

then within 1, 5, and 10 days post-MTBI; these
individuals were contrasted with control athletes
tested preseason and at 1, 5, and 10 days post-
trauma. Inspection of group mean performance
showed no significant performance difference
compared to baseline at 24 hours post-trauma;
however, the MTBI group did differ when their
change scores (pre- to post-injury) were com-
pared to the change scores of the noninjured
control group. At 10 days, there were essentially
no differences in the MTBI group versus the
control group.
Collins et al. (1999) found that college football
players who were concussed showed significantly
poorer Hopkins Verbal Learning Test perfor-
mance compared to noninjured players at 24
hours after injury. Moderate differences in perfor-
mance persisted until at least 5 days post-trauma.
Echemendia, Putukian, Mackin, Julian, and
Shoss (2001) found significant differences in neu-
ropsychological test performance for athletes sus-
taining MTBI in comparison to nonconcussed
control athletes at 2 hours and 48 hours post-
trauma. There were no multivariate group differ-
ences at 1 week post-trauma, although univariate
differences were seen on a few measures. At 1
month post-injury, a statistically significant dif-
ference was found on one measure, with the
injured athletes marginally outperforming the
noninjured athlete control subjects.
McCrea et al. (2003) found that concussed
collegiate football players showed recovery over
the first week post-trauma. Symptoms of concus-
sion (e.g., headache, dizziness) gradually resolved
by Day 7. Directly measured cognitive function
improved to baseline (preinjury) levels within 5 to
7 days following concussion, and balance deficits
dissipated within 3 to 5 days post-trauma. The
mild impairments in cognitive processing and
verbal memory that were apparent on neuropsy-
chological testing 2 days post-trauma resolved by
Day 7. McCrea et al. (2003) found no significant
differences in symptoms or functional impair-
ments in the concussed and nonconcussed athlete
controls 90 days following concussion.
In a meta-analysis of sports-related concus-
sion based on 21 studies involving 790 cases of
concussion and 2014 control cases, Belanger and
Vanderploeg (2005) found acute effects of con-
cussion within the first 24 hours post-injury of
approximately one standard deviation or more on
measures of delayed memory, memory acquisi-
tion, and global cognitive function. No residual
deficits were seen on testing conducted 10 days or
more post-trauma.
Mild Traumatic Brain Injury 237
McCrea (2008), in a comprehensive review of
MTBI and post-concussion syndrome, provides a
summary figure of recovery from MTBI. This is
reproduced as Figure 9.1, and shows how symp-
tomatic recovery, cognitive recovery, recovery of
balance, and recovery from the reversible meta-
bolic effects of MTBI converge, with normaliza-
tion at 7 days post-trauma. McCrea et al. (2009),
in a subsequent review, note that fMRI studies
suggest a hypothesis that MTBI physiologically
manifests in a pattern of decreased cerebral acti-
vation in select attention-related neural circuits
during the earliest acute period, 12 to 24 hours
post-injury, likely relating to the acute physiologi-
cal mechanisms of injury. Increased activation
then becomes evident during the subacute phase,
up to 1 month post-injury, apparently in relation
to compensatory mechanisms, with return to
normal activation patterns beyond one month
post-trauma. Similar data have been subsequently
published for symptom report, cognitive func-
tion, balance, and quantitative EEG by McCrea,
Prichep, Powell, Chabot, and Barr (2010).
Compared to control subjects, symptom report,
cognitive function, and balance differences,
apparent on day of injury, normalized by eight
days post-trauma and did not differ from values
reported for noninjured controls. Quantitative
EEG differences were significant in comparison to
controls on day of injury, 3 days, and 8 days post-
trauma, but were not significantly different at
45 days post-trauma.
The good long-term outcome of a single,
uncomplicated MTBI appears to extend across
the age range. Full recovery from MTBI is gener-
ally expected for children (Bijur, et al., 1996;
Satz et al., 1997). Very young children, aged 3 to 7
years, also make good recovery for intellectual
skills, receptive language, and everyday and spa-
tial memory, although they may have persistent
problems in higher linguistic skills (Anderson,
Catroppa, Morse, Haritou, & Rosenfeld, 2001).
Older adults also showed good outcome from
a single, uncomplicated MTBI. Goldstein, Levin,
Goldman, Clark, and Altonen (2001) found that
older adults (average age 62.3 years) suffering
MTBI performed at similar levels to older adults
not suffering MTBI; this was examined on mea-
sures of attention, memory, and executive func-
tion when tested, on average, 25 days post-trauma.
The only difference between the older adults with
MTBI and control subjects was seen on the
Controlled Oral Word Association test. Both the
individuals with MTBI and noninjured controls
outperformed a group of older adults suffering
 Symptom Recovery Cognitive Recovery Postural Stability Recovery
30 30 24
Concussion 22 Concussion
25 Control 29 Control
20

BESS Total Score

GSC Total Score

SAC Total Score

20 28 18
16
15 27
14
Concussion
10 26 Control 12

5 25 10
8
0 24 6
Baseline CC PG 1 2 3 4 5 6 7 90 Baseline CC PG 1 2 3 4 5 6 7 90 Baseline CC PG 1 2 3 4 5 6 7 90
Day Day Day
Assessment Point Assessment Point Assessment Point

500

Ca2+
400
K+
% Control

300

CMRgluc
200
lactate
100

glutamate CBF
0
0 1 2 4 6 8 12 16 20 25 30 1 6 12 24 2 3 4 6 8 10
Time (minutes) (hours) (days)

FIGURE 9.1: Recovery curves for symptoms, cognitive functioning, and postural stability following MTBI. Higher scores on the GSC indicate more severe symp-
toms. Lower scores on the SAC indicate more severe cognitive dysfunction. Higher scores on the Balance Error Scoring System (BESS) indicate more severe balance
problems. Error bars indicate 95% confidence intervals. Baseline is preinjury. CC, time of concussion; PG, postgame/postpractice. From McCrea (2008), McCrea
et al. (2003), and Giza and Hovda (2001), with permission.

moderate TBI on all measures of language, atten-
tion, memory, and executive dysfunction.
In a subsequent article, Goldstein and Levin
(2001) reviewed extensive literature on cognitive
outcome following mild and moderate TBI in
adults over 50 years of age. These authors
concluded that patients suffering MTBI, unlike
those suffering moderate TBI, exhibited cognitive
functioning similar to noninjured controls by 1 to
2 months post-trauma. Despite evidence of full
neuropsychological recovery, MTBI patients
continued to report significant anxiety, depres-
sion, and somatic preoccupation. Goldstein and
Levin found that the lowest post-resuscitation
GCS and the presence of intracranial pathology
were more strongly associated with outcome than
durations of PTA and impaired consciousness.
Schretlen and Shapiro (2003) included sports
concussion studies with traditional prospective
clinical studies in their meta-analysis and found
that persons with MTBI essentially returned to a
baseline level of performance within 1 to 3 months
post-trauma. Indeed, there was a 97% overlap of
control and MTBI test performance by 1 month
post-trauma, and the 95% confidence intervals
of effect size estimates at both 30–89 days and
more than 89 days post-trauma included zero.
Schretlen and Shapiro interpreted these data as
showing that the overall cognitive test perfor-
mance of those with MTBI was essentially
indistinguishable from that of matched controls
by 1 month post-trauma.
Similar findings demonstrating full recovery
within 1 to 3 months post-MTBI have been
reported in meta-analyses conducted by
Frencham et al. (2005), and Belanger et al. (2005).
Frencham et al. reported an effect size of 0.11 in
persons assessed over three months post-MTBI,
with time-since-injury a significant moderator
variable, and effect sizes tending to zero with
increasing time post-injury. Belanger et al. found
no residual neuropsychological impairment by
3 months post-injury (d = 0.04) in unselected or
prospective samples of MTBI cases.
Pertab, James, and Bigler (2009) reported a
re-analysis of the Binder et al. (1997) and
Frencham et al. (2005) meta-analyses that they
interpreted as showing a clinically lasting effect, 3
months post-injury, on select subsets of neuro-
psychological measures, including Digit Span
(d = 0.31), Coding (d = 0.33), and Verbal Paired
Memory (d = 0.52). However, they omitted 7 of
the 25 studies (28%) analyzed by Binder et al.
and Frencham et al., and reported other negative
Mild Traumatic Brain Injury 239
findings on measures known to be sensitive to
acute effects of MTBI as well as to residual deficits
following moderate to severe TBI, including Trail
Making B (d = 0.05) and List Learning and
Memory (d = 0.00; note that this category included
the Dikmen et al., 1995 study in which Verbal
Selective Reminding had an effect size of 0.11).
The Pertab et al. results are clearly discrepant
from other meta-analytic results (Belanger &
Vanderploeg, 2005; Belanger et al., 2005; Binder
et al., 1997; Frencham et al., 2005; and Schretlen &
Shapiro, 2003). Their data are also discrepant
from expectation relative to the known sensitivity
of specific neuropsychological tests to acute effects
of MTBI as well as sensitive to long-term residual
effects of moderate and severe TBI.
Further underscoring the atypical findings of
Pertab et al. (2009) are two studies also published
in 2009: Ettenhofer and Abels (2009), and Ivins,
Kane, and Schwab (2009). Ettenhofer and Abels
(2009) compared samples of college students
with a) history of MTBI, n = 63, and b) orthope-
dic injury, n = 63, studied an average of 36.75
months post-trauma. The only significant group
difference on neuropsychological testing was on
Trial 2 of the Delis Kaplan Trail Making Test, on
which the MTBI sample performed better than
the orthopedic trauma sample. There were no
group differences on a Post-concussion Symptom
Checklist (PCSC; Gouvier, Cubic, Jones, Grantley,
& Cutlip (1992), nor were there group differences
in psychiatric symptoms on the Brief Symptom
Inventory (BSI; Derogotis & Spencer, 1982).
Interestingly, the total scores on the PSC and BSI
were strongly correlated with one another, at a
similar level of magnitude within both the MTBI
and orthopedic trauma samples.
Ivins, et al. (2009) compared computerized
test scores (ANAM measures of working memory,
processing speed, and reaction time) and post-
concussion symptoms of soldiers with self-
reported MTBI occurring up to two years prior to
testing (n = 124; median time since injury of 19
months; 7 months = 25th percentile; 44 months =
75th percentile), to those of noninjured service
persons (n = 703), and service persons who
sustained injury not involving TBI (n = 129), all of
whom had served in Iraq or Afghanistan. Also
evaluated was history of prior MTBIs. Data were
screened using predetermined cutoffs for invalid
performance (i.e., screened for “bad data”). There
were no differences among the groups in terms of
their endorsement of post-concussion symptoms,
with the exception of the noninjured group
240 forensic neuropsychology
showing a higher rate of endorsement of one
problematic post-concussion symptom compared
to the MTBI or injured without TBI. There was
no effect of one or two or more prior TBIs on
post-concussion symptom endorsement, and no
evidence of poorer ANAM performance by those
with MTBI versus those with injury but no TBI
and those without injury. Interestingly, those
who sustained TBI in Iraq or Afghanistan were
less likely to have “bad data” on the ANAM math-
ematical processing test than those who were
uninjured, and those with a lifetime history of
multiple TBI were less likely to have bad data on
the matching to sample test than those with no
lifetime history of TBI.
Ivins et al. (2009) also reported no differences
on ANAM performance for moderate or severe
TBI; however, they used a criterion of loss of
consciousness of greater than 20 minutes and/or
post-traumatic amnesia of greater than 24 hours
to define moderate injury or worse; they did not
base this on typical GCS criteria of 9–12 for mod-
erate, and 8 or below for severe. Moreover, 98% of
their sample qualified for a self-reported diagno-
sis of MTBI. Given Dikmen et al.’s findings of no
differences in comparison to orthopedic controls
at one year post-trauma in subjects who took up
to one hour to follow commands, it is likely that
some proportion of the small percentage of
cases considered “moderate” or “severe” by Ivins
et al. actually would have fallen in the range of
Dikmen et al.’s “mild” category. This inference is
supported by lack of report by Ivins et al. of medi-
cal services provided to any of their TBI sample.
Although persons with MTBI may escape medical
surveillance, it is unlikely that those with moder-
ate or severe TBI would escape such surveillance.
Thus, the Ivins et al. investigation also highlights
some of the problems associated with research on
self-reported history of TBI.
A meta-analysis focusing specifically on emo-
tional symptoms after MTBI has also demon-
strated absence of significant persisting problems
(Panayiotou, Jackson, & Crowe, 2010). Eleven
studies were analyzed, including a total of 352
MTBI and 765 control participants, examined an
average of 12.1 months post-injury, considering
scores from measures of depression, anxiety,
coping, and psychosocial disability. Data were
analyzed such that positive values of d were asso-
ciated with greater symptom report in MTBI rela-
tive to control subjects. Analysis of Cohen’s d with
effect sizes weighted by the inverse variance to
correct for sample size differences across different
studies, yielded effect sizes ranging from 0.26
(depression) to −.28 (anxiety), with an overall
effect size of 0.05. None of the inverse variance-
weighted effect sizes were significantly different
from zero. Panayiotou et al. concluded that their
results lent additional support to the argument
that symptoms of PCS are not unique to MTBI
patients, occurring commonly in the general
population, non-brain-injured trauma patients,
personal injury claimants, chronic pain patients,
and psychiatric patients. They observed that
premorbid psychological health, expectation of
symptoms, emotional reactions to the experience
of a traumatic event, expression of a predisposed
disorder as a result of a traumatic stressor, ineffec-
tive coping strategies, and poor motivation may
better explain the enduring subjective complaints
of MTBI patients, than any specific effects of
MTBI.
The above findings showing essentially full
neuropsychological and psychological recovery
following a single, uncomplicated MTBI for most
patients also appear to extend to return to work
following MTBI. Dikmen et al. (1994) found that
82% of TBI patients who took 5 or fewer hours
to follow commands had returned to work by
12 months, with 84% back to work by 24 months,
compared to 87% of orthopedic trauma controls
who had returned to work in the first year post-
trauma.
Other summaries support the typical outcome
of good recovery following a single, uncompli-
cated MTBI. The Institute of Medicine (2008)
convened a group of expert scientists to review
literature concerning the long-term consequences
of traumatic brain injury of all severities, includ-
ing both closed head trauma and penetrating
brain injuries. In the summary of findings regard-
ing evidence for causal association, the following
levels of evidence were identified: 1) sufficient
evidence of a causal relationship, 2) sufficient evi-
dence of an association, 3) limited/suggestive
evidence of an association, 4) inadequate/insuffi-
cient evidence to determine whether an associa-
tion exists, and 5) limited/suggestive evidence of
no association. Most of the conclusions regarding
MTBI fell in category 4 (inadequate/insufficient
evidence of association), including MTBI and
neurocognitive deficits, MTBI without loss of
consciousness and dementia of the Alzheimer-
type, MTBI and PTSD, MTBI and long-term
adverse social functioning (e.g., unemployment,
diminished social relationships, decrease in the
ability to live independently), and all levels of

TBI in reference to mania or bipolar disorder,
attempted suicide, multiple sclerosis, amyotrophic
lateral sclerosis, as well as TBI survived for
6 or more months and premature death. Carroll
et al. (2004), in a review conducted under the
auspices of the World Health Organization
(WHO), concluded that for adults, cognitive
deficits and symptoms are common in the acute
stages of MTBI, but the majority of studies
report recovery for most persons within 3–12
months.
McCrae et al. (2009) presented an integrated
model of recovery after uncomplicated MTBI
encompassing three time periods post-trauma:
acute (immediately post-trauma to approximately
5 days), subacute (approximately 5 days to 30
days), and chronic period (greater than 30 days).
For the chronic period, a relatively small percent-
age of patients were observed to report persistent
symptoms and cognitive or other complaints
which may be influenced by injury (e.g. cases of
complicated MTBI with abnormal structural
imaging findings), or non-injury-related factors
(e.g., depression, chronic pain, PTSD, life stress or
secondary gain); the brain returned to a normal
state of cerebral function (e.g., normal activation
on functional neuroimaging); persistent post-
concussion symptoms may be observed in a small
percentage (<5%) of MTBI cases, significantly
influenced by noninjury factors.
FA C T O R S P O T E N T I A L LY
R E L AT E D T O P E R S I S T E N T
P RO B L E M S F O L L OW I N G
M I L D T R A U M AT I C
B R A I N I N J U RY
Wilson, Teasdale, Hadley, Wiedman, and Lang
(1994) demonstrated the need to consider GCS
and PTA in evaluating MTBI. These investigators
found a close association between GCS and PTA
for those patients who experienced 6 hours or
more of coma following TBI (note that 6 hours of
coma is beyond what would be considered
MTBI). Eight patients had coma less than 6 hours
with PTA greater than 7 days, and three of these
eight were only briefly unconscious, if at all. These
data demonstrated the importance of basing
diagnosis of MTBI on both circumscribed loss of
consciousness and circumscribed PTA.
Williams et al. (1990) found that patients with
GCS of 13–15 and CT evidence of structural
lesion were more similar in neuropsychological
outcome to patients with moderate TBI (GCS
9–12) than they were similar to those with MTBI
Mild Traumatic Brain Injury 241
(GCS 13–15 without CT scan abnormalities). The
GCS 13–15 group with CT-identified lesions was
identified as mild/complicated by Williams et al.
(1990).
Magnetic resonance imaging (MRI) is more
sensitive than CT scan in detecting lesions follow-
ing mild-to-moderate TBI (Levin, Amparo, et al.,
1987; Levin, Williams, Eisenberg, High, & Guinto,
1992). Levin et al. (1992) found that although
MRI-identified lesions were more prevalent than
those identified by CT in mild-to-moderate head
injury and more prominent in moderate (GCS
9–12) relative to mild (GCS 13–15) TBI, these
lesions resolved over 1 to 3 months follow-up,
paralleling the recovery seen in neuropsycho-
logical test scores. For some of the subjects with
acute MRI-identified lesions, however, neuro-
psychological impairment persisted despite
resolution of the lesion on MRI.
Dikmen, Machamer, and Temkin (2001)
further addressed factors related to presence and
persistence of deficits following MTBI, including
patients with complicated MTBI. Four groups of
subjects were formed, characterized by decreasing
sample size as a function of stringency of defini-
tion of the groups. The most inclusive group was
identified by GCS of 13–15, followed by a group
defined by GCS and time-to-follow commands of
less than 1 hour, followed by a group who met the
prior conditions with the added condition of
normal CT scan, followed by the most restrictive
classification that met all preceding criteria plus
had PTA less than or equal to 24 hours. At 1
month post-trauma, the group defined by GCS
13–15 alone differed on the Verbal Selective
Reminding Test from all other MTBI groups,
which did not differ from one another or from a
group of control patients with non-TBI trauma.
There were no 1-month group differences on
measures of attention, psychomotor speed, or
Performance IQ. At 1 year post-trauma, there
were no group differences on any measures.
In a subsequent investigation, Dikmen,
Machamer, and Temkin (2003) found that TBI
patients with GCS of 13–15 who also had abnor-
mal CT scans differed from TBI patients with
GCS of 13–15 without abnormal CT scans for
both level of consciousness and neuropsycholo-
gical outcome. The individuals with GCS 13–15
with positive CT scans had fewer cases with
GCS of 15, with a corresponding greater number
of cases with GCS 13 and 14; had longer time
to follow commands; and had longer PTA than
the group with GCS 13–15 without CT scan
242 forensic neuropsychology
abnormality. Similarly, the GCS 13–15 CT-positive
group had lower verbal memory (Selective
Reminding), Performance IQ, Trail Making B,
and Halstead Impairment Index at testing 1 month
post-trauma than the group of GCS 13–15
with normal CT, which itself did not differ from a
control group with non-TBI trauma. At 1 year
post-trauma follow-up, the CT-positive group
had lower Selective Reminding than the trauma
control group, with no differences between the
CT-negative and trauma control group.
Based on the research of Levin and colleagues
(Levin et al., 1992; Williams et al., 1990) and
Dikmen and colleagues (Dikmen et al., 2001,
2003), TBI patients with GCS of 13–15 who also
have CT scan or MRI abnormalities may not have
a truly MTBI. Moreover, the Dikmen et al. (2001,
2003) and Wilson et al. (1994) investigations
showed the importance of considering duration
of PTA in differentiating true MTBI from those
with apparent cases of MTBI who actually have
more severe injuries.
Radiologic abnormalities in cases with GCS of
13 to 15 have not always been associated with
poorer outcome. Hanlon, Demery, Martinovich,
and Kelly (1999) found no difference with respect
to neuropsychological status or vocational out-
come between patients who had positive findings
on CT scan versus those who were CT negative at
testing conducted approximately 6 months post-
trauma. Hughes et al. (2004) found neuropsycho-
logical differences at 72 hours post-trauma
between those MTBI with MRI abnormalities and
those without such findings; however, neither
group differed at 6 month follow-up on either
return to work or on post-concussion symptom
endorsement. In a study with small sample sizes
(n = 14 for uncomplicated MTBI, complicated
MTBI and normal controls), the complicated
MTBI group differed in cognitive function from
the uncomplicated MTBI group and control
groups, which did not differ from one another on
testing done within 40 days post-trauma (Borgaro,
Prigatano, Kwasnica, & Rexer, 2003). Both the
complicated and uncomplicated MTBI differed
from the control group on affective measures, but
did not differ from one another. On admission to
hospital, persons with GCS 14–15 and intracranial
abnormalities on CT scan did not perform differ-
ently on neuropsychological tests at time of admis-
sion or show GCS differences in comparison to
those with GCS 14–15 and no CT abnormalities,
although at one year follow-up those with CT
abnormalities were more likely to have persistent
symptomatic complaints and not be fully recov-
ered (Sadowski-Cron et al., 2006). Subjects meet-
ing criteria for MTBI who had evidence for
traumatic lesion on MRI performed less well
within 96 hours of injury on post-admission test-
ing than those who had MTBI without MRI evi-
dence of traumatic lesion (Kurca, Sivak & Kucera,
2006). Iverson (2006) found that those with com-
plicated MTBI performed less well on some tests
of a neuropsychological battery than those with
uncomplicated MTBI when evaluated within 2
weeks of injury, but the effect sizes were small to
medium, and the two groups could not be differ-
entiated using logistic regression analysis. Lange,
Iverson, and Franzen (2009) found that patients
with complicated MTBI performed less well on 3
of 13 cognitive measures, but had no significant
differences in the proportion of impaired scores,
with the exception of delayed verbal recall, on test-
ing conducted an average of 3.5 days post-trauma.
Returning to the original conceptualization of
complicated MTBI as equivalent to moderate TBI
suggested by Williams et al. (1990), Kashluba,
Hanks, Casey, and Millis (2008) found few
neuropsychological differences between these
groups either at rehabilitation discharge, or at
1-year follow-up. The only exception was that the
complicated MTBI group showed less severely
impaired information-processing speed and
verbal learning than did the moderate TBI group.
Both groups exhibited evidence of incomplete
recovery at 1-year follow-up.
To summarize, MTBI with radiologic evidence
of space-occupying lesion may or may not make
full neuropsychological recovery, similar to find-
ings characterizing moderate TBI. This contrasts
with the typical finding of full recovery within
3 months that characterizes patients suffering
uncomplicated MTBI.
Some investigators have presented data
suggesting that MTBI results in a reduction in
cerebral reserve (see Satz, 1993, for a general
discussion of brain reserve capacity following
brain injury). Ewing, McCarthy, Gronwall, and
Wrightson (1980) found evidence for persisting
cognitive deficits in apparently recovered MTBI
patients who were subjected to hypoxic stress.
This finding appears consistent with evidence
from the same laboratory demonstrating a longer
recovery time for persons following MTBI if there
was a history of prior concussion (Gronwall, 1989;
Gronwall & Wrightson, 1975).
Reduced cerebral reserve was also suggested
by the Collins et al. (1999) sports concussion

investigation, which found that collegiate football
players with one or more prior concussions who
also had preexisting learning disability had poorer
baseline (preseason) test results on the Trail
Making Test Part B and on the Symbol Digit
Modalities Test than did football players without
history of prior concussion. Guskiewicz et al.
(2003) found that football players with a history
of three or more concussions were three times
more likely to experience a subsequent concus-
sion than football players without history of
prior concussion. There was a dose effect of prior
concussion with length of recovery: 30% of play-
ers with history of three or more prior concus-
sions had symptoms lasting greater than 1 week
compared to 14.6% of players with one previous
concussion. Subsequently, Guskiewicz et al.
(2005), employing a questionnaire methodology
(but no direct neuropsychological evaluation),
found a significant association between recurrent
concussion (3 or more) and clinically diagnosed
mild cognitive impairment, and self-reported
memory impairments in retired professional
football players. Although there was no assoc-
iation between recurrent concussion and
Alzheimer’s disease, there was an earlier onset of
Alzheimer’s disease in the retired football players
relative to the general American male population.
Data also exist that challenge the hypothesis of
reduced cerebral reserve. Alterman et al. (1985)
found no significant neuropsychological perfor-
mance differences between alcoholic patients
with and without history of a prior MTBI.
Dikmen, Donovan, Loberg, Machamer, and
Temkin (1993) found no significant interactions
between alcohol use and head trauma severity in
relation to neuropsychological outcome in their
study of the full range of head trauma severity
(i.e., MTBI, moderate and severe TBI). Bornstein
et al. (1993) found no significant neuropsy-
chological differences between those HIV-positive
patients with a history of MTBI and those without
history of MTBI.
Others have not found convincing evidence of
poorer outcome in persons sustaining multiple
MTBIs. Bijur et al. (1996) did not find evidence
for cumulative effects of MTBI in comparing chil-
dren with a history of one, two, or three MTBIs
with non-head-injured orthopedic controls
with history of one, two, or three orthopedic
injuries. Bijur et al. suggested that cognitive defi-
cits associated with multiple MTBI were second-
ary to social and personal factors related to
multiple injuries rather than resulting from
Mild Traumatic Brain Injury 243
damage to the head. Cullum and Thompson
(1999) referenced an ongoing investigation that
found that MTBI patients with and without
history of prior MTBI did not differ from one
another or from a group of non-TBI trauma
control subjects when tested within 1 week and
within 2 months of the accident. Iverson, Brooks,
Lovell, & Collins (2005) found no measurable
effect of one or two previous self-reported
concussions on high school or college athletes’
preseason neuropsychological test performance
or symptom reporting. Collie, McCrory, and
Makdissi (2006) found no association between
self-reported history of up to four or more prior
concussions and performance on a computerized
cognitive assessment battery for a large sample of
Australian rules football players. Bruce and
Echemendia (2008) found no differences in
performance on a computerized cognitive battery
or in symptom report for a large sample of
collegiate male athletes who had no, one, two, or
more prior self-reported concussions. Ivins et al.
(2009) found no differences in neuropsychologi-
cal performance or post-concussive symptom
report for persons with no, one, or two, or more
prior TBIs in military veterans with no injury,
injury but no MTBI, and MTBI tested upon return
from deployment in Afghanistan or Iraq.
Belanger, Spiegel, and Vanderploeg (2010)
conducted a meta-analysis of the sports concus-
sion literature based on eight studies, involving
614 cases of multiple MTBI and 926 control cases
suffering a single, self-reported MTBI. The overall
effect of multiple self-reported MTBIs was mini-
mal and not significant (d = 0.06). Belanger et al.
found significant heterogeneity of results using
the Q statistic, and therefore conducted subse-
quent meta-analysis by test domain. Significant
heterogeneity remained for six of eight ability and
symptom report domains. Per subtest domain,
executive function (d = 0.24) and delayed memory
(d = 0.16) showed small but significant effect sizes.
Although Belanger et al noted little association
between two or more MTBIs and persistent
problems, they did hypothesize that there may
still be a “threshold effect” yet to be determined
that could lead to persistent sequelae as a function
of multiple prior concussion, calling to mind
dementia pugilistica and a prior meta-analysis
(Belanger & Vanderploeg, 2005) that showed a
significant effect (d = 0.71) using number of
boxing bouts, length of boxing career, and/or
frequency of heading in soccer as the measure of
exposure.
244 forensic neuropsychology
To summarize, there is no consistent evidence
at the present time showing an association of
multiple MTBI with increased neuropsychologi-
cal impairment in comparison to cases with a
single MTBI. It is important to consider that
some persons suffering multiple MTBI may differ
neuropsychologically on a premorbid basis, as
suggested by Bijur et al. (1996). Additional
research using orthopedic trauma control subjects
with histories of one, two, or three prior injuries
may provide further clarification of this issue.
The use of improvised explosive devices (IEDs)
in the wars in Afghanistan and Iraq have led
to blast injury as the hallmark injury of these
conflicts (Belanger, Kretzmer, Yoash-Gantz,
Pickett, & Tupler, 2009). Belanger et al. observed
that the primary mechanism of brain injury from
explosion is over-pressurization or blast wave
effect, contrasted with the acceleration/decelera-
tion effects characteristic of typical closed head
injury, raising the possibility that blast injury
results in a different type of brain trauma. To
examine these issues further, Belanger et al. (2009)
compared the neuropsychological test results of
patients suffering mild or moderate/severe TBI
from blast injury to groups of patients suffering
mild or moderate TBI from nonblast trauma
effects. Overall, there were no neuropsychological
differences as a function of blast versus non-blast
injury. Effects were observed for injury severity
(mild vs. moderate/severe), but these were mod-
erated also by presence of PTSD symptomatology.
Only the CVLT-II showed a continuing signifi-
cant difference between mild and moderate/
severe TBI following covariation of time-since-
injury and PTSD symptom report. Belanger et al.
(2009) concluded that cognitive sequelae follo-
wing TBI were determined more by severity of
injury than mechanism of injury on verbal learn-
ing and memory measures.
In a study of blast-related MTBI alone,
Brenner et al. (2010) studied a total of 45 soldiers,
all of whom reported a blast-caused MTBI, 28 of
whom had persisting symptoms, and 17 of whom
presented with symptoms of PTSD. The group
with persisting symptoms of MTBI did not differ
on neuropsychological test performance from the
subjects denying persisting problems. Similarly,
the subjects with PTSD symptoms did not differ
on neuropsychological test performance from
those without PTSD. To date, the results of
Brenner et al. (2010) and Belanger et al. (2009) do
not provide any support for an atypical outcome
following blast-related MTBI.
S Y M P T O M AT I C C O M P L A I N T
I N M I L D T R A U M AT I C
B R A I N I N J U RY : T H E
POSTCONCUS SION
SYNDROME
Post-concussion syndrome (PCS) refers to a con-
stellation of somatic (e.g., headache), cognitive
(e.g., memory), and emotional (e.g., irritability)
symptoms following MTBI (Alexander, 1995;
Axelrod et al., 1996). There has been a longstand-
ing controversy over whether PCS results from
neurological or physiogenic factors versus non-
neurological or psychogenic factors (Gasquoine,
1997; Lishman, 1988). Physiogenic factors are likely
operative in the first month post-trauma, during
the time when ongoing neuropsychological
deficits are resolving, as per Figure 9.1, whereas
psychogenic factors are more likely related to
chronic PCS, also known as persistent post-concus-
sion syndrome (PPCS), persisting several months
after MTBI (Alexander, 1995; Binder, 1997).
For example, Dikmen, McLean, and Temkin
(1986) found that, 1 month after trauma, 3 of 12
PCS symptoms (bothered by noise, insomnia, and
memory difficulties) discriminated MTBI from
control subjects, but at 1 year, there were no dif-
ferences in symptom endorsement. Binder (1997)
reported that 7–8% of MTBI patients remained
symptomatic on a chronic basis, a value slightly
higher than the 5% rate of persistent neuropsy-
chological deficit reported by Binder et al. (1997).
Noninjury factors have been reported in asso-
ciation with either severity of symptom report
and/or persistence of symptom report. Kashluba,
Paniak, and Casey (2008) compared high and low
symptom severity MTBI groups and found that
the groups were not differentiated by loss of con-
sciousness, length of loss of consciousness, dura-
tion of PTA or injury severity score, but the groups
did differ on the percentage seeking or receiving
compensation (60.0% for high severity, 23.8% for
low severity). The high severity group also showed
a greater number of pre-injury life stressors,
pre-injury treatment for psychological problems,
and pre-injury use of analgesic, psychotropic,
or neurological medication. Stulemeijer, Vos,
Bleijenberg, and van der Werf (2007) found that
PCS cognitive complaints were strongly related
to lower educational levels, emotional distress,
personality, and poorer physical functioning, but
not to injury characteristics, concluding that
self-reported cognitive complaints were more
strongly related to premorbid traits and physical
and emotional state factors than to actual

cognitive impairments on formal neuropsycho-
logical testing. Kirsch et al. (2010) compared an
outlier subgroup of MTBI with extreme persisting
distress on the Rivermead Post-concussion
Symptoms Questionnaire to a group without per-
sisting complaints and found that the outlier
group had a history of prior head injury, preinjury
disability, history of substance use, unemploy-
ment, and elevated somatic symptoms when ini-
tially seen in the emergency department. At 12
months, the outlier group had a higher use of
health services and presence of litigation in the
post-injury period than the non-outlier group.
It is noteworthy that although prior head injury
was a characteristic of the outlier group, 39 of 45
non-outliers had prior history of head injury
and did not convert to outlier status, with report
of good recovery at 12 months. Last, Lange,
Iverson, Brooks, and Rennison (2010) found that
MTBI subjects receiving workers’ compensation
who failed the Test of Memory Malingering
(TOMM; Tombaugh, 1996), endorsed more post-
concussive complaints, reported poorer cognitive
performance, and performed less well on tests of
attention, memory, and executive functioning
than did MTBI patients receiving workers’ com-
pensation who passed the TOMM, demonstrating
a clear association between poor effort (failed
TOMM), elevated symptom report and reduced
cognitive performance.
There is increasing evidence that questions
the validity of the PCS symptom constellation.
To qualify as a syndrome, a condition must
demonstrate a set of specifically associated symp-
toms broadly present in persons who have the
condition and absent in those who do not have it
(note the relevance to sensitivity and specificity).
Symptoms thought to be representative of PCS,
such as headache, memory difficulty, and irrita-
bility, are also seen in persons with suspected neu-
rotoxic exposure (Larrabee, 1990; Lees-Haley &
Brown, 1993) and in persons who have chronic
pain but no history of TBI (Iverson & McCracken,
1997). Level of depression is more strongly associ-
ated with PCS report than is head injury status
(Brulot, Strauss, & Spellacy, 1997; Gunstad &
Suhr, 2001; Trahan, Ross, & Trahan, 2001). These
symptoms occur frequently in the non-brain-
injured population; for example, Lees-Haley
and Brown (1993) found that 62% of outpatient
family practice patients endorsed headache, 20%
endorsed memory problems, and 38% endorsed
irritability. Subsequently, Garden and Sullivan
(2010) reported high rates of PCS symptom
Mild Traumatic Brain Injury 245
endorsement in healthy university students and
healthy community volunteers, for example, 81%
endorsed headache, 52% endorsed dizziness, 78%
endorsed irritability, 73% endorsed concentration
problems, and 56% endorsed memory problems.
In a subsample of depressed participants, endorse-
ment of PCS symptoms increased, with 96%
reporting headaches, 75% reporting dizziness,
62% reporting nausea, 83% reporting poor con-
centration, and 75% reporting memory problems
(Garden & Sullivan, 2010). Lees-Haley and Brown
(1993) found very high endorsement of PCS
symptoms in persons in litigation for emotional
distress or industrial stress, without neurological
claims or injuries, with 89% reporting headaches,
53% reporting memory problems, and 77%
reporting irritability. In this vein, litigating MTBI
subjects endorsed more symptoms than nonliti-
gants, despite not differing on demographic char-
acteristics, TBI severity ratings, or premorbid risk
factors for poor outcome (Feinstein, Ouchterlony,
Somerville, & Jardine, 2001). PCS-type symptoms
increase in relation to stress, independent of pres-
ence or absence of history of MTBI (Gouvier
et al., 1992). As noted in an earlier section of this
chapter, Ettenhofer and Abels (2009) found no
differences in PCS symptom endorsement on the
Gouvier et al. (1992) PCSC for MTBI compared
to an orthopedic injury sample, on testing done
approximately 3 years post-trauma, but that PCSC
endorsement was related to psychiatric symptom
endorsement on the Derogatis and Spencer (1982)
BSI for both groups of subjects. Moreover, BSI
Somatization correlated with PCSC Dizziness and
Fatigue; BSI Hostility correlated with PCSC
Irritibility; BSI Obsessive-Compulsive Symptoms
correlated with PCSC Memory Problems and
Difficulty Concentrating, and BSI Total correlated
with PCSC Anxiety.
Table 9.2 displays PCS-type complaints for the
Lees-Haley and Brown (1993) outpatient medical
patients, nonneurological litigants, and a sample
of individuals with MTBI reported by Mittenberg,
DiGuilio, Perrin, and Bass (1992). These data
clearly demonstrate the poor specificity for pur-
ported PCS symptomatic complaints, which can
occur with high frequency in nonconcussed
persons, such that relying on these symptoms as
indicative of PCS would result in abnormally
high false-positive diagnoses. In this vein, it is
noteworthy that of the eight symptoms proposed
in the Diagnostic and Statistical Manual of Mental
Disorders, fourth edition (DSM-IV; American
Psychiatric Association, 1994) as part of the
246 forensic neuropsychology

TABLE 9.2 COMPLAINT BASE RATES

Percent Endorsing Complaint

Symptom Mild Medical Non-neurologic
Traumatic Outpatientsb Litigantsb
Brain Injurya

Headache 59.1 62 88
Anxiety 58.3 54 93
Depression 63.2 32 89
Poor 70.5 26 78
Concentration
Dizziness 52.0 26 44
Visual Problems 45.4 22 32
Irritability 65.9 38 77
Fatigue 63.9 58 79
Trouble Thinking 57.6 16 59c
Poor Memory 50.6d 20 53
a
Mittenberg et al., 1992; 100 persons with MTBI
b
Lees-Haley & Brown, 1993; 50 nonlitigating medical outpatients and 170 per-
sons in litigation for psychological stress or distress, without neurological claims
or injuries
c
“Confusion” in Lees-Haley & Brown
d
“Forgets why they entered a room,” the most frequent of 20 memory complaints
in Mittenberg et al.

research criteria for PCS, only one—disordered
sleep—discriminated individuals with MTBI
from control subjects at 1 month post-trauma in
the Dikmen et al. (1986) study. This same symp-
tom of disturbed sleep was endorsed by 59% of
the Iverson and McCracken (1997) non-TBI
chronic pain patients. All eight DSM-IV PCS
symptoms also had high rates of occurrence in the
Lees-Haley and Brown (1993) non-head-injured
litigants, ranging from 44% (dizziness) to over
80% (disordered sleep, 92%; headache, 88%; anxi-
ety, 93%). Gunstad and Suhr (2004) reported
higher PCS endorsement rates in depressed
subjects and headache sufferers than in control
subjects and subjects with history of MTBI, who
did not differ from one another.
In addition, different diagnostic criteria result
in differing numbers of MTBI subjects classified
as showing persistent post-concussional disorder.
Boake et al. (2004) found that fewer MTBI sub-
jects met DSM-IV criteria of both cognitive defi-
cit and symptoms interfering with social role
functioning than met the ICD-10 criteria, which
were limited to history of TBI plus persistent
symptom report. Boake et al. opined that in the
absence of evidence about the relative advantages
of the DSM-IV and ICD-10 diagnostic criteria
for post-concussional syndrome, there was
minimal justification for preferring either set of
diagnostic criteria. In a subsequent investigation,
McCauley et al. (2008) found that persistent
post-concussional syndrome (PCS) criteria of the
ICD-10 were met 3.1 times more frequently than
the persistent post-concussional disorder (PCD)
criteria of DSM-IV. Potential compensation was
an equally significant factor in both criteria sets,
and there was a higher frequency of major depres-
sive episode and PTSD in subjects meeting PCS
and PCD criteria, lending support to the hypoth-
esis that psychological factors play a significant
role in persistent PCS/PCD.
Post-concussion syndrome and other “neuro-
logical” symptoms are poorly correlated with
actual neuropsychological test performance for a
variety of clinical samples. Patients with severe
TBI, Alzheimer-type dementia, and nontraumatic
focal hemispheric brain disease frequently dem-
onstrate anosognosia or denial or minimization
of deficit (Feher, Larrabee, Sudilovsky, & Crook,
1994; Prigatano, 1996; Prigatano & Altman, 1990).
Conversely, persons without neuropsychological
deficit may misreport memory dysfunction
secondary to depression (Larrabee & Levin, 1986;
Larrabee, West, & Crook, 1991; Williams, Little,
Scates, & Blockman, 1987) or secondary to soma-
tization (Hanninen et al., 1994). Brulot et al.

(1997) found no correlation between Minnesota
Multiphasic Personality Inventory 2 (MMPI-2)
neurocorrection items (i.e., those items purport-
edly related to neurological dysfunction) and
initial GCS, duration of PTA, or neuropsychologi-
cal test performance in a large sample of TBI
patients comprised primarily of subjects with
MTBI. Rather, the purported neurocorrection
items were significantly associated with elevations
on the MMPI-2 Depression Content Scale.
Given these findings, the presence of an asso-
ciation between cognitive symptom complaint
and actual test performance should raise suspi-
cions regarding the accuracy of both symptom
report and test performance. Indeed, Gervais,
Ben-Porath, Wygant and Green (2008) found that
a significant association between scores on a
Memory Complaint Inventory and performance
on the California Verbal Learning Test actually
disappeared when subjects who failed symptom
validity testing were excluded from the analysis.
Mittenberg et al. (1992) found that head
trauma-naıve normal subjects, when asked to
imagine they had sustained an MTBI, endorsed
the same set of PCS symptoms as did persons with
actual MTBI. Of particular interest, the subjects
with MTBI underestimated the frequency at
which these symptoms occurred prior to their
trauma (note that this “good old days” bias
reported by Mittenberg et al. has been replicated
by Gunstad & Suhr, 2001; 2004, and Iverson,
Lange, Brooks, & Rennison, 2010). Mittenberg
et al. (1992) related their results to a process of
selective attentional bias to common internal
states, stress, and arousal. Putnam and Millis
(1994) provided a similar explanation, charac-
terized PPCS as a somatoform disorder, and
drew parallels between selective attentional
bias in persons with MTBI and the self-directed
selective attention to bodily sensations in persons
with elevated health concerns (see Watson &
Pennebaker, 1989; also see Mittenberg &
Strauman, 2000). Subsequently, Delis and Wetter
(2007), influenced by the work of Mittenberg
et al. (1992), Putnam and Millis (1994), and
Watson and Pennebaker (1989), proposed criteria
for cogniform disorder and cogniform condition,
which delineate a type of somatoform disorder
characterized by excessive or atypical symptom
report in the absence of otherwise demonstrated
neurological abnormality or evidence for malin-
gering. PPCS would fit nicely into the cogniform
criteria proposed by Delis and Wetter (Larrabee,
2007).
Mild Traumatic Brain Injury 247
Failure to appreciate the nonspecificity of
PCS symptoms can lead to misdiagnosis and
iatrogenesis of persistent complaints (Larrabee,
1997; Newcombe, Rabbitt, & Briggs, 1994). If a
patient is prone to attend selectively to common
phenomenon and incorrectly attribute these to
“brain injury,” then “diagnosing” these symptoms
as PCS can be quite damaging. Such a patient,
who on a premorbid basis manifests tendencies
toward excessive health concerns, may focus
excessively on common daily symptoms such as
irritability and forgetfulness and become more
anxious regarding these “symptoms,” fearing that
these are the result of their recent MTBI. The
problem is compounded if these individuals are
informed by a variety of health care professionals
that they have suffered TBI.
Consistent with the above conceptualization of
PPCS, Mittenberg, Tremont, Zielinski, Fichera, and
Rayls (1996) found that providing a patient with
MTBI with a printed cognitive behavioral manual
and having the patient meet with a therapist prior
to hospital discharge resulted in shorter duration of
symptoms and lower symptom endorsement rates
at 6-month follow-up in comparison to a nontreat-
ment control group who received routine hospital
treatment and discharge recommendations. The
cognitive behavioral manual reviewed the nature
and incidence of expected symptoms, the cognitive
behavioral model of symptom maintenance and
treatment, as well as techniques for reducing symp-
toms and instructions for gradual resumption of
premorbid activities (see Mittenberg, Zielinski, &
Fichera, 1993).
Negative expectations about outcome of MTBI
can also affect neuropsychological test perfor-
mance in addition to maintaining or increasing
PCS symptom report. Suhr and Gunstad (2002)
found that those MTBI subjects who had their
attention called to their prior head injury history
and who were advised of the potential effects of
head injury on cognition (“diagnosis threat”) per-
formed less well on measures of general intellect
and memory than did a group of MTBI subjects
provided with neutral test instructions. Moreover,
the diagnosis threat group rated themselves as
putting forth less effort on the tests, and their self-
rated degree of effort correlated with their perfor-
mance on the Rey Auditory Verbal Learning Test
and with their performance on the Complex
Figure Test. Although Suhr and Gundstad did not
administer symptom validity testing, the scores
reported in their Table 2 are not consistent with
the presence of malingering in the diagnosis threat
248 forensic neuropsychology
group (e.g., their mean age-scaled score on
Digit Span was 11.1). Hence, the motivational
factors affecting the diagnosis threat group’s
performance appear to be unintentional and out-
side their conscious control. In a subsequent
investigation, Suhr and Gunstad (2005) replicated
the finding of poorer performance in their “diag-
nosis threat” group in comparison to the group
receiving neutral test instructions. Contrary to
their earlier findings, the “diagnosis threat” group
did not rate themselves as putting forth less effort
on testing than the neutral instruction group.
Moreover, they did not perform differently from
the neutral group on an objective measure of per-
formance validity, the Word Memory Test (Green
et al., 1996), nor was their performance related to
increased anxiety or depression. In summary, the
“diagnosis threat” research of Suhr and Gunstad
(2002; 2005) is a compelling demonstration of
iatrogenesis in MTBI.
Last, persistent symptomatic complaint of
persons having sustained MTBI has been used to
characterize a group of subjects thought to repre-
sent a “miserable minority,” who are suffering
from continuing effects of their MTBI (Bigler,
2008; Ruff, Camenzuli, & Mueller, 1996; Ruff &
Richardson, 1999). The estimate typically associ-
ated with the prevalence of this “miserable minor-
ity” is 15% (Alexander, 1995). As Greiffenstein
(2009) has observed, this prevalence rate is inac-
curate, as it was based on a material misunder-
standing of two studies: McClean, Temkin,
Dikmen, and Wyler (1983), and Rutherford,
Merret, and McDonald, (1979). Greiffenstein
clarified that the McClean et al. investigation fol-
lowed only 20 patients for 1 month; there was no
1-year follow-up (i.e., no chronic follow-up data).
For the Rutherford et al. cases, 19 (14.5%) still
reported complaints at 1-year follow-up, but eight
were involved in lawsuits, six showed malingering
signs at 6 months, and most complained of new
symptoms at 1 year that were not reported at 6
weeks post-injury. Moreover, Greiffenstein noted
that there was no control group, which made it
difficult to draw conclusions about population
base rates for symptoms which, as already dis-
cussed in this section and demonstrated in
Table 9.2, are nonspecific for MTBI. Interestingly,
Rutherford (1989), in a follow-up to his earlier
work, concluded that the presence of litigation
was associated with more than doubling the
long-term symptom rate. Rutherford’s conclusion,
over 20 years ago, has been echoed by the meta-
analysis of Belanger et al. (2005) which found
litigation to be associated with persistent com-
plaints and poorer neuropsychological test per-
formance in MTBI, and by the best-evidence
synthesis conducted by the World Health
Organization, which concluded that where symp-
toms of MTBI persisted, compensation/litigation
was the only consistent factor, with little evidence
for other predictors (Carroll et al., 2004).
DIFFERENTIAL DIAGNO SIS
O F T H E PAT I E N T W I T H M I L D
T R A U M AT I C B R A I N I N J U RY
As noted by Binder et al. (1997), the low base rate
(5%) of persistent impairment following MTBI,
results in positive predictive power of less than
50%, indicating a clinician is more likely to be
incorrect than correct in diagnosing brain damage
as the cause of persistent impairment. These data
do not indicate that persistent impairment cannot
occur, but do strongly underscore the need for the
clinician to perform a careful differential diagno-
sis of the individual MTBI patient because the risk
of false-positive diagnosis is high (Binder, 1997).
The necessity of careful differential diagnosis is
underscored by the data in Figure 9.2 from Iverson
(2005), which displays effect sizes (mean of MTBI
group minus the mean of the comparison group,
divided by the pooled standard deviation) for
MTBI at various points of recovery (0–6 days,
7–30 days, 1–3 months), in comparison to effect
sizes for acute and chronic moderate/severe TBI,
cannabis use, dysthymia, benzodiazepine with-
drawal, depression, litigation, ADHD, bipolar
disorder, chronic benzodiazepine use, and exag-
geration/malingering. Figure 9.2 clearly shows
how a patient’s clinical history and disorders other
than MTBI provide an important framework for
interpretation of neuropsychological test data.
Risk factors for persistent problems following
MTBI were reviewed in the section, “Factors
Potentially Related to Persistent Problems Follo-
wing Mild Traumatic Brain Injury.” These factors
include the possible effects of prior MTBIs on
increased symptoms or prolonged recovery time
following a subsequent MTBI. If such effects do
occur, they should be manifested early on,
with demonstration of prolonged confusion/
disorientation or other PCS symptoms in the
acute and subacute period following an MTBI
(cf. Guskiewicz et al., 2003). Conversely, a very
rapid return to orientation and processing of
ongoing memory following an MTBI would
appear to contradict any potential additive effects
of a prior MTBI.
 Mild Traumatic Brain Injury 249

1.1
1
0.9
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0

AD tion
C rate ver

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Ex ic b er
M

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M

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an

hr
ys

ep
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tig on

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od

od e-
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TB

ag en
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nz ia

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th

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er

e se
I
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I

od
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ra
ia

i
z

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-
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ys

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e

in
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ith

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rin
24 nt

aw

g
al
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s

FIGURE 9.2: Neuropsychological effect sizes for MTBI at different points of recovery, in comparison to
moderate-severe TBI, and various other disorders, drug use/withdrawal, litigation, and exaggeration/malin-
gering. Effect sizes less than 0.3 are very small and difficult to detect in individual patients because the patient
and control groups largely overlap (overlap for an effect size of 0.3 is 78.7%). From Iverson (2005) and
McCrea (2008), with permission.

As noted, individuals with apparent MTBI
who may have admission GCS values in the MTBI
range of 13 to 15, who also have CT or MRI abnor-
malities, focal neurological findings on day of
injury, or PTA lasting longer than 24 hours are
not actually individuals with MTBI. Rather, these
are cases of complicated MTBI. Such cases may
have recovery patterns more similar to moderate
TBI as opposed to MTBI; that is, these cases may
have persistent neuropsychological deficits on a
chronic basis.
Thus, the careful differential diagnosis of the
patient with MTBI must begin with the acute
injury characteristics (Alexander, 1995). Records
from EMS rescue runs and hospital ER records
are important for characterizing day-of-injury
TBI severity. These records will provide informa-
tion on level of orientation, GCS rating, time of
accident, and time spent in the hospital, as well as
procedures conducted in the hospital. The
memory and orientation of the patient with MTBI
can be evaluated during clinical interview and
later cross-checked against the EMS and ER
records. Statements characterizing a patient as
“oriented times three” actually describe the
highest level of verbal response on the GCS.
Moreover, orientation to time is typically the last
component of orientation to recover during the
resolution of PTA (High, Levin, & Gary, 1990).
Hence, someone who is oriented times three
(time, place, and person) is most likely no longer
in PTA. The ER records will also contain informa-
tion on presence/absence of focal neurological
signs and whether a CT scan was done, as well as
the results of any CT scan.
The section on PCS, which reviewed the
nonspecificity of symptoms for MTBI, demon-
strated the relationship of these symptoms to
factors of depression, stress, and somatization.
Consequently, any careful differential diagnosis of
the individual MTBI case should also consider the
possibility of symptom expression and mainte-
nance because of a diagnosable psychiatric disor-
der. Binder (1997) cited Symonds (1937), who
stated that, “It is not only the kind of injury that
matters, but the kind of head” (p. 1092). As Binder
observed, the kind of head is virtually as broad as
the DSM-IV.
250 forensic neuropsychology
In addition to being sensitive to neurological
dysfunction, performance on neuropsychological
tests is also affected by a variety of psychiatric
disorders, particularly disorders such as depres-
sion that affect attention and effortful processing
(Cohen, Weingartner, Smallberg, Pickar, &
Murphy, 1982; Cohen, 1993). Several DSM-IV
disorders, including schizophrenia, mood disor-
ders, anxiety disorders, and particularly posttrau-
matic stress disorder (PTSD), are characterized by
accompanying cognitive symptoms (American
Psychiatric Association, 1994; also see Figure 9.2).
Levin et al. (2001) found no neuropsychologi-
cal differences at 3 months post-trauma between
trauma controls and a group of patients with
mild-to-moderate TBI. In contrast, when the
trauma control and MTBI groups were combined,
then divided on the basis of presence/absence of
either PTSD or major depressive disorder (MDD),
differences emerged on neuropsychological test-
ing. Patients with PTSD performed significantly
less well on the Wisconsin Card Sorting Test than
did patients without PTSD. Patients with MDD
performed significantly less well on the Symbol
Digit Modality Test, Rey Complex Figure, Verbal
Selective Reminding Test, and Wisconsin Card
Sorting Test than did patients without MDD. In
particular, Levin et al. found that MDD was
comorbid with PTSD, in addition to the afore-
mentioned neuropsychological abnormalities,
and associated with disability measured by the
Glasgow Outcome Scale and Community
Integration Questionnaire.
Chapter 13 in this volume reviews somato-
form stress disorders, which must also be consid-
ered in any differential diagnosis of suspected
MTBI. Mittenberg and Strauman (2000) consid-
ered PPCS following MTBI as a unique somato-
form disorder specific to concussion. Alternatively,
significant overlap of PCS symptoms with other
disorders not characterized by history of concus-
sion (e.g., chronic pain, Iverson & McCracken,
1997; litigants claiming psychological injuries,
Lees-Haley & Brown, 1993) suggests that PPCS
may be one of many exemplars of a more general
category of somatoform stress disorder rather
than specific to MTBI. This conclusion was sup-
ported in particular by Gouvier et al. (1992), who
found no difference in rates of PCS symptom
endorsement in college students who had history
of MTBI compared with students who did not
have history of MTBI. Moreover, both the MTBI
and non-MTBI students experienced increased
PCS symptom endorsement under periods of
heightened daily stress. Cogniform disorder, as
proposed by Delis and Wetter (2007) and dis-
cussed earlier in this chapter, may explain PPCS
as a specific type of somatoform disorder charac-
terized by atypical and/or excessive cognitive
complaints.
Developmental disorders (Spreen, Risser, &
Edgell, 1995; Yeates, Ris, Taylor, & Pennington,
2010) can also affect symptomatic complaints
and neuropsychological test performance. Deve-
lopmental learning disorders can present with
specific reduction in verbal cognitive, calcula-
tional, and memory skills (Fletcher, Lyon, Fuchs,
& Barnes, 2007; Rourke, 1991). Developmental
nonverbal learning disability can result in signifi-
cant social interaction difficulties in addition to
specific reductions in nonverbal visual perceptual
skills (Rourke, 1995). Persons with preexisting
diagnoses of attention-deficit/hyperactivity disor-
der can show neuropsychological deficits in atten-
tion, as well as problems in impulse control
(Barkley, 2006; also see Figure 9.2).
Chronic pain and pharmacological treatment
of pain are also related to symptomatic complaints
similar to those in PCS (Iverson & McCracken,
1997) as well as to changes in neuropsychological
test performance (Taylor, Cox, & Mailis, 1996;
Uomoto & Esselman, 1993). Chronic pain com-
plaints, particularly headache and neck/shoulder
and back pain, are significantly more frequent in
those with MTBI relative to moderate or severe
TBI; for instance, 95% of those with MTBI in one
series had pain complaints, in contrast to only 22%
of individuals with moderate-to-severe TBI with
pain complaints (Uomoto & Esselman, 1993).
Taylor et al. (1996) compared the information-
processing performance of three groups of
patients, those with (a) whiplash, (b) chronic pain
without history of whiplash or head injury, and
(c) moderate-to-severe TBI. The whiplash and
chronic pain groups were carefully matched on
IQ, WMS-R Digit and Visual Span, pain severity
ratings, and MMPI-2 profiles. Taylor et al. found
no group differences on either the Paced Auditory
Serial Addition Test (PASAT) or Auditory
Consonant Trigrams procedures. Both the chronic
pain and whiplash groups had higher pain ratings
and MMPI-2 Depression scales than the moder-
ate-to-severe TBI group, but did not differ from
one another. These data demonstrate the effects of
chronic pain on symptom report and neuropsy-
chological test performance. Moreover, these data
contradict the association between whiplash and
brain dysfunction secondary to MTBI claimed by

some investigators (Sweeney, 1992). Indeed,
Taylor et al. (1996) concluded that their results
demonstrated poor specificity for detecting subtle
effects of brain trauma and did not support the
theory of neuronal degeneration as the etiology of
whiplash-related cognitive complaints.
Substance abuse, particularly alcohol abuse, is
a significant differential diagnostic consideration,
particularly given the known association of alco-
hol use with motor vehicle accidents. As reviewed,
alcohol use does not appear to affect outcome
adversely in MTBI (Alterman et al., 1985; Dikmen
et al., 1993). Alcohol abuse, in and of itself, how-
ever, is certainly associated with neuropsychologi-
cal deficits (Parsons, Butters, & Nathan, 1987).
Data also exist demonstrating that nonalcoholic
progeny of alcoholic parents perform more poorly
on neuropsychological testing than do nonalco-
holic progeny of nonalcoholic parents (see Parsons,
1987, for a review of these findings; also see
Montserrat, Rodriguez-Holguin, & Cadaveira,
1999). Bolla reviews the neuropsychological effects
of drugs of abuse in chapter 11 of this volume.
A major consideration in any differential diag-
nosis of MTBI is the possibility that deficits and
complaints are the result of malingering.
Malingering, the exaggeration or fabrication of
symptoms or deficits for external incentives in
adversarial circumstances, is reviewed by Larrabee
in chapter 5 of this volume. Malingering is a fre-
quent occurrence in litigated MTBI cases.
Larrabee (2003) and Mittenberg et al. (2002)
found, using different methodologies, an approxi-
mate 40% base rate of malingering in litigated
MTBI cases, suggesting that this is a reliable esti-
mate of malingering base rate on average.
Larrabee, Millis, and Meyers (2009) reviewed
additional research that further supports an aver-
age base rate of malingering of 40% in settings
with external incentive, including MTBI as well as
other alleged conditions. The base rate of 40% is
eight times the 5% frequency of persistent neu-
ropsychological deficits in individuals with MTBI
who were followed prospectively since the time of
their injury and reported by Binder et al. (1997).
Indeed, Mittenberg et al. (2002) argued that, given
Binder et al.’s 5% base rate of persistent deficit
following MTBI and their survey data indicating a
malingering base rate of 40%, the actual base
rate of malingering in litigants showing neuro-
psychological deficits following MTBI may be as
high as 88%. Refer to chapter 5 in this volume for
further discussion of the evaluation and diagnosis
of malingering.
Mild Traumatic Brain Injury 251
FUTURE DIRECTIONS
There are two main areas for which additional
research will be of interest: (a) developing a better
understanding of the persons falling in the miser-
able minority who have less than the expected
full recovery following MTBI and (b) additional
research into the consequences of multiple
MTBIs. Do persons in the miserable minority
have preexisting problems that predispose to
experiencing less than full recovery from MTBI?
Following how many MTBIs does someone need
to become concerned about potential permanent
neuropsychological deficits?
Research on identification of persons who are
going to fall in the miserable minority needs to be
conducted on a prospective basis from the time of
injury forward, rather than on the basis of samples
of convenience collected from persons presenting
for clinical services 1 or 2 years post-trauma.
As discussed in this chapter, following patients
prospectively, from the time they enter the emer-
gency room, ensures a study of a representative
sample of MTBI.
Given the strong evidence emerging from the
sports concussion research of full recovery from a
single MTBI (Belanger et al., 2009; Collins et al.,
1999; Echemendia et al., 2001; Macciocci et al.,
1996; McCrea, 2008; McCrea et al., 2003) and the
strong evidence, in prospective research, of full
recovery (Belanger et al., 2005; Binder et al., 1997;
Dikmen et al., 1995; Frencham et al., 2005;
Schretlen & Shapiro, 2003), it may develop that
persons falling in the miserable minority have
persisting complaints and problems on a psycho-
logical basis as part of a somatoform equivalent
disorder (Delis & Wetter, 2007; Mittenberg et al.,
1992, 1996; Putnam & Millis, 1994; Suhr &
Gundstad, 2002; 2005), as a consequence of
post-traumatic stress disorder (Levin et al., 2001),
or as a consequence of preexisting psychiatric or
neurological conditions (Dikmen et al., 2001;
Luis, Vanderploeg, & Curtiss, 2003).
Alternatively, it may develop that, as a func-
tion of greater neurological insult, persons with
GCS of 13 are at greater risk for less-than-full
recovery than are persons who have GCS of 15
(Culotta et al., 1996). Consequently, efforts
directed at grading the severity of MTBI, such as
have been developed for sports concussion
(American Academy of Neurology, 1997) or
criteria developed by Ruff and Richardson (1999)
that emphasize duration of PTA and persistence
of neurological symptoms in the first 24 hours
post-trauma, may yield information useful in
252 forensic neuropsychology
predicting who will become part of the miserable
minority. Of interest, Vanderploeg, Curtiss, and
Belanger (2005) reported data showing no signifi-
cant differences between veterans reporting
a history of MTBI compared to those reporting
history of injury in a motor vehicle accident and
those reporting no injury history on 15 separate
neuropsychological tests (mean effect size = −.03,
consistent with meta-analytic outcome data on
chronic effects of MTBI); rather, there was
evidence for a subgroup characterized by prob-
lems with left-sided inattention and gait distur-
bance. In particular, subtle attention problems
(defined as examinee request to discontinue the
PASAT) were associated with left-sided visual
imperceptions, and excessive proactive inhibition
on the CVLT (Trial 1 minus Trial B difference
of 3 or more) was associated with impaired
tandem gait. These data suggest greater neuro-
logic insult in those MTBI subjects manifesting
these difficulties which, since subjects were
identified based on a self-reported rather than
medically documented history of MTBI, may
have characterized individuals who actually had
sustained a complicated MTBI.
MRI diffusion tensor imaging (DTI) holds
promise as a means for identifying those MTBI
subjects who may have sustained relatively greater
initial trauma. Rutgers et al. (2008) found differ-
ences in corpus callosum DTI measures of
fractional anisotropy (FA) and apparent diffusion
coefficient (ADC) in subjects with MTBI in com-
parison to healthy control subjects, when scanned
less than 3 months post-trauma. For those MTBI
subjects who were scanned 3 months or greater
post-trauma, there were no FA or ADC differ-
ences relative to healthy controls. Mayer et al.
(2010) found that DTI FA differences in the left
and right hemisphere discriminated between an
MTBI group scanned an average of 12 days post-
trauma and a healthy control group, following
correction for differences in premorbid intellec-
tual functioning. Interestingly, neuropsycholo-
gical test scores did not discriminate these two
groups, after controlling for premorbid intellec-
tual function. A subset of the subjects were seen at
3–5 month follow-up, and showed a trend towards
normalization of DTI FA. The Rutgers et al. (2008)
and Mayer et al. (2010) studies show a heightened
sensitivity of DTI to subacute effects of MTBI,
with follow-up data suggesting a parallel with
neuropsychological outcome, given an apparent
normalization of DTI values at 3 months or more
post-trauma. Of note per earlier discussion of
appropriate research designs, neither investiga-
tion employed an orthopedic trauma control
group. Given evidence that orthopedic trauma
controls may differ in neuropsychological test
performance relative to a noninjured healthy
population (Dikmen et al., 1995; Bijur et al. 1996),
it would appear prudent to incorporate such
subjects in DTI studies of MTBI, to control for
possible premorbid differences in white matter
density that could underlie these apparent non-
TBI differences in neuropsychological abilities.
Importantly, the role of psychological factors
(Delis & Kaplan, 2007; Mittenberg et al., 1992;
Suhr & Gunstad, 2002; 2005) and litigation
(Belanger et al., 2005; Binder & Rohling, 1996;
Carroll et al., 2004) in persistence of MTBI symp-
tomatology must be explored further. Per the
information reviewed in the present chapter, as
well as in other reviews of MTBI (Carroll et al.,
2004; McCrea, 2008), psychological and litigation
factors are most strongly associated with persis-
tence of symptomatic complaints in cases of
uncomplicated MTBI.
Additional research is needed on the relation-
ship of multiple MTBIs to the likelihood of
persistent neuropsychological deficits. Gronwall’s
laboratory (Gronwall, 1989; Gronwall &
Wrightson, 1975) showed that persons with
a history of prior MTBI took longer to recover
than persons with a single MTBI. The issue of per-
sistence of deficit was not addressed. Collins et al.
(2002) reported that concussed high school
athletes with three or more prior concussions
were 9.3 times more likely than concussed
athletes with no prior history of concussion to
demonstrate three to four abnormal on-field
markers of concussion severity. McCrea et al.
(2003) found greater risk of sustaining a subse-
quent concussion in football players with history
of preexisting concussion and longer time for
symptom resolution in patients with history of
three as opposed to one prior concussion. As
noted earlier, cumulative effects of multiple MTBI
have not been consistently demonstrated in the
literature (cf. Belanger et al., 2010).
Of particular interest in relation to evaluating
the effects of multiple MTBIs is the work of Bijur
et al. (1996), who found that an apparent cumula-
tive effect of multiple MTBIs in children did not
reflect cumulative neuropsychological deficit;
rather, the lower performance of children with
multiple MTBI paralleled the performance of
children with multiple orthopedic injuries. In
other words, children at risk for multiple injuries

(head or orthopedic) had lower neuropsychologi-
cal scores than those children with a single injury
(head or orthopedic), showing Satz et al.’s (1999)
“general injury effect, head and body,” but not
showing evidence for head injury effect.
The optimal “laboratories” for evaluation of
the effects of multiple MTBIs are the sports
concussion programs currently in place in
professional and collegiate sports programs.
Preseason baseline neuropsychological testing
allows more accurate measurement of post-MTBI
cognitive change. Per Bijur et al.’s (1996) research,
a control group of athletes suffering one or
more significant orthopedic injuries would be of
interest as a control for general injury (head
and nonhead) effects on neuropsychological test
performance.
AC K N OW L E D G M E N T
I acknowledge the assistance of Matthew Miliano
in the preparation of this chapter.
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 10
Moderate and Severe Traumatic Brain Injury
TRESA ROEBUCK-SPENCER AND MARK SHERER
Mortality and morbidity due to trauma are major
public health problems in the United States. Data
from the National Center for Health Statistics
(Kung, Hoyert, Xu, & Murphy, 2008) indicate that
accidents are the fifth leading cause of death for all
Americans with motor vehicle accidents and falls
accounting for a large proportion of these deaths.
The most recent Centers for Disease Control
(CDC) data indicate that there are over 1.5 million
new cases of traumatic brain injury (TBI) a year,
and that as a result of TBI, 1,224,000 Americans
were treated in hospital emergency departments,
290,000 were hospitalized, and 51,000 died
(Rutland-Brown, Langlois, Thomas, & Xi, 2006).
It is estimated that 80,000 to 90,000 persons have
new onset of disability each year due to TBI
(Thurman, Alverson, Dunn, Guerrero, & Sniezek,
1999), and that at least 5.3 million Americans live
with disability due to TBI (Langlois, Rutland-
Brown, & Wald, 2006). When considering medi-
cal costs and lost productivity, the lifetime cost of
TBI in the United States is an estimated 60 billion
dollars annually (Finkelstein, Corso, & Miller,
2006). This estimate does not take into account
the emotional cost of TBI or the indirect impact
on families, caregivers, and the community.
Given this high incidence and the likelihood
of persistent impairments, neuropsychologists
often play an important role in the evaluation and
treatment of persons with TBI. Patients with
moderate and severe TBI are much more likely
than patients with mild TBI to require inpatient
(Harrison-Felix, Newton, Hall, & Kreutzer, 1996)
or post-acute rehabilitation (Malec & Moessner,
2000; Sherer, Bergloff, High, & Nick, 1999) and
are often first seen by neuropsychologists in
these settings. Patients with mild TBI may be
more likely to be seen in forensic or other com-
pensation-related settings where determination of
whether the patient has any brain impairment or
persisting sequelae is the focus of the evaluation
(Binder, 1997; Binder & Willis, 1991). As a group,
patients with moderate and severe TBI have
poorer outcome both in terms of mortality and
morbidity than patients with mild TBI (Dikmen,
Machamer, Winn, & Temkin, 1995; Dikmen
et al., 1994; Levin, 1993; Levin, 1995; Zhang, Jiang,
Zhong, Yu, & Zhu, 2001) and may require
longer-term outpatient evaluation and treatment
by neuropsychologists to address these issues. In
contrast, the long-term effects of mild TBI remain
controversial. Most consecutive series of trauma
center patients with uncomplicated mild TBI
show that cognitive symptoms and deficits are
resolved by 3 months post-injury (Dikmen,
McLean, & Temkin, 1986; Institute of Medicine,
2009; Levin et al., 1987; Williams, Levin, &
Eisenberg, 1990). However, other investigators
have found significant self-report of neurobehav-
ioral symptoms in samples of patients with mild
TBI who are referred for services in the post-acute
period (Alexander, 1992; Cicerone & Kalmar,
1995). These persistent complaints have been
referred to as post-concussion syndrome, which
is viewed by some as maintained by psychological
rather than neurological factors (McCrea, 2008;
Mittenberg & Strauman, 2000). Recent reviews
confirm that incomplete recovery from mild TBI
is often associated with preexisting psychiatric or
substance abuse problems, poor general health,
concurrent orthopedic injuries, or comorbid
problems such as chronic pain, life stress, unem-
ployment, and protracted litigation (Iverson,
2005; McCrea, 2008).
Forensic issues in mild TBI are addressed in
chapter 9 by Larrabee. The present chapter will
focus on moderate to severe TBI and will review:
(1) classification of TBI; (2) incidence of moder-
ate and severe TBI; (3) course of recovery after
moderate and severe TBI; (4) neuropsychological
assessment of patients with moderate and severe
TBI; (5) outcome after moderate and severe TBI
 Moderate and Severe Traumatic Brain Injury
including mortality as well as physical, cognitive,
neurobehavioral, and functional status outcomes;
and (6) prediction of outcome after TBI.
C L A S S I F I C AT I O N O F
TBI SEVERITY
The CDC define TBI as “an occurrence of injury to
the head that is documented in a medical record
with one of the following conditions attributed to
head injury: 1) observed or self-reported decreased
level of consciousness, 2) amnesia, 3) skull fracture,
or 4) objective neurological or neuropsychological
abnormality or diagnosed intracranial lesion”
(Marr & Coronado, 2004). Notably, some authors
do not find that skull fracture is always associated
with brain impairment (Williams et al., 1990). TBI
severity is generally determined based on the depth
of impaired consciousness or duration of impaired
consciousness. The most commonly used measure
of depth of impaired consciousness is the Glasgow
Coma Scale (GCS) (Teasdale & Jennett, 1974). The
GCS measures levels of responsiveness in eye open-
ing, motor movement, and verbal communication.
Scores range from 3 to 15 with higher scores indi-
cating more intact functioning. Patients with scores
of 7 and below are definitely in coma and over 50%
of those with scores of 8 are in coma (Jennett &
Teasdale, 1977). GCS scores used for classification
of TBI severity should be obtained immediately
post-resuscitation or at admission to the emer-
gency department. Patients with post-resuscitation
GCS scores of 3 to 8 are classified as having had
severe TBI and those with scores from 9 to 12 are
classified as having had moderate injuries (Clifton,
Hayes, Levin, Michel, & Choi, 1992; Hannay &
Sherer, 1996; Levin & Eisenberg, 1991). Some
researchers further divide the severe group into very
severe (GCS 3 to 5) and severe (GCS 6 to 8) (Zhang,
et al., 2001). Patients with GCS scores between 13
and 15 are classified as having had mild injuries, but
outcomes of these patients depend on the presence
or absence of depressed skull fracture or intracra-
nial pathology as shown on the initial CT scan.
Patients with GCS scores between 13 and 15 with no
depressed skull fracture or pathology on initial CT
scan have uncomplicated mild TBI and have very
favorable outcomes (Dikmen, Machamer, &
Temkin, 2003; Williams et al., 1990). Patients with
initial GCS scores between 13 and 15 who do have
depressed skull fractures or CT scan abnormalities
have complicated mild TBI and their outcomes are
more similar to patients with moderate TBI
(Dikmen, Machamer, & Temkin, 2003; Williams
et al., 1990).
261
Return to a conscious or responsive state
after TBI is indicated by ability to follow simple
commands, indicate yes/no reliably through
words or gestures, give intelligible verbalizations,
or other purposeful behaviors (Giacino, et al.,
2002). Most studies of recovery from TBI have
used ability to follow commands as the primary
indication of return to a conscious state, but some
have used purposeful withdrawal from a painful
stimulus (Levin, 1995; Whyte, Cifu, Dikmen, &
Temkin, 2001). Whyte and colleagues (2001)
found that ability to follow commands was the
more useful of the two indices. The interval from
onset of injury to recovery of ability to follow
commands has proven to be a useful index in
determining injury severity. While “time to follow
commands” is the most accurate term for this
interval, some authors use the term “duration of
unconsciousness.” This term may be inaccurate,
as some aphasic patients may clearly be “con-
scious,” but fail to demonstrate command follow-
ing (Levin, 1995). Poorer outcomes are associated
with longer intervals from time of injury to time
of recovery of ability to follow commands. Time
to follow commands has been shown to be predic-
tive of global outcome, neuropsychological func-
tioning, personal independence, and employment
outcome after TBI (Dikmen & Machamer, 1995;
Dikmen, McLean, Temkin, & Wyler, 1986;
Dikmen et al., 1994). The usefulness of this index
of TBI severity is limited by the lack of a com-
monly agreed upon classification scheme. Also, it
may not be possible to determine time to follow
command intervals that map neatly onto severity
categories as determined by GCS ratings. While
duration of time to follow commands shows
the expected dose-response relationship to GCS
severity categories with more severe injuries
having longer time to follow commands intervals,
there is substantial overlap in time to follow com-
mands durations among extremely severe, severe,
moderate, and mild GCS categories (Sherer,
Struchen, Yablon, Wang, & Nick, 2008).
Another index of TBI severity is duration of
post-traumatic amnesia (PTA). PTA refers to the
phase of recovery from TBI during which the
patient is responsive, but is acutely confused and
disoriented and is unable to form and retain new
memories (Russell, 1932; Symonds, 1937). While
virtually all authors define PTA duration as the
interval from injury to recovery of orientation, a
few (e.g., Ellenberg, Levin, & Saydjari, 1996; Sherer,
Hart, Whyte, Nick, & Yablon, 2005) define PTA
duration as the interval from recovery of ability
262 forensic neuropsychology
to follow commands to recovery of orientation.
While disorientation and memory disturbance
are hallmarks of this phase of recovery, recent
researchers have noted the similarity of this state
to delirium and have recommended use of the
term “post-traumatic confusional state” (Sherer,
Nakase-Thompson, Yablon, & Gontkovsky, 2005;
Sherer, Yablon, Nakase-Richardson, & Nick, 2008;
Stuss et al., 1999). Numerous studies have shown
that duration of PTA is predictive of various
aspects of outcome after TBI including neuro-
psychological outcome, independent living status,
and return to work (Dikmen et al., 1994; Ellenberg
et al., 1996; Sherer, Sander, et al., 2002).
Duration of PTA can be assessed retrospec-
tively by waiting until the patient is no longer con-
fused and asking him/her to report the first
memory that he/she can recall following the brain
injury (Symonds & Russell, 1943). Additionally,
based on review of medical records, some
researchers have used documentation of consis-
tent orientation in all spheres as evidence that an
individual has cleared PTA (Traumatic Brain
Injury Model Systems National Data Center,
1999). This practice is consistent with research
showing that orientation improves in a predict-
able manner with orientation to time being a
potential marker for clearing PTA (High, Levin, &
Gary, 1990). More commonly, duration of PTA is
determined prospectively by serial assessment of
the patient’s degree of disorientation. The most
commonly used measure for this purpose is the
Galveston Orientation and Amnesia Scale
(GOAT) (Levin, O’Donnell, & Grossman, 1979).
Other similar scales include the Orientation Log
(Jackson, Novack, & Dowler, 1998), the Oxford
Scale (Fortuny, Briggs, Newcombe, Ratcliff, &
Thomas, 1980), and the Westmead Scale (Shores,
Marosszeky, Sandanam, & Batchelor, 1986).
Although the reliability of retrospective assess-
ment of PTA duration has been criticized, esti-
mates of PTA duration have been shown to be
similar across these two assessment methods
(McMillan, Jongen, & Greenwood, 1996).
As with time to follow commands, the useful-
ness of duration of PTA as an index of TBI sever-
ity is limited by the lack of commonly agreed
upon criteria for intervals indicating severe, mod-
erate, and mild injuries. Perhaps the most com-
monly used criteria were developed by Russell
and Smith (1961). In this scheme, patients with
PTA less than one hour are classified as having
had slight concussion, patients with PTA of one to
24 hours are classified as having had moderate
concussion, patients with PTA of one to seven
days are classified as having had severe concus-
sion, and patients with PTA greater than seven
days are classified as having had very severe con-
cussion. Unfortunately, TBI severity classification
based on the Russell and Smith schema is mark-
edly different than classification based on initial
GCS scores. As with time to follow commands,
there is a clear dose-response effect for PTA dura-
tion between GCS severity categories, but there is
marked overlap in PTA duration among GCS
severity categories. Thus, use of the Russell and
Smith criteria will result in misclassification of
many persons with mild or moderate injuries
based on initial GCS scores as severe (Sherer,
Struchen, et al., 2008). Thus, clinicians should be
wary of classifying patient injury severity based
on PTA duration. It is strongly recommended that
investigators not determine injury severity for
some subjects based on GCS scores and for others
based on PTA duration. This practice will likely
result in misleading findings.
There are only a few investigations comparing
PTA duration and time to follow commands as
indices of TBI severity. Dikmen and colleagues
(1986) found that time to follow commands and
GCS were more predictive of cognitive status at 1
month post-TBI than was PTA duration. However,
Katz and Alexander (1994) found that PTA dura-
tion accounted for significantly more of the vari-
ability in Glasgow Outcome Scale scores at 6
months and at 12 months post-injury than did
time to follow commands. In multivariable regres-
sion models predicting outcome at 6 and 12
months, PTA duration entered the model while
time to follow commands did not. Based on these
limited data, it is not possible to determine
whether PTA duration or time to follow com-
mands is the better predictor of outcome after
TBI. This likely depends on the time frame of the
prediction and the outcome being predicted.
I N C I D E N C E O F M O D E R AT E
AND SEVERE TBI
The overall incidence rate of TBI is difficult to
determine. This is because many individuals with
mild TBI may not seek medical care and if they do
seek care they may not be admitted to a hospital.
A CDC study covering the year 2003 estimated
the total incidence of TBI at 1.6 million and that
1,224,000 persons sought medical care following
TBI (Rutland-Brown, et al., 2006). TBI rates were
the highest among young children (ages 0–4) and
then peaked again in adolescence. Visits to the
 Moderate and Severe Traumatic Brain Injury
emergency department were highest among
children between the ages of 0 and 14, and hospi-
talization and death rates were the highest among
older adults (age 65 and older). Consistent with
past data, rates for men were higher than rates for
women, with approximately 1.5 times as many
TBIs in males as females. Falls and motor vehicle
accidents were found to be the leading causes of
TBI. Falls account for the largest number of
TBIs in the very young and very old, while motor
vehicle accidents account for most of the TBIs
in adolescence and young adulthood (Langlois,
Rutland-Brown, & Thomas, 2006; Rutland-Brown
et al., 2006). These numbers are likely to underes-
timate the true incidence of TBI, as they do not
account for persons with TBIs treated in private
doctor’s offices or outpatient care settings, or
persons that did not seek medical care.
Incidence varies widely due to methodological
differences across studies. A review by Kraus and
Chu (2005) demonstrated that the incidence of
brain injury ranged from 92 cases per 100,000
persons to 618 per 100,000 with an average rate
of fatal plus nonfatal hospitalized brain injuries
estimated at 150 per 100,000 persons per year.
Emergency-department-based studies report
higher rates of TBI. For instance, Jager and col-
leagues (2000) indicated that 444 persons per
100,000 seek medical care for TBI each year. The
vast majority of these injuries would have been
mild and would not have required hospitalization.
With changes in health care provision, there has
been a trend for fewer patients with mild TBI to
be admitted to hospitals (Thurman & Guerrero,
1999). However, the hospitalization rates for
patients with moderate and severe TBI remain
largely unchanged from earlier reports. CDC esti-
mates from the year 2000 documented that of
patients hospitalized due to TBI, over 50% had
mild injuries, while 21% had moderate injuries,
and 19% had severe injuries, resulting in about
102,500 moderate and severe TBIs per year. These
rates do not include patients who expired prior to
hospitalization (Thurman & Guerrero, 1999).
CDC estimates that approximately 56,000 persons
die from TBI each year and 80,000 to 90,000 are
left with persistent disability due to TBI each year
(Thurman, et al., 1999).
C O U R S E O F R E C O V E RY
FROM TBI
Significant TBI results in some degree of impaired
consciousness (Levin, 1992; Ommaya &
Gennarelli, 1974). Patients with severe injuries
263
have coma (Ommaya & Gennarelli, 1974). Coma
is a temporary nonresponsive state in which the
patient has closed eyes, follows no instructions,
gives no communication, and shows no purpose-
ful movements (Teasdale & Jennett, 1974). Recent
large consecutive series of patients admitted to
emergency departments with severe TBI indicate
that 23% to 49% of patients do not recover from
coma (Murray et al., 1999; Zhang et al., 2001).
Those patients who do survive almost always
recover to a more responsive state. A small per-
centage of surviving patients, 1% to 5%, may
remain in a nonresponsive vegetative state
(Murray, et al., 1999), but even these patients
show recovery of some brainstem functioning
and have return of sleep/wake cycles with periods
of eye opening.
Surviving, nonvegetative patients recover to
some degree of responsiveness to the environ-
ment. This level of responsiveness may be mark-
edly reduced at first as in the minimally conscious
state (Giacino, et al., 2002). Patients in this state
show minimal, but definite evidence of awareness
of self or the environment. Examples include
localized motor responses to noxious stimuli or
sounds, sustained visual fixation, vocalization in
response to a stimulus, smiling or crying in
response to a stimulus, and inconsistent com-
mand following. Resolution of the minimally
conscious state is indicated by consistent com-
mand following, verbal or gestural yes/no
responding, intelligible verbalization, or some
other evidence of consistent purposeful behavior
such as functional use of objects. This state is
generally temporary but may be permanent in a
small subset of patients.
Most commonly, resolution of coma is
followed by a responsive, but markedly confused
state. Patients with moderate TBI may have loss
of consciousness at the time of injury, but (by def-
inition) are responsive but confused at presenta-
tion to the emergency department. The period of
acute confusion following TBI is a temporary
phase of recovery (Levin, 1993). Most patients
recover from the confused state, at least to some
degree, though they may be left with persistent
cognitive and behavioral impairments (Levin,
1992). The confused phase of recovery after TBI is
a complex state that manifests in a variety of neu-
robehavioral impairments. Early writers (Russell,
1932; Symonds, 1937) described deficits in
arousal, memory, orientation, attention, language,
behavior, mood, and perception. The period of
confusion is now commonly called post-traumatic
264 forensic neuropsychology
amnesia (PTA), but early writers used many terms
including acute traumatic psychosis, after effects
of concussion, traumatic confusion, and delirium
Many previous investigations of the period of
confusion after TBI have primarily focused on
disorientation and memory impairment. High
and colleagues (1990) found that orientation after
TBI recovers sequentially with initial recovery of
orientation to person followed by orientation to
place and time. Memory disturbance after head
trauma is characterized by some loss of ability
to recall events immediately preceding injury
(retrograde amnesia) as well as a period of inabi-
lity to encode and later recall new memories
(anterograde amnesia) (Levin, 1992). Memory
impairment during post-traumatic confusion is
greatest for explicit, episodic memory with some
sparing of implicit and procedural memory
(Ewert, Levin, Watson, & Kalisky, 1989).
Attentional impairments during early recov-
ery from TBI include difficulties focusing
attention on the examiner, sustaining attention,
processing information, and excessive distracti-
bility (Levin, 1993). In their investigation of
attentional functions in confused patients, Stuss
and colleagues (1999) demonstrated that atten-
tional abilities recover in an orderly manner after
TBI. Performance on attentional tasks improved
prior to obtaining a GOAT score in target range or
ability to recall three words at a 24-hour delay.
Stuss and colleagues argued that attentional
disturbance is a key aspect of impaired conscious-
ness after TBI. They noted the similarity of this
state to delirium and proposed the term “post-
traumatic confusional state” (PTCS) to replace
the more commonly used PTA.
Other investigators have studied motor
restlessness (agitation) in confused patients after
TBI. These investigations have found an associa-
tion of restlessness with cognitive impairment.
Agitation is common in patients with low levels
of cognitive function, but rare in patients with
higher levels of cognitive function (Corrigan &
Mysiw, 1988). Patients with intermediate levels of
cognitive function are equally likely to be agitated
or nonagitated. Patients experience cognitive
improvement prior to resolution of agitation as
opposed to resolution of agitation followed by
cognitive recovery.
Work by Sherer and colleagues (2005; Sherer,
Yablon, et al., 2008) has provided additional
support for considering the period of confusion
after TBI to be a complex neurobehavioral
state similar to delirium as opposed to a state
primarily characterized by memory impairment
as suggested by the term PTA. Using their assess-
ment procedure for confusion, the Confusion
Assessment Protocol (CAP), Sherer and col-
leagues (2005) found that seven key symptoms
characterize the confused state after TBI. These
are: (1) disorientation, (2) impaired cognition,
(3) restlessness, (4) fluctuation of symptom
presentation, (5) sleep disturbance, (6) decreased
daytime level of arousal, and (7) psychotic-type
symptoms. Diagnosis of PTCS using the CAP
showed 87% agreement with a clinical diagnosis
on delirium. Presence of confusion at admission
to inpatient rehabilitation made a unique contri-
bution to functional status at discharge after
adjustment for other known predictors of TBI
outcome.
More recently, Sherer and colleagues (2008)
showed that severity of confusion at a fixed time
(21 days) post-injury made a contribution to
prediction of early and late outcome after TBI.
In addition, presence or absence of each of seven
symptoms of confusion 21 days post-injury was
predictive of early outcome and, in most cases,
late outcome. Of particular importance, this
investigation showed that psychotic-type symp-
toms occur in approximately 40% of patients in
early recovery from TBI. Even though these symp-
toms resolve in almost all patients, patients with
early psychotic-type symptoms were at markedly
increased risk for poor long-term outcome. These
findings support the position of Stuss and
colleagues (1999) that this early phase of recovery
after TBI is better characterized as PTCS as
opposed to PTA.
After resolution of PTA (or PTCS), patients
continue to show progressive resolution of physi-
cal, cognitive, and behavioral impairments. There
is general agreement that recovery continues for
up to 18 months after moderate or severe TBI
(Dikmen, Reitan, & Temkin, 1983; Levin, 1995;
Tabaddor, Mattis, & Zazula, 1984) and there is
some evidence that some cognitive functions
may continue to recover after this 18 months’
timeframe (Millis et al., 2001; van Zomeren &
Deelman, 1978).
In a few patients, recovery may be compromi-
sed by late complications such as post-traumatic
epilepsy or post-traumatic hydrocephalus. Late
seizures (greater than two weeks post-injury)
occur in only about 4% to 7% of survivors of non-
penetrating TBI, but the incidence may be as high
as 50% for patients with penetrating TBI
(Annegers, Hauser, Coan, & Rocca, 1998; Yablon,
 Moderate and Severe Traumatic Brain Injury
1996). The incidence of post-traumatic hydro-
cephalus is not well known due to wide variation
in the degree of monitoring for this condition.
One prospective series in which all patients with
moderate or severe TBI admitted for inpatient
rehabilitation received head CT scans found an
incidence of 13% (Yu, Yablon, Ivanhoe, & Boake,
1995).
TBI patients with large focal hemispheric
lesions or certain subcortical, brain stem, or cere-
bellar lesions may have persistent motor impair-
ments (Bontke, Zasler, & Boake, 1996; Horn &
Sherer, 1999). Such impairments may include
spasticity, dysphagia (impaired swallowing),
dysarthria, balance disturbances, or hemiparesis.
Most patients with moderate or severe TBI show
good resolution of motor impairments.
The prognosis for recovery of cognitive
abilities after moderate and severe TBI is less
favorable than for motor functions. Risk for per-
sistent cognitive impairment is related to initial
injury severity as indicated by post-resuscitation
GCS score or time to follow commands (Dikmen,
Machamer, et al., 1995; Tabaddor et al., 1984).
Even at one year post-injury, all patients with very
severe TBI (time to follow commands ≥ 14 days)
have residual cognitive impairments while more
than one-half of those with time to follow com-
mands between one hour and 13 days have resid-
ual deficits (Dikmen, Machamer, et al., 1995).
While the general course of recovery of cognitive
abilities is for continuing improvements for about
18 months post-injury, a subgroup of patients
shows improvement beyond this period (Millis
et al., 2001). There is limited evidence that another
subgroup of patients may show late decline (Millis
et al., 2001; Ruff et al., 1991). Age at time of injury
appears to be a risk factor for late decline with
older age at time of injury indicating greater risk
for late decline.
The typical pattern of impairments after blunt
head trauma includes slowed fine motor move-
ments, decreased attention, decreased cognitive
speed, memory impairment, impaired complex
language skills and discourse, and impaired exec-
utive functions (Levin, 1993). Severe persistent
aphasia or visual perceptual impairment are
uncommon after diffuse injuries but may occur in
patients with focal injuries (Levin, 1993).
Patients with moderate and severe TBI may
also show persistent neurobehavioral impair-
ments and emotional changes (Oddy, Humphrey,
& Uttley, 1978; Satz et al., 1998). Neurobehavioral
changes include problems with disinhibition,
265
decreased initiation, and poor awareness of these
and other changes (for review see Roebuck-
Spencer, Banos, Sherer, & Novack, 2010).
Behavioral manifestations of disinhibition may
include aggression/agitation, social disinhibition,
impulsivity, risk-taking behavior, and affective
lability (Grafman et al., 1996; Kim, 2002).
Impaired self-awareness is common after moder-
ate and severe TBI both in the acute (Sherer, Hart,
et al., 2003) and the post-acute periods (Sherer,
et al., 1998). This tendency for some TBI survi-
vors to be partially or totally unaware of problems
can be a primary source of family member stress
and contributes to poor functional outcome and
return to previous activities, including work
(Prigatano, Altman, & O’Brien, 1990; Sherer et al.,
1998; Sherer, Hart, et al., 2003). Patients with poor
self-awareness have poor motivation to change as
they do not perceive the need to change (Malec &
Moessner, 2000). The most common emotional
changes following moderate to severe TBI include
depression with prevalence rates ranging from
15% to 60% (Kim, et al., 2007; Rogers & Read,
2007) and anxiety with prevalence rates ranging
from 2% to 44% (Rogers & Read, 2007). Rates of
psychotic disorders after TBI are less clear due to
inconsistent definitions and methodology, but are
generally not considered to be common following
TBI (Kim et al., 2007).
Patients and family members are more likely
to report these neurobehavioral and emotional
impairments than either cognitive or physical
impairments in the post-acute period (Brooks,
Campsie, Symington, Beattie, & McKinlay, 1987;
Lezak, 1987, 1989). Family members report that
these neurobehavioral symptoms, particularly
personality change and threats of violence, cause
more stress than cognitive or physical impair-
ments (Brooks, Campsie, Symington, Beattie, &
McKinlay, 1986; Riley, 2007). There is some evi-
dence that family member report of these symp-
toms may actually increase with the passage of
time (Brooks et al., 1986). It is unclear whether
this is due to an actual increase in the frequency or
severity of behavioral problems as opposed to a
greater sensitivity to the effects of these problems.
NEUROPSYCHOLOGICAL
A S S E S S M E N T O F PAT I E N T S
W I T H M O D E R AT E A N D
SEVERE TBI
There are a number of contributions that neuro-
psychological assessment can make to the care of
persons with moderate and severe TBI. Such
266 forensic neuropsychology
evaluations provide documentation of cognitive,
behavioral, and emotional status and may also
assist with determination of patients’ ability to
function independently (Sherer & Novack, 2003).
Documentation of status is useful to provide
feedback to family members, improve patient
self-awareness, guide treatment efforts, and assess
the effectiveness of medication trials. Areas of
functional ability that may be assessed include
decision-making capacity, capacity for safe and
independent home functioning, driving capacity,
and ability to return to work.
The focus of neuropsychological assessment is
determined both by the goals of the assessment
and the stage of recovery of the patient. Early neu-
ropsychological assessment may focus on deter-
mining level of responsiveness and documenting
changes in level of responsiveness in minimally
conscious patients. Measures such as the Coma
Recovery Scale (Giacino, Kezmarsky, DeLuca, &
Cicerone, 1991) provide a structured repeatable
protocol for assessing low-level patients. Areas
assessed include arousal and attention, auditory
perception, visual perception, motor function,
oromotor ability, communication, and initiation.
With responsive but confused patients, assess-
ment focuses on orientation, attentional skills,
ability to form new memories, and level of agita-
tion. Measures such as the GOAT (Levin, et al.,
1979) or Orientation Log (Jackson, et al., 1998)
can be used to assess orientation. The Toronto
Test of Acute Recovery After TBI (Stuss, et al.,
1999) includes simple measures of attentional
skills and ability to form and retain new memo-
ries. The Agitated Behavior Scale (Corrigan, 1989)
is the most commonly used measure of agitation
after TBI. The Confusion Assessment Protocol
(Sherer, Nakase-Thompson, et al., 2005) includes
elements of all these areas and preliminary find-
ings indicate that it may be useful in assessing a
wide range of symptoms of confusion after TBI.
Some writers recommend delaying adminis-
tration of formal neuropsychological tests until
the patient has emerged from PTA (Clifton, et al.,
1992). This recommendation is based on the
assumption that confused, disoriented patients
will perform poorly on all tests and, thus, little
additional information will be obtained.
Nonetheless, there is some evidence that adminis-
tration of selected neuropsychological measures
to patients still in PTA can result in useful data
that are predictive of later functional status
(Hannay & Sherer, 1996; Pastorek, Hannay, &
Contant, 2004). Such tests should be relatively
simple in terms of test directions, processing
demands, and response requirements in order to
enhance chances of test completion. Neuro-
psychological tests measuring language compre-
hension, attention, short-term memory, visual
acuity, and tracking may be useful. Examples of
specific neuropsychological tests used in acute
batteries for individuals in later stages of PTA
(e.g., GOAT scores > 40) include Complex
Ideational Material from the Boston Diagnostic
Aphasia Exam, the Mini Token Test, Auditory
Number Search Test, Visual Number Search Test,
Digit Span, and the Trailmaking Test (Hannay &
Sherer, 1996; Pastorek et al., 2004).
While a range of neuropsychological batteries
have been used in the literature to assess the
cognitive effects of TBI, no specific battery of tests
for TBI has been proposed and widely accepted.
Initial and follow-up comprehensive neuro-
psychological evaluations of persons with moder-
ate or severe TBI should nonetheless assess a wide
range of abilities including orientation, fine motor
skills, divided and sustained attention, cognitive
speed, memory, language skills, visual-perceptual
skills, and executive functions (Clifton et al., 1992;
Dikmen, Machamer, et al., 1995; Hannay & Sherer,
1996; Traumatic Brain Injury Model Systems
National Data Center, 1999). Key impairments
shown by almost all patients with moderate
to severe TBI include attentional difficulties,
slowed information processing speed, verbal
learning and memory, and executive functioning.
Thus, tests assessing these domains are particu-
larly important to include in any battery assessing
these patients and may be the most predictive of
outcome (see prediction of outcome section
included later in this chapter). Table 10.1 provides
a list of neuropsychological tests organized by cog-
nitive domain that have been used frequently in
the research literature on moderate to severe TBI.
Neurobehavioral problems such as mental
flexibility, planning, unusual thought content,
agitation, disinhibition, emotional withdrawal,
hostility, depression, anxiety, and motor slowing
should also be assessed (McCauley et al., 2001).
Measures such as the Neurobehavioral Rating
Scale (Levin et al., 1987) and the Neurobehavioral
Functioning Inventory (Kreutzer, Marwitz, Seel,
& Serio, 1996) are helpful with assessment of
neurobehavioral impairments. Because of fre-
quent problems with poor self-awareness follow-
ing moderate to severe TBI, it is helpful to collect
this information from a family member or
caregiver, in addition to the patient.
 Moderate and Severe Traumatic Brain Injury
TABLE 10.1 EX AMPLES OF COMMONLY USED TESTS
BY COGNITIVE DOMAIN FOR NEUROPSYCHOLOGICAL
ASSESSMENT OF TBI
Cognitive Domain
Orientation:
Attention/Processing Speed/Flexibility:
Memory:
Language:
Visuospatial Skills:
Problem Solving/Reasoning:
Motor:
Behavior:
1
(Clifton, et al., 1992)
2
(Traumatic Brain Injury Model Systems National Data Center, 1999)
3
(Dikmen, Machamer, et al., 1995)
4
(Dikmen, Machamer, Powell, & Temkin, 2003)
Descriptions of these tests can be found in reference volumes on neuropsychological assessment such as
(Lezak, Howieson, Loring, Hannay, & Fischer, 2004) and (Spreen & Strauss, 1998).
The relationship between cognitive function-
ing and personal independence and employment
is complex. While neuropsychological findings
are related to functional outcomes such as
personal independence (Hart et al., 2003) and
employment (Dikmen et al., 1994; Sherer, Novack,
et al., 2002; Sherer, Sander, et al., 2002), these
functional outcomes are also influenced by
a variety of other factors such as premorbid func-
tioning, demographic variables, environmental
supports, and family support (Sherer, Nick, et al.,
2003). There are a number of instruments that can
be used to directly rate patient functioning in
267
Tests Utilized
Galveston Orientation and Amnesia Test2
Paced Auditory Serial Addition Test1,4
Digit Span2
Seashore Rhythm Test3
Stroop Color Word Test3
Trail Making Test, Parts A2 and B1,2
Symbol Digit Modalities Test2
Digit Symbol1
Rey Complex Figure Test1
Selective Reminding Test1,3
Rey Auditory Verbal Learning Test2
WMS-Logical Memory Test2,3
WMS-Visual Reproduction3
California Verbal Learning Test4
Controlled Oral Word Association Test1,2
Token Test2
WAIS-VIQ3
Benton Visual Form Discrimination Test2
Block Design Test2
WAIS-PIQ3
Tactual Performance Test3
Wisconsin Card Sorting Test1,2
Category Test3
Grooved Peg Board Test1,2
Finger Tapping Test3
Namewriting3
Neurobehavioral Rating Scale1
Neurobehavioral Functioning Inventory2
these areas. Three scales that have been included
in the TBI Model Systems protocol (Traumatic
Brain Injury Model Systems National Data Center,
1999) are described below.
The Disability Rating Scale (DRS) (Rappaport,
Hall, Hopkins, Belleza, & Cope, 1982) was devel-
oped to track patient progress after TBI from
coma to return to community activities. The DRS
is a 30-point scale which rates eight areas of
functioning: eye opening; verbalization; motor
response; level of cognitive ability for daily activi-
ties of feeding, toileting, and grooming; overall
level of dependence; and employability. Higher
268 forensic neuropsychology
scores indicate greater disability. Inter-rater
reliability has been shown to range from 0.97 to
0.98 (Gouvier, Blanton, LaPorte, & Nepomuceno,
1987; Rappaport et al., 1982). The DRS has been
shown to be sensitive to improvements in func-
tioning between two and six months post-injury,
as well as between six months and one year (Hall,
Cope, & Rappaport, 1985).
The Supervision Rating Scale (SRS) (Boake,
1996) can be used to quantify the level of personal
independence. The level of supervision received is
rated on a 13-point ordinal scale ranging from
“independent” to “full-time direct supervision
(with patient in physical restraints).” The SRS has
been shown to have satisfactory inter-rater reli-
ability (Boake, 1996). SRS scores are related to
patient living arrangement and to skills in activi-
ties of daily living.
The Community Integration Questionnaire
(CIQ) (Willer, Rosenthal, Kreutzer, Gordon, &
Rempel, 1993) was used in the TBI Model Systems
battery in the past and was developed to assess
degree of community integration after TBI.
Community functioning is rated in three areas:
home integration, social integration, and produc-
tive activity. Studies of inter-rater reliability have
found moderate to strong reliability (Sander et al.,
1997; Willer, Ottenbacher, & Coad, 1994). Validity
studies have shown that CIQ scores are correlated
with other measures of functional status such as
the DRS (Sander, et al., 1999).
In an attempt to provide some guidance regard-
ing timing of neuropsychological evaluations for
patients with TBI of different severities, Sherer
and Novack (2003) conducted a survey of 41 neu-
ropsychologists. Survey participants were selected
based on board certification, published research
on TBI, and current participation in TBI research.
Thirty-three of those surveyed responded. These
TABLE 10.2 SCHEDULE FOR NEUROPSYCHOLOGICAL
EVALUATIONS AFTER TBI
Time of Evaluation Severe TBI
At resolution of PTA
1 week to 1 month post-injury
3 months post-injury
6 months post-injury
1 year post-injury
2 years post-injury
respondents reported a median of 20 years of clin-
ical experience with patients with TBI (range = 7
to 35 years). Guidelines for timing of assessments
based on this survey are summarized in Table 10.2.
These guidelines provide general suggestions.
Timing of testing for any specific patient should be
determined by clinician judgment based on evalu-
ation of factors unique to that patient.
In cases of moderate or severe TBI, there
will generally be clear-cut medical evidence indi-
cating that the patient sustained brain injury.
This may be in the form of radiological findings,
medical documentation of loss of consciousness,
coma, or sustained confusion, or operative reports.
Nonetheless, such patients may occasionally
exaggerate symptoms when seen for follow-up
evaluations, particularly if they are engaged in
litigation. Consequently, the symptom validity
measures described by Larrabee in chapter 5
should also be administered for those moderate
or severe TBI patients involved in litigation or
compensation actions.
OUTCOME AFTER
M O D E R AT E A N D S E V E R E T B I
Outcome after moderate and severe TBI can be
assessed in many ways. Neurosurgical studies may
focus on early survival while rehabilitation studies
may focus on return to work or independent
living. The Glasgow Outcome Scale (GOS)
(Jennett & Bond, 1975) is the most commonly
used measure of overall outcome after TBI. With
the GOS, outcomes are rated in five categories:
(1) Death, (2) Vegetative State (unable to
follow commands or communicate), (3) Severe
Disability (conscious but requiring assistance to
meet basic physical and cognitive needs such
feeding, toileting, grooming, or personal safety),
(4) Moderate Disability (able to meet basic
Moderate TBI Mild TBI
X X X
X
X X X
X X
X X X
X X
 Moderate and Severe Traumatic Brain Injury
physical and cognitive needs and use public trans-
portation and work in a sheltered workshop, but
unable to return to nonsheltered work or resume
other major societal roles), and (5) Good Recovery
(able to return to nonsheltered work though
perhaps in a decreased capacity and resume social
roles though some neurologic or psychologic
impairments may remain).
Death is a common outcome after severe TBI.
Death rates for severe TBI patients who have been
hospitalized range from 23% to 50% (Braakman,
Gelpke, Habbema, Maas, & Minderhoud, 1980;
Jiang, Gao, Li, Yu, & Zhu, 2002; Marion, 1996;
Murray et al., 1999; Zhang et al., 2001). The most
typical death rate is about 40%. Causes of early
death after TBI include brain swelling, diffuse
axonal injury, increased intracranial pressure, and
intracranial hematomas (Graham, Adams, &
Gennarelli, 1993; Marion, 1996).
Only a few patients remain in a vegetative state
after severe TBI. At 3 months post-injury, less
than 10% of patients are in a vegetative state (Choi
& Barnes, 1996; Choi et al., 1994) and by 6 months,
only 4% remain vegetative (Murray, et al., 1999).
Of those who are vegetative at 3 months, 50%
improve, 25% expire, and 25% remain in a vegeta-
tive state so that, by one year post-injury, the inci-
dence of vegetative state ranges from less than 1%
(Jiang et al., 2002) to 2% or 3% (Choi & Barnes,
1996; Choi et al., 1994) of severe TBI survivors.
Outcome proportions for patients with severe
disability, moderate disability, and good recovery
below are for patients with severe TBI who sur-
vived their acute hospitalizations excluding those
who expired. At 3 months post-injury, approxi-
mately 31% to 32% of surviving patients initially
hospitalized with severe TBI remain with severe
disability (Choi & Barnes, 1996; Choi et al., 1994).
By 6 months post-injury, only about 22% remain
with severe disability (Choi & Barnes, 1996; Choi
et al., 1994; Murray et al., 1999). By one year post-
injury, many patients who experienced severe dis-
ability at 3 months post-injury have recovered to
moderate disability or good recovery. Only about
17% of surviving patients remain with severe dis-
ability (Choi & Barnes, 1996; Choi et al., 1994).
Approximately 30% of severe TBI patients
have moderate disability at 3 and 6 months post-
injury (Choi & Barnes, 1996; Choi et al., 1994;
Murray et al., 1999). However, some of the patients
who had moderate disability at 3 months have
achieved good recovery by 6 months while some
patients who were vegetative or had severe dis-
ability at 3 months have recovered to moderate
269
disability by 6 months. By one year post-injury,
17% to 22% of patients with severe TBI remain
with moderate disability (Choi et al., 1994; Zhang
et al., 2001).
Good recovery is achieved by only 22% of
patients with severe TBI by 3 months post-injury
(Choi & Barnes, 1996; Choi et al., 1994). By 6
months post-injury, this has increased to over
35% (Choi et al., 1994; Zhang et al., 2001). At one
year after severe TBI, 46% to 54% of patients with
severe TBI have reached good recovery (Choi
et al., 1994; Zhang et al., 2001). Thus, for patients
who survive severe TBI, good recovery is the most
likely GOS outcome by one year post-injury. Note
that these patients may remain with significant
cognitive or neurobehavioral problems even
though they have recovered well enough to return
to work.
Death is a rare outcome after moderate TBI,
occurring in fewer than 10% of cases (Murray
et al., 1999; Stein, 1996). When death does occur,
it is likely to be due to associated trauma or medi-
cal complications (Signorini, Andrews, Jones,
Wardlaw, & Miller, 1999). Vegetative state is even
a rarer outcome after moderate TBI with some
large trauma series reporting no cases (Murray
et al., 1999).
Severe disability does occur after moderate
TBI, though it is uncommon. Some reports
indicate that no moderately injured patients
remain with severe disability at 6 months post-
injury (Williams et al., 1990) while others find
that 6% (Stein, 1996) to 14% (Murray et al., 1999)
have severe disability. Moderate disability is a
more common outcome and is seen in about 25%
of patients at 6 months post-injury (Jain, Layton,
& Murray, 2000; Stein, 1996; Williams et al., 1990).
Good recovery is by far the most common out-
come after moderate TBI with 53% (Murray et al.,
1999) to 73% (Williams et al., 1990) of cases
showing good recovery by 6 months post-injury.
As with severe TBI patients, good recovery cannot
be taken to mean complete recovery.
While data on GOS outcome categories are
informative, clinicians, family, and patients are
more likely to be concerned about the likelihood
that a patient will return to work and/or to inde-
pendent living. Employment outcomes have been
studied more intensively than independent living
outcomes. Perhaps this is because of the greater
ease of characterizing employment status as
opposed to degree of personal independence.
Reported return to work rates following TBI
range from 22% to 66% (Sander, Kreutzer,
270 forensic neuropsychology
Rosenthal, Delmonico, & Young, 1996). The wide
range of rates is contributed to by inter-study
differences in injury classification, populations
sampled, time from injury to follow-up, and
differing definitions of employment. Previous
investigations have focused on two populations of
patients with TBI, consecutive cases seen at
trauma centers and patients seen for inpatient
rehabilitation. Both populations are important,
but findings based on one population should not
be generalized to the other. The subset of TBI
patients admitted for inpatient rehabilitation
excludes those with very poor outcomes such as
vegetative patients and those with very good out-
comes such as those who are oriented and inde-
pendent with activities of daily living prior to
discharge from the acute care hospital.
Brooks and colleagues (1987) reported on a
series of 134 patients with severe TBI seen on an
acute neurosurgical service. Most patients (75%)
were employed at time of injury but only 25%
were employed at follow-up, assessed from two to
seven years post-injury. Dikmen and colleagues
(1994) reported on a series of 366 patients with
TBI who were admitted to a trauma center.
Patients who were not employed at time of injury
were excluded from study. At one year post-injury,
26% of patients with severe injuries had returned
to work and 56% of patients with moderate
injuries had returned to work. By two years post-
injury, 37% of patients with severe injuries were
working while 64% of patients with moderate
injuries were working. Age, education, pre-injury
work history, injury severity, and neuropsycho-
logical test performance, including ability to
undergo testing at one month were all strongly
related to the amount of time it took patients to
return to work after sustaining a TBI. Doctor and
colleagues (2005) examined unemployment rates
at one year post-injury after adjusting for unem-
ployment rates in the general population and
found that 42% of individuals with TBI were
unemployed compared with a 9% expected unem-
ployment rate.
Sherer and colleagues (2003) reported on 1615
patients with TBI who were admitted to 17 TBI
Model Systems sites for inpatient rehabilitation.
Of this population, 72% were employed at the
time of injury. One year employment outcome
data were available on 1083 patients. Of these
1083 patients, 63% had severe injuries, 16% had
moderate injuries, and 20% had complicated mild
injuries. Patients who were available at follow-up
had a higher pre-injury employment rate (76%)
than those lost to follow-up (68%). This suggests
that the one-year post-injury employment rate for
the 1083 patients is likely to overestimate the
overall one-year post-injury employment rate.
For the 1083 patients with available one-year
post-injury employment data, the employment
rate was 35%.
Moderate and severe TBI results in decreased
personal independence. Persons with moderate
and severe TBI have a markedly increased risk for
institutional (usually nursing home) placement as
compared to noninjured controls (Dikmen,
Machamer, & Temkin, 1993; Kersel, Marsh, Havill,
& Sleigh, 2001). Even so, only about 5% require
institutional care at one year post-injury (Dikmen
et al., 1993; Kersel et al., 2001). More commonly,
persons who were living independently prior to
injury reside with a family member or significant
other post-injury. In one series, almost half of
persons with moderate and severe TBI who were
living independently prior to injury are living
with parents at one year post-injury (Dikmen,
et al., 1993).
In a study of caregiver supervision, Hart and
colleagues (2003) reported on a series of 563
patients with TBI who were seen for inpatient
rehabilitation. Patients who were could not com-
plete a neuropsychological evaluation during
inpatient rehabilitation were excluded from the
study meaning that patients with more severe
injuries may be under-represented in this study
sample. Sixty-nine percent of this sample were
rated as receiving no supervision at one year fol-
low-up. Twenty-four percent received varying
degrees of part-time supervision and 7% received
full-time supervision. Amount of supervision
received at follow-up was generally related to ini-
tial injury severity as determined by GCS rating
with those having more impaired initial GCS rat-
ings receiving more supervision at follow-up.
However, initial GCS scores for those who were
independent at follow-up ranged from 3 to 15, as
did initial GCS scores for those receiving the
highest levels of supervision at follow-up.
The literature on very long-term outcome fol-
lowing history of moderate to severe TBI is grow-
ing due to evidence that some individuals with
TBI show a decline in cognitive functioning later
in life. History of moderate to severe TBI has now
been accepted as a risk factor for degenerative
neurological diseases (Institute of Medicine,
2009). A study by Plassman and colleagues (2000)
found greater risk for dementia and specifically
for Alzheimer’s disease in WWII veterans who
 Moderate and Severe Traumatic Brain Injury
had a history of medically documented moderate
to severe TBI. This relationship was not found for
mild TBI. Other studies have also found an
increased risk for Alzheimer’s type dementia fol-
lowing history of TBI (French et al., 1985; Guo
et al., 2000; Heyman et al., 1984; Schofield et al.,
1997). Higher rates of past TBI also have been
found in studies of patients with Parkinson’s dis-
ease or probable Parkinson’s disease (Bower et al.,
2003; Goldman et al., 2006; Taylor et al., 1999).
The relationship between TBI and later neurode-
generative disease may be driven by the accumu-
lation of multiple proteins in the brains of
individuals with TBI that is presumed to be trig-
gered by the injury (Uryu et al., 2007). Although
manifestation of neurodegenerative disease does
not occur until later in life, this accumulation of
proteins appears to start early in the course of
injury. Other studies propose a genetic vulnera-
bility that increases the association between TBI
and neurodegenerative disease (Guo et al., 2000;
Mayeux et al., 1995). However, this relationship
remains inconclusive (Millar, Nicoll, Thornhill,
Murray, & Teasdale, 2003).
PREDICTION OF OUTCOME
There is a very large literature on prediction of
outcome after moderate and severe TBI.
Interpretation of this literature is complicated by
the wide variety of populations sampled, time
frames of outcomes, and outcomes studied.
Factors predictive of a given outcome in a partic-
ular sample over a specified timeframe may not be
at all predictive of apparently related outcomes in
a different sample over a different timeframe. This
is particularly the case for subsamples that are
highly selected (e.g., patients admitted for post-
acute rehabilitation services). We will briefly
review predictors of death after TBI and func-
tional status at follow-up.
Factors most predictive of death after TBI are
those that directly indicate neurologic and physi-
ologic status early after injury. Such factors
include: (1) level of responsiveness as indicated by
admission GCS score (Eisenberg & Weiner, 1987;
Mosenthal et al., 2002), (2) pupillary responses
(Andrews et al., 2002; Jiang et al., 2002; Wardlaw,
Easton, & Statham, 2002), (3) initial CT scan find-
ings (particularly presence of subarachnoid blood
or mass lesion such as subdural hematoma)
(Eisenberg & Weiner, 1987; Mataro et al., 2001;
Wardlaw et al., 2002), (4) elevated temperature
(Andrews et al., 2002; Jiang et al., 2002), (5) elec-
trophysiologic findings (Claassen & Hansen,
271
2001; Vespa et al., 2002), (6) elevated intracranial
pressure (Eisenberg & Weiner, 1987; Jiang et al.,
2002), and (7) hypoxia (Andrews et al., 2002;
Eisenberg & Weiner, 1987; Jiang et al., 2002). Of
demographic variables, age is most predictive of
death with older age being associated with greater
risk of death (Jiang et al., 2002; Mosenthal et al.,
2002; Susman et al., 2002). Early neurosurgical
management also affects death rates. Centers that
managed patients aggressively, as indicated by
intracranial monitor placement, had 40% lower
mortality rates than centers with less aggressive
management (Bulger et al., 2002).
Late functional status (return to work, return
to school, and personal independence) after TBI
is affected by even more factors than early out-
come. As time from injury to outcome becomes
greater, injury characteristics become less impor-
tant and other factors such as premorbid func-
tioning and environmental supports become
more important. Factors predictive of functional
outcome can be categorized into pre-injury fac-
tors (including demographic variables), injury
severity variables, neuroanatomical variables,
physical impairments, cognitive and neurobehav-
ioral impairments, and environmental supports.
See Table 10.3 for a review of studies using these
variables to predict functional outcome. These
factors are generally studied by examining predic-
tion of outcome for groups of patients using
multivariable regression models. While these
models account for substantial variability in func-
tional outcomes after TBI, substantial additional
variability remains unexplained. Further, results
may be specific to the sample or particular data
set utilized. In each data set there are individual
outcomes that are better or worse than predicted
by the regression models. Consequently, clini-
cians must be cautious in applying findings from
these studies to the prediction of a specific out-
come for a specific patient.
Compared to the number of studies on
predicting return to school and personal indepen-
dence after TBI, the literature on return to work
after TBI is quite extensive. It should be noted that
many studies define work broadly and may include
return to school as indicating a return to produc-
tivity after TBI. Unfortunately, these studies do
not provide separate analyses for return to school.
Injury severity as indicated by initial GCS score,
time to follow commands, or duration of PTA is
predictive of employment outcome with those
with more severe injuries having poorer outcomes
(Dikmen et al., 1994; Doctor et al., 2005). Time to
272 forensic neuropsychology

TABLE 10.3 FACTORS PREDICTIVE OF FUNCTIONAL OUTCOME AFTER TBI

Predictors References
Pre-injury factors
Age (Brown, et al., 2005; Dikmen, et al., 1994; Donders &
Warschausky, 2007; Keyser-Marcus, et al., 2002; Poon,
Zhu, Ng, & Wong, 2005; Ruff, et al., 1993; Sherer, Nick,
et al., 2003; Testa, Malec, Moessner, & Brown, 2005)
Years of education (Hart, et al., 2003; Sherer, et al., 1999; Sherer, Sander, et al.,
2002)
Pre-injury employment (Dikmen, et al., 1994; Keyser-Marcus, et al., 2002; Sherer,
Nick, et al., 2003; Sherer, Sander, et al., 2002)
Substance use (MacMillan, Hart, Martelli, & Zasler, 2002; Sherer, et al.,
1999)
Injury severity variables
Initial GCS (Dikmen, et al., 1994; Levin, et al., 1990; Poon, et al., 2005)
Time to follow commands (Dikmen, Ross, et al., 1995; Dikmen, et al., 1994; Hart, et al.,
2003; Ruff, et al., 1993)
Duration of PTA (Boake, et al., 2001; Brown, et al., 2005; Sherer, Sander, et al.,
2002; Sherer, Yablon, et al., 2008)
Neuroanatomical variables (Hanlon, Demery, Kuczen, & Kelly, 2005; T. W. Teasdale &
Engberg, 2005; Wedekind & Lippert-Gruner, 2005)
Physical impairments (Brown, et al., 2005)
Cognitive and neurobehavioral impairments
Early cognitive status (Boake, et al., 2001; Dikmen, et al., 1994; Sherer, Novack,
et al., 2002; Sherer, Sander, et al., 2002)
Neuropsychological testing (Boake, et al., 2001; Doctor, et al., 2005; Hanks, et al., 2008;
Hart, et al., 2003; Kinsella, et al., 1997)
Post-injury depression (Ruff, et al., 1993; Seel, et al., 2003)
Impaired self-awareness (Sherer, et al., 1998; Trudel, Tryon, & Purdum, 1998)
Early functional status (Gollaher, et al., 1998; Ponsford, Olver, Curran, & Ng, 1995)
Environmental supports
Family functioning (Catroppa, et al., 2008; Ewing-Cobbs, et al., 2006; Prigatano,
et al., 1994)
Post-acute brain injury rehabilitation (High, Roebuck-Spencer, Sander, Struchen, & Sherer, 2006;
Malec & Basford, 1996; Sander, Roebuck, Struchen, Sherer,
& High, 2001)

follow commands and PTA duration are generally
more predictive of outcome than initial GCS
score, particularly for patients who undergo inpa-
tient brain injury rehabilitation (Sherer, Sander,
et al., 2002; Sherer, Yablon, et al., 2008). Of demo-
graphic characteristics, age and years of education
have the strongest associations with employment
outcome with age at injury greater than 50 years
predicting poorer outcome (Dikmen et al., 1994)
and higher years of education predicting more
favorable outcome (Sherer, Sander, et al., 2002).
Pre-injury adjustment, particularly pre-injury
employment status, also has substantial impact on
employment outcomes (Dikmen et al., 1994;
Sherer, Nick, et al., 2003).
Neuropsychological assessment makes a
unique contribution to prediction of employment
beyond that made by injury and demographic
variables with more intact early cognitive status
predicting more favorable long-term employment
outcome (Sherer, Novack, et al., 2002). A recent
prospective study found that a brief battery of
neuropsychological tests administered early in the
recovery course was predictive of employability at
 Moderate and Severe Traumatic Brain Injury
one year (Hanks et al., 2008). Neuropsychological
tests were able to predict functional outcome
above and beyond functional and injury severity
variables providing support for the incremental
validity of neuropsychological testing in moderate
to severe TBI. Tasks requiring rapid cognitive
processing and cognitive flexibility appear to be
particularly useful in making these predictions
(Boake et al., 2001). For instance, Doctor and
colleagues (2005) found that greater risk of unem-
ployment at one year post-injury was associated
with poor performance on the Trailmaking Test
Part B and the Digit Symbol subtest of the Wechsler
Adult Intelligence Scale administered at one
month post-injury.
Significant TBI has a number of effects on
school performance. TBI survivors are more
likely to fail grades, are more likely to receive
special education services, have more behavioral
problems, have poorer academic performance,
and score more poorly on cognitive tests than
children with no TBI (Ewing-Cobbs et al., 2006;
Hawley, 2004). Contrary to some early thoughts,
younger age at injury is associated with poorer
outcome due to interference with skills acquisi-
tion during key developmental phases (Donders
& Warschausky, 2007). For older (college-aged)
patients, return to school is often considered a
productive outcome and combined with return to
work in outcome studies (e.g., Ip, Dornan, &
Schentag, 1995) so that there is little or no unique
investigation of factors that predict return to
school for this age group. Prediction of return to
school for younger patients may be a moot point
as these children have a legal right to an appropri-
ate educational program regardless of degree of
impairment. Nonetheless, school performance for
children is predicted by injury severity (Catroppa,
Anderson, Morse, Haritou, & Rosenfeld, 2008)
and neuropsychological assessment (Kinsella
et al., 1997). Even children with mild TBI have
poorer adaptive skills though academic perfor-
mance may be less affected (Catroppa et al., 2008).
Effects of brain injury are moderated by pre-injury
functioning, socio-economic status, and family
functioning (Catroppa et al., 2008; Ewing-Cobbs
et al., 2006).
TBI also has a marked effect on personal
independence. Greater injury severity, as indi-
cated by longer time to follow commands interval,
is associated with decreased personal indepen-
dence after TBI. Residential placement may be
considered a proxy for personal independence.
Over 40% of those with time to follow commands
greater than 28 days require institutional
273
placement at one year post-injury (Dikmen, Ross,
Machamer, & Temkin, 1995). Institutional place-
ment in the post-acute period is a less frequent
outcome than dependence on others for supervi-
sion and assistance with household management.
This dependence results in many persons who
lived independently prior to TBI living with par-
ents or others at one and two year post-injury
follow-up. As with institutional placement, initial
injury severity predicts likelihood of living with
others after injury (Dikmen, Ross, et al., 1995).
Degree of cognitive impairment as assessed by
neuropsychological tests makes a unique contri-
bution to prediction of supervision requirements
after TBI (Hanks et al., 2008; Hart et al., 2003).
As with other functional outcomes, personal
independence after TBI is affected by a number
of noninjury factors such as sex, marital status,
and ethnicity (Chang, Ostir, Kuo, Granger, &
Ottenbacher, 2008).
In conclusion, moderate to severe TBI is dis-
tinct in its initial presentation, course of symp-
toms, and outcome as compared to milder forms
of TBI. These individuals sustain a wide range of
neuropsychological and neurobehavioral impair-
ments that can be long lasting and affect their
ability to return to previous levels of personal,
social, and occupational functioning. Factors pre-
dicting short and long-term outcome are varied
and complex in nature. This chapter was intended
to assist neuropsychologists in understanding the
expected course of recovery, the expected out-
comes, and the factors that help to predict out-
come following moderate to severe TBI. By
understanding these factors, the neuropsycholo-
gist will be better suited to evaluate these patients,
provide psychoeducation and treatment, and help
patients and families plan for the future. Finally,
knowledge of these factors is essential for the neu-
ropsychologist working with these patients in
forensic settings by allowing for identification of
expected behavioral and performance patterns
and using this knowledge to make informed
decisions and predictions about the future.
AC K N OW L E D G M E N T
Completion of this chapter was partially sup-
ported by the National Institute on Disability and
Rehabilitation Research Grant #H133A070043,
the Texas TBI Model System of TIRR
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 11
Neurotoxic Injury
KAREN I. BOLLA
INTRODUCTION
This chapter focuses on the determination of
neurotoxic injury subsequent to possible expo-
sure to specific neurotoxicants. A neurotoxin is a
chemical or substance that is harmful or fatal to
the central nervous system of biological organ-
isms when introduced in certain quantities or
doses (Loomis & Hayes, 1996). It is important to
remember that even the most innocuous of
substances can have harmful effects if introduced
into the body in high enough doses. For example,
even water can be toxic if ingested in large enough
quantities. Also, a chemical can be harmful or
have adverse effects that are species specific. That
is, a chemical that is lethal to an insect may be
harmless to a human.
The associations between neurologic symp-
toms and exposure to some specific chemicals are
still controversial. In fact, much of the research on
the neurological sequelae of neurotoxicants has
been litigation-fueled (Lees-Haley & Williams,
1997). While the literature continues to debate
whether low-level chronic exposure results in
neurotoxic insult, it is generally accepted that
higher levels of exposure to certain chemicals can
result in neurocognitive sequelae. Even with
higher levels of exposure, the association between
exposure and central nervous system effects may
be reported by some studies, while other studies
fail to find a similar relationship. A prime example
of this is the relationship between solvent expo-
sure and toxic encephalopathy.
Both the scientific and lay communities
accept that exposure to solvents causes chronic
painter’s syndrome or solvent encephalopathy.
This well-known syndrome is characterized by
headache, fatigue, difficulty concentrating, poor
memory, depressed mood, sleep disturbance,
decreased libido, and irritability. In fact, in 1985,
a World Health Organization (WHO) working
group on the chronic effects of organic solvents
on the central nervous system categorized the
neurobehavioral effects associated with solvent
exposure. These categories were based on the
severity of symptoms, and categories are pre-
sented in Table 11.1).
Painter’s syndrome originated in 1979 when
Arlein-Soborg et al. (1979) from Denmark
reported a brain syndrome that they termed
chronic painter’s syndrome. This report was based
on 70 house painters who had an average of 24
years of job-related exposure to solvents and
who were referred for medical evaluation for sus-
pected organic solvent intoxication or dementia.
Following the release of this report, governments
in the Scandinavian countries began to compen-
sate workers for cognitive and psychiatric disabil-
ities that were determined to be work related.
Although its impact was enormous, this initial
description of chronic solvent encephalopathy did
not include a control group, made no attempt to
control for background variables such as level of
education or intelligence, and based its conclu-
sions solely on clinical judgments about the
subjective complaints of patients seeking medical
treatment. For the most part, reports of neuro-
behavioral difficulties in workers exposed to
solvents are of questionable validity because many
of the studies published in the scientific literature
contain methodological limitations. Inconsist-
encies in the literature can be attributed to differ-
ences in the populations studied (control and
exposed groups) with respect to pre-morbid level
of cognitive and psychiatric functioning, age of
the sample, and severity of the exposure (i.e.,
intensity and duration). Furthermore, many stud-
ies make no attempt to control for alcohol use,
associated medical disorders (e.g., diabetes,
hypertension), educational level, or level of intel-
ligence. For example, when Gade et al., attempted
282 forensic neuropsychology

TABLE 11.1. CATEGORIES OF THE T YPES OF SOLVENT ENCEPHALOPATHY

Type I Subjective nonspecific encephalopathy symptoms only

Type IIa Sustained personality and mood change. Negative neurobehavioral findings. Unclear if symptoms
are reversible.
Type IIb Impairment of intellectual function documented by objective neurobehavioral test results and
possible mild neurologic signs. After removal from exposure, symptoms should remain stable or
improve, not become worse.
Type III Dementia with neurologic signs, neurobehavioral deficits and possible neuroradiologic findings
(e.g., frontal lobe atrophy). Related to repeated severe exposure (i.e., paint huffers). May be
irreversible but generally does not progress.

Cranmer and Goldberg, 1987.

to replicate the data of Arlien-Soborg et al. (Gade
et al., 1988; Arlien-Soborg et al., 1982), they added
a control group that was matched to the workers
in terms of sex, age, education, and intelligence.
When they re-analyzed the test data of 20 patients
reported on by Arlien-Soborg et al. (1982) using
this control group, the neurometric test scores no
longer showed any significant difference between
the exposed group and the controls. A similar
result was obtained by Cherry et al. in a group of
workers exposed to methyl-N-butyl ketone
(MBK) and toluene for an average of 11.7 years
(Cherry et al., 1985). When these authors matched
a control group of workers to their exposed work-
ers on the basis of a verbal intelligence test
(NAART), the association between poor neuro-
behavioral test performance and exposure to
solvents disappeared. Also, many studies use
biased sampling by allowing subjects to self-select
into their study groups; for example, they may
report only on workers who present to a medical
clinic with symptoms or complaints, or only on
workers involved in litigation (Morrow et al.,
1989; Morrow et al., 1990). Similar methodologi-
cal mistakes are also seen in investigations of
potential neurotoxins other than solvents, such as
the heavy metal, manganese (Lees-Haley et al.,
2004). Studies that use such nonrandom samples
are fatally flawed in their methodology and their
findings cannot be viewed as scientifically sound.
Nevertheless, these faulty studies can be used by
attorneys during litigation to influence judges,
juries, and the media.
Two critical reviews of the literature (World
Health Organization, 1985; Cranmer & Goldberg,
1986) concluded that at least 10 years of exposure
are necessary to produce an increased risk of
neurobehavioral sequelae from solvent exposure.
A number of methodologically sound studies
found statistically significant dose-related associ-
ations between exposure to solvents and decre-
ments in neurobehavioral test scores although the
magnitude of the effects suggests that they are
probably clinically insignificant (Cherry et al.,
1985; Maizlish et al., 1987; Gade et al., 1988;
Triebig et al., 1988; Bolla et al., 1990 ; Bleecker
et al., 1991; Bolla et al., 1995). It therefore appears
that, while 10 years or more of exposure may
increase an individual’s risk of developing neu-
robehavioral symptoms, few significant adverse
effects may ever actually develop. This finding
emphasizes that if an individual was exposed to a
neurotoxicant, the exposure would have had to be
of significant intensity and duration to cause
symptoms. If there is no evidence of exposure, no
relationship can be established between symp-
toms and exposure to toxicants. Also, if an indi-
vidual was exposed to sufficiently elevated levels
of neurotoxicants, they should have acute physical
symptoms, such as headaches, dizziness, and
fatigue, prior to developing chronic symptoms,
such as neurocognitive deficits. Recent evidence
suggests a caveat to this pattern. As discussed later
in this chapter, neurotoxicant exposure may result
in “accelerated aging” of neurological function
and structure.
As with any diagnostic process, the ability to
make a differential diagnosis between neurotoxi-
cant exposure, neurological disease, psychiatric
disturbance, or malingering (see Dr. Larrabee’s
chapter) is based on the combined evidence taken
from the industrial hygiene data, occupational,
medical, social, and academic histories, as well as
the physical and neurological examinations,
biological monitoring, nerve conduction studies,
EEG, CT/MRI, and the neuropsychological evalu-
ation. It is therefore essential that patients with
potential neurotoxic exposure are evaluated by an

interdisciplinary team of health care professionals
with expertise in neurotoxicology. Ideally, this
“dream team” should be comprised of a neuro-
psychologist, a neurologist, an occupational
medicine physician/internist, an industrial
hygienist, and other medical specialties as neces-
sary (i.e., pulmonologist).
Whereas some health effects such as pulmo-
nary distress and gastrointestinal symptoms are
noticed immediately by the affected individual,
neurocognitive effects may go unrecognized while
the individual is acutely ill. Acute, high-level
exposure to a toxicant often results in clearly iden-
tifiable signs (e.g., delirium, seizures, flu-like
symptoms, or unconsciousness), but the residual
effects, involving alterations in cognition, mood,
and personality, are usually quite subtle. The most
common clinical presentation is one of poor con-
centration, short-term memory loss, depressed
mood, anxiety, restlessness, loss of interest in
work and hobbies, decreased libido, irritability,
headaches, weakness, sleep disturbances ranging
from insomnia to somnambulism, and symptoms
consistent with peripheral neuropathy. Since this
constellation of symptoms is nonspecific and
could be related to a host of neurological as well as
psychiatric etiologies, determining if these symp-
toms are a result of neurotoxic injury can be
extraordinarily challenging.
CATEGORIES OF TOXINS LEADING
TO REFERRAL FOR EVALUATION
The main categories of chemicals that have been
associated with CNS injury are the heavy metals
(e.g., lead, mercury), solvents (e.g., mixed solvents,
toluene), pesticides (organophosphates), and
gases (e.g., carbon monoxide). In addition, recent
work has shown that very heavy doses of drugs of
abuse (e.g., alcohol, cocaine, MDMA, marijuana,
methamphetamine) are also associated with
lower scores on neuropsychological measures
(Gonzalez, 2007; Bolla et al., 1998; Bolla et al.,
1999; Bolla et al., 2002) and abnormalities in brain
activity (Bolla et al., 2003; Eldreth et al., 2004;
Nestor et al., 2008) and brain density (Matochik
et al., 2003; Matochik et al., 2005) and neural
integrity (Cowan et al., 2008) when measured
using neuroimaging methods.
Most recently, so-called “toxic mold” in homes,
schools, and office buildings has been a promi-
nent topic in the news and is increasingly becom-
ing the basis for litigation. Notably, mold growth
has become a major public health concern in
the greater New Orleans area after the flooding
Neurotoxic Injury 283
associated with Hurricane Katrina (Riggs et al.,
2008). As with other neurotoxicants, the link
between mold and health effects is still controver-
sial. A statement published by the American
College of Occupational and Environmental
Health Medicine (2002) concludes that there is no
scientific evidence linking serious human health
effects, which include neurocognitive effects, to
inhaled mycotoxins (a secondary metabolite of
mold) in the home, school, or office environment.
Moreover, in 2004, the Institute of Medicine
(IOM) concluded that mold exposure is associ-
ated with respiratory illness and that immuno-
compromised persons are at risk for fungal-related
infections (IOM Committee on Damp Indoor
Spaces and Health, 2004). Of note, research on the
possible neurocognitive sequelae of mold expo-
sure is still needed as there are currently no avail-
able scientifically rigorous studies (see Dr. Binder’s
chapter for further discussion of toxic mold).
An in-depth discussion of the physical, cogni-
tive, and neuropsychiatric symptoms associated
with significant exposure to specific neurotoxicants
and drugs of abuse is beyond the scope of this
chapter but several reviews are available (Bolla &
Roca, 1994; Rosenstock et al., 2004; Hartman DE,
1995; Bolla & Cadet, 2007). However, Tables 11.2–
11.4 summarize the main categories of identified
neurotoxicants and the physical and cognitive dif-
ficulties generally associated with significant expo-
sure to these substances (Bolla & Roca, 1994; Bolla
& Cadet, 2007). Table 11.5 presents symptoms
associated with drugs of abuse (Bolla & Cadet,
2007). Neurotoxicant-symptom relationships sum-
marized in the tables were extracted from a review
of numerous epidemiological studies of effects of
various neurotoxicants on the nervous system. The
reader is cautioned that, as with any brain injury,
there is large individual variability in the develop-
ment of symptoms and therefore, not all symptoms
will be present in a single individual. Also readily
apparent in these tables is that the symptoms result-
ing from significant exposure to a specific neuro-
toxicant are quite generic. For example, several
neurotoxicants can produce memory, perceptuo-
motor, and emotional symptoms.
In summary, individuals with known signifi-
cant neurotoxicant exposures have reported
cognitive, physical, and affective changes. With
acute, high-level exposure, the physical symptoms
appear to be immediate, prominent, and
primary. Other primary symptoms may include
confusion and mood alterations. Conversely,
with low-level exposure, mood and cognitive
 TABLE 11.2. SYMPTOMS ASSOCIATED WITH HEAVY METAL EXPOSURE

Metal Associated Symptoms Neurologic Findings Neurocognitive Findings

Aluminum Respiratory dysfunction Cognitive decline; halting speech; ataxia Personality change; fatigue; memory;
attention/executive function

Arsenic
Acute GI distress; respiratory distress; cardiac Headache; nervousness; vertigo; paralysis; seizures; Verbal memory; drowsiness; confusion; stupor;
distress; elevated temperature; Mee’s lines myelopathy; hyperreflexia; neuropathy organic psychosis resembling paranoid
schizophrenia; delirium; agitation; emotional
lability
Chronic Abdominal pain; dermatitis; increased risk Headaches; fatigue; restlessness; vertigo; cognitive Verbal memory; drowsiness; confusion; stupor;
of cancer decline; visual changes or optic neuropathy; organic psychosis resembling paranoid
seizures; painful sensorimotor peripheral schizophrenia; delirium; agitation; emotional
neuropathy lability

Lead
Acute
Children Respiratory distress; flu-like symptoms Lethargy; cognitive decline; gait disorder; ataxia; Lethargy; hyperactivity
seizures
Adults GI distress; miscarriages; joint pain; flu-like Fatigue; delirium; seizures Delirium
symptoms

Lead (continued)
Chronic
Children Changes in auditory threshold; behavioral Learning disorders Intelligence; reaction time; perceptual motor
problems; cognitive decline; learning performance; memory; reading; spelling;
disabilities; attention deficit hyperactivity auditory processing; attention;
disorder (ADHD)
Adults Miscarriage/stillbirth; arthralgia; anemia; Scoptic visual effects; depression; irritability; sleep Depression; apathy; confusion; fatigue; tension;
hypertension; gout; renal effects; disturbance; decline in libido; cognition (learning restlessness; anger; visual intelligence;
decreased sperm count and memory); fasciculations; paresthesias; visuomotor; general intelligence; memory;
sensorimotor polyneuropathy; changes in auditory psychomotor speed; rate of learning; attention;
threshold visuoconstruction; manual dexterity
Manganese Anorexia; manganese pneumonia
Mercury
Inorganic
Acute Bronchial irritation; chills; gingivitis; GI
distress; bloody diarrhea; brownish
mouth lesions; metallic breath;
respiratory distress; renal failures
Chronic Salivary gland swelling; excessive salivation;
gingivitis; renal dysfunction
Organic Primarily affects the nervous system
Bolla and Roca, 1994; Bolla and Cadet, 2003.
Headaches; apathy; fatigue; depression;
hyperexcitability; dysarthria; psychotic behavior;
tremor; gait disorders; microphagia; parkinsonism
Weakness; irritability; delirium; psychosis
Shyness; fatigue; weakness; personality changes;
hyper-irritability; insomnia; depression; cognitive
decline; visual disturbance; intentional tremor;
parkinsonism; seizures; painful paresthesias;
peripheral polyneuropathy (sensorimotor
axonopathy)
Cognitive decline; neurasthenia; paresthesias;
ataxia; restricted visual fields; cortical blindness;
peripheral polyneuropathy; intention tremor;
motor neuron disease (ALS-like)
Sleepiness; asthenia; anorexia; impaired speech;
insomnia; hallucinations; mental excitement;
aggression; mania; dementia; frontal lobe
dysfunction; emotional lability; parkinsonism;
judgment; memory
Confusion
Irritability; avoidant behavior; overly sensitive
interpersonal behavior; shyness; depression;
lassitude; fatigue; agitation; visuospatial; visual
memory; reaction time; learning
 TABLE 11.3. SYMPTOMS ASSOCIATED WITH ORGANIC SOLVENT EXPOSURE
Organic Solvents Associated Symptoms Neurologic Findings Neurocognitive Findings
Mixtures Irritant effects; contact dermatitis Headaches; fatigue; irritability; depression; Executive functions; eye-hand coordination/
sleep difficulties; cognitive decline; decreased manual dexterity; visuoconstruction; odor
olfaction; peripheral neuropathy; myopathy identification

Carbon Disulfide Pulmonary and dermal irritants; cardiac
effects; toxic threshold lowered in
alcoholism; diabetes mellitus; renal and
hepatic diseases
Headaches; irritability; cognitive decline;
psychosis; delirium; hearing loss; loss of
corneal reflex; parkinsonism; peripheral
polyneuropathy
Psychosis; depression; personality change;
insomnia; eye-hand coordination; motor
speed, emotionality; energy level; psychomotor
performance; reaction time; vigilance;
visuomotor functions, construction; retarded
speech

Carbon Tetrachloride GI distress; hiccups; liver and kidney Intoxication; headaches; vertigo; delirium; Lethargy; confusion
damage; toxic threshold lowered in seizures; parkinsonism; optic atrophy; visual
alcoholism; obesity; diabetes; liver and difficulties
kidney disease

Ethylene Glycol Renal effects; cardiopulmonary effects Restlessness; agitation; seizures; absent corneal Fatigue; personality changes; depression
reflexes; coma

Methyl Alcohol (methanol) GI distress Headache; weakness; incoordination; delirium;

hallucinations; visual loss; stupor; seizures;
parkinsonism; death

Methyl-N-Butyl Euphoria Weight loss; sensorimotor polyneuropathy Personality changes; depression

Ketone (MBK)

N-Hexane Euphoria Headaches; poor appetite; mild euphoria; Headaches; appetite; depression; euphoria
peripheral polyneuropathy
Toluene (Methyl Benzene) Pulmonary effects; cardiac effects Euphoria; fatigue; ataxia; dizziness; tremor; Acute exposure: Excitation at lower or shorter
cognitive decline; seizures; delirium concentrations; depression at higher
concentrations; fatigue; confusion; anxiety;
reaction time; concentration

Olfaction; optic atrophy; hearing loss; peripheral Chronic exposure: Huffing exhileration; euphoria;
neuropathy (in cases w/associated N-hexane disinhibition; performance IQ; memory; motor
exposure); alcohol intolerance control; dementia; attention; visuospatial
function; apathy; flattened affect

Trichlorethylene (TCE) Cardiopulmonary effects; toxic threshold Headaches; insomnia; fatigue; anxiety; trigeminal Headaches; dizziness; fatigue; diplopia; alcohol
reduced with alcohol nerve damage; neuro-ophthalmological intolerance; neurasthenia; anxiety; lability;
findings; alcohol intolerance; cognitive insomnia; concentration; manual dexterity;
decline; hearing loss; peripheral neuropathy visuospatial accuracy; reaction time; memory

Bolla and Roca, 1994; Bolla and Cadet, 2003.

288 forensic neuropsychology

TABLE 11.4. SYMPTOMS ASSOCIATED WITH EXPOSURE TO

MISCELLANEOUS NEUROTOXINS

Neurotoxin Associated Symptoms Neurologic Findings Neurocognitive Findings

Carbon Monoxide None Headache; irritability; “Apathetic mask-like facial

dizziness; cognitive
decline; impaired vision;
blindness; deafness;
seizures; parkinsonism;
coma
expression”; dementia;
amnesia; disorientation;
irritability; cognitive
efficiency and flexibility;
verbal and visual memory,
spatial deficits

Organophosphates GI distress; excessive Headache; fatigue; dizziness; Confusion; fatigue;

sweating and salivation;
hypothermia; liver
dysfunction
decreased consciousness;
sleep disturbance;
cognitive decline; blurred
vision; absent papillary
response; muscular
fasciculations; tremor;
delayed polyneuropathy
(OPIDP)
headache; vigilance;
concentration; information
processing; depression;
anxiety; irritability;
memory and learning;
visuoconstruction; tension;
restlessness; anxiety;
apprehension

Bolla and Roca, 1994; Bolla and Cadet, 2003.

TABLE 11.5. SYMPTOMS ASSOCIATED WITH DRUGS OF ABUSE

Drug Neurological Symptoms Neurocognitive Findings
Alcohol Peripheral neuropathy Memory; executive function; visuospatial
function
Amphetamine Meth-induced psychosis; hyperactivity; Verbal memory; executive function; attention
euphoria; headaches; confusion;
vasculitis; strokes
Cocaine Vasoconstriction; stroke Executive function; visuoperception;
psychomotor speed; manual dexterity
MDMA Psychiatric disturbance; sleep disturbance; Visual and verbal memory;
Ectasy pupillary dilation; tremors; possible executive function
seizures; strokes
Marijuana Vasoconstriction Memory; executive function; psychomotor
speed; manual dexterity
Opiates Peripheral neuropathy Memory; executive function

Bolla and Cadet, 2003.

changes appear to be the primary symptoms.
Individuals exposed to neurotoxicants have
reported difficulties in the areas of concentration
and short-term memory. These individuals also
complain of disorientation, depression, irritabil-
ity, fatigue and sleep disturbances, decreased
libido, headaches, and weakness (Bolla & Cadet,
2007).
Once health effects have been detected, it can
be problematic to relate these in a causal fashion
to a specific neurotoxicant exposure. The diagno-
sis of neurotoxicant-related damage is generally
one of exclusion. Therefore, other causes of cen-
tral and peripheral nervous system dysfunction
must be ruled out, and a history of significant
exposure must be substantiated.

PRINCIPLES OF
N E U ROTOX I C O L O G Y
In behavioral neurotoxicology, the ability to make
accurate causal-inferences about a possible expo-
sure and the presence of adverse neurologic symp-
toms relies on how well the available data complies
with the principles of neurotoxicology. These
include the presence of a dose-response relation-
ship, the biological plausibility of symptoms, and
the occurrence of symptoms in close proximity to
an exposure. Of paramount importance is the pres-
ence of a dose-response relationship. This encom-
passes the idea that as the degree of exposure
increases (intensity/concentration or duration) the
symptoms (physical, cognitive, and psychological)
should also become more severe. That is, there
should be a direct relationship between the dose of
a chemical agent and the response obtained.
Therefore, if a patient reports exposure to a chemi-
cal in a well-ventilated area, for a short duration of
time, and claims subsequent severe neurocognitive
difficulties, then the symptoms are out of propor-
tion to the level of exposure.
Another principle of neurotoxicology relates
to biological plausibility. For example, if all of the
animal studies show that an extremely high level
of exposure to a specific chemical does not pro-
duce any health effects in animals, then there
would be little reason to suspect that health effects
would be produced in humans at a lower level.
Another prime example is the waxing and waning
of specific symptoms with solvent exposure. Acute
significant exposure to solvents almost always
results in headaches which then resolve once
removed from the source of exposure. Therefore,
the characteristic pattern of solvent-induced
headaches is that they develop after the individual
arrives at work in the morning and resolve after
they leave work, on the weekends, and when away
Cognitive Function
Neurotoxicant
Exposure
0 15 25 35
FIGURE 11.1: A decline in cognitive function may begin earlier (B); occur at a steeper slope (C),
or both (A), normal cognitive decline dotted line (D).
Neurotoxic Injury 289
on vacations. Biological plausibility is absent if the
patient claims that his headaches are related to
solvent exposure and reports that these headaches
last all day and night, seven days a week, and never
remit.
It has generally been accepted that, except for
carbon monoxide (CO) exposure and organophos-
phate (i.e., pesticide and nerve-agent exposure)
exposures, neurological and other physical symp-
toms will occur acutely at the time of high-level
exposure. Once the source of the exposure is elimi-
nated, these symptoms will begin to remit or at the
least remain constant over time. The proximity to
exposure principle posits that symptoms will not
increase after removal from exposure and do not
develop after a delayed time interval. As mentioned
previously, the only two chemicals where symp-
toms may worsen following significant exposure
are in cases of CO and organophosphate exposure
(Parkinson et al., 2002; Senanayake et al., 1982).
This viewpoint may need to be modified in
light of the availability of new information. In
recent years, a number of important studies have
documented that lead exposure in adults may
hasten cognitive decline with advancing age. In
three longitudinal studies of occupational or envi-
ronmental lead exposure in 3,052 adults, higher
tibia lead level was consistently associated with
persistent and possibly progressive changes in cog-
nition and brain structure long after exposure had
ended and lead levels had declined (Schwartz et al.,
2000; Schwartz et al., 2001; Schwartz et al., 2005).
Older adults with higher tibia lead levels showed
greater longitudinal declines in the domains of
verbal memory and learning, visual memory, and
executive function. This line of evidence provides
convincing evidence that adult lead exposure could
modify the rate and slope of cognitive decline that
occurs naturally with aging (Figure 11.1).
Adult Exposure
A D
B C
Dementia Threshold
45 55 65 75 85 95 105
Age (years)
290 forensic neuropsychology
New state-of-the art neuroimaging techniques
are also increasing our understanding of the
effects of neurotoxicants on the brain. For instance,
higher tibia lead was associated with a decrease in
volume of total brain, parietal white and gray
matter, temporal white matter, and the cingulate
gyrus, and insula (Stewart et al., 2006). These
changes in brain volume may mediate those cog-
nitive changes that have been well documented
(Caffo et al., 2008). Furthermore, although not
widely used, magnetic resonance spectroscopy
(MRS) can be utilized to examine neuronal loss,
possibly contributing to deficits in cognitive
functioning. In a case example, one individual
with significant past lead exposure had a lower
N-acetylaspartate: creatine ratio, a marker of
neuronal density (Weisskopf et al., 2004). These
neuroimaging results highlight the potential
future usefulness of these state-of-the-art tech-
niques for examining long-term, residual neuro-
logical consequences of exposure to lead as well as
to other neurotoxicants. However, it is imperative
to acknowledge that these techniques can be used
presently only in research settings and it would be
a serious error to prematurely use these investiga-
tional techniques in clinical or medical-legal
arenas.
EXPOSURE AS SES SMENT
Are the patient’s symptom complaints caused by
exposure to a neurotoxic substance?
Establishing Exposure
This is the primary referral question addressed to
the neuropsychologist in the context of toxic tort
litigation. To answer this question with any degree
of certainty, it must first be established that an
individual has been exposed to a neurotoxicant
and second, if the exposure to the neurotoxicant
was sufficient enough to cause CNS injury.
Without empirical evidence documenting an
exposure, it is difficult to address the question of
causality. In the context of forensic neuropsychol-
ogy, the inability to establish a strong association
between an exposure and neurologic effects will
not be useful to a plaintiff. On the other hand, the
defense can use this absence of empirical exposure
data to its advantage. Therefore, it is paramount to
establish if an exposure can be documented early
in the evaluation process, preferably prior to the
initial interview with the patient.
In general, both plaintiff and defense attorneys
will already possess or have access to industrial
hygiene data. Industrial hygienists collect air,
water, soil, and environmental samples in homes,
schools, office buildings, and industrial sites. These
samples are analyzed by sophisticated analytical
chemistry methods (e.g., mass spectroscopy) to
ascertain the composition of chemicals in the sam-
ples and if the concentrations of the identified
chemicals are above the acceptable threshold limit
values (TLV) set by the American Conference of
Governmental Industrial Hygienists (American
Conference of Governmental Industrial Hygienists
(ACGIH), 2008). The TLVs refer to airborne con-
centrations of substances, in conditions that nearly
all workers may be exposed on a daily basis. TLVs
are intended to be used only as guidelines in the
practice of industrial hygiene in the control of
potential workplace health hazards. TLVs can not
be used as an absolute value above which someone
will develop adverse health effects because of the
wide variation in individual susceptibility.
In addition to industrial hygiene sampling,
other sources documenting exposure level infor-
mation can be utilized. For example, in cases of
carbon monoxide (CO) poisoning, the fire depart-
ment will often have records of CO levels in the
dwelling where the person was exposed. In addi-
tion, emergency room records will contain labo-
ratory data on carboxyhemoglobin levels, which if
elevated, will provide evidence that a significant
exposure has occurred. Since carboxyhemoglobin
levels are elevated in smokers, smoking status
must be considered when interpreting this infor-
mation. In a nonsmoker, carboxyhemoglobin
levels higher than 8–10% are considered elevated;
greater than 50% life-threatening; and greater
than 70–75% usually fatal (Bolla & Cadet, 2007).
However, for CO exposure, carboxyhemoglobin
levels will drop rapidly once the person is removed
from the source of exposure. Therefore, it is
important to gain knowledge about the time
period that has elapsed between the suspected
exposure and the person’s treatment in the ER,
including the time of the blood draw for carboxy-
hemoglobin levels. This explains why documenta-
tion of a significant exposure is of utmost
importance and is the first step in determining if
CNS symptoms are related to the exposure.
Furthermore, if air samples of CO are higher
than the TLV of 50 ppm, then a case for a CO
exposure can be made. If, however, the dwelling
has been ventilated and the carboxyhemoglobin
levels are taken a few hours or days after the max-
imum exposure, then there will be little industrial
hygiene or biological data to support significant
CO exposure even if significant exposure has

occurred. Without data to verify an exposure, it is
difficult to determine the intensity of current and
past exposure, or even if an individual has been
exposed to a toxic chemical. However, knowledge
of the toxokinetics of the neurotoxicant is required
to interpret this type of information. If there is no
empirical evidence of an exposure, it will gener-
ally be difficult to relate neurologic symptoms to a
neurotoxic origin.
E S TA B L I S H I N G S U F F I C I E N T
EXPOSURE
“The most important tenet of establishing
a neurotoxic cause of any neurologic problem is
that the opportunity for exposure does not prove
that the symptoms were caused by the exposure”
(London & Albers, 2007). Often patients will
complain of residual neurocognitive effects
following exposure to an unknown chemical,
usually one with a strong, unpleasant odor. One
such substance is tar used in roofing and highway
repair. Many individuals report becoming ill when
exposed to tar and claim neurocognitive sequelae
as a result of this exposure. However, there is no
scientific evidence showing that tar is a neuro-
toxicant. These odorous chemical irritants may
produce allergy-type symptoms (e.g., runny eyes
and nose, congestion) but do not cause perma-
nent brain injury. There are an unlimited number
of chemical substances that we encounter in
everyday life where there is no evidence of neuro-
toxicity.
Once it has been established that an exposure
to a potentially neurotoxic chemical has occurred,
it then needs to be determined if the exposure
was of sufficient duration or intensity to produce
neurologic injury. To accomplish this task, a bio-
logical measurement (a biomarker) of exposure
is required. Unfortunately, with the exception
of the heavy metals, biomarkers for many neuro-
toxicants are either difficult to obtain or non-
existent. For example, solvents are difficult to
measure because of their rapid metabolism and
clearance. N-hexane, an aliphatic hydrocarbon,
has a half-life in fat tissue of about 64 hours.
Therefore, N-hexane and other organic solvents
are not cumulative chemicals, which means that
only recent exposure (i.e., end of work shift) can
be evaluated by a biological marker. Even if a
patient had elevated levels of N-hexane at one
time, the levels would not be elevated after only a
few days with no exposure. Cases of solvent expo-
sure can be akin to cases of mild traumatic brain
injury with respect to the paucity of empirical
Neurotoxic Injury 291
data linking neurological injury to an adverse
event.
H I S T O RY
Since there is often no definitive evidence (i.e.,
biomarkers, industrial hygiene data) to make
causal inferences about negative neurologic effects
of a neurotoxic exposure, in-depth histories must
be obtained. These histories should include infor-
mation within the medical, occupational, envi-
ronmental, social, academic, and psychiatric
domains, to allow ruling out factors accounting
for symptoms and test performance other than
the alleged exposure.
M E D I C A L H I S T O RY
A detailed medical history is essential to deter-
mine if there are alternative explanations for the
patient’s symptom complaints. Patients should be
asked specific questions about previous neuro-
logic problems including head injury, the pres-
ence of migraines, sleep disorders, substance use
(especially alcohol use), previous learning dis-
abilities (i.e., were they ever held back a grade in
school), symptoms of attention deficit disorder
with and without hyperactivity, and symptoms
compatible with carpal tunnel syndrome, which
can be confused with symptoms of neurotoxicant-
associated polyneuropathy. It is particularly
important to review the patient’s medical records.
It is informative if the patient reports a long series
of severe medical complaints that they believe are
caused by neurotoxicant exposure but there is no
history that the patient ever sought medical atten-
tion for these symptoms, or if they saw physicians
for other concerns and did not mention the
alleged symptoms.
O C C U PAT I O N A L A N D
E N V I R O N M E N TA L H I S T O RY
We must rely on the occupational and environ-
mental history to determine if there was sufficient
exposure to a neurotoxicant to produce neuro-
logic effects. An in-depth history relating to a per-
son’s occupational setting and specifics of the
duties required by the job must be obtained not
only from the patient but from other sources.
Questions that must be addressed are aimed at
assessing the work environment where the poten-
tial exposure occurred. The reader is referred to
Kilbourne and Weiner (1990) for an occupational
history questionnaire. Does the person work in an
industry with potential exposure to a neurotoxi-
cant? Does the person have a job which places
292 forensic neuropsychology
him in close proximity to an exposure? Since the
routes of absorption of neurotoxicants are inhala-
tion, ingestion, and dermal absorption, does the
person have a significant exposure that is biologi-
cally plausible? For example, although a person
lives in a house with lead paint, if the paint is in
good shape (i.e., not peeling) and is not disturbed,
then there is no potential source of significant
exposure. Did the person come in contact with a
neurotoxicant? Does the employer enforce safety
standards? Is there medical monitoring (i.e., rou-
tine testing for elevated lead levels)? If the com-
pany does not medically monitor or enforce safety
standards, it may not be because of negligence, it
may be because the work environment has been
determined to be safe. Has the patient experi-
enced symptoms while at work? Have co-workers
complained of similar symptoms?
It is also important to determine if individuals
claiming neurotoxic exposure are disgruntled
workers who have unstable work histories. How
many jobs has the patient had? What kind of work
performance evaluations has the individual
received? Does the patient show unexplained
poor job performance evaluations and excessive
absenteeism from work long before a claim for
exposure is made?
Environmental sources of exposure must also
be explored since these may be responsible for the
exposure, rather than the work site. What is the
person’s living situation? Do they live in an old or
relatively new home? Do they live in the country
or the city? What is the source of water? If water
comes from a well, the well may be contaminated.
Do they live in old housing in the city which could
be contaminated with lead paint, is the paint in
poor repair, and if so, have they tried to remove
the lead paint? Does the patient garden? Gardening
may be associated with exposure to excessive
amounts of pesticides. Has their home been
treated with pesticides lately? What are the indi-
vidual’s hobbies? Patients can become ill from
high exposure in poorly ventilated areas to paint
thinners used in refinishing antique furniture,
become lead exposed from lead solder used in
making stained glass, and may be exposed to
heavy metals from glazes if they make ceramics.
SOCIAL, ACADEMIC, AND
P S Y C H I AT R I C H I S T O RY
The collection of social history is important to
gain a feel for psychological stability. Individuals
claiming exposure to neurotoxicants may have a
long history of antisocial personality disorder,
somatoform disorder, major depressive disorder,
and childhood traumas. Therefore, it is important
to obtain information about the number of mar-
riages, past and current treatments for psychiatric
illness, and if there were any instances of physical
or sexual childhood trauma. In particular, history
of childhood physical or sexual trauma is associ-
ated with increased risk for somatization disorder
in adulthood (see Binder chapter).
It is also important to ascertain whether
there has been a change in neurological status.
School records, if available, can provide critical
information about premorbid level of functioning
(especially National Standardized Test results).
For example, it is not uncommon for a patient to
claim that they are having difficulty in mathemat-
ics or reading as a result of their potential expo-
sure. However, very poor grades in these subjects
as well as poor scores on a national standardized
test compared to a national sample would indicate
that the individual has always had trouble in
these areas.
T H E E VA L UAT I O N
Historically, neuropsychological techniques have
consisted of oral and written tests that are admin-
istered by a trained examiner on a one-to-one
basis. A number of computerized test batteries
have also been developed (e.g., the World Health
Organization Neurobehavioral Test Battery and
the Neurobehavioral Evaluation System-NES-2;
Letz & Baker, 1985) specifically for the evaluation
of neurocognitive sequelae of neurotoxicant
exposure.
Advantages and disadvantages exist for both
interviewer-administered and computer-admin-
istered tests (Kane & Kay, 1992). For interviewer-
administered tests, the advantages include human
interaction and encouragement by the examiner,
the ability to determine problem-solving strate-
gies by actually observing the individual perform
the tests, and the ability to administer tasks requir-
ing verbal presentation and verbal responses. For
example, verbal memory cannot be adequately
assessed by a computer without sophisticated
computer hardware. The disadvantages of inter-
viewer-administered tests include standardization
of administration between different testers and
between testing sessions. In epidemiological
investigations, interviewer-administered tests are
more labor intensive and require a large study
team to administer the tests.
Computerized testing offers excellent stan-
dardization in administering and scoring. Further-
more, in epidemiological studies, multiple work
stations and computers can be set up to test groups

of workers simultaneously. However, extensive
normative populations may not be available
for computer-administered tests, which is not
the case for interviewer-administered tests. The
normative values for interviewer-administered
tests cannot be used to compare the results of
written tests adapted for the computer because
the performance demands of the tasks change
even though the tests appear to be similar (Kane
& Kay, 1992).
A thorough assessment includes tests that
assess the cognitive domains of Intelligence, Lan-
guage, Verbal and Visual Learning and Memory,
Perception, Motor/Tactile skills, Attention, Psycho-
motor Speed, Executive Function and Personality
(Lezak et al., 2004; Spreen & Strauss, 1998). The
cognitive areas most often reported to be adversely
affected by neurotoxicants are manual dexterity,
psychomotor speed, verbal and visual memory
and learning, attention, and executive functions
(refer to Tables 11.2–11.5).
Verbal intelligence can be assessed using the
Verbal Subtests from the Wechsler Adult
Intelligence Scale (WAIS-IV) (Wechsler, 2008).
For brevity of testing, the Vocabulary Subtest can
be used alone to obtain a good estimate of verbal
intelligence because it correlates highly with the
Full-Scale IQ score.
Although there are many standardized tests to
evaluate language and aphasia, such as the Western
Aphasia Battery (Kertesz, 2006) and the Boston
Diagnostic Aphasia Battery (Goodglass et al.,
2000), extensive evaluation of language function-
ing in suspected cases of neurotoxic exposure is
unnecessary because most neurotoxins do not
selectively impair language. Therefore, deficits in
language (e.g., paraphasias) suggest an alternative
etiology for symptoms. The significant aspects of
language can be quickly assessed by confronta-
tional naming, repetition of words and phrases,
spontaneous writing of a sentence, writing a sen-
tence to dictation, and rating verbal expression.
At low levels, neurotoxins affect new learning
and recent memory, and they do not affect remote
memory. If gaps exist in the individual’s early
memories, then a neurotoxic etiology is unlikely.
Remote memory can be assessed by asking about
significant early life events (wedding or occupa-
tional details, or historical events).
Difficulties with anterograde memory (ability
to learn new information) is one of the character-
istics of neurotoxic exposure (Bleecker et al., 1991;
Schwartz et al., 1993; Schwartz et al., 2000; Bolla
et al., 1995; Stewart et al., 1999; Schwartz et al.,
2005). Therefore, it is important to evaluate this
Neurotoxic Injury 293
cognitive domain thoroughly with procedures
such as the California Verbal Learning Test-II
(CVLT-II) (Delis et al., 2000) and the Rey Auditory
Verbal Learning Test (RAVLT) (Rey, 1964). Close
inspection of performance patterns on the RAVLT
or the CVLT-II in individuals with neurotoxic
exposure show a learning effect over the trials, but
at a lower rate than expected. Performance on the
RAVLT (trial 1–5) also declines as years of expo-
sure to lead increases (Bolla et al., 1995) and peak
tibia lead levels increase (Schwartz et al., 2000;
Schwartz et al., 2005). These tests also allow exam-
ination for signs of malingering. For example, the
person may be embellishing symptoms if they
recall a word consistently on the free recall learn-
ing trials but then fail to recognize it on the
Recognition Subtest (Binder et al., 2003; Wiggins
& Brandt, 1988; Bernard, 1990).
Visual memory can also be assessed with tests
such as the Symbol Digit Paired Associate
Learning Task (Kapur & Butters, 1977a; Kapur &
Butters, 1977b) or the Rey Complex Figure
(Osterrieth, 1944).
Sustained attention and executive/motor skills
have been reported to be affected by neurotoxic
exposure, as well. Two tests that are sensitive in
detecting not only neurotoxic exposure, but any
type of CNS damage, are the Digit-Symbol
Substitution Test from the WAIS-III (now the
Coding subtest from the WAIS-IV) and the Trail
Making Test (Trails A and B) from the Halstead
Reitan Neuropsychological Test Battery (Reitan &
Davison, 1974). The Wisconsin Card Sorting Test
and the Category Test are also sensitive to deficits
in executive function and reasoning (Lezak et al.,
2004). The Stroop Test and Consonant Trigrams
are measures of divided attention as well as execu-
tive functions (Lezak et al., 2004).
Simple Visual Reaction Time is another
test that has been shown to be affected by neuro-
toxins (Balbus et al., 1997). Reaction time can be
measured by using either a reaction-time device
or a computer. Stimuli are randomly presented
so that the presentation of the next stimulus
cannot be anticipated. When this task is given
over 44 or more trials, an index of vigilance, sus-
tained attention, and response variability can be
determined. In addition to examining the mean
or median reaction, the standard deviation has
been shown to be especially sensitive for measur-
ing variability in rate of response which appears to
be strongly affected by lead exposure (Balbus
et al., 1997).
Manual dexterity and coordination have been
shown to deteriorate with exposure to various
294 forensic neuropsychology
neurotoxins, especially to a combination of
organic and inorganic lead (Bolla et al., 1995;
Stewart et al., 1999; Schwartz et al., 1993; Schwartz
et al., 2000; Schwartz et al., 2001a; Schwartz et al.,
2001b). The Purdue Pegboard (Purdue Research
Foundation, 1948; Agnew et al., 1988) and the
Grooved Pegboard (Klove, 1963; Klove, 1963) are
measures of fine motor speed and dexterity. The
Finger Oscillation Task (Finger Tapping) (Reitan
& Davison, 1974) is a measure of dexterity/simple
motor speed. Brain damage from most neurotox-
ins is diffuse, and significantly faster scores on one
hand compared to the other (greater than 10%
difference) may suggest a lateralized dysfunction
and would therefore be incongruent with a diag-
nosis of a neurotoxic exposure. Although, epide-
miological studies find that nondominant hand
performance may be more sensitive to lead expo-
sure, the effect is small (Bolla et al., 1995; Stewart
et al., 1999; Schwartz et al., 2002).
Not only is it important to use tests that have
been shown to be sensitive to detecting subtle
neurocognitive effects from exposures, but tests
sensitive enough to show a dose-response asso-
ciation are favorable. Significant dose-related
associations (increased exposure, poorer perfor-
mance) between quantitative measures of expo-
sure to a mixture of organic and inorganic lead or
to only inorganic lead (duration of exposure, peak
tibia bone lead, current blood lead) have been
reported for the RAVLT, Serial Digit Learning
test, Rey Complex Figure Delayed, Trails A and B,
Stroop, Block Design, Purdue Pegboard, and
Finger Tapping (Bolla et al., 1995; Stewart et al.,
1999; Schwartz et al., 2000; Schwartz et al., 2005).
Likewise, increased lifetime weighted average
exposure to a mixture of solvents was associate
with decreased performance on the Digit Symbol
substitution, Serial Digit learning, Reaction time,
Trails A and B, and bilateral finger tapping
(Bleecker et al., 1991). Establishing evidence of
dose-related associations on the neuropsycholo-
gical assessment helps rule out non-neurologic
psychiatric factors and malingering. Systematically
evaluating for malingering must be included in
every evaluation of a potential case of neurotoxic
exposure. The reader is referenced to Dr. Larrabee’s
chapter on malingering for guidelines.
I N T R P R E TAT I O N
OF FINDINGS
Adequate Normative Values for Reference
Speculation about the cause of poor performance
on a neurobehavioral test must be made with
caution. To determine if a score falls outside the
normal range, adequate norms must be used for
comparison. For example, intellectual ability can
predict test performance for verbal, perceptual,
executive function, and psychomotor speed tasks
(Larrabee, 2000), but few norms are currently
available for individuals with low levels or high
levels of intellectual functioning. Comparing the
test results of an individual with lower intellectual
ability with normative values based on a more
intelligent group could lead to the erroneous con-
clusion of CNS injury where none exists. This is
especially problematic in behavioral neurotoxi-
cology because there are few norms available for
unskilled laborers (i.e., blue-collar workers), many
of whom never finished high school. Conversely,
performance decrements in highly intelligent
people may be missed, since even their diminished
performance may still meet or exceed the upper
limits of a normative group representing a more
average level of intellectual functioning. In addi-
tion, cognitive performance is also influenced
by age and sex. Therefore, to ensure an accurate
diagnosis, the clinician must use norms that
have been adjusted to include the effects of
modifying variables such as education, intelli-
gence, age, and sex.
Base Rates
When attempting to determine if a patient’s
cognitive complaints are consistent with those
that have been reported with exposure to neuro-
toxicants, one must consider the base rate of the
complaint in the general population. For example,
in a study of 40–90-year-old community-dwelling
healthy individuals, 83% complained of difficulty
remembering names, 60% complained that they
misplaced items, and 53% complained of word-
finding problems (Bolla et al., 1991). These base
rates increase moderately when associated with
head injury of toxic exposure, but increase dra-
matically once someone enters the legal arena to
become a personal injury claimant (Lees-Haley &
Brown, 1993; Dunn et al., 1995). Table 11.6 is
taken from the work of Dunn et al. (1995) and
shows the frequency of symptom complaints in
samples of controls, head-injured and/or toxic-
injured individuals, and personal-injury claim-
ants. Therefore, it is paramount to remember that
just because a patient complains of a specific
symptom and that symptom has been reported
with exposure to a specific neurotoxicant, this
does not mean that the individual was exposed to
a chemical that permanently injured her/his
nervous system.
 TABLE 11.6. BASE RATES OF COMPLAINTS
SYMPTOM FREQUENCY
Symptom Medical Controls Head Injured/ Personal Injury
(n=113) Toxic (n=68) (n=156)
Anxiety 41 56 87
Trouble sleeping 30 40 81
Headaches 50 57 77
Depression 27 41 76
Tension 24 40 74
Concentration problems 21 34 71
Fatigue 37 56 71
Difficulty concentrating 18 32 69
Impatience 33 41 64
Irritability 27 31 63
Restlessness 16 37 63
Confusion 5 18 58
Feeling disorganized 20 32 58
Thinking clearly 11 27 57
Neck pain* 31 40 56
Loss of interest 13 15 51
Easily distracted 15 24 49
Loss of efficiency 10 13 49
Loss of temper 11 19 49
Attention problems 10 25 48
Word finding 12 24 46
Feeling partially disabled 4 16 44
Weakness 6 15 44
Dizziness 21 28 41
Nausea 20 32 39
Sexual problems 8 18 39
Shoulder pain* 14 24 38
Slowed thinking 5 16 38
Blurred vision 18 32 37
Rapid heartbeat 15 19 37
Poor judgment 4 16 35
Recent memory problems 5 18 35
Chest pressure 13 13 34
Trouble hearing 12 28 34
Numbness 5 21 34
Painful tingling 5 16 34
Visual problems 7 21 34
Trouble reading 1 6 33
Fear of non-cancer illness 6 19 33
Trouble walking 4 6 32
Trembling 5 15 31
Feeling totally disabled 3 3 30
Bumping into things 14 13 30
Diarrhea* 26 47 28
Perspiring for no reason 5 13 26
Loss of common sense 4 6 24
Marital problems 9 12 24
Fine motor coordination 2 4 20
(Continued)

296 forensic neuropsychology
TABLE 11.6. Continued
Long-term memory problems
Speech problems
Slurred speech
Elbow pain*
Impotence
Not knowing where I am
= Mean No. Symptoms
Dunn et al., 1995;
*indicates that the symptom is a distractor.
It is important to note that neurobehavioral
tests can have high sensitivity, but low specificity,
meaning that they can be very effective in detect-
ing deficits, but less effective in identifying the
causes of those deficits (see Larrabee chapter on
scientific approach). It is important to determine
if cognitive decrements are related to neuro-
toxicant exposure or to another CNS, medical,
or neuropsychiatric disorder. Alterations in per-
formance can be related to age, sex, educational
level, native intelligence, cultural differences,
cultural deprivation, motivation, involvement in
litigation, frustration, fatigue, emotional prob-
lems like anxiety and depression, and personality
characteristics.
Consequently, while some individual tests are
sensitive, they are of little value when attempting
to delineate the precise etiology of a person’s defi-
cits. The neuropsychological evaluation cannot be
used in isolation to make a diagnosis, but rather
must be used in combination with medical, social,
school, and occupational histories. Although
patients may report a recent onset of cognitive
difficulties, review of school records and prior
employment evaluations might indicate long-
standing problems (i.e., subnormal intelligence or
learning disability).
Furthermore, long-term or heavy alcohol use
(Bondi et al., 1998; Parsons, 1998), heavy cocaine
use (Bolla et al., 1999), heavy MDMA (Ecstasy)
use (Bolla et al., 1998), or even very heavy
marijuana use (Bolla et al., 2003; Gonzalez, 2007)
may produce a number of cognitive deficits.
Medical conditions such as diabetes can cause
symptoms of peripheral neuropathy as well as
cognitive deficits (Bruce et al., 2003). Other
medical conditions to consider in the differential
diagnosis are past history of head injury, hyper-
tension, thyroid disease, and renal or hepatic
disorders. Depression or anxiety can also produce
0 7 18
2 6 17
1 6 15
8 22 14
4 2 14
0 4 12
9 14 25
decrements in neuropsychological test perfor-
mance. These decrements are usually observed in
the areas of attention, learning and memory,
processing speed, and psychomotor speed. Since
similar cognitive domains are affected by both
neurotoxicants and alterations in mood, it can be
difficult to determine the relative contribution of
each to decrements in neuropsychological test
performance. More specifically, such symptoma-
tology could be related to neurotoxic exposure, to
the patient’s emotional state, to the patient’s per-
sonality characteristics, or to some combination
of the three.
In order to determine the etiology of com-
plaints, patterns of performance and inconsisten-
cies during testing (such as superior performance
on harder tasks with poor performance on easier
ones, or lower than chance performance on all of
the tasks) must be examined carefully. Repeat
testing will also assist in this area, since test
performance should remain relatively static over
the course of several days. If significant alterations
in test scores are indicated, an affective or motiva-
tional disturbance is the likely culprit. If test
performance declines without re-exposure, then a
progressive disease or secondary psychological
reaction to the exposure is suspect (Bolla &
Rignani, 1997).
Emotional reactions to a perceived exposure
may be as important as, or even more important
than, the direct physiological effects of the chemi-
cals, especially when considering etiology and
persistence of symptoms. Figures 11.2 and 11.3
illustrate the complex relationships between
exposure and neurologic sequelae (Bolla, 1996b;
Bolla, 1996a; Bolla & Rignani, 1997). The fear
associated with suspected exposures can be
stressful enough to cause significant mental disor-
ders such as somatoform disorders, anxiety disor-
ders, adjustment disorders, typical and atypical
 Neurotoxic Injury 297

EXPOSURE TO NEUROTOXICANTS

ACUTE, HIGH INTENSITY

Cognitive Symptoms Physical Symptoms

(acute confusional (peripheral neuropathy)
state) (nausea)

Hypersensitivity to Anxiety/Depression
Endogenous Stimuli

Primary symptoms Secondary symptoms

FIGURE 11.2: Schematic representation of the development and persistence of physical, cognitive, and
affective symptoms following acute, high-intensity chemical exposure. Solid lines are primary symptoms, and
dotted lines are secondary symptoms.

post-traumatic stress disorders, and idiopathic hypersensitive to endogenous stimuli. Expecta-

environmental intolerance (IEI). In addition, spe-
cific inherent personality characteristics may pre-
dispose an individual to develop physical,
cognitive, and psychological symptoms (Bolla-
Wilson et al., 1988; Kellner, 1985; Mechanic,
1972). Clinical observation suggests that more
perfectionist and anxious individuals may be
tions by susceptible individuals that exposure to
chemicals has adversely affected their health may
result in enhanced awareness of normal bodily
sensations. This normal physiological activity may
then be erroneously attributed to neurotoxic-
related abnormal physical, cognitive, and affective
symptoms (Bolla-Wilson et al., 1988). The degree

EXPOSURE TO NEUROTOXICANTS

CHRONIC, LOW INTENSITY

Cognitive Symptoms Physical Symptoms

(memory, psychomotor, (headaches, fatigue)
speed) (attention deficits)

Hypersensitivity to Anxiety/Depression
Endogenous Stimuli

Primary symptoms Secondary symptoms

FIGURE 11.3: Schematic representation of the development and persistence of physical, cognitive, and
affective symptoms following chronic, low-intensity chemical exposure. Solid lines are primary symptoms
and dotted lines are secondary symptoms.
298 forensic neuropsychology
to which an individual is hypersensitive to endog-
enous stimuli (normal bodily sensations) may
determine the duration and intensity of symp-
toms. Those psychological mechanisms have been
observed in toxic exposure, as well as in persistent
post-concussion syndrome (Bolla-Wilson et al.,
1988; Mittenberg et al., 1992) and in idiopathic
environmental intolerance (a. k. a. multiple chem-
ical sensitivity [MCS]; see Dr. Binder’s chapter for
further discussion).
The neuropsychological evaluation provides
unique information on the functional integrity of
the CNS. As with any diagnostic process, the
ability to make a differential diagnosis between
neurotoxicant exposure, neurologic disease, med-
ical illness, or neuropsychiatric disturbance is
based on the combined evidence taken from the
medical, occupational, social, and academic his-
tories, physical and neurologic exams, biological
monitoring, EEG, CT/MRI, and the neuropsycho-
logical evaluation.
Central nervous system effects are best
discovered with neuropsychological assessment.
However, interpretation of decrements in
performance on these tests is often erroneous if
made by individuals who lack specific expertise
in neurobehavioral toxicology. This is illustrated
nicely by the N-hexane example presented
earlier in this chapter. If the clinician is not
knowledgeable about the specific symptoms asso-
ciated with specific neurotoxic agents, they may
conclude that a mild deficit in verbal memory
(without having the patient examined for periph-
eral neuropathy) was due to exposure to N-hexane
when this conclusion would not be biologically
plausible.
The neurological examination, electroenceph-
alogram (EEG), computed tomography (CT) scan,
and magnetic resonance imaging (MRI) scans are
generally not helpful in making a specific diagno-
sis of toxic encephalopathy but are helpful in
ruling out other causes of the patient’s symptoms.
In contrast, nerve conduction studies are useful in
detecting peripheral neuropathies that are often
associated with exposure to specific chemicals.
For example, the predominant neurologic feature
of N-hexane exposure is peripheral neuropathy,
not cognitive disturbance. Symmetrical sensory
dysfunction in the hands and feet is the usual pre-
senting complaint. Weakness in the lower extrem-
ities is also a common symptom. Decreased
response to pin, vibration, and thermal stimula-
tion is found on examination. The clinician should
become suspicious if no symptoms of peripheral
neuropathy were ever reported to any doctor by
the patient, and the patient is only claiming
cognitive problems. If there are no acute effects, it
would be highly unlikely to have chronic effects.
After discontinuation of exposure, both CNS and
PNS effects recover.
When evaluating patients who present with
symptoms of a possible neurotoxicant exposure,
it is irresponsible to routinely attribute their
symptoms to the presence of a neuropsychiatric
disorder. It is equally irresponsible to attribute
neurotoxic-like symptoms to neurotoxicant
exposure without rigorously exploring other
etiologies. If other causes for the symptoms are
not considered, then many treatable conditions
will remain unidentified and untreated.
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 12
The Psychological Assessment of
Persons with Chronic Pain
K E V I N W. G R E V E , K E V I N J . B I A N C H I N I ,
A N D J O N AT H A N S . O R D
Pain is no evil unless it conquers us.
He that is uneasy at every little pain is never without some ache.
INTRODUCTION
The International Association for the Study of
Pain (IASP) defines pain as “an unpleasant
sensory and emotional experience associated
with actual or potential tissue damage, or
described in terms of such damage” (Merskey &
Bogduk, 1994, p. 212). Importantly, the IASP’s
definition considers pain a subjective experience
influenced by both psychological and contextual
factors that is not necessarily dependent on tissue
damage or specific nociceptive activation. Pain is
usually termed chronic when symptoms do not
follow the natural course of healing after injury or
persist for longer than three months without
biological value (Merskey & Bogduk, 1994). As
described by Pappagallo and Werner (2008),
“Acute pain ordinarily has a useful purpose, such
as signaling damage or that something is wrong.
By contrast, chronic pain has no such value, but is
a disease in its own right, causing widespread
suffering, distress, and disability” (p. 17).
Scope of the Problem
Chronic pain is a widespread problem estimated
to affect between 10% and 20% of the general
population (Verhaak, Kerssens, Dekker, Sorbi, &
Bensing, 1998) and 20% to 25% of primary care
patients (Gureje, Von Korff, Simon, & Gater,
1998). Spine-related pain is a particularly common
problem with over half of adults experiencing an
episode of spine-related pain (Andersson, 1998;
— george eliot
—proverb
Frymoyer, 1988; Rubin, 2007) and approximately
one-third experiencing chronic spinal pain in
their lifetime (Von Korff et al., 2005).
Financially, the direct and indirect costs of
chronic pain are substantial. Pain complaints
result in millions of physician office visits per year
(Woodwell, 2004) and Americans spend an esti-
mated $70 billion per year in health care costs
related to chronic pain (American Academy of
Pain Management, 2003). Pain has a large impact
on health-related quality of life (Morken et al.,
2002) and back pain alone is thought to contrib-
ute to over 100 million lost workdays yearly (Guo,
Tanaka, Halperin, & Cameron, 1999). The total
economic burden of pain-related health care and
disability has been estimated by some to exceed
$150 billion a year (Gatchel & Okifuji, 2006;
Mayer, Gatchel, & Polatin, 2000).
Neuropsychologists will almost inevitably be
confronted with issues of pain and pain-related
disability in their practice. Pain is a feature of a
variety of conditions commonly encountered by
neuropsychologists such as multiple sclerosis,
Parkinson’s disease, and traumatic brain injury
(TBI). Chronic pain after TBI, for example, occurs
in 75% of mild TBI patients and 32% of moderate-
severe TBI patients (Nampiaparampil, 2008). Pain
is an important prognostic indicator for injury
recovery (Alexander, 1995; Mooney, Speed, &
Sheppard, 2005) and should be addressed in
order to reduce residual disability and maximize
 The Psychological Assessment of Persons with Chronic Pain
functional outcomes. Therefore, an understanding
of pain and the factors that influence pain-related
disability is essential for the neuropsychologist;
particularly when evaluating cases in the context
of workers’ compensation claims or personal
injury litigation, where pain can directly influence
the assessment of disability.
Physical Factors Alone Are Inadequate
to Explain Outcome
A strict physical reductionist school of thought
holds that all pain is entirely physically based and
that all treatment should follow from this assump-
tion (see Thompson, 2005). This reductionist
thought runs counter to current mainstream sci-
ence which views symptoms and disability result-
ing from pain-related conditions (see appendix
A) as a product of biological, psychological, and
social factors (Gatchel, Peng, Peters, Fuchs, &
Turk, 2007). Research has increasingly demon-
strated that pathological findings from commonly
used medical diagnostic techniques (see appendix
B) are not sufficient to explain current or future
pain-related symptoms or disability.
For example, pathology of the spine is associ-
ated with pain generation (Schwarzer, Aprill,
Derby, Fortin, Kine, & Bogduk, 1995). However,
objective evidence of physical pathology does not
always correlate with pain symptoms or disability,
nor does it reliably predict who will become symp-
tomatic in the future. Cervical and lumbar disc
abnormalities including some that would be con-
sidered surgical lesions have been found in the
cervical and lumbar spines of asymptomatic
patients (Boden, Davis, Dina, Patronas, & Wiesel,
1990; Boden, McCowin, Davis, Dina, Mark, &
Wiesel, 1990; Jarvik, Hollingworth, Heagerty,
Haynor, & Deyo, 2001). Additionally, the presence
of an identifiable abnormality of the disc or spinal
canal in the lumbar spine of asymptomatic patients
does not predict subsequent low back pain seven
years later (Borenstein et al., 2001). What did pre-
dict the development of low back pain after three
years in cases asymptomatic at baseline was self-
reported depression at baseline (Jarvik,
Hollingworth, Heagerty, Haynor, Boyko, & Deyo,
2005). Those cases with depression at baseline
consistently reported greater experienced pain.
This applies not just to spine pain but to other
types of pain as well. Incidental meniscal findings
on MRI of the knee are common in the general
population (Englund et al., 2008) and more than
60% of persons with one or more meniscal tears
are asymptomatic. Further, a finding of meniscal
303
pathology without frequent symptoms at baseline
did not have a significant relationship with the
development of knee symptomology 15 months
later (Englund et al., 2007). Similarly, among
persons with carpal tunnel syndrome there was
no association between electrodiagnostic findings
and symptoms/disability (Chan et al., 2007).
Conversely, many people present to physicians
with a range of physical symptoms for which no
medical explanation can be found. Seventy-two
percent of the Englund et al. (2008) sample with-
out meniscal pathology or radiographic evidence
of osteoarthritis were symptomatic. Nearly 20% of
patients seen in primary care clinics present with
medically unexplained symptoms, a finding not
explained by comorbid depression or anxiety
(Barsky, Orav, & Bates, 2005). Among first-time
referrals to a neurology service, 61% (59% of
females, 63% of males) had at least one medically
unexplained symptom (Fink, Steen Hansen, &
Sondergaard, 2005). Thirty-four percent (41.3%
of females, 27.7% of males; 20.5% of inpatients,
43.2% of outpatients) of the Fink et al. (2005)
cases met the diagnostic criteria an ICD-10 soma-
toform disorder. In this context, neuropsycholo-
gists are particularly familiar with psychogenic
nonepileptic seizures which are diagnosed in
approximately 30% of patients evaluated using
video-EEG monitoring (Benbadis, O’Neill, Tatum,
& Heriaud, 2004; Gates, Ramani, Whalen, &
Loewenson, 1985; Martin, Burneo, Prasad, et al.,
2003). Please refer to the chapter by Binder in
the present volume for further discussion of
unexplained medical symptoms.
Summary
In short, objective physical findings do not fully
explain the symptom presentation of a large
proportion of patients seen by physicians for
complaints of pain. In fact, psychosocial factors
may predict important outcomes (e.g., return to
work) better than physical variables such as MRI-
identified morphologic abnormalities (Schade,
Semmer, Main, Hora, & Boos, 1999). Linton
(2000) has shown that multiple psychological
factors are important in the transition from acute
to chronic pain. Pain is a complex biopsychoso-
cial phenomenon and consideration of psychoso-
cial factors is essential for a comprehensive
understanding and appropriate treatment of pain
and patients with pain (Gatchel & Okifuji, 2006).
These findings emphasize the point that the
pathophysiology and psychosocial factors
underlying pain-related disability are complex
304 forensic neuropsychology
individually and in combination and that an
understanding of both is important in the clinical
management of the pain patient (Gatchel &
Okifuji, 2006). The remainder of this chapter will
review these psychosocial factors along with
relevant contextual factors and the evidence for
their association with chronic pain and their
relevance for the clinical management of the
chronic pain patient. Issues pertaining to assess-
ment and diagnosis will then be discussed. Finally,
we will discuss the treatment of patients with pain
and the role of the psychological evaluation in
those interventions.
P S Y C H O S O C I A L FA C T O R S
I N PA I N
There has now developed a voluminous empirical
literature demonstrating that consideration of
psychosocial factors is essential for a comprehen-
sive understanding and appropriate treatment of
patients with pain (see the following for detailed
reviews: Gatchel, 2004; Keefe, Rumble, Scipio,
Giordano, & Perri, 2004; Linton, 2000). The rela-
tionship between psychosocial factors and pain-
related disability is not simple cause-and-effect
but is instead reciprocal and complex. Linton
(2000) concluded that these factors are related to
every aspect and phase of neck and back pain and
particularly important in the transition between
acute and chronic pain.
The following section will review several of
these factors and their relationship to outcome in
pain-related conditions. The subsequent section
will review the influence of socioeconomic factors
in pain. While this chapter presents these factors
in discrete sections, this should not imply inde-
pendence. Many of the factors are closely linked
conceptually and functionally, and recognition of
their interrelatedness is important.
Childhood Adversity
Childhood adversity in the form of abuse, neglect,
and abandonment has proven an important
predictor of current and future mental health
(Arnow, 2004; Taylor & Jason, 2002; Widom,
DuMont, & Czaja, 2007). For example, childhood
adversity is associated with the presence of medi-
cally unexplained symptoms. Brown, Schrag, and
Trimble (2005) found that physical/emotional
abuse was more common and more extreme in
patients with unexplained neurological symptoms
who met Diagnostic and Statistical Manual of
Mental Disorders (DSM) criteria for somatization
disorder than in those with a neurologically based
dystonia. A higher degree of family conflict was
present in the somatization group; however, there
were no group differences for neglect, sexual
abuse, or witnessing violence. Exposure to emo-
tional abuse accounted for 50% of the variance in
unexplained symptoms. These effects are not
simply explained by psychiatric comorbidity, as
Spitzer, Barnow, Gau, Freyberger, and Grabe
(2008) found that the odds of having been sexu-
ally abused in childhood were nine times higher
in persons who met DSM criteria for somatiza-
tion disorder than in those meeting criteria for
major depressive disorder.
Childhood adversity is also an important
predictor of pain symptoms (Davis, Luecken, &
Zautra, 2005). For example, Walker, Gelfand,
Gelfand, Green, and Katon (1996) found that
women with both irritable bowel syndrome and
chronic pelvic pain were significantly more likely
to have a history of childhood sexual abuse as well
as a variety of mood and anxiety disorders, soma-
tization disorder, and hysterectomy. Childhood
adversities are more common in somatoform
pain disorder and fibroymalgia is particularly
associated with severe maltreatment in childhood
(Imbierowicz & Egle, 2003; Walker, Keegan,
Gardner, Sullivan, Bernstein, & Katon, 1997;
Wolfe & Hawley, 1998). Brown, Berenson,
and Cohen (2005) surveyed a community sample
(n = 649) and found that adult chronic pain was
associated with a history of sexual abuse and that
this effect was not attributable to the presence of
depression at the time the survey was completed.
Walsh, Jamieson, Macmillan, and Boyle (2007)
found that a history of physical and sexual abuse
differentiated adult chronic pain patients with
disability in some aspect of their life from those
with pain but without disability.
A history of childhood adversity is also associ-
ated with outcomes in the treatment of pain
(Linton, 2000). Two studies are particularly
revealing. In the first study, Schofferman,
Anderson, Hines, Smith, and White (1992) retro-
spectively examined 86 patients who underwent
lumbar spine surgery. Five types of childhood
trauma were considered: 1) physical abuse;
2) sexual abuse; 3) emotional neglect or abuse;
4) abandonment; and, 5) chemically dependent
caregiver. Of patients who had experienced three
or more of these types of trauma, 85% had unsuc-
cessful surgical outcomes. In contrast, only 5% of
the patients who had experienced none of these
traumas had unsuccessful surgery. A similar study
of patients who had undergone multidisciplinary
 The Psychological Assessment of Persons with Chronic Pain
evaluation for refractory back pain also found a
high incidence of childhood traumas, especially
in patients with minimal signs of pathology
(Schofferman, Anderson, Hines, Smith, & Keane,
1993).
Not surprisingly, health care utilization is
greater in persons with a history of abuse, neglect,
or serious family dysfunction in childhood
(Arnow, 2004; Arnow, Hart, Hayward, Dea, &
Barr-Taylor, 2000). Even disability retirement is
associated with childhood adversity. Of nearly
9,000 community survey respondents ranging in
age from 40 to 54, those with multiple childhood
adversities were more than three times as likely to
take disability retirement compared to those with
no history of such adversity (Harkonmaki et al.,
2007). Spitzer et al. (2008) concluded “childhood
sexual abuse is an important factor in the multi-
factorial aetiopathogenesis of somatization disor-
der” (p. 335) and Arnow (2004) stated that “the
more severe the abuse, the stronger the associa-
tion with poor outcomes in adulthood” (p. 10).
The mechanisms underlying the translation of
adverse childhood experiences into health-related
phenomena are complex and multifactorial
(Spitzer et al., 2008). Physiologically, it is known
that childhood adversity causes acute and chronic
disruption of the hypothalamic-pituitary-adrenal
(HPA) axis (Bremner & Vermetten, 2001; Tarullo,
& Gunnar, 2006; Teicher, Andersen, Polcari,
Anderson, Navalta, & Kim, 2003) and is associ-
ated with the development of psychopathology
and certain pain syndromes (i.e., chronic pelvic
pain; Heim, Ehlert, Hanker, & Hellhammer, 1998).
Behaviorally, Waldinger et al. (2006) found that in
women, fearful attachment mediated the link
between childhood trauma and somatization. In
men, attachment style and trauma each contrib-
uted independently to the development of soma-
tization. The authors concluded that “childhood
trauma shapes patients’ styles of relating to others
in times of need, and these styles, in turn, influ-
ence the somatization process” (p. 129). The pro-
cess of somatization may be one link between
childhood psychological trauma and problematic
pain outcomes (Roelofs & Spinhoven, 2007).
Somatization
Somatization and related terms (e.g., somatoform
disorder) have a complex and sometimes contro-
versial history (Lamberty, 2008). Nonetheless, as a
narrow concept, somatization is a central factor in
understanding disability attributed to chronic
pain. Somatization refers to the way “certain
305
patients use their physical symptoms as a way of
dealing with, and communicating about, their
emotional lives . . . in this type of symptom mag-
nification, physical symptoms may be easier to
accept as causing current unhappiness and
discontent than admitting that some psychologi-
cal reason is contributing to it” (p. 204; Gatchel,
2004). In short, somatization reflects the expres-
sion of psychological problems manifested in
physical symptoms and complaints, a tendency to
complain of or develop physical symptoms and
illness when under emotional stress, and be exces-
sively focused on one’s physical functioning.
Somatization may be best viewed as a potentially
maladaptive personality and/or coping style. That
is, as used here, somatization refers not to a diag-
nostic entity but to a mode of thinking about one’s
self and world that contributes to medically unex-
plained illness and excess disability.
The MMPI (Hathaway & McKinley, 1943) and
its revision, the MMPI-2 (Butcher et al., 1989), are
the most widely used psychological assessment
instruments (Lubin, Larsen, & Matarazzo, 1984)
and are among the most commonly used in evalu-
ating chronic pain patients (e.g., Robinson,
Swimmer, & Rallof, 1989; Keller & Butcher, 1991;
Deardorff, Chino, & Scott, 1993; Slesinger, Archer,
& Duane, 2002). The MMPI has been used in the
evaluation of chronic pain patients to predict
response to treatment (Love & Peck, 1987), likeli-
hood of return to work (e.g., Bigos et al., 1991;
Vendrig, Derken, & de Mey 1999), and outcome
from spinal surgery (Block, Gatchel, Deardorff,
& Guyer, 2003). Classically, elevations on scales
1 (Hypochondriasis) and 3 (Hysteria) of the
MMPI have been ascribed to factors such as som-
atization (Block et al, 2003; Blumetti & Modesti,
1976; Friedman, Gleser, Smeltzer, Wakefield, &
Schwartz, 1983; Marks & Seeman, 1963).
Studies by Bigos et al. (1991) and Applegate
et al. (2005) showed that early (pre-injury) ten-
dencies or predispositions for somatization, as
measured by the MMPI, are linked to subsequent
development of physical symptoms including
back pain. Bigos et al. (1991) conducted a longitu-
dinal study of 3,020 aircraft employees to identify
risk factors for reporting acute back pain at work,
about 16% of whom developed back problems
over the four-year follow-up period. During
slightly more than 4 years of follow-up, 279
subjects reported back problems. The 20% of
participants with the highest Scale 3 scores were
twice as likely to report back problems as those
with lower scores. Applegate et al. (2005) found
306 forensic neuropsychology
that the MMPI at college admission (n = 2332)
predicted pain-related conditions at 30 year
follow-up. Among men, Scales 1, 3, and 5
(Masculinity/Femininity) were most predictive of
the number of chronic pain conditions. Among
women, Scales 1, 3, and 6 (Paranoia) were most
predictive. Thus, for both men and women, Scales
1 and 3 predict chronic pain 30 years later.
In patients with chronic pain, somatization is
associated with more medically unexplained
symptoms, poorer response to treatment, and
future development of disability. For example,
Block, Vanharanta, Ohnmeiss, and Guyer (1996)
found a higher incidence of nonorganic symptom
responses on discograms in patients with eleva-
tion on Scales 1 and 3, suggesting that these scales
are related to psychological mechanisms of pain
complaints, including somatization, rather than
purely physiological processes. Block et al. also
found that these Scale elevations were associated
with poorer response to both surgery and conser-
vative care. Gatchel, Polatin, Mayer, and Garcy
(1994) examined acute back pain patients (n =
152) and found that elevations on Scale 3 pre-
dicted higher levels of disability one year later.
Catastrophizing
Over the past 25 years “pain catastrophizing” has
emerged as an important predictor of pain experi-
ence and pain-related disability (Sullivan et al.,
2001). Pain catastrophizing has been defined as a
tendency to fear pain, have a fear-inducing under-
standing of the meaning of pain (e.g., the presence
of pain is an indication of harm), and/or a ten-
dency to allow pain to be a dominant focus of
one’s life (Proctor, Gatchel, & Robinson, 2000).
More simply, it is the interpretation of pain as
being extremely threatening (Crombez, Eccleston,
Baeyens, & Eelen, 1998). Psychometrically, pain
catastrophizing has proven to be a stable construct
that is related to but not redundant with depres-
sion and other forms of psychological distress
(Sullivan et al., 2001).
Turner and Aaron (2001) suggest that cata-
strophizing reflects a relatively stable personality
disposition whose manifestation may be influ-
enced by situational variables such as changes in
physical condition or implementation of specific
cognitive interventions. Theoretical formulations
to explain pain catastrophizing and hypotheses
regarding the mechanisms by which pain cata-
strophizing influence reports of pain and pain-
related disability have only begun to emerge
(Sullivan et al., 2001; Turner & Aaron, 2001).
Edwards, Bingham, Bathon, and Haythornthwaite
(2006) reviewed four mechanisms by which pain
catastrophizing may act: 1) interfering with pain
coping and beneficial health behaviors; 2) increas-
ing attention to pain; 3) amplifying pain process-
ing in the central nervous system; and, 4)
maladaptive impacts on the social environment.
Pain catastrophizing predicts the development
of chronic pain complaints in the general popula-
tion (Severeijns, Vlaeyen, van den Hout, & Picavet,
2005). Pain catastrophizing is associated with
greater pain vigilance and preoccupation with pain
and physical problems (Goubert, Crombez, & Van
Damme, 2004) and may mediate the reduced activ-
ity level seen in some clinical patients (Sullivan,
Stanish, Sullivan, & Tripp, 2002). Pain catastroph-
izing is also related to variety of important func-
tional and outcome variables, pain intensity,
psychological distress, and level of disability
(Severeijns, Vlaeyen, van den Hout, & Weber, 2001;
Turner, Jensen, Warms, & Cardenas, 2002; Woby,
Watson, Roach, & Urmston (2004). This relation-
ship is independent of level of physical injury or
impairment (Severeijns et al., 2001). For reviews of
pain catastrophizing, see Sullivan et al. (2001) and
Edwards et al. (2006). There is evidence that pain
catastrophizing is a precursor to the development
of pain-related fear (Leeuw et al., 2007).
Personality Disorder
The prevalence of personality disorder in the
chronic pain population ranges from 31% to 60%
(Gatchel et al., 1996; Fishbain et al., 1986; Reich,
Tupin, & Abramowitz, 1983; Large, 1986; Monti
et al., 1998; Polatin et al., 1993). There is consider-
able variability in rates of specific disorders, prob-
ably due to issues of diagnostic and assessment
reliability (Adams, Luscher, & Bernat, 2001). The
most common specific disorders are paranoid,
histrionic, borderline, avoidant, and dependent.
Others have identified a sense of entitlement
(Bellamy, 1997; Cook & Degood, 2006) and the
presence of embitterment (Swirtun & Renstrom,
2008) as important personality factors in patients
with pain. Personality disorders are considered to
be long-standing patterns of interaction and thus
not a consequence of a specific event (DSM-
IV-TR; American Psychiatric Association, 2000).
However, there is evidence that the report of life-
time symptomology may be influenced by state
factors (Fishbain et al., 2006; Weisberg, 2000a)
and contextual factors such as financial incentive.
We have examined the effect of malingering in
pain patients on Axis II scale scores from the
 The Psychological Assessment of Persons with Chronic Pain
Millon Multiaxial Clinical Inventory-III (MCMI-
III; Millon, Davis, & Millon, 1997). Chronic pain
patients who met published criteria for either
Definite or Probable Malingered Pain-Related
Disability (MPRD; Bianchini, Greve & Glynn,
2005) scored significantly higher than nonmalin-
gering pain patients on the Avoidant, Depressive,
Dependent, Negativistic, Masochistic, Schizoty-
pal, and Borderline scales (Aguerrevere, Greve,
Bianchini, & Meyers, 2009). They also tended to
score higher on the Schizoid and Paranoid scales.
In contrast, those who showed no evidence of
malingering scored higher on the scales associ-
ated with narcissistic, histrionic, and compulsive
personality disorders. Neither group tended to
elevate the Antisocial and Sadistic scales. These
data show that malingering is associated with self-
report that emphasizes distress and disability.
When personality issues are present in nonmalin-
gering pain patients the tendency is toward their
having a sense of specialness (narcissistic), dra-
matic over-reaction and need for attention (histri-
onic), and emotional/behavioral over-control
(compulsive).
Consideration of personality disorders in pain
is important because “the treatment success
(defined by decreased pain perception, increased
function, and decreased health care use) with
patients with personality disorders is low, and any
way to maximize compliance, independence,
decreased emotionality, and other features of per-
sonality disorders are [sic] likely to result in
improved outcomes” (Weisberg, 2000b; p. 235).
Weisberg (2000b) goes on to outline several rea-
sons for assessing for personality disorder in
patients with pain. First, identification of long-
standing personality features helps determine
changes in interaction style that are attributable to
the painful condition and thus provides a clearer
target for treatment. Second, identification of
maladaptive interaction styles can help the
clinician adjust their reactions to the patient
so as to facilitate the development of a therapeutic
relationship. Finally, the treatment itself can be
modified to better fit the patient’s character.
Mood and Anxiety Disorders
Mood and anxiety disorders are common in
patients with chronic pain. In a large survey of the
general population, approximately 18% of persons
reporting chronic spinal pain were diagnosed
with a comorbid mood disorder, while approxi-
mately 27% were diagnosed with some form of
anxiety disorder (Von Korff et al., 2005). Patients
307
seeking treatment for pain-related conditions
are particularly likely to report symptoms of
depression, as the prevalence of major depression
in this population has been reported to be over
50% (Dersh et al., 2006; Mayer, Towns, Neblett,
Theodore, & Gatchel, 2008).
Depression is a particularly important consid-
eration in patients with chronic pain, as studies
have shown a near linear association between
self-reported pain intensity and depressive symp-
toms (Carroll, Cassidy, & Cote, 2000; Currie &
Wang, 2004). However, depression and chronic
pain have a complex, reciprocal, relationship as:
(a) there is some overlap between symptoms (e.g.,
sleep disturbances or reduced activity levels);
(b) they may share physiological mechanisms,
specifically norepinephrine (NE) and 5-HT
serotonin dysregulation (Bair, Robinson, Katon,
& Kroenke, 2003); (c) the presence of either pre-
dicts future development of the other (Gureje,
Simon, & Von Korff, 2001); and (d) comorbidity
complicates treatment for both conditions
(Moultry & Poon, 2009). Depression may be a
particularly important predictor of pain-related
disability (Alshuler, Theisen-Goodvich, Haig, &
Geisser, 2008), with studies suggesting that it may
serve as a moderator for the relationships between
other psychological vulnerabilities discussed in
this section and self-perceived disability (Boersma
& Linton, 2005, 2006).
Anxiety can also influence perceptions of pain
and response to treatment. Anxious expectations
have been found to significantly increase the per-
ceived intensity of painful stimuli by directly
facilitating nociceptive transmission (Colloca &
Benedetti, 2007). Anxiety also impacts outcome
following surgery, as higher pre-surgical anxiety
is associated with slower recovery and more com-
plications post-surgery (Kiecolt-Glaser, Page,
Marucha, MacCallum, & Glaser, 1998). Similarly,
Trief, Grant, and Fredrickson (2000) found that
higher levels of pre-surgical anxiety significantly
predicted poorer functional outcome one year
after receiving lumbar spine surgery to relieve
pain. The negative effects of anxiety on patient
outcome may be explained in part by the relation-
ship between anxiety sensitivity and fear of pain
(Martin, McGrath, Brown, & Katz, 2007).
Fear-Avoidance Model of
Pain-Related Disability
Fear is a reaction that occurs in the presence of a
specific, identifiable, immediate threat; often lead-
ing to escape or avoidance behaviors (Rachman,
308 forensic neuropsychology

1998). Fear-avoidance models of chronic pain-
related disability have been proposed whereby the
emotional, cognitive, and behavioral factors dis-
cussed above interact with the pain experience to
contribute to a reinforcing cycle of fear and anxi-
ety towards pain-related stimuli (see Asmundson,
Vlaeyen, & Crombez, 2004; Vlaeyen, Kole-
Snijders, Boeren, & van Eek, 1995; Vlaeyen &
Linton, 2000). Fears can be directed towards pain
itself, reinjury, or specific activities such as move-
ment (i.e., kinesiophobia). Avoidance of activities,
in turn, contributes to the development and main-
tenance of functional disability (Leeuw et al.,
2007; Woby, Watson, Roach, & Urmston, 2004).
Fear-avoidance models of pain-related disability
are similar to models of the development and
maintenance of panic disorder and agoraphobia
(Klein & Gorman, 1987).
Figure 12.1 illustrates Leeuw et al.’s (2007)
version of this model. Importantly, this model
explicitly includes physical injury and pain sever-
ity. The maladaptive element of the Fear-Avoidance
model is reciprocal which allows for increasing
disability and the development of comorbid
depression. Pain catastrophizing appears to be a
critical element, or trigger, in the development of
pain-related fear and anxiety (Vlaeyen et al.,
2004). It is the emotional and coping response to
the injury which determines whether recovery
will be complicated. Coping strategies account for
adjustment to chronic pain above and beyond
what is predicted by pain-related history and
tendency to somaticize (Rosenstiel & Keefe, 1983).
Regardless of the specific trigger, fear-avoidance is
an obstacle to functional improvement in chronic
pain patients (Smeets, van Geel, & Verbunt, 2009;
Turner et al., 2006; Vlaeyen et al., 1995; Vlaeyen &
Linton, 2000).
Summary
Psychological factors serve as important prog-
nostic indicators of cases that transition from
acute to chronic pain (Carragee, Alamin, Miller,
& Carragee, 2005; Dersh, Gatchel, & Polatin, 2001;
Keefe et al., 2004; Linton, 2000; Pincus, Burton,
Vogel, & Field, 2002). Psychopathology can
increase perceived pain intensity, hamper reha-
bilitation efforts, and magnify perceived disabili-
ties, all of which serve to reinforce and perpetuate
pain-related dysfunction (Gatchel & Dersh, 2002;
Holzberg, Robinson, Geisser, & Gremillion, 1996;
Leeuw et al., 2007).

INJURY
DISUSE
DISABILITY
DEPRESSION
RECOVERY

AVOIDANCE
ESCAPE
PR TIV
MO
L

EV ATI
SA

EN ON
OU

CONFRONTATION
TA
AR

PAIN PAIN EXPERIENCE

TIV

DE TIV

ANXIETY
MO
E

FE ATI
L
SA

HYPERVIGILANCE
NS ON
OU

IVE

FEAR
AR

OF PAIN
THREAT PERCEPTION

CATASTROPHIZING LOW FEAR

NEGATIVE AFFECTIVITY
THREATENING ILLNESS INFORMATION

FIGURE 12.1: Fear-avoidance model of pain-related disability. Science+Business Media: Leeuw, M.,
Goossens, M. E., Linton, S. J., Crombez, G., Boersma, K., & Vlaeyen, J. W. (2007). The fear-avoidance
model of musculoskeletal pain: Current state of scientific evidence. Reproduced from Journal of Behavioral
Medicine, 30, 77–94, with kind permission from Springer.
 The Psychological Assessment of Persons with Chronic Pain
C O N T E X T UA L R I S K
FA C T O R S
In the past twenty years a sizeable literature has
developed examining noninjury characteristics/
risk factors, of patient or context, and how these
affect symptomatic and functional outcomes. For
example, injury recovery is affected by physical
characteristics such as age and weight, as well as
demographic factors such as education and
income (Rubin, 2007). It is also important to keep
in mind that recovery from injury often occurs in
the context of a complex social network, a consid-
eration that is particularly essential when it comes
to compensable injuries, where complications can
arise from a number of sources including the
patient’s attitudes about their work or company,
the relationship with the insurance and claims
adjusters, treatment delays, attorney involvement,
and litigation. This effect is not limited to injuries
that are clearly altered or contaminated by psy-
chological factors. Rather, contextual factors are
known to impact injury results even in patients
with well-described and documented physical
injuries. The effect has been shown in patients
with more significant and documented physical
injuries and in patients with less clearly docu-
mented physical injury, including whiplash (Atlas
et al., 2000, 2006; Carroll et al., 2008; Cassidy,
Carroll, Cote, Berglund, & Nygren, 2003; Cassidy
et al., 2000).
Education
Lower education has been identified as a prognos-
tic indicator of work-related disability (Breslin
et al., 2008; Hagen, Holte, Tambs, & Bjerkedal,
2000). A review by Dionne et al. (2001) found that
lower education is associated with longer pain
duration following back injury and a higher rate of
pain recurrence. Even after controlling for age,
pain duration, sex, and incentive status, lower
education was significant associated with higher
self-perceived disability (Roth & Geisser, 2002).
This relationship may be explained by the finding
that lower education is associated with more mis-
conceptions about back pain (Goubert, Crombez,
& De Boudeauhuij, 2004), as Roth and Geisser
found that the relationship between education
and disability was mediated by maladaptive pain
beliefs and coping strategies (e.g., catastrophizing).
Occupation and Work-Related Factors
Physical work load and job satisfaction both are
prognostic indicators of back-pain-related work
absences and disability (Bigos et al., 1991; Hagen
309
et al., 2002; Hoogendoorn et al., 2002; Shaw et al.,
2005). A study by Hagen et al. (2000) found that
unskilled workers are two to three times more
likely to retire due to disability than professionals
and concluded that this relationship may be
partly due to a social class effect, rather than just
physical job demands, as the relationship between
professional level and disability retirement
remained consistent at higher levels of levels of
the socioeconomic scale. Volinn, Van Koevering,
and Loeser (1991) also found that lower pay is
associated with longer back-pain chronicity.
Similarly, Tate (1992) found that younger workers
with higher preinjury wages, greater seniority,
and less severe injuries were more likely to return
to work post injury.
Elements of the relationship between the
worker and the company, including job satisfac-
tion and availability of accommodations, can also
impact outcome and even the initiation of symp-
tom reports. For example, in a study of 3,020
aircraft industry employees, those who reported
that they “hardly ever” enjoyed their work were
2.5 times more likely to report a back injury than
those who reported more positive feelings about
their job/work (Bigos et al., 1991). Shaw, Pransky,
Patterson, and Winters (2005) examined psycho-
social factors in patients referred to an occupa-
tional medicine clinic for back pain and found
that some elements of the patient’s job character-
istics, including job tenure, physical work
demands, availability of modified duty, and earlier
reporting to employer, were more predictive of
outcome than physical examination. Similarly,
Turner, Franklin, Fulton-Kehoe, Sheppard,
Wickizer, and Wu (2007) found that baseline
demographic variables, symptom severity, func-
tional limitations, lack of job accommodation,
job physical demands, job psychosocial condi-
tions, and psychosocial characteristics predicted
chronic disability following a claim for carpal
tunnel syndrome. Each domain of variables
(sociodemographic, clinical, psychosocial, work-
related) added significantly to the prediction of
chronic disability.
Aside from the complexities of these interac-
tions, the injured worker who is attempting to
return to work may encounter obstacles. For the
subset of patients that have performed heavy
physical labor, returning to their previous level of
work may no longer be possible and a return to
even modified work can pose considerable chal-
lenges. The sometimes daunting obstacles for a
worker to return to work include: insufficient
310 forensic neuropsychology
training or education to do work other than heavy
work, advanced age, a feeling of uncertainty about
other job tasks, poor information or misinforma-
tion about what would be required for a work
return, unavailability of vocational rehabilitation,
and financial disincentives for returning to
work; all superimposed on the other risk factors
discussed in this chapter.
Financial Incentive Effects
It is not uncommon for chronic pain cases to be
seen in a context involving financial compensa-
tion such as personal injury litigation, workers
compensation, or disability determinations. Over
the years, the presence of financial incentive has
been shown to be a robust factor related to out-
come in patients with pain. Patients seen in a
compensatory context report significantly more
pain, depression, and disability than patients not
involved in compensation (Chibnall & Tait, 1994;
Rainville, Sobel, Hartigan, & Wright, 1997;
Rohling, Binder, & Langhinrichsen-Rohling,
1995). Further, compensation status is associated
with overall decreased treatment efficacy (Gatchel,
Polatin, & Mayer, 1995; Rainville et al., 1997;
Rohling et al., 1995) including worse surgical out-
comes (Harris, Mulford, Solomon, van Gelder, &
Young, 2005), even for clearly defined spinal
pathology (Atlas et al., 2000; Atlas et al., 2006). As
an example of the systemic effects of compensa-
tory context, recent changes to a “no fault” com-
pensation system in Canada were found to result
in a lower incidence of lower-back pain and whip-
lash injuries following accidents and better prog-
nosis for recovery (Cameron et al., 2008; Cassidy,
Carroll, Cote, Berglund, & Nygren, 2003).
There is evidence that at least some of the rela-
tionship between compensation and injury recov-
ery for some patients may be due to alterations in
their clinical presentations. For example, a longi-
tudinal study by Overland et al. (2008) found that
reports of pain, anxiety, depression, sleep distur-
bances, and somatic symptoms steadily increased
as a financial disability determination neared,
only to steadily decrease after the determination
was made. In fact, a study by our group found that
a sizeable minority of chronic pain patients seen
in a compensatory context were exaggerating
symptoms and disability during psychological
evaluation (Greve et al., 2009). However, the
relationship between compensable injury and
recovery is complex and cannot be fully explained
by patient presentation. The following discussion
will focus on the contributions of delays in
treatment and patient dissatisfaction with care
that can arise in some treatment systems.
Delays in Treatment
When an injury occurs within a compensatory
context there are a number of different sources for
delays in the ultimate rehabilitation of the patient.
For example, in many state worker’s compensa-
tion systems second opinions can be required
before surgeries or rehabilitation can be funded.
On the other side of things, Bernacki and Tao
(2008) found that the presence of attorney
representation is associated with longer claim
duration, suggesting some mechanism of delay.
Thus, either “side” can contribute to delays. It
should be mentioned that these delays are not
minor or inconsequential: Following the switch
from a tort-compensation system to a no-fault
system in Canada, Cassidy et al. (2000) observed
that the average time between injury and claim
resolution for whiplash was more than halved.
Crook and Moldofsky (1994) conducted a
prospective, longitudinal, cohort study of patients
with musculoskeletal soft tissue impairment fol-
lowing a work-related injury. They looked at prog-
nostic factors for the likelihood that the injured
worker would return to work or remain on work
disability at a given point in time. Factors included
gender, age, return to work attempts, and site of
injury. They showed a strong relationship between
the passage of time and persistent disability.
Efforts to return early to work contributed to a
decrease in overall work disability.
McIntosh, Frank, Hogg-Johnson, Bombardier,
& Hall (2000) examined compensation claimants
seen for rehabilitation to determine prognostic
factors of chronicity. They found several factors
predicted work disability: 1) working in the con-
struction industry; 2) older age; 3) lag time from
injury to treatment; 4) pain referred into the leg;
and 5) three or more positive Waddell’s nonor-
ganic signs. They identified protective factors,
including a higher score on a modified version of
the low back outcome score, intermittent pain,
and prior history of back problems. They listed
several possibilities to explain the apparent coun-
terintuitive problem of a prior history of back
problems, including a prior history of learning
through physical therapy leading to increased
coping skills abilities, and also noted that, although
this group may have additional future problems,
once a patient has had back problems and returned
to work this may predict a shorter duration of
future problems.
 The Psychological Assessment of Persons with Chronic Pain
Olney, Quenzer, and Makowsky (1999) exam-
ined patients who underwent carpal tunnel release
in three different contexts: 1) no worker’s com-
pensation claim; 2) uncontested worker’s com-
pensation claim; and 3) a contested worker’s
compensation claim that required the interven-
tion of an attorney. There were no statistically sig-
nificant differences in postoperative return of grip
strength and in postoperative return to work
intervals in comparing the non-work-related
patients with the uncontested worker’s compensa-
tion patients. However, the contested worker’s
compensation patients were much less likely and
slower to return to light-duty and to return to full
duty. Return of grip strength was slower and less
in the contested worker’s compensation patients.
These examiners concluded that within worker’s
compensation, contested claims were associated
with a higher risk of poor outcome; while patients
with uncontested worker’s compensation claims
had outcomes nearly as good as noncompensa-
tion patients.
Similar results were reported by Stover,
Wickizer, Zimmerman, Fulton-Kehoe, and
Franklin (2007) in a larger prospective cohort
sample of workers’ compensation claimants with
more diverse injuries. These examiners studied
population-based retrospective inception cohort
of 81,077 workers who had four or more days of
work disability resulting from workplace injuries
over six years’ time. They found similar predictors
of long-term disability in this different and larger
population including: delay between injury and
first medical treatment, older age, construction
industry, logging occupation, longer time for
medical treatment to claim filing, back injury,
smaller firm size, female gender, higher unem-
ployment rate, and having dependents.
Satisfaction with Care
Wickizer, Franklin, Fulton-Kehoe, Turner, Mootz,
and Smith-Weller (2004) examined injured
worker satisfaction with their care and the impact
of these feelings on important outcome variables.
Their sample included 681 workers who had
ongoing follow-up care after initial treatment
and examined their satisfaction with interper-
sonal and technical aspects of care, finding that
satisfaction with interpersonal technical aspects
of care was strongly and positively associated with
their ratings of their overall treatment experience.
As a group they found that the satisfaction mea-
sures explain 3% of the variance in the patient’s
reports of the overall treatment experience after
311
controlling for demographics, satisfaction with
medical care prior to injury, job satisfaction, type
of injury, and provider type. They found the
injured workers who reported less favorable treat-
ment experiences were 3.54 times as likely (95%
confidence interval, 1.20–10.95, P = .021) to be
receiving time lost compensation for inability to
work due to injury 6 or 12 months after filing
the claim compared to patients whose treatment
experience was more positive. This is important
because it shows not only the relationship with the
company but also that the relationship with treat-
ment providers can be important for understand-
ing and predicting outcome in injured workers.
The same group (Wickizer et al., 2004) also
examined the relationship between patient
satisfaction and retention of an attorney. They
found that patient satisfaction was a significant
predictor of attorney retention by an injured
worker. However, since the mean date from claim
initiation to attorney retention was so long (368
days) they conclude that attorney retention was a
correlate rather than a predictor of disability.
Summary
An understanding of the context of the care of
patients with pain is of demonstrable importance
given the relationship, described in this section,
between some of these variables and measures of
symptoms and outcomes. This may be particu-
larly important in patients who are treated in a
context where financial incentive is present, as
these situations are commonly accompanied by
complex interrelationships between various mem-
bers of the claims environment (e.g., companies,
insurance adjusters, attorneys). Thus, these rela-
tionships can be the source of good or bad effects
on outcome and some patients may have increased
vulnerability to the potential negative effects.
DIAGNO STIC AND
AS SES SMENT IS SUES
Diagnostic Considerations
From a psychological perspective there are a
number of different clinical/diagnostic phenom-
ena/entities that are relevant in the assessment
and treatment of the chronic pain patient. Many
of those have been discussed in the preceding
sections. The following section addresses the
three major conditions which would be associated
with nonorganic or nonphysiological presen-
tations by persons claiming chronic pain:
somatoform disorders, factitious disorder, and
312 forensic neuropsychology
malingering. All of these are particularly impor-
tant, not just because they complicate treatment
and recovery, but also because they can lead to
invasive treatment efforts (e.g., surgery) which
themselves can be physically damaging and cause
disability. These conditions may also contribute to
over-prescribing and over-use of narcotic pain
medications and other medications with addic-
tion potential (e.g., benzodiazepines).
Somatoform Disorders
The somatoform disorders category of the
DSM-IV includes somatization disorder, undif-
ferentiated somatoform disorder, conversion dis-
order, pain disorder, hypochondriasis, body
dysmorphic disorder, and somatoform disorder
NOS. The common feature of these disorders is
that they are characterized by persistent com-
plaints of physical symptoms that suggest a medi-
cal condition, but for which there is either no
identifiable physiological cause or, in the case of
pain disorder, where medical findings do not
explain all of the symptoms or degree of disability.
As such, psychological factors are thought to play
a role in the onset, severity, and maintenance of
physical symptoms.
Nearly half (45%) of medical inpatients have
at least one medically unexplained symptom and
approximately 20% meet DSM-IV criteria for a
somatoform disorder (Fink, Hansen, & Oxhoj,
2004). Prevalence is generally higher in women
than in men and approximately half of somaticiz-
ing patients have comorbid anxiety or depression
(Barsky, Orav, & Bates, 2005). However, while the
construct of somatization is important for under-
standing chronic pain, somatoform diagnoses
based on DSM-IV criteria can be problematic
considering that many patients seeking treatment
for chronic pain meet criteria for somatoform
pain disorder while almost none meet criteria for
somatization disorder (Polatin et al., 1993; Dersh
et al., 2006).
Somatoform tendencies (the tendencies
common to somatoform patients) include com-
ponents that are cognitive, perceptual, and behav-
ioral in nature. Elements include excessive worry
about serious illness (i.e., hypochondriasis),
hypervigilence towards bodily sensations, nega-
tive interpretations or disease attributions for
benign sensations, sensitization to averse somatic
sensations, and excessive care-seeking or need for
illness validation. These factors are often viewed
as a cycle in which cognitions, perceptions, and
behaviors mutually reinforce and strengthen each
other (Barsky & Borus, 1999). Importantly,
patients with somatoform disorders are not con-
sciously feigning or exaggerating symptoms, as is
seen with factitious disorders and malingering.
Factitious Disorder
Factitious disorder is the consistent intentional
production of signs or symptoms of illness in the
absence of external incentives. Symptom presen-
tation is deliberate and motivation comes from
internal sources such as a need to assume the sick
role. Presentation may include symptom fabrica-
tion (e.g., subjective complaints that do not exist),
symptom production (e.g., intentional self-harm),
symptom exaggeration, or manipulation of objec-
tive medical signs (e.g., warming a thermometer).
Pain complaints are the most commonly reported
symptom in patients with factitious disorder
(Krahn, Li, & O’Conner, 2003).
Establishing the prevalence of factitious
disorder is made difficult by the deceptive
nature of the condition, reluctance to assign the
“factitious disorder” label, and the possibility that
some factitious patients may be counted multiple
times. Estimates have placed the prevalence of
factitious disorder at around 1% for patients seen
in a general hospital setting (Sutherland & Rodin,
1990). An extreme form of factitious disorder
known as Munchausen syndrome is thought to
account for approximately 10% of these cases.
Overall, factitious disorder is thought to be about
twice as prevalent in females as in males (Krahn,
Li, & O’Conner, 2003).
Factitious disorder is differentiated from
somatoform disorders, where symptom produc-
tion is unconscious; and malingering, where
external incentives are present. However, it should
be noted that it is not always possible to defini-
tively differentiate factitious disorder from malin-
gering. For example, a feigned illness could be
motivated by a need for attention (internal
incentive), a desire to avoid household or work
duties (external incentive), or both. In these cases
the DSM-IV allows for reasonable inferences to
be made regarding the source of individual’s
motivation (i.e., internal versus external) as direct
evidence is not always available.
Patients with factitious disorder have been
observed to intentionally engage in self-injurious
behavior and seek out unnecessary medical treat-
ment (Eastwood & Bisson, 2008; Lande, 1996;
Masterton, 1995; Paar, 1994; Wise & Ford, 1999).
However, factitious disorder and malingering are
not necessarily as distinct as the DSM–IV seems
 The Psychological Assessment of Persons with Chronic Pain
to suggest. Eisendrath (1996) presented several
cases in which the self-injurious behavior of
patients with factitious disorder served as the
basis of civil litigation. In these particular cases,
the symptom production not only met the intra-
psychic needs of the factitious patient but was also
reinforced by the potential secondary gain associ-
ated with litigation. Similarly, Greve, Bianchini,
and Ameduri (2003) reported a patient with a
psychological profile consistent with factitious
disorder who intentionally feigned sensory loss
that she attributed to a work injury.
Eisendrath and McNeil (2004) discuss the
complex cases of four factitious disorder patients
who also had financial incentive in the form of
civil litigation and who died as a result of their
factitious behavior. Since both factitious disorder
and malingering involve intentional exaggeration
of symptoms these cases illustrate that the line
between malingering and factitious disorder can
sometimes be blurred. More specifically, the
source of motivation for intentional exaggeration
can come from both the desire to assume the sick
role and the desire for external gain, potentially in
the same patient.
It is reasonable to assume that factitious
disorder reflects greater psychopathology than
that seen in most persons who choose to malin-
ger. However, there is no reason to believe that
patients with factitious tendencies are any less
subject to the influences of the potential second-
ary gain available in the medico-legal context than
persons without the intrapsychic needs character-
istic of factitious disorder. Moreover, the level of
premorbid psychopathology in some patients
who do malinger may approach that more charac-
teristic of factitious patients, yet their behavior
still reflects malingering. Put simply, some malin-
gerers will engage in potentially self-injurious
behavior and malingering should not be ruled out
simply on the basis that a person is seeking medi-
cally unnecessary treatment including surgery
(Bianchini, Heinly, & Greve 2004; Bianchini &
Greve, 2009).
Factitious disorder presents an unusual but
important form of psychological complication of
physical symptom complaints. Of particular
interest is the characteristic willingness of some
factitious patients to engage in self-harm. The
Eisendrath and McNeil (2004) paper cited above
includes patients whose factitious tendencies
ultimately resulted in their death. Thus detection
of this form of psychological complication is
important for the life and sometimes survival of
313
the factitious patient. Of course these patients
often actively try to avoid detection.
Malingering
Malingering is a potential problem in contexts
where there are financial incentives to appear
disabled. Malingering is “the intentional produc-
tion of false or grossly exaggerated physical or
psychological symptoms, motivated by external
incentives such as avoiding military duty, avoid-
ing work, obtaining financial compensation,
evading criminal prosecution, or obtaining drugs”
(DSM-IV-TR; American Psychiatric Association,
2000; p. 739). Pain often occurs in the context of a
legally compensable event such as a work-related
injury or incident in which some other party is
potentially liable. In fact, back pain is the most
common reason for filing a workers compensa-
tion claim (Guo, Tanaka, Halperin, & Cameron,
1999).
The prevalence of malingering in patients with
pain is between 20% and 50% (Mittenberg, Patton,
Canyock, & Condit, 2002; Greve, Ord, Bianchini,
& Curtis, 2009; Kay & Morris-Jones, 1998),
depending on the method of assessment and case-
specific factors. These rates are consistent with
those reported in other compensable conditions
and contexts such as criminal forensic settings
(Ardolf, Denney, & Houston, 2007), social secu-
rity disability evaluations (Chafetz, 2008), toxic
exposure (Greve, Bianchini, Black et al., 2006),
traumatic brain injury (Larrabee, 2003), and
among Vietnam-era veterans receiving services
within the Veterans Administration system
(Larrabee, Millis, & Meyers, 2008). These studies
demonstrate that overall malingering, including
in patients with pain, is not a rare event or trivial
phenomenon despite claims to the contrary
(e.g., Fishbain, Cutler, Rosomoff, & Rosomoff,
1999; Sears, Wickizer, & Franklin, 2008). In
patients with pain, malingering potentially has a
very large economic impact given the prevalence
of pain-related complaints.
DSM-IV-TR does not provide criteria for the
diagnosis of malingering; instead it describes
circumstances under which “malingering should
be strongly suspected” (p. 739). There are,
however, published criteria for the diagnosis of
malingering. The Slick, Sherman, and Iverson
(1999) criteria for Malingered Neurocognitive
Dysfunction (MND) can be used with patients
with pain though this system is narrowly focused
on malingering of cognitive deficits and is thus
limited in application to pain patients (Bianchini,
314 forensic neuropsychology
Etherton, & Greve, 2004; Greve, Bianchini, Black
et al., 2006; Greve, Bianchini, Love, Brennan, &
Heinly, 2006). Bianchini, Greve, and Glynn (2005)
modified the Slick et al. system to address the
multidimensional (e.g., cognitive, emotional,
physical) clinical presentation of patients with
pain. Their approach differed conceptually from
earlier diagnostic systems by focusing on disabil-
ity attributed to the compensable injury or illness
rather than the injury or illness itself. In this view,
the question of interest in addressing malingering
in pain is not just about the veracity of the pain
complaint itself, but of the degree of disability that
is attributed to the pain.
Thus, the magnitude of disability becomes the
central forensic issue because how disabled a
person is or claims to be dramatically affects the
monetary value of his or her claim. Malingered
pain-related disability (MPRD) refers to the inten-
tional exaggeration or fabrication of cognitive,
emotional, behavioral, or physical dysfunction
attributed to pain for the purposes of obtaining
financial gain, to avoid work, or to obtain drugs
(incentive). As with any malingering diagnosis, a
diagnosis of MPRD requires evidence of external
incentive and intentional symptom production.
Typically, it is not difficult to identify the presence
and nature of external incentives in a given case.
Determination of intent is a more difficult task.
At the heart of the issue of malingering is the
question “is the patient intentionally performing
below his or her true capacity or manifesting more
disability/symptoms than is actually the case?”
Importantly, neither the Slick et al. (1999)
criteria for MND nor the Bianchini et al. (2005)
criteria for MPRD require that the clinician deter-
mine whether or not a specific/single behavior is
diagnostic of malingering. Instead, the ultimate
determination of intent is dealt with in a more
comprehensive manner by considering multiple,
highly improbable events as indicative of intent.
Thus, it is not necessary to rely on single events
that unequivocally demonstrate intent because
the MND and MPRD criteria are based on behav-
iors and symptom report that are atypical for and
not representative of expected clinical findings in
legitimate, unequivocal neurological, psychiatric,
or developmental disorders. Thus, intent is
inferred as a result of the combined improbability
of events rather than necessarily relying on a
single definitive indication of intent (Larrabee,
Greiffenstein, Greve, & Bianchini, 2007).
Generally speaking, “improbability” is deter-
mined empirically by comparing clinical patients
who have been diagnosed as malingering using
explicit criteria (usually based on the Slick et al.,
1999, or Bianchini et al., 2005, systems) to
etiologically similar patients, often ones with
greater objective pathology than the malingering
group. This method is referred to as “known-
groups” (Greve & Bianchini, 2004; Rogers, 1997)
or “criterion-groups” (Frederick, 2000; Dawes &
Meehl, 1966) validation. Using this approach one
can identify score levels beyond which few or
no nonmalingering patients perform. Thus, the
degree of “improbability” is expressed as the false
positive error rate at a given score level. Over the
last decade and a half numerous techniques for
the detection of poor effort, response bias, under-
performance, and malingering have been devel-
oped and empirically validated. A review of this
research is beyond the scope of this chapter and
the reader is referred to two recently published
texts on this topic for more information (Boone,
2007; Larrabee, 2007), as well as the chapter by
Larrabee in the present volume.
While the data on cognitive malingering in
traumatic brain injury patients can be generalized
to patients with pain these results may result in an
increased false negative error rate in pain patients
who lack objective brain pathology (Bianchini,
Etherton, & Greve, 2004). Moreover, the numerous
psychosocial factors that can complicate a chronic
pain presentation may result in high false
positive error rates on self-report measures sensi-
tive to somatization (Aguerrevere, Guise, Greve,
Bianchini, Meyers, 2008; Bianchini, Etherton,
Greve, Heinly, & Meyers, 2008). Therefore, a
number of indicators of malingered cognitive,
emotional, and physical disability have now been
validated in patients with chronic pain (some of
these methods are discussed in the assessment sec-
tion below). Validation of physical capacity mea-
sures for the detection of malingering is currently
under way in our laboratory and in Europe (J. Kool,
personal communication, January 28, 2009).
A striking feature of some of these data is that
the rate of positive findings (i.e., test failure) is
associated in a dose-response fashion with
increasing objective evidence of malingering and
not with injury characteristics (Ben-Porath,
Greve, Bianchini, & Kaufmann, 2009; Greve,
Bianchini, Etherton, Meyers, Curtis, & Ord, 2009;
Greve, Bianchini, Etherton, Ord, & Curtis, 2009;
Greve, Etherton, Ord, Bianchini, & Curtis, 2009).
This finding in pain patients is complemented
by the finding in TBI patients that the magnitude
of potential compensation is associated with
 The Psychological Assessment of Persons with Chronic Pain
malingering test failures (Bianchini, Curtis, &
Greve, 2006). Interestingly, in Canada, a change in
personal injury liability law was followed by a nearly
50% decline in disability claims related to back pain
(Cassidy, Carroll, Cote, Berglund, & Nygren, 2003).
Taken together, these findings support the conclu-
sion that empirically defined “improbable” test per-
formance is motivated by financial incentive.
Assessment
This section is intended to provide an overview of
the conceptual approach to the assessment of the
chronic pain patient and not to discuss in detail
the many psychological tests which might be
included in such an evaluation. The psychological
evaluation must be capable of separating symp-
toms/disabilities involving psychological reac-
tions to physical symptoms, including pain, from
somatization and from intentional exaggeration
(e.g., malingering, factitious disorder) at a level
consistent with currently available techniques and
research. Given the importance of psychological
factors in various forms in cases with chronic
pain, when properly conducted, the psychological
evaluation has the potential to shed important
light on the clinical circumstances of a given
patient and provide important guidance to treat-
ment efforts. However, in order to do this prop-
erly, a comprehensive approach is required, one
that actively considers all of the differential diag-
nostic possibilities.
As with any psychological evaluation, the psy-
chological pain evaluation requires a careful
review of all available medical records and, when
possible, any other records which may have bear-
ing on subsequent conclusions (e.g., accident
reports, personnel records, depositions). Like any
psychological evaluation, the pain psychological
evaluation will typically begin with a clinical inter-
view. This will generally address the nature of the
accident, efforts at treatment, and current status
including symptoms and complaints. However,
the interview should also assess the variety of
complicating factors such as recent and ongoing
psychosocial stressors, past psychiatric history,
childhood psychological trauma, and job factors
that might predict poor outcome from treatments.
Ideally, patients should not be given information
regarding pain-related symptoms, including
symptom checklists and direct questioning about
symptoms, until after they have been asked to
spontaneously report all of their symptoms in all
domains so as to reduce the risk of suggesting
symptoms that may bias subjective report.
315
After the clinical interview the patient is
administered standardized psychological and neu-
ropsychological tests and procedures. Pain patients
may report disabling problems in multiple domains
(e.g., physical, emotional, and cognitive; Schnurr
& MacDonald, 1995; Myers & Diep, 2000; Ericsson
et al., 2002; Wilson, Eriksson, D’Eon, Mikail &
Emery, 2002), all of which may have important
implications for the decision-making of various
clinicians (Gatchel, 2004). Therefore, the psycho-
logical pain evaluation should be designed to
objectively assess the common cognitive, psycho-
logical, emotional, and physical complaints of
patients with pain and pain-related disability
including attention and concentration, processing
speed, learning and memory, general knowledge,
intelligence and problem solving skills, physical
complaints, and physical capacity, current emo-
tional state, and personality style. It is helpful to
use broad measures of intelligence such as the
WAIS-III/IV or WASI as well as well-validated
neuropsychological tests of memory and related
cognitive functions, omnibus personality tests and
behavioral health measures. The inclusion of
narrow measures of constructs not tapped by the
broader personality tests (e.g. pain catastrophiz-
ing, coping skills) is important as well.
Moreover, because the results of psychological
tests can be invalidated by biased responding and/
or poor effort, the psychological pain evaluation
should contain indicators over-reporting of sub-
jective symptoms (e.g. MMPI-2 validity scales)
and under-performance on ability tests (both
stand-alone SVTs and embedded indicators of
performance validity). The comprehensive assess-
ment of response and performance validity is
important even in cases not seen in a compensa-
tion-seeking context because exaggeration of
pain-related disability may also be motivated by
the desire to obtain pain medication. Unlike many
psychological assessments of patients with pain
that tend to focus on emotional function alone,
this multidimensional battery approach allows a
comprehensive assessment of an individual’s
functional status that can lead to detailed recom-
mendations regarding the management of
their pain and pain-related disability and supply
valuable information to vocational experts and
life-care planners. This approach to the assess-
ment of the chronic pain patient that incorporates
SVTs and neuropsychological tests of memory,
working memory, processing speed, and intellec-
tual and problem solving skills, is similar to that
of Meyers and Diep (2000).
316 forensic neuropsychology
I N T E RV E N T I O N A L I S S U E S
Pre-procedure Psychological Screening
This chapter summarizes the literature showing
that psychosocial factors influence pain complaints
and pain-related disability. The importance of con-
sidering such factors in the context of invasive
medical efforts to relieve pain, which do involve
damaging tissue and thus have the potential to do
harm, is essential.
“Spine surgery’s ultimate effectiveness . . .
depends on much more than the surgeons’
diagnostic acumen and technological skill.
Psychological factors exert very strong influ-
ences–ones that can improve, or inhibit, the
patient’s ultimate recovery . . . surgical results
can be greatly augmented by the inclusion of
psychological components in the assessment
and preparation of patients for spine surgery,
as well as in post-operative rehabilitation” (p. 4;
Block et al., 2003).
The psychological assessment of surgical risk
is not simply a matter of determining if a patient
is psychotic, has a pathological body image, has
somatic delusions, or is depressed. While the pres-
ence of significant psychopathology which might
lead to post-surgical psychological instability or
problems with medical compliance is an issue of
importance, this type of problem may be a minor-
ity in presurgical pain cases, particularly those
seen in a medicolegal context. There is now strong
empirical research regarding what psychological
factors predict outcome from surgery (e.g., Block
et al., 2003; Bruns & Disorbio, 2009; Voorhies,
Jiang, & Thomas, 2007).
Nelson, Novy, Averill, and Berry (1996) have
argued that in addition to active psychosis, sui-
cidality, untreated major depression, and sub-
stance dependence, factors such as somatization,
lack of social support, and cognitive deficits
should exclude patients from receiving a spinal
cord stimulator. They also noted that disincentive
to recover related to compensation or litigation
issues was a factor that would require exclusion.
Similarly, Block and colleagues (Block et al., 2001;
Epker & Block, 2001) have demonstrated that the
presence of certain psychosocial factors predicts
poor outcome from lumbar disc surgery. Among
these factors are financial incentive, history of
abuse or abandonment, job dissatisfaction, prob-
lems with social support, substance abuse, pre-
existing psychopathology, depression/anxiety,
and pain catastrophizing as well as compliance
problems and deception.
These risk factors have been summarized and
integrated into a presurgical screen risk factor
check list by Block et al. (2001). A similar medical
risk factor checklist is part of their comprehensive
presurgical screen. See Table 12.1 for both. The
presurgical screening approach developed by
Block et al. (2001) has been thoroughly explicated
in Block et al. (2003) and the ultimate process is
laid out in the form of a flowchart (see Figure 12.2;
flowchart from Block et al., 2003, pg. 108). Similar
approaches have been reported for screening of
patients being considered for morphine pump
and dorsal column stimulator implantation
(Bruns & Disorbio, 2009) though these have not
yet been subjected to the same level of research. It
is likely that similar evaluation of all pain patients
will identify those who would be expected to have
complicated course and delayed outcomes regard-
less of the specific interventions.
Block et al. (2003) have argued that pre-
procedure psychological screening is an essential
component in the medical diagnostic process
of spine surgery candidates, especially when the
major goal is symptomatic pain reduction. Fur-
ther emphasizing this point, Lebovits (2000) has
stated that
“although the treatment of a patient with
chronic pain mandates a comprehensive evalu-
ation of the medical as well as psychological
contributions to the etiology, maintenance,
and exacerbation of pain, evaluating and
treating patients with chronic pain with a uni-
modal, strictly medical approach still occurs.
This, unfortunately, often leads to iatrogenic
effects, such as failed surgical interventions
and activity restriction” (p. 126).
Psychological factors and presurgical screen-
ing may provide a very specific benefit for those
managing a pain case. Psychological factors are
important to surgery outcome even in the context
of clear and objective indications for surgery
(Voorhies et al., 2007). In cases where there is
disagreement about the physical indications for
surgery, the results of a presurgical psychological
screen may provide even more valuable guidance.
Specifically, a psychological evaluation that
identifies factors in a patient that would predict
higher risk of poor outcome from surgical inter-
vention may encourage continued conservative
interventions and even a shift to functional
 The Psychological Assessment of Persons with Chronic Pain 317

TABLE 12.1 CHECKLIST OF MEDICAL AND PSYCHOLOGICAL

RISK FACTORS FROM BLOCK ET AL., 2001 

Medical Risk Factors Score Psychological Risk Factors Score

Chronicity Litigation
< 6 months 0 Pending litigation 2
6–12 months 1 Workers’ compensation
12 + months 2 Currently receiving 2
Job dissatisfaction
Previous spine surgery Moderate 1
0 0 Extreme 2
1 1 Heavy job demands
2+ 2 > 50-pound frequent lift 2
Substance abuse
Surgery type Pre-injury 1
Laminectomy/discectomy 1 Current 2
Fusion 2 Family reinforcement of pain
Moderate 1
Nonorganic signs Extreme 2
Present 2 Marital dissatisfaction
Moderate to extreme 1
Nonspine medical treatment Physical or sexual abuse
Some treatment 1 Pre-injury 1
Multiple hospitalizations 2 Current 2
Pre-injury psychological treatment
Smoking Outpatient 1
< 1 pack per day 1 Inpatient 2
> 1 pack per day 2 MMPI Elevations >70 (maximum score 4)
Hypochondriasis 2
Obesity Hysteria 2
< 50% overweight 1 Depression (pre-existing) 2
Depression (reactive) 2
Psychopathic deviate 2
Psychasthenia 1
Coping Strategies Questionnaire (max score 2)
Low self-reliance 2
Poor pain control 2

Medical total score: Psychological total score:

High risk threshold = 8 High risk threshold = 10
Total maximum = 13 Total maximum = 23

restoration that incorporates active management
of psychological risk factors and comorbidities
(see discussion below).
Behavioral Pain Treatments
Patients with pain conditions, particularly
chronic conditions, have a higher incidence of
affective disorders than the general public (Dersh,
Gatchel, Mayer, Polatin, & Temple, 2006; Mayer,
Towns, Neblett, Theodore, & Gatchel, 2008). This
recognition has led to the utilization of a variety
of psychiatric and psychological therapies for the
treatment of pain, pain related disability, and
psychiatric comorbidities to pain conditions.
A full review of the role of psychopharmacology
management strategies for pain and pain-related
affective disorders is beyond the scope of this
chapter. The reader is referred to Polatin and
318 forensic neuropsychology

8+ Present
6+ Poor Prognosis
Total Discharge
Total
psychosocial Adverse recommended
medical
4 –7 clinical
risk risk
features

Absent Poor Prognosis

0–5 Noninvasive
treatment
0–3 recommended

Interview Risk Factors Total 6+

Factor Pts. medical Present Fair Prognosis
Job dissatisfaction 2 risk Compliance and
Worker’s comp. 2 motivation
Litigation 2 Adverse measures
Spousal solicit. 1 clinical recommended
No spouse support 1 features
Abuse & abandon. 1
Substance abuse 2 0–5 Absent
Good Prognosis
Psych. history 2
Postoperative
psychological
treatment
Testing Risk Factorsa recommended
Factor Pts. Medical Risk Factors
Pain sensitivity 2 Factor Pts.
Depression-chronic 2 Pain 6–12 mos. 1
Depression-reactive 1 Pain > 12 mos. 2 Adverse Clinical Features
Highly destructive surgery 2 Good Prognosis
Anger 2
Nonorganic signs 2 Inconsistency No psych.
Anxiety 2
Abnormal pain drawing 2 Medication seeking treatment
Depressed-pathol. 4
Prior spine surgeries Staff splitting needed
Catastrophizing 2 2 or more 2 Compliance issues
1 1 Threatening
aMaximum of 4 points for MMPI Prior medical probs. 2 Resignation
items + 2 points for Smoking 2 Deception
catastrophizing Obesity 1 Personality disorders

FIGURE 12.2: Algorithm for determining presurgical psychological screening prognosis. MMPI =
Minnesota Multiphasic Personality Inventory. Reproduced from Block, Gatchel, Deardorff, & Guyer, 2003,
with permission from the APA.

Dersh (2004) for a review of relevant issues and
applications of these interventions.
Psychological treatments, including cognitive
behavior therapy (CBT) and behavior therapy
(BT), have been studied for their efficacy in
dealing with pain, pain disability, and affective
comorbidities, including depression. Applied in
isolation these treatments have a weak effect on
pain and disability, although they may be of some
help in altering mood outcomes (Eccleston,
Williams, & Morley, 2009). In contrast, combin-
ing therapies in a multidisciplinary rehabilitation
format has shown promise, particularly for treat-
ing patients at higher risk for poor outcome. The
central features of these approaches include mul-
tidisciplinary symptom treatment, including
physical therapy treatment and psychological
assessment and treatment for psychological com-
orbidities, an assessment of psychological and
other risk factors for poor outcome, the system-
atic management of the risk factors, and an orga-
nized and systematic approach to work return
(Westman et al., 2006).
Guzman et al. (2002), working through
the Cochrane Database System, recently con-
cluded that multiple reviewed studies provide
“strong” evidence that intensive multidisciplinary
biopsychosocial rehabilitation with a functional
restoration approach improves pain and function.
They also indicate that less intensive interventions
did not show improvements in clinically relevant
outcomes. They also indicate there was contra-
dictory evidence regarding vocational outcomes
of intensive intervention, some trials reported
improvements in work readiness, but others
showed no significant reduction in sickness
leaves. They note that particularly the less inten-
sive outpatient psychophysical treatments did not
improve pain function or vocational outcomes
when compared with non-multidisciplinary out-
patient therapy or usual care.
Recently, Howard, Mayer, and Gatchel (2009)
studied one important component of this
approach: the emphasis on a work return. Injured
workers who stayed at work (“presentees”)
were more likely than “absentees” to complete a
 The Psychological Assessment of Persons with Chronic Pain
functional restoration treatment program, to
return to work, to retain work 1-year post treat-
ment, and to not have a decreasing job demand
from preinjury to post-treatment time periods.
Thus, the emphasis on early work return may be a
particular critical factor in the rehabilitation of
patients with pain. Ultimately, consideration of
psychosocial and socioeconomic complexities of
patients with pain in a comprehensive pain man-
agement program with a functional restoration
focus can lead to a reduction in the need for inva-
sive treatment procedures and overall improved
outcomes (Gatchel & Okifuji, 2006).
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 Appendix
The following sections will provide a brief review
of chronic pain conditions along with relevant
medical diagnostic procedures and treatments.
This review is not meant to be exhaustive but
rather is intended as a brief introduction to some
of the more common conditions and procedures
that a psychologist is likely to encounter in the
assessment of chronic pain patients. The focus
will be on chronic nonmalignant conditions
rather than acute pain or pain related to cancer or
terminal illness.
APPENDIX A: REVIEW
O F PA I N - R E L AT E D
CONDITIONS
Arthritis
Arthritis refers to a large group of joint disorders
with symptoms that often include swelling,
stiffness, and pain. The two most common types
are osteoarthritis and rheumatoid arthritis.
Osteoarthritis (OA) is a degenerative condition
involving the breakdown of cartilage in the joints
as well as pathophysiologic changes in the under-
lying bone and joint capsule. OA is primarily
found in load-bearing joints and the phalanges.
Onset of symptoms is typically gradual and
worsens with activity. The incidence of OA
increases with age, affecting over half of men and
women over age 65 and nearly all over age 80
(D’Ambrosia, 2005).
Rheumatoid arthritis (RA) is a systemic
inflammatory disease that causes a number of
problems including joint degeneration and pain,
primarily in peripheral regions. Other common
symptoms include fatigue, malaise, and stiffness.
Symptom onset is typically gradual but in a minor-
ity of cases onset may be abrupt. The prevalence
rate of RA in the US is approximately 1% (Gabriel,
Crowson, & O’Fallon, 1999). While the exact
etiology is unknown, a genetic link has been
identified and infectious agents have been specu-
lated to contribute.
Carpal Tunnel
Carpal tunnel syndrome is caused by compres-
sion of the median nerve which runs from the
forearm to the hand. Symptoms may include tin-
gling, numbness, and pain in the hand and wrist
which may also radiate up the arm. Many factors
can contribute to the development of carpal tunnel
syndrome including congenital predisposition,
wrist trauma, or any number of conditions that
result in narrowing of the carpal tunnel passage-
way in the wrist. The estimated incidence of
carpal tunnel syndrome in the U.S. population is
approximately 400 per 100,000 person-years
(Gelfman et al., 2009). While hand-arm vibra-
tions and some types of repetitive motions are
thought to be causal agents, contrary to common
perception no evidence has been found to
support a connection between computer use and
the development of carpal tunnel syndrome
(Thomsen, Gerr, & Atroshi, 2008).
Chronic Widespread Pain/
Fibromyalgia
Chronic widespread pain is typically defined as
pain in three or more body segments that persists
for at least three months. Chronic widespread
pain is the core feature of fibromyalgia, a condi-
tion that commonly also presents with fatigue,
sleep disturbances, and stiffness. Clinical diagno-
sis of fibromyalgia relies on pain elicited from
pressure on discrete anatomical areas referred to
as tender points, although the diagnostic useful-
ness of tender points has been criticized (Clauw,
2007). Some have questioned the clinical useful-
ness of fibromyalgia as a diagnosis (e.g., Bohr,
1995), and the condition is now often viewed as
one end of a spectrum of chronic pain conditions
rather than a distinct clinical entity. The self-
reported point prevalence of chronic widespread
pain is approximately 11% (Croft, Rigby, Boswell,
Schollum, & Silman, 1993) while an estimated 2%
of the population meets criteria for fibromyalgia
(Wolfe, Ross, Anderson, Russell, & Herbert,
330 forensic neuropsychology
1995). Both conditions are more prevalent in
females.
While the exact pathophysiological mecha-
nisms underlying chronic widespread pain and
fibromyalgia are not known, abnormalities in
CNS pain processing are thought to play a role in
sensitization to pain. Psychosocial factors includ-
ing adverse childhood experiences, vulnerability
to stress, mood and anxiety disorders, somatiza-
tion, and catastrophizing are thought to underlie
the development of these conditions and are pre-
dictive of patient prognosis (Gupta et al., 2007;
Winfield, 2000). While trauma is sometimes
reported as a trigger for fibromyalgia, current
conceptions do not support a direct biomechani-
cal link. Instead, trauma is thought to act as a gen-
eral stressor which can trigger fibromyalgia only if
the necessary underlying factors are present
(McLean, Williams, & Clauw, 2005).
Complex Regional Pain Syndrome
Complex regional pain syndrome (CRPS) involves
a heterogeneous group of symptoms that typically
occur in a limb following trauma. Symptoms are
disproportionate to the initial injury and may
include radiating pain, swelling, altered skin color
or temperature, reduced range of motion, and
sensory or motor disturbances. CRPS I (reflex
sympathetic dystrophy) is diagnosed in the
absence of major nerve damage, and CRPS II
(causalgia) is diagnosed if nerve damage is pres-
ent. The estimated incidence rate of CRPS is 5 to
26 per 100,000 person years, with females out-
numbering males 4:1 (de Mos et al., 2007;
Sandroni, Benrud-Larson, McClelland, & Low,
2003). Diagnosis of CRPS is difficult, however,
due to the lack of objective diagnostic signs.
Current clinical criteria proposed by the
International Association for the Study of Pain
allow for a diagnosis of CRPS based solely on
symptom report. These criteria have been criti-
cized for having low specificity (. 36) and over-
diagnosis may be a problem (Harden & Bruehl,
2006).
The pathophysiology underlying CRPS is not
well understood. A number of physiological alter-
ations have been observed in the central and
peripheral nervous system, immune system, and
vascular system, but the cause of these changes,
particularly in the absence of neuropathy, in not
clear. Prolonged disuse of a limb can reproduce
many of the features of CRPS in healthy individu-
als (Butler, 2001) and cases of self inflicted CRPS
have been documented (Mailis-Gagnon,
Nicholson, Blumberger, & Zurowski, 2008). It is
now understood that behavioral factors can play a
role in the development and maintenance of CRPS
symptoms and psychological evaluation and
intervention is recommended for chronic CRPS
cases (Bruehl & Chung, 2006).
Disc Bulge and Herniation
The spine is composed of vertebrae segments that
are connected to each other by a complex consist-
ing of two facet joints and an intervertebral disc.
The disc is composed of a nucleus surrounded by
layers of fibrous cartilage called the annulus and
interfaces with the verterbral bodies at the disc
endplate. Over time, vertebral discs may naturally
begin to bulge outward beyond the vertebral body
margins as they lose elasticity and expand hori-
zontally. If the disc continues to degenerate or is
exposed to traumatic mechanical stress, a hernia-
tion may occur as the annular fibers tear and allow
the disc nucleus to protrude against or through
the annulus wall. In these conditions, pain may
result directly from the annulus tears, from irrita-
tion caused by the release of chemicals from the
nucleus, or by compression of the nerve root.
However, disc bulges and herniations are rela-
tively common, especially in older populations,
and are unlikely to be symptomatic unless neural
compromise is involved (Boos et al., 1995; Jensen
et al., 1994).
Facet Joint Syndrome
The facet, or zygapophyseal, joints are also thought
to be a common contributor to back pain. This
joint pain may be caused directly through arthritic
processes, or indirectly by impinging on nearby
structures such as the nerve root. The processes
responsible for the development of facet joint pain
often co-occur with disc degeneration and thus
distinguishing the specific etiology of pain symp-
toms is often difficult.
Meniscal Tears
Meniscal tears may occur due to knee trauma or
due to age-related degenerative processes. Each
knee contains two menisci which are tough carti-
lage structures located between the femur and
tibia. The menisci serve to absorb shock and dis-
tribute mechanical stress evenly across the knee
joint. Meniscal tears are common in asymptom-
atic adults and evidence suggests that meniscal
tears do not directly cause pain symptoms, but
 The Psychological Assessment of Persons with Chronic Pain
they may contribute to the development of
osteoarthritis (Englund et al., 2007).
Migraine
Migraines are characterized by recurrent severe
head pain that may be accompanied by neuro-
logical disturbances. Pain may be unilateral or
bilateral, is often described as throbbing, and may
be accompanied by sensitivity to stimuli and/or
nausea. In a minority of patients, onset may be
preceded by prodromes (premonitory symptoms)
such as mood changes or aura (focal neurologic
symptoms) such as visual disturbances. Migraines
are classified according to whether aura is
present (classic migraine) or absent (common
migraine). Approximately 10% of the general
population is thought to be affected (Jensen &
Stovner, 2008). While the mechanisms underlying
migraine are not completely understood, evidence
has suggested neurotransmitter and neuromor-
phological abnormalities play a role (Filippi &
Rocca, 2008).
Muscle Ligament Injuries
Muscle sprains and strains are relatively common
consequences of strenuous physical activity.
Sprains are injuries involving ligaments, which
are bands of cartilage that connect bones and hold
them in alignment. Sprains are usually caused by
trauma that displaces a joint resulting in stretch-
ing or tearing of the associated ligament(s). Strains
are injuries involving muscles or the tendons that
attach muscles to bone. Strains are usually caused
by a quick movement that over-stretches or over-
contracts a muscle resulting in damage or tearing
to the muscle or tendon. Treatment and recovery
depend on the severity of injury. Mild to moder-
ate injuries will typically heal with self-care and
rest while severe cases may require immobiliza-
tion or surgery.
Myofascial Pain Syndrome
Myofascial pain syndrome refers to musculoskele-
tal pain arising from localized trigger points in a
taut band of muscle. These focal trigger points are
tender to palpation and may cause muscle weak-
ness or reduced range of motion. If the trigger
point is active, as opposed to latent, application of
pressure is said to produce referred pain in a pre-
dictable pattern. Myofascial trigger points are
reportedly found in 30% of patients seeking treat-
ment for pain (Skootsky, Jaeger, & Oye, 1989).
However, there are currently no well-validated
331
criteria for the identification of trigger points or the
diagnosis of myofascial pain syndrome (Bennett,
2007).
Radiculopathy/Sciatica
Radiculopathy refers to a disruption of (or near)
the nerve root that can result in pain as well as
sensory or motor disturbances. An important fea-
ture of radiculopathy is that symptoms are often
referred to the limb associated with the disrupted
nerve. Radiculopathy involving the sciatic nerve,
often referred to as sciatica, is relatively common
with a lifetime prevalence of around 25%
(Konstantinou & Dunn, 2008). Sciatic symptoms
typically manifest unilaterally in the lower back
and legs.
Rotator Cuff Tears
The rotator cuff is composed of a group of four
muscles that provide mobility and stabilization to
the shoulder area. Tears in the rotator cuff tendons
usually occur at the point at which they attach to
the humeral head (the ball of the shoulder joint).
Rotator cuff tears can be classified according to
severity as partial thickness tears, full thickness
tears, or full thickness tears with complete detach-
ment. Rotator cuff tears are relatively common in
asymptomatic patients (Tempelhof, Rupp, & Seil,
1999) and it is not completely understood what
factors contribute to the development and mainte-
nance of symptoms (Williams, Rockwood, Bigliani,
Iannotti, & Stanwood, 2004).
Spinal Stenosis
Spinal stenosis refers to a narrowing of the spinal
canal, nerve root canal, or foraminal openings
from which nerve roots exit the canal. Symptoms
typically occur when these nerve fibers become
impinged. An estimated 5% of the adult popula-
tion shows signs of spinal stenosis, with the preva-
lence increasing with age (Lee, Cassinelli, & Riew,
2007). The condition can be congenital, but is
more commonly acquired through degenerative
processes. Cervical stenosis is associated with
radiating arm pain, numbness, and paresthesia.
Lumbar stenosis is associated with lower back pain
and radiating bilateral or unilateral leg pain. More
severe cases may present with other symptoms
including myelopathy (spinal cord dysfunction).
Spondylolysis & Spondylolisthesis
Spondylolysis refers to a stress fracture of the pars
interarticularis, the narrow bridge between the
332 forensic neuropsychology
upper and lower facet joint of a vertebrae. A con-
dition known as spondylolisthesis can occur if the
fracture is bilateral and the vertebrae slip out of
alignment. Most consider spondylolysis to repre-
sent a fatigue fracture resulting from chronic
mechanical stress rather than a single traumatic
event, though trauma may worsen a condition.
Spondylolysis is relatively common, particularly
in athletes, and most cases are asymptomatic.
When pain is present it is thought to be caused by
nerve root compression, intervetebral disc pain,
or facet joint pain.
Spondylosis
Spondylosis is a condition caused by age-related
disc degeneration that causes a number of patho-
logical processes that can ultimately result in a
narrowing of the spinal canal. One mechanism is
the formation of osteophytic bars along the
ventral spinal canal caused by increased mechani-
cal stress. Pain may result from compression or
irritation of the cauda equine or nerve root.
Temporomandibular Disorder
Temporomandibular disorder (TMD), also
referred to as temporomandibular joint (TMJ)
syndrome, involves pain originating from the
TMJ, a complex joint that connects the mandible
to the skull at points just in front of the ear. Most
people will show signs and symptoms of TMD at
some point in their life and approximately 5% will
seek treatment (Poveda Roda et al., 2007). TMD
can be broadly categorized into two potentially
overlapping syndromes according to the etiology
of symptoms: myogenous (muscle-related) TMD
and arthrogenous (joint-related) TMD. The cause
of myogenous TMD is not completely under-
stood; however, it is commonly comorbid with
bruxism and jaw clenching and has been linked to
stress and anxiety (Poveda Roda et al., 2007).
Arthrogenous TMD can result from a number of
joint conditions including disc displacement,
degenerative joint disorders, recurrent disloca-
tions, and arthritis.
Tension-Type Headaches
Tension-type headaches involve mild to moderate
bilateral frontal-occipital head pain that is often
described as pressure or tightening. Episodic
tension headaches are very common, with 90% of
the general population experiencing them at some
point in life (Smith, 2004). The condition is typi-
cally considered chronic if a patient experiences
more than 15 episodes per month. The incidence
of chronic headaches is reported to be 3 per 100
person-years (Midgette & Scher, 2009). Muscular
contractions as well as psychogenic factors (e.g.,
stress or anxiety) are thought to have an etiological
role. Head and neck injuries have been shown to
increase the odds of developing chronic daily head-
aches (Couch, Lipton, Stewart, & Scher, 2007).
Whiplash-associated Disorder (WAD)
Whiplash-associated disorders (WAD) refer to a
collection of symptoms resulting from rapid
hyperextension/flexion of the neck, often associ-
ated with motor vehicle accidents. The Quebec
Task Force classifies WAD into grades (I-III)
based on symptom report and clinical findings
(Spitzer et al., 1995). Grade I includes complaints
of neck pain or stiffness with no physical
signs; Grade II includes neck complaints as well as
musculoskeletal signs such as decreased range
of motion or point tenderness; and Grade III
includes neck complaints along with neurological
signs such as motor or sensory disturbances. An
injury involving a fracture or dislocation may be
referred to as a Grade 4; however, the terms “whip-
lash” and “WAD” are generally reserved for cases
in which observable pathology is not present.
Clinical manifestations of WAD may include a
number of diverse symptoms including deafness,
dizziness, tinnitus, and headache. Acute neck
pain, the primary symptom of WAD, is thought to
result from soft tissue injury and there is little evi-
dence that whiplash injuries differ from any other
musculoskeletal sprain or strain (Pearce, 1999).
WAD typically resolves quickly and chronic and/
or late onset symptoms in the absence of pathol-
ogy are not expected. Psychosocial risk factors
such as compensation status, injury perceptions,
and coping styles are a stronger predictor of out-
come than collision severity (Buitenhuis, de Jong,
Jaspers, & Groothoff, 2008; Carroll et al., 2008;
Carroll, Holm, Ferrari, Ozegovic, & Cassidy, 2009;
Ferrari & Schrader, 2001; Richter et al., 2004).
APPENDIX B: DIAGNO STIC
PROCEDURES
Diagnostic Injections
Injection of local anesthetics, steroids, neural
blockades, or even irritants can be useful for
determining the source of pain symptoms. A typi-
cal procedure involves the injection of the agent
into a target location, after which changes in the
 The Psychological Assessment of Persons with Chronic Pain
patient’s pain symptoms are noted. These tech-
niques can help identify the source of pain symp-
toms and allow for differentiation between local
versus referred pain, somatic versus visceral pain,
and peripheral versus central etiologies. While
diagnostic injections can offer the advantage of
pinpointing a specific cause of symptoms, it
should be noted that these procedures rely on the
patient’s accurate report of symptoms and some
have been criticized for having poor specificity in
patient populations with external incentives.
Discography, Myelography, &
Arthrography
Injections can also be used to introduce contrast
materials to enhance standard imaging tech-
niques. Arthograms involve the injection contrast
agents into a joint to better image interior soft tis-
sues. In a myelogram, contrast agent is introduced
into the dura surrounding the spinal cord and
nerves, which allows for a detailed view of nerve
arrangement and impingements. Discograms
involve the injection of contrast material into the
nucleus of an intervertebral disc to highlight any
defects in the disc’s structural integrity. Often dis-
cograms also serve as a diagnostic injection due to
the mildly irritating nature of the contrast mate-
rial. If the injection elicits symptoms that are sim-
ilar to those normally experienced, it is considered
an indication that the targeted disc is responsible.
However, as with all diagnostic injections, reli-
ance on patient report can call the accuracy of the
procedure into question when used in patient
populations with external incentive.
Electrodiagnosis
Electrodiagnostics involves the study of human
physiology using devices that produce and mea-
sure electrical current in the body. An electro-
myogram (EMG) uses a needle to directly measure
the electrical activity of a muscle during different
stages of activity. Abnormal electrical activity
can indicate nerve and muscle pathologies.
A nerve conduction study (NCS) delivers an
electrical charge to a peripheral nerve while a
recording electrode is placed in the innervated
muscle. This arrangement allows for the determi-
nation of the nerve conduction velocity which is a
sensitive indicator of nerve damage. An NCS also
has the advantage of being able to isolate the spe-
cific site of nerve damage or impingement by
stimulating the nerve at various locations along
its path.
333
Imaging
Radiography and magnetic resonance imaging
(MRI) are the most common forms of imaging.
Radiography involves the use of X-ray to view
internal tissue and is particularly useful for exam-
ining bony structures in the body. The three main
categories of radiography are: 1) static images, 2)
fluoroscopy, and 3) computed tomography (CT).
Static images are classic X-ray snapshots on film.
Fluoroscopy is the use of X-rays to provide real-
time dynamic internal imaging—a technique
often used to guide the placement of instruments
during surgical procedures. CT scanning uses
X-rays to collect numerous image slices which are
then assembled into a detailed three-dimensional
structural view. MRI uses strong magnetic fields
to provide what is essentially an image of water
distribution in the body. MRI is particularly suited
to examining soft tissue structures and the
high-definition images allow for very accurate
identification of spinal disc herniation and nerve
root compression.
While imaging is undoubtedly a useful medi-
cal tool, there are some reasons to interpret imag-
ing findings with caution. Imaging “abnormalities”
are common in asymptomatic individuals (Jensen
et al., 1994) and may not necessarily predict future
symptoms. For example, Jarvik et al. (2005) found
that MRI findings are not significant prognostic
indicators for the development of low back pain.
A review of the diagnostic accuracy of imaging
for patients with low back pain determined that
these procedures are not called for unless a patient
is over the age of 50 or signs of systemic disease
are present (Jarvik & Deyo, 2002). In fact, early
imaging for acute back pain was found to have no
benefit to outcome and knowledge of the imaging
results was actually detrimental to patients’ sense
of well-being (Ash et al., 2008).
Physical Examination/
Functional Capacity Exams (FCEs)
Physical examination can aid in diagnosis as well
as provide information about the type and degree
of functional limitations. Musculoskeletal aspects
examined may include gait, posture, sensitivity to
palpation, range of motion, and strength.
Neurological aspects examined may include focal
CNS signs, motor disturbances, reflexes, and
muscle tone. In patients without clear pathology,
physical examination can also provide evidence of
nonorganic illness behaviors. Waddell signs are
often used as an indication of psychosocial
334 forensic neuropsychology
involvement in the clinical presentation of patients
with back pain (Waddell, McCulloch, Kummel, &
Venner, 1980). Most formal functional capacity
evaluations (FCEs) include a variety of indicators
that allow the determination of whether the results
are valid. However, their reliability in detecting
malingering has not yet been established.
APPENDIX C: MEDICAL
T R E AT M E N T S
Electrical Stimulation
Electrical stimulation is thought to provide anal-
gesia through presynaptic dorsal horn inhibition,
activation of endogenous pain-control pathways,
modulation of nerve activity, or some combina-
tion of these processes. Transcutaneous electrical
nerve stimulation (TENS) is used to treat a variety
of pain conditions by the application of a mild
electric current to the surface of the skin. A TENS
unit is attached to the targeted location via
electrodes and is generally worn throughout the
day. Patients typically have control over the acti-
vation of the unit and the amplitude, duration,
and frequency of the electric pulse. There is wide
variation among patients regarding optimal TENS
settings as well as the onset, degree, and duration
of analgesia provided. Evidence for the overall
effectiveness of TENS treatments has been mixed
(Nnoaham & Kumbang, 2008).
Surgically implantable stimulation devices
may also be used to directly deliver electrical
impulses to the dorsal column, peripheral
nerves, or the spinal nerve root. Since not all
patients respond to spinal cord stimulation, a trial
phase is usually implemented before internaliza-
tion of the device. In patients who achieve analge-
sia during the trial period and have been properly
screened for psychological risk factors, implant-
able stimulation devices have generally proved a
safe and effective form of pain control (Cameron,
2004).
Medication
Analgesic medication for the treatment of chronic
pain is typically divided into three progressive
steps depending on the severity of symptoms:
1) nonsteriodal anti-inflammatories (NSAIDs);
2) weak opiates such as codeine or hydrocodone;
and 3) strong opiates such as oxycodone or mor-
phine. Opiates are often combined with NSAIDs
to increase effectiveness. In addition to analgesics,
adjuvants such as tricyclic antidepressants, SSRIs,
anticonvulsants, anxiolytics, muscle relaxants, or
corticosteroids have also proved effective for some
types of chronic pain. An implantable intrathecal
pump may be used to deliver analgesic medica-
tion directly into the spinal fluid in cases of
chronic intractable pain. The targeted delivery
system allows for smaller doses to be delivered at
regular intervals and can avoid some complica-
tions associated with systemic routes of adminis-
tration.
Nerve Decompression
There is a variety of procedures used to relieve
nerve impingement depending on the pathology
involved. Discectomy is a relatively common sur-
gical intervention used to treat disc herniations.
The procedure involves the removal or ablation of
a portion of disc nucleus in an effort to relieve
pressure on the nerve root. Laminectomy involves
the removal of a small amount of bone from the
lamina, which is commonly used to help decom-
press the nerve root in treating spinal stenosis.
Neurolytic Blockade/Neurotomy
Neurolytic blockades work by interrupting the
transmission of nociceptive signals to the brain
by damaging specific nerve fibers. Methods
include chemical neurolysis, cryocoagulation,
radiofrequency coagulation, and neuroablation.
The most significant challenge to these procedures
is to disable nociceptive transmission while spar-
ing motor and sensory nerves. Pain relief after
successful treatment is often long lasting but not
necessarily permanent, as targeted nerves may
regenerate.
Spinal Fusion
Spinal fusion is used to treat spinal instability by
eliminating motion in a segment of two or more
adjacent vertebral bodies. Methods of fusion vary
depending on the number and location of joints
to be fused. In a lumbar fusion, the most common
method of fixation is to attach rods or plates to the
vertebrae by inserting screws into the pedicle. In
an inter-body fusion, the disc is removed and
replaced by an implant. Fusion of two or three
vertebrae can often be achieved with little or no
impact on overall flexibility or mobility.
Therapeutic Injections
Corticosteroid injections are the most frequently
used type of therapeutic injection and provide
pain relief primarily by reducing inflammation.
 The Psychological Assessment of Persons with Chronic Pain 335

Epidural steroid injections can relieve local pain
and reduce nerve impingement. In some cases,
these treatments can halt the cycle of irritation
and inflammation and provide relatively long-
lasting relief.
Trigger point injections involve injections into
specific trigger points for the relief of musculosk-
eletal pain. Many different types and methods
exist ranging from the injection of local anesthet-
ics or corticosteroids directly into trigger points
to superficial “dry” injections similar to acupunc-
ture. The variety of methods and lack of appropri-
ately controlled studies makes it difficult to draw
any conclusions about the effectiveness of trigger
point injections (Scott, Guo, Barton, & Gerwin,
2008).
 13
Forensic Assessment of Medically
Unexplained Symptoms
L AU R E N C E M . B I N D E R
Disorders of medically unexplained symptoms
without clearly demonstrated pathophysiological
origin are characterized more by disability,
symptoms, and suffering than by objective medi-
cal findings and pathology (Deary, Chalder, &
Sharpe, 2007; Labarge & McCaffrey, 2000; Rief &
Broadbent, 2007). Illnesses including fibromyal-
gia (Bohr, 1996; Grace, Nielson, Hopkins, & Berg,
1999), chronic fatigue syndrome (Abbey &
Garfinkel, 1991; Buchwald & Garrity, 1994;
DeLuca, Johnson, Ellis & Natelson, 1997; DiPino
& Kane, 1996; Fukuda et al., 1994), multiple
chemical sensitivities (Black, 2000; Bolla, 2000;
McCaffrey & Yantz, 2007; Sparks, 2000), symp-
toms following war and terrorism incidents
(Clauw, Engel, Aronowitz et al., 2003), and toxic
mold syndrome and sick building syndrome
(Burge, 2001; Hardin, Kelman, & Saxon, 2003;
Hodgson, 2000; Khali & Bardana, 2005; Kuhn &
Ghannoum, 2003; Lees-Haley, 2003; 2004;
McCaffrey & Yantz, 2007; Reijula & Tuomi, 2003;
Robbins et al., 2000) have been referred to as
functional somatic syndromes (Barsky & Borus,
1999) and as collections of medically unexplained
symptoms (Binder & Campbell, 2004; Deary et al.,
2007; Rief & Broadbent, 2007). This review dis-
cusses neuropsychological assessment of medi-
cally unexplained symptoms. I am not attempting
to provide comprehensive reviews of the above
disorders, but I have focused on certain largely
medically unexplained disorders that either are
commonly encountered in the practice of forensic
clinical neuropsychology in adults, or that are
particular exemplars of functional somatic
syndromes in the neuropsychological setting.
Portions of this chapter were based on previous
work (Binder & Campbell, 2004). This chapter is
organized in terms of the common assessment
issues associated with these disorders.
Forensic neuropsychologists encounter these
disorders in two ways. First, persons seeking
disability from private insurers or from govern-
ment entitlement programs often claim one or
more of these conditions as an explanation of
their inability to work. Second, some of these dis-
orders are common and may be seen concurrently
with other potentially compensable problems
such as alleged toxic encephalopathy (Bolla, this
volume) or traumatic brain injury (Larrabee, this
volume; Roebuck-Spencer & Sherer, this volume).
In addition, experience suggests that medically
unexplained symptoms are common in many
clinical neuropsychological settings.
A LT E R N AT I V E
E X P L A N AT I O N F O R
S Y M P TO M S
Cognitive symptoms are not signs of cognitive
impairment. Negative emotions were more
strongly predictive of subjective cognitive symp-
toms than were objective cognitive problems in
some study populations (Dux, Woodard, Calamari
et al., 2008; Hoppe, Elger, & Helmstaedter, 2007;
Larrabee & Levin, 1986; Rohling, Green, Allen, &
Iverson, 2002; Seidenberg, Taylor, & Haltiner,
1994; Williams, Little, Scates, & Blockman, 1987).
For example, subjective cognitive impairment was
more strongly related to scores on the Beck
Depression and Anxiety Inventories than to
objective cognitive performance in veterans with
Persian Gulf War-related illnesses (Binder,
Storzbach, Anger et al., 1999). Fibromyalgia and
chronic fatigue syndrome patients also have
cognitive complaints more severe than their
objective deficits (Grace, Nielson, Hopkins, &
Berg, 1999; Tiersky, Johnson, Lange et al., 1997).
Cognitive complaints in some persons are
an index of and surrogate for emotional
 Forensic Assessment of Medically Unexplained Symptoms
distress—emotional distress communicated in
different language than the complaints typically
associated with depression and anxiety. Neuro-
cognitive symptoms warrant investigation that
may show objective abnormalities and disease
(Babiloni, Visser, Frisoni et al., 2008; Kearney-
Schwartz, Rossignol, Bracard et al., 2009; Mitchell,
2008), but symptoms are not signs of disease.
Rather, symptoms are an expression of “dis-ease.”
Symptoms, whether they are cognitive or somatic,
are expressions of unease about one’s health. The
term “cogniform” has been proposed to describe
patients with a pervasive belief that they have
cognitive impairment despite no neuropsycho-
logical or neurological evidence of cognitive
impairment (Delis & Wetter, 2007).
Reports of headaches, memory loss, irritabi-
lity, dizziness, and other physical, cognitive, and
emotional complaints are nonspecific. These
symptoms are not diagnostic of mild traumatic
brain injury, toxic encephalopathy, or other forms
of brain dysfunction (Fox, Lees-Haley, Earnest, &
Dolezal-Wood, 1995). Symptoms that often are
associated with brain dysfunction are not diag-
nostic of brain dysfunction, an issue often of inter-
est to researchers on mild traumatic brain injury.
Normal control subjects frequently complained
of symptoms of traumatic brain injury (TBI) such
as memory loss, irritability, headaches, and
dizziness (Gouvier, Uddo-Crane, & Brown, 1988).
Post-concussive syndrome (PCS) symptoms were
at least partly attributable to stress and did not
distinguish between TBI and control subjects
(Gouvier, Cubic, Jones, Brantly, & Cutlip, 1992).
Among college student controls, many symptoms
were as common among controls as among TBI
patients (Gouvier et al., 1988). In the Gouvier
et al. study, normal controls had these symptom
frequencies: memory loss, 20%; loss of interest,
36%; temper problems, 37%; fatigue, 28%. The
relatives of the same college student participants
also observed high rates of “PCS symptoms” in
the control group, an observation that suggests
that reports of significant others may provide mis-
leading information after suspected mild TBI
(Gouvier et al., 1988).
The symptoms of depression overlap with
symptoms thought to be associated with brain
dysfunction. In college students without history
of head injury, symptoms considered typical of
post-concussive syndrome had a correlation with
depressive symptoms of 0.76 (Iverson & Lange,
2003). Clinically depressed patients met conser-
vative criteria for post-concussive syndrome in
337
about 50% of the cases and met liberal criteria
for post-concussive syndrome in about 90% of the
cases (Iverson, 2006).
Litigation, like depression, is associated with
neurological complaints despite the absence of
any neurological history. Patients in litigation
claiming psychological and physical damage who
did not have neuropsychological histories or
claims reported the following symptoms on a
questionnaire: concentration problems, 78%; con-
fusion, 59%; memory loss, 53%; dizziness, 44%;
and word finding problems, 34% (Lees-Haley &
Brown, 1993). Persons with pain complaints that
they attributed to work-related injuries had more
cognitive complaints than pain patients with
non-work-related problems and as many cogni-
tive complaints as head-injured persons not
involved in litigation (Iverson, King, Scott, &
Adams, 2001).
The hypothesis that post-concussive syndrome
complaints were unrelated to suspected mild TBI
was indirectly tested by comparing mild TBI and
more severely head-injured patients (Novack,
Daniel, & Long, 1984). Mild TBI patients were
nearly twice as likely as the more severely injured
to have elevations on the MMPI HS and HY
scales, which assess physical complaints. The
number of post-concussive symptoms was more
strongly associated with elevations of these two
MMPI scales than with neuropsychological data.
Novack et al. suggested that the number of post-
concussive symptoms was an index of emotional
adjustment. This inverse relationship between
acute severity of head injury and MMPI/MMPI-2
abnormality has been replicated—the less severely
head-injured patients had greater MMPI/MMPI-2
elevations, especially on scales HS and HY
(Leininger, Kreutzer, & Hill, 1991; Scott, Emick, &
Adams, 1999; Youngjohn, Davis, & Wolf, 1997).
Pseudoneurological symptoms are conceiv-
ably neurological complaints, such as limb weak-
ness, dizziness, memory loss, or weakness of a
limb, that are not correlated with any objective
neurological findings. Pseudoneurological com-
plaints are increased by stressors and can continue
chronically (Cardena & Spiegel, 1993; Escobar,
Canino, Rubio-Stipec, & Bravo, 1992). One week
after the San Francisco Bay area earthquake
of 1989, 30% of exposed persons complained of
dizziness and 71% of concentration difficulty
(Cardena & Spiegel, 1993). One year after a flood
there were more pseudoneurological symptoms
in persons exposed to the flood than in nonex-
posed persons (Escobar et al., 1992). Neurological
338 forensic neuropsychology
symptoms were more common in firefighters with
post-traumatic stress disorder (PTSD) than in
those without this disorder (McFarlane, Atchison,
Rafalowicz, & Papay, 1994). Dizziness was seven
times more common and headaches three times
more common in returned Iraqi veterans with a
diagnosis of PTSD than in veterans without PTSD
(Hoge, Terkahopian, Castro et al., 2007). Non-
neurological somatic symptoms such as pseudo-
cardiac problems also were far more common in
veterans with PTSD (Hoge et al. 2007).
Expectations and attributions have an impor-
tant role in the generation of medically unex-
plained symptoms (Deary et al., 2007; Rief &
Broadbent, 2007). There is evidence that symp-
toms simply are misattributed to certain events
when the symptoms actually are explained by
other events or are preexisting. Mittenberg and
colleagues introduced the notion of “expectation
as etiology” in connection with symptoms after
mild TBI, showing that nonpatient controls were
able to predict symptoms reported by patients
(Mittenberg, DiGuilio, Perrin, et al., 1992) and
later showing that simple reassurance and educa-
tion significantly reduced symptoms (Mittenberg,
Tremont, Zielinski, et al., 1996). In another study,
prolonged symptoms after mild TBI were pre-
dicted by patients’ expectations about prognosis
(Whittaker, Kemp, & House, 2007).
Expectations of illness also affect symptoms
after exposure to manmade devices. In a study of
Vietnam War veterans, self-reported herbicide
exposure to Agent Orange was related to greater
psychological and medical problems, but objec-
tive history of exposure was unrelated (Korgeski
& Leon, 1983). This study of Vietnam veterans
may have been weakened by imprecise objective
measurement of Agent Orange exposure, how-
ever. In an experimental study, the belief of
Norwegian patients who suffered from chronic
headaches that their laboratory-induced head-
aches were caused by radio frequency waves ema-
nating from mobile phones was associated with
both actual and sham mobile phone usage
(Oftedal, Straume, Johnsson, & Stovner, 2007). A
New Zealand study assessed the effect of beliefs
about the effects on human health of technologies
such as microwave radiation, hormone additives
in food, and fluoridated water (Petrie, Broadbent,
Kley, et al., 2005). Belief that such technologies
were harmful was associated with more symp-
toms. Furthermore, participants who believed
that such technologies were harmful reported
more adverse health effects from a local pesticide
spray project than those participants with a more
benign view of these technologies.
Negative expectations can have an effect on
cognitive test performance. Negative expectations
and stereotyping regarding associations between
one’s demographic group and performance
appears to explain the inferior performance of
females compared with males on tests of mathe-
matical abilities (Spencer, Steele, & Quinn, 1999;
Steele, 1997). Suhr and Gunstad (2002; 2005)
demonstrated that college students with a history
of mild TBI performed worse on neuropsy-
chological measures when their injury and its
possible effect on test performance was empha-
sized prior to testing than students with similar
injury history who received instructions that did
not include information linking mild TBI to
cognitive problems. Suhr and Gunstad termed
this phenomenon “diagnosis threat.” Just as a
demographic group stereotype was associated
with lower performance (Spencer et al., 1999;
Steele, 1997), beliefs about the effects of medical
history and diagnosis had a neuropsychological
effect in these studies of students with prior mild
TBIs. Negative expectations also influenced neu-
ropsychological performance in persons with
multiple chemical sensitivities (Smith & Sullivan,
2003). This research on the effect of negative
expectations on performance is consistent with
the work of Bandura and others on self-efficacy.
Bandura and Locke (2003) summarized several
meta-analytic studies showing that beliefs in one’s
competence had salutary effects on academic, cog-
nitive, athletic, and other types of tasks and wrote:
The evidence from these meta-analyses is
consistent in showing that efficacy beliefs con-
tribute significantly to the level of motivation
and performance. Efficacy beliefs predict not
only the behavioral functioning between indi-
viduals at different levels of perceived self-
efficacy but also changes in functioning in
individuals at different levels of efficacy over
time and even variation within the same indi-
vidual in the tasks performed and those
shunned or attempted but failed (p. 87).
A LT E R N AT I V E
E X P L A N AT I O N S F O R
COGNITIVE DEFICITS
Like cognitive complaints, cognitive deficits also
are not specific to neurological disease or injury.
Objective neuropsychological deficits are common
in a host of psychiatric disorders. Cognitive
 Forensic Assessment of Medically Unexplained Symptoms
deficits occur in affective disorders (reviewed in
Burt, Zembar, & Niederehe, 1995; Cassens, Wolfe,
& Zola, 1990; Johnson & Magaro, 1987;
Langenecker, Lee, & Bieliauskas, 2009; Rogers,
Kasai, Koji, et al., 2004). Patients with depression,
particularly inpatients, may have difficulties with
attention, abstract thinking, processing speed,
memory, manual dexterity, visuospatial skills
(Burt et al., 1995; Cassens et al., 1990), executive
dysfunction (Langenecker et al., 2009; Rogers
et al., 2004), and intellectual decline (Sackeim
et al., 1992). Patients with depression or history of
depression are neuropsychologically heteroge-
neous (Langenecker et al., 2009). Patients with
pseudoneurological symptoms perform poorly on
neuropsychological tests. These findings will be
summarized in detail later in this chapter.
GENERAL
CHARACTERISTICS
OF DISORDERS WITH
M E D I C A L LY U N E X P L A I N E D
S Y M P TO M S
Barsky and Borus (1999) describe characteristics
of these conditions. The amount of disability
contrasts markedly with the degree of measured
physical limitations and examination and labora-
tory abnormalities. Some patients with these
conditions tend to view themselves as severely
disabled (Hadler, 1999; Moss-Morris, Petrie, &
Weinman, 1995; Wolfe et al., 1997), and they often
apply for disability payments (Van der Werf,
Prins, Jongen, van der Meer, & Bleijenberg, 2000;
Wolfe et al., 1997). The degree of disability often
contrasts with the degree of disability reported by
patients with demonstrable medical pathology,
for example, patients with heart disease, amputa-
tions, cancer, or rheumatoid arthritis. According
to Barsky and Borus, the fact that subjective dis-
tress so often exceeds objective medical findings
suggests that symptom magnification is a primary
feature of these disorders.
Ford (1997) described similar characteristics
in what he labeled as “fashionable illnesses.”
Fashionable illnesses are characterized by vague,
subjective multi-system complaints, a lack of
objective laboratory findings, quasi-scientific
explanations, overlap from one fashionable diag-
nosis to another, symptoms consistent with
depression or anxiety or both, and denial of psy-
chosocial distress or attribution of it to the illness.
According to Ford, fashionable diagnoses repre-
sent a heterogeneous collection of physical dis-
eases, somatization, and anxiety or depression.
339
Patients with medically unexplained symp-
toms obtain knowledge and beliefs about their
conditions from a variety of sources. Often, these
patients express skepticism with mainstream
medicine (Staudenmayer, 2001). This rejection of
mainstream medical thinking is unsurprising,
because many recognized experts believe that
these conditions are either of disputed origin or
surrogates for psychological disorders (Abbey &
Garfinkel, 1991; Albers & Berent, 2000; Barsky &
Borus, 1999; Binder & Campbell, 2004; Black,
2000; Bohr, 1996; Ferguson, 1997; Gabriel et al.,
1994; Hadler, 1997; Hennekens et al., 1996;
Hyams, Wignall, & Roswell, 1996; Katon &
Walker, 1993; Kroenke & Price, 1993; Rief &
Broadbent, 2007; Sanchez-Guerrero, Schur,
Sergent, & Liang, 1994; Staudenmayer, 2001;
Walker, Keegan, Gardner, Sullivan, Katon, &
Bernstein, 1997; Youngjohn, Spector, & Mapou,
1997). Patients with these disorders often reject
psychological explanations for their symptoms,
preferring biomedical and somatic explanations
(Butler, Chalder & Wessely, 2001; Ford, 1997;
Nimnuan, Hotopf, & Wessely, 2001). The doctor-
patient relationship becomes more problematic
when there is disagreement about causation of
symptoms, as often occurs in medicolegal cases
(Engel, Adkins, & Cowan, 2002). Therefore,
patients seek out health care professionals who
share their belief system and who are likely to rec-
ommend alternative medical treatment or expla-
nations (Black, 1996; Nimnuan, et al., 2001). The
general tendency of physicians to provide medical
explanations (Nimnuan, Hotopf, & Wessely, 2000)
and the proliferation of alternative medicine
explanations for symptoms help patients avoid
treatment by physicians who interpret somatic
symptoms as stress related in origin. Patients often
have educated and diagnosed themselves through
self-help groups, books and pamphlets, and
the Internet (Wessely, 1997), and unexplained
illnesses are more likely in adults whose parents
suffered from serious illnesses (Hotopf, Mayou,
Wadsworth, & Wessely, 1999).
Many of these disorders have overlapping
symptoms, reducing the reliability and validity of
their diagnoses (Deary, 1999; Wessely, Nimuan, &
Sharpe, 1999), and they may not be distinct enti-
ties. The same patient could receive a diagnosis of
fibromyalgia from a rheumatologist, a diagnosis
of chronic fatigue syndrome from an internist,
and a diagnosis of multiple chemical sensitivity
from a clinician interested in that disorder
(Buchwald & Garrity, 1994). The complaints of
340 forensic neuropsychology
fatigue and joint pain are common to chronic
fatigue syndrome, fibromyalgia, toxic mold
illness, silicone breast-implant-related illness, and
Gulf War-related illnesses.
Not only do the symptoms of these illnesses
overlap, but many of the symptoms are common
in healthy samples. Clearly, purportedly “neuro-
logical” symptoms such as headaches, fatigue,
memory loss, and dizziness occur commonly in
the general population (Ferguson, Mittenberg,
Barone, & Schneider, 1999; Gouvier, Uddo-Crane,
& Brown, 1988; Kroenke & Price, 1993; Sawchyn,
Brulot, & Strauss, 2000). Healthy control partici-
pants reported the following frequencies of
neurological symptoms: fatigue, 33%; headaches,
58%; forgetfulness, 58%; poor concentration, 35%
(Paniak et al., 2002). Pain also is commonly expe-
rienced. In one large survey, joint pains (37%),
back pain (32%), headaches (25%), chest pain
(25%), arm or leg pain (24%), and abdominal pain
(24%) were reported by community dwellers
(Kroenke & Price, 1993). The oft-replicated find-
ing that these symptoms are common in various
control samples implies that people who view
themselves as able-bodied usually do not find
these symptoms to be disabling or pay undue
attention to them. Although people with disor-
ders that are medically unexplained may experi-
ence some of these symptoms to a more extreme
degree than people who consider themselves
healthy, clinical observation suggests that some of
them also seem to view common symptoms as
signs of a serious illness, and some believe their
outcome will be bad (Sharpe, Chalder, Palmer, &
Wessely, 1997).
Shorter (1992) provided a historical view of
illnesses of mysterious origin. He maintained that
historical eras and cultures shaped the symptoms
of illnesses. The individual is pressured to produce
symptoms that are considered legitimate. Different
symptoms are considered socially acceptable in
different eras. As symptom legitimacy changes
over time, people respond by producing different
symptoms. Paralysis, for example, no longer is
accepted in the mainstream North American cul-
ture. In recent years, pain and fatigue have been
accepted by our culture. Shorter posited that
chronic fatigue syndrome and fibromyalgia repre-
sent contemporary prototypes of culturally
induced illnesses.
Shorter also argued that medical authority has
declined and the influence of the media on popu-
lar opinions regarding illness has increased. The
media, always searching for new and sensational
stories, promotes some illnesses. Rather than
depending solely on medical authority for infor-
mation, support groups also are viewed as sources
of information. Shorter noted that advocacy
groups were responsible for the name change
from chronic fatigue syndrome to chronic
immune dysfunction syndrome, despite the lack
of evidence of immune dysfunction in this illness
(Wessely, 1997). Shorter’s work predated the wide-
spread availability of medical information and
opinion on the Internet, which perhaps has con-
tributed to the contemporary media trend that
Shorter described.
According to Shorter, the increasing degree of
social isolation may play a role in culturally
induced illnesses. He noted that people were less
likely to receive consensual validation and feed-
back regarding the unimportance of common
symptoms such as fatigue and headache from, for
example, a wise aunt or friend. In the absence of
sensible social input about normal symptoms,
people may worry excessively about their signifi-
cance. Medical care providers with scientifically
unsupported explanations also are sources of
beliefs about illnesses, and they may be iatrogenic
causes of symptom production and maintenance
(Black, 2000).
In contrast to many of these arguments,
Ferguson and Cassaday (2001-2002) hypothesized
that conditions labeled in this chapter as unex-
plained are caused by a complex interaction of
biological, psychological, and environmental
influences. They emphasized the role of the
immune system and its responsiveness to psycho-
logical factors and stressors. Ferguson and
Cassaday suggested that some of these illnesses
could by caused by what they call a “bio-associa-
tive” mechanism or what psychologists refer to as
Pavlovian or classical conditioning. An illness ini-
tially caused by a pathogen could be associated
with a trigger such as an odor. Later, the illness
could be triggered by another odor. In this expla-
nation, the unconditioned stimulus is the patho-
gen and the conditioned stimulus is the odor. This
theory has received empirical support in the case
of multiple chemical sensitivities (Sorg, Tschirgi,
Swindell, et al., 2001; Van den Bergh, et al., 2001;
Winters, Devriese, Van Diest, et al., 2003). Others
have rejected a dualistic mind-body distinction in
attempting to understand medically unexplained
symptoms (Rief & Broadbent, 2007).
Illnesses with medically unexplained symp-
toms may be multiply determined (Ford,
1997). For example, a small percentage of veterans
 Forensic Assessment of Medically Unexplained Symptoms
with Gulf War illnesses suffered from leshma-
niasis, a parasitic disease. Some Gulf War
veterans have diagnoses of chronic fatigue
syndrome or fibromyalgia. There may be multiple
etiologies for chronic fatigue syndrome, both
pathophysiological and psychiatric (Afari &
Buchwald, 2003).
Rief and Broadbent (2007), while not viewing
illnesses such as fibromyalgia and chronic fatigue
syndrome as having pathophysiological causes
as do diseases such as cancers and pneumonias,
also believe that an explanation of medically
unexplained symptoms as purely psychogenic is
overly simplistic. They believe that some symp-
toms, at least initially, may have pathophysio-
logical (e.g., influenza) or psychophysiological
(e.g., stress of wartime deployment or battle
trauma) causes. However, patients with chronic
medically unexplained symptoms overemphasize
the role of organic causes, an explanation that
is unhelpful and countertherapeutic. Rief and
Broadbent reviewed many psychological contri-
butions to physical complaints, including tenden-
cies to adapt catastrophic interpretations of bodily
sensations, to overestimate the probabilities of
negative outcomes, to distort the probabilities of
organic causes of their symptoms provided by
their physicians, and to exhibit anxious attach-
ment behaviors in their interactions with health
care personnel in a way that leads to overutiliza-
tion of health care. They also note the importance
of rewards from the social system, including social
reinforcement from family and health care pro-
viders and financial incentives for illness.
Excessive anxiety about health often underlies
medically unexplained symptoms (Taylor &
Asmundson, 2004). The cognitive behavioral
approach to health anxiety assumes that health
anxiety is developed and maintained by cata-
strophic interpretations of relatively normal or
minor bodily signs and symptoms. People with
medically unexplained symptoms attempt to
cope by excessively checking their bodies, over-
attending to bodily sensations, and seeking reas-
surance. Autonomic arousal, the physiological
component of anxiety, often plays a role, both in
creating more bodily sensations and in arousing
fear about them. Excessive and medically unnec-
essary pursuit of health care often ensues.
Unnecessary diagnostic tests and medications
may lead to additional, iatrogenic symptoms.
Focus on disability may lead to inactivity, with
numerous negative health consequences for mus-
culoskeletal and other systems of the body.
341
PSEUDONEUROLOGICAL
ILLNES S
Pseudoneurological symptoms are complaints
such as dizziness, numbness, weakness, and
memory loss that are not associated with objec-
tive evidence of neurological disease. Research in
this area is useful in the understanding of all med-
ically unexplained symptoms.
Many years ago, evidence of authentic neuro-
logical disease sometimes could not be found
using the existing primitive diagnostic tools,
potentially leading to incorrect diagnosis of
pseudoneurological disease. In longitudinal
research that began not long after World War II,
Slater (1965) showed that many patients in his era
diagnosed with hysteria ultimately were proven to
have genuine neurological disease. After the
advent of more advanced neurodiagnostic tools,
there were similar studies. In one investigation, 56
patients with diagnoses of conversion disorder
were followed an average of 4.5 years later. Only
two patients later developed an organic deficit
that might have been related to the original epi-
sode of illness (Couprie, Wijdicks, Rooijmans, &
van Gijn, 1995). Others have reported similar
findings in longitudinal research suggesting that
incorrect diagnoses of somatoform problems
prove uncommon (Kent, Tomasson, & Coryell,
1995; Mace & Trimble, 1996; Crimlisk, Bhatia,
Cope, David, Marsden, & Ron, 1998). In contrast
to the primitive workups of Slater’s era, these more
recent studies confirmed the correctness of the
diagnoses in the vast majority of patients diag-
nosed by neurological evaluation as suffering
from pseudoneurological illness.
Despite the absence of neurological disease,
patients with pseudoneurological complaints
often have measurable neuropsychological
deficits. In the first of these studies (Matthews,
Shaw, & Klove, 1966), neurological and pseudo-
neurological patients were compared on the
Halstead-Reitan battery and the WAIS. Statistical
comparisons yielded significant differences on 17
of 26 variables. However, the authors stated, “In
spite of the relatively high levels of statistical sig-
nificance obtained by many of the comparison
variables, the use of any single one of them to clas-
sify individuals remains a doubtful procedure.
Useful cutoff points for the comparison variables
could not be established . . .” (Matthews et al.,1966,
p. 250). In a mixed group of pseudoneurological
cases, 54% were misclassified as brain damaged
based on the Generalized Neuropsychological
Deficit Scale of the Halstead Reitan Battery, 34%
342 forensic neuropsychology
misclassified based on the Halstead Impairment
Index, and 22% misclassified using the Average
Impairment Rating (Sherer & Adams, 1993).
Pseudoneurological patients also were impaired
on a verbal learning task (Sherer, Nixon, Parsons,
& Adams, 1992).
More recent neuropsychological investiga-
tions of pseudoneurological patients often have
studied patients with nonepileptic seizures and
consistently have documented poor performance.
In these studies, patients were diagnosed with
either epileptic or nonepileptic seizures after
intensive EEG video telemetry monitoring.
Criteria for classification were described in detail
in these studies. The first of these studies (Wilkus,
Dodrill, & Thompson, 1984) used a structured
test battery with cutoff scores previously estab-
lished in the same population. The test battery did
not show any significant differences between the
groups with epileptic and nonepileptic seizures.
The epileptic group performed abnormally on an
average of 46% of the tests, and the nonepileptic
seizure patients produced abnormal scores on an
average of 51% of the tests, a nonsignificant differ-
ence. A similar study found no significant differ-
ences between patients with epileptic and
nonepileptic seizures on 16 neuropsychological
measures (Brown, Levin, Ramsay, Katz, &
Duchowny, 1991). Based on a qualitative analysis
of test data, Brown et al. concluded that the non-
epileptic patients had inconsistent abnormalities
characteristic of non-neurological conditions.
In another investigation, Binder, Kindermann,
Heaton, and Salinsky (1998) compared control
participants with epileptic and nonepileptic
seizure patients. The two patient groups with
seizures performed similarly and demonstrated
significant impairment compared with the con-
trol group; for example, the nonepileptic seizure
patients had a mean WAIS-R Full Scale IQ of
92.0, a mean score 9.9 points lower than the con-
trol group. The difference between nonepileptic
seizure patients and healthy controls on Trail
Making Part B was 31.0 seconds. The mean for the
nonepileptic seizure group on Logical Memory I
of the Wechsler Memory Scale-Revised was at
the 31st percentile with no data available on this
measure from the control group.
Factors other than neurological disease
explain neuropsychological abnormalities in
patients with psychogenic nonepileptic seizures.
There are studies suggesting the influence of
motivational and emotional factors. Nonepileptic
seizure patients performed more poorly than
epileptic seizure patients on the Portland Digit
Recognition Test (PDRT), a measure of motiva-
tion to remember (Binder, Salinksy & Smith,
1994), but they generally did not perform in the
range typically associated with malingering on
this measure. The PDRT findings in the non-
epileptic group (Binder et al., 1994) were consis-
tent with earlier qualitative observations judged
to imply inconsistent effort (Brown et al., 1991)
and with data showing frequent failures in patients
with nonepileptic events on another measure of
motivation, the Word Memory Test (Williamson,
Drane, & Stroup, 2007). One study, however,
failed to find differences between patients with
epileptic and psychogenic nonepileptic seizures
on measures of effort (Cragar, Berry, Fakhoury,
et al., 2006). The influence of emotional factors on
neuropsychological performance was supported
in a study showing that patients with psychogenic
seizures and emotional problems as measured by
the MMPI-2 performed worse on cognitive
testing than patients with psychogenic seizures
with either relatively normal or purely somato-
form MMPI-2 profiles (Cragar, Berry, Fakhoury,
et al., 2002).
In addition to measurable neuropsychological
impairment, there is significant disability associ-
ated with pseudoneurological conditions. Many
nonepileptic seizure patients never work again
(Barry et al., 1998). The cause of nonepileptic
seizures usually is psychiatric. Hence, the cause of
disability associated with nonepileptic seizures
also is psychiatric.
Investigators have studied the relationships
between mild head injury, seizure type, and the
opportunity for financial compensation. Epileptic
seizures were not commonly found after mild
head injury in an epidemiological study, and they
were more common after moderate and especially
severe head injury (Annegers, Hauser, Coan, &
Rocca, 1998). The prevailing opinion is that trau-
matic seizures of epileptic origin can be caused by
cortical contusions. These contusions can be con-
sistent with a head injury defined as mild solely by
Glasgow Coma Scale criteria, however, a head
injury with a Glasgow score of 13–15 and a contu-
sion is often classified as a complicated mild head
injury. If there is no evidence of contusions from
acute neuroimaging, and if the head injury was
trivial with little or no loss of consciousness and
little or no post-traumatic amnesia, post-injury
seizures in a forensic setting usually will be of
nonepileptic origin. Nonepileptic seizures, in con-
trast with epileptic seizures, commonly follow
 Forensic Assessment of Medically Unexplained Symptoms
mild head injuries that offer the opportunity for
financial compensation (Westbrook, Devinsky, &
Geocadin, 1998).
Diagnosis of seizures is within the domain of
neurology, particularly the subspecialty of epilep-
tology. Intensive EEG monitoring remains the
gold standard method of diagnosis of seizure type.
Neuropsychological assessment can aid in the
evaluation of post-injury seizures by identifying
which patients fit the psychological profile of non-
epileptic seizure patients or are likely to be diag-
nosed as nonepileptic with appropriate diagnostic
tools. Persons with neuropsychological correlates
of nonepileptic seizures are candidates for inten-
sive EEG monitoring where definitive diagnosis is
possible. The MMPI-2 is the best single predictor
for this purpose. In settings with high base rates of
nonepileptic seizures, the MMPI-2 is about 70%
accurate in predicting the differential of epileptic
or nonepileptic seizures as diagnosed by neurol-
ogy through intensive EEG monitoring, accord-
ing to a review of studies (Dodrill, Wilkus, &
Batzel, 1993). Conversion V profiles and scores on
HS or HY above 79 are associated with nonepilep-
tic seizures. Epileptic seizure groups score about
10 points lower on HS and HY than nonepileptic
groups (Dodrill et al., 1993). In adult settings, sei-
zure onset generally is more recent in nonepilep-
tic than epileptic seizures. Chronicity of seizures
and routine EEGs were combined with the
MMPI-2 to yield 86% accuracy in predicting sei-
zure diagnosis with approximately equal accuracy
for both types of seizures (Storzbach, Binder,
Salinsky, Campbell, & Mueller, 2000).
F I B R O M YA L G I A
Fibromyalgia is characterized by widespread joint
pain, insomnia (Bohr, 1996), and nonrestorative
sleep. The diagnosis of fibromyalgia is based upon
the trigger point exam. In response to four kilo-
grams of finger pressure applied by the examiner
(pressure sufficient to blanch the fingernail of the
examiner), the patient must report pain in at least
11 of 18 trigger points, including sites both above
and below the waist. These criteria have proved
problematic (Bohr, 1996; Hadler, 1997) for two
reasons. First, it is difficult for a clinician to
consistently apply four kilograms of pressure and
second, it is not likely that patients will reliably
report the experience of pain, an inherently
subjective event. The illness can be viewed as
entirely subjective (Hadler, 1997).
The etiology of fibromyalgia is unknown.
It is believed by some investigators that there are
343
neuroendocrine abnormalities associated with
fibromyalgia and that the illness is caused by
abnormal sensory processing (Bennett, 1999).
However, emotional problems also are associated
with neuroendocrine disorders (Barlow, 2000),
and it is not clear that there are neuroendocrine
abnormalities in fibromyalgia specific to that
condition. Some investigators have reported
reduced cerebral blood flow in the subcortical
and brainstem regions in patients with fibromyal-
gia (Kwiatek, Barnden, Tedman, et al., 2000), but
similar findings are nonspecific and occur in psy-
chiatric patients (Hakala, Karlsson, Ruotsalainen,
et al., 2002; Lange, Wang, DeLuca, & Natelson,
1998). Posterior fossa decompression has been
used as neurosurgical treatment of fibromyalgia
based solely on the rationale of overlapping
symptoms with Chiari type I malformation, but
this practice is controversial (Nash, Cheng, Meyer,
& Remler, 2002).
There are some well-established facts regard-
ing fibromyalgia. It is far more frequent in females
than in males (Wolfe et al., 1995) and often is the
basis for claims of disability (Wolfe et al., 1997).
The condition sometimes is associated with mild
neuropsychological deficits (Hart, Martelli, &
Zasler, 2000), but the reason for this association,
when it exists, is unclear. In one study the fibro-
myalgia group performed within the normal
range on all cognitive measures although there
were some differences between fibromyalgia
patients and controls (Grace et al., 1999). Other
investigators found that more than a third of the
fibromyalgia patients who either were seeking
disability payments or who already were receiving
them scored below the cutoffs on measures of
motivation to remember (Gervais, Russell, Green,
et al., 2001). When participants with evidence of
poor effort were eliminated, there were no differ-
ences between fibromyalgia patients and controls
(Suhr, 2003). Subjective cognitive complaints out-
stripped objective abnormalities (Grace et al.,
1999) when only patients who passed a measure
of effort were included (Suhr, 2003). In a study
that requires replication, fibromyalgia patients,
compared with controls with memory complaints,
were slower on measures of naming speed but
were better than controls on some measures of
visuomotor speed (Leavitt & Katz, 2008).
Fibromyalgia patients were more likely than
control subjects to have a history of psychiatric
problems including mood and anxiety disorders,
according to a meta-analytic review (Henningsen,
Zimmerman, & Sattel, 2003), and more medically
344 forensic neuropsychology
unexplained physical symptoms across several
organ systems (Walker, Keegan, Gardner, Sullivan,
Katon, & Bernstein, 1997). Fibromyalgia patients
had more evidence of abuse and trauma in both
childhood and adulthood, compared with patients
with rheumatoid arthritis (Walker, Keegan,
Gardner, Sullivan, Bernstein, & Katon, 1997).
C H R O N I C FAT I G U E
SYNDROME
Diagnostic criteria for chronic fatigue syndrome
(CFS) in the United States include chronic
disabling fatigue and at least four of eight other
features including muscle ache, joint pain, subjec-
tive cognitive problems, sore throat, new head-
ache, nonrestorative sleep, post-exertion malaise,
and swollen lymph glands (Fukuda et al., 1994).
These symptoms are similar to those associated
with fibromyalgia. Although some symptoms of
chronic fatigue are similar to the symptoms of
depression, the emotional aspects of depression
such as sadness, anhedonia, and low self-esteem
often seem to be absent in CFS (Jason et al., 1997).
Afari and Buchwald (2003) reviewed CFS. Like
fibromyalgia and multiple chemical sensitivities,
it is more prevalent in females than males (Jason
et al., 1999).
Neuropsychological impairment in CFS has
been reviewed (DiPino & Kane, 1996; Tiersky
et al., 1997). Intellect and complex problem-
solving abilities are preserved, but CFS patients
suffer from a deficit in complex information pro-
cessing (Tiersky et al., 1997). Clearly, subjective
ratings of cognitive impairment are more pro-
nounced than objective neuropsychological find-
ings (Tiersky et al., 1997). There is mixed evidence
of motivational problems on neuropsychological
testing in patients with CFS. A deficit was found
on a forced choice measure of motivation to
remember in a clinical sample (Van der Werf et al.,
2000), but not on a similar measure in a research
sample composed largely of people who did not
consider themselves disabled (Binder, Storzbach,
Campbell, Rohlman, & Anger, 2001). A meta-ana-
lytic review showed that chronic fatigue syndrome
often is associated with a history of anxiety and
depression (Henningsen et al., 2003), but cogni-
tive deficits were found in another study despite
controlling for history of psychiatric illness
(DeLuca, Johnson, Ellis, & Natelson, 1997). The
same study (DeLuca et al., 1997) found that CFS
of gradual onset was associated with more psychi-
atric illness but less severe memory problems than
CFS of sudden onset. The need to consider the
heterogeneity of the illness was amplified by the
finding that CFS of sudden onset was associated
with slower information processing speed (Clay-
poole, Noonan, Mahurin, et al., 2007). Exercise
caused a more severe decline in cognition in
people with CFS than controls (LaManca et al.,
1998). Subsequently, an investigation using mono-
zygotic twins discordant for the illness found little
evidence of vulnerability to cognitive problems
soon after exercise in people with CFS (Claypoole,
Mahurin, Fischer, et al., 2001).
Factors independent of the symptoms of CFS
may be responsible for the association found in
many studies between neuropsychological deficits
and the illness. Monozygotic twins discordant for
CFS showed no cognitive differences (Mahurin,
Claypoole, Goldberg, et al., 2004). In the Mahurin
et al. study, however, both healthy twins and
twins with CFS performed worse than controls on
measures of information processing speed, and
their findings suggested that the cognitive deficits
preexisted the onset of illness. Although premor-
bid mental aptitude differences were found as
measured by the Armed Forces Qualification Test
between CFS and control participants after the
Persian Gulf War, these premorbid differences
did not explain the impaired performance of the
CFS group compared with and controls on some
measures of information processing speed and
attention (Binder et al., 2001).
Several investigators have studied regional
cerebral blood flow in CFS, typically with single
photon emitted computerized tomography
(SPECT). Early studies suggested that the illness
was associated with reductions in cerebral blood
flow (Ichise et al., 1992; Schwartz et al., 1994).
Subsequent studies parallel results previously
reviewed for fibromyalgia: Either there are no
abnormalities in CFS (Fischler et al., 1996; Lewis
et al., 2001) or the abnormalities are nonspecific
and similar to those found in psychiatric groups
(Lange et al., 1998). A fluorine-deoxyglucose
positron emission tomography (PET) study
suggested that hypometabolism in the brainstem
was found only in CFS and not in depression
(Tirelli et al., 1998), but a study using the same
technique found no differences between a group
with CFS and a group with somatization disorder
(Hakala et al., 2002).
Controversies regarding the etiology of CFS
have been reviewed (Afari & Buchwald, 2003;
Tiersky et al., 1997). Various hypotheses have
been advanced including viral, limbic system, and
immune system explanations, all lacking basic
 Forensic Assessment of Medically Unexplained Symptoms
scientific support. There is no evidence of a spe-
cific viral etiologic agent. In some quarters, CFS is
viewed as the equivalent of a psychiatric condi-
tion. According to this view, patients with CFS are
engaging in illness behavior and have normal
complaints (Barsky & Borus, 1999). In the view of
others (Henningsen et al., 2003), the lack of unity
between diagnoses of CFS and depression and/or
anxiety suggests that CFS should not be consid-
ered a psychiatric entity.
Wessely and colleagues (Sharpe et al., 1997)
have adopted a complex view of the etiology of
CFS, emphasizing the distinction among factors
that may have predisposed patients to develop the
illness such as lifestyle, work stress, and personal-
ity; factors that may have triggered the illness such
as viral infection or life events; and factors that
may have perpetuated the illness such as cerebral
dysfunction, sleep disorder, depression, inconsis-
tent activity, and misunderstanding of the illness
and fear of making it worse.
It also is hypothesized that the low levels of
natural killer cells in the immune system explain
the illness (Whiteside & Friberg, 1998), although
the relationship between low-level immune
system activation and CFS symptoms is unclear
(Afari & Buchwald, 2003; Wessely, 1997). More
controversial is the posterior fossa decompression
surgery that also has been performed on fibromy-
algia patients (Nash et al., 2002). Just as neuropsy-
chological findings differ in subgroups (Claypoole
et al., 2007; DeLuca et al., 1997), the etiology of
CFS may be heterogenous (Afari & Buchwald,
2003).
M U LT I P L E C H E M I C A L
SENSITIVITIES
The term “multiple chemical sensitivities” (MCS)
has been discarded by some authorities (Sparks,
2000) for several reasons, including the lack of
conclusive pathophysiological evidence that
people with the diagnosis are abnormally sensi-
tive to specific chemicals (Dalton & Hummel,
2000), because the relationship between symp-
toms and exposures is unproven, and because
MCS is not a clinically defined disease with gener-
ally accepted underlying pathophysiological
mechanisms or validated criteria for diagnosis. As
discussed by Sparks (2000), the term “idiopathic
environmental intolerance” has been proposed as
a replacement. Although MCS is the term com-
monly employed by many clinicians, the condi-
tion has other labels, including chemical
intolerance, environmental illness, and total
345
allergy syndrome. MCS was reviewed compre-
hensively in an edited volume (Sparks, 2000), and
Labarge and McCaffrey (2000), Staudenmeyer
(2001), and McCaffrey and Yantz (2007) have
reviewed the topic from neuropsychological and
psychological perspectives. The illness is charac-
terized by symptoms in multiple organ systems in
reaction to a variety of low levels of chemically
unrelated common odors at doses that do not
cause symptoms in the general population. The
substances causing discomfort in people with
MCS are irritants rather than neurotoxicants
(Bolla, 2000). Symptoms of MCS include fatigue,
confusion, dizziness, and gastrointestinal, muscu-
loskeletal, and respiratory problems. These symp-
toms may last for days or weeks. Patients with
MCS believe they are sensitive to certain odors
and they avoid common odors such as perfume,
gasoline and other petroleum products, new
carpets, and ordinary household cleansers. Some
people with MCS attempt to avoid close contact
with printed matter because of perceived sensi-
tivity to ink. Food allergies are common in this
population. The avoidance of so many common
substances often leads to disability. Many patients
with MCS also are diagnosed with CFS and
fibromyalgia (Bell, Baldwin, & Schwartz, 1998;
Buchwald & Garrity, 1994; Sparks, 2000), because
the symptoms overlap among these disorders.
MCS may follow the misperception of exposure to
toxins, such as occurred in the Persian Gulf War
of 1991 (Reid, Hotopf, Hull, et al., 2001) and
during construction of a chemical weapons incin-
erator in Umatilla, Oregon (Binder, Storzbach, &
Salinsky, 2006). Expectations that a particular
odor is harmful clearly play a role in the deve-
lopment of symptoms (Das-Munshi, Rubin, &
Wessely, 2006; Winters et al., 2003).
This clinical entity is controversial, indeed.
The clinical ecological approach views the illness
as organic and caused by chemical exposure and
recommends costly lifestyle changes and other
interventions. Mainstream medicine has been
particularly critical of the clinical ecological
approach (American Academy of Allergy and
Immunology, 1986; American College of Phys-
icians, 1989). Laboratory provocation in patients
diagnosed with MCS with the chemicals identi-
fied as incitants yielded extremely low sensitivity
and specificity values, data strongly suggesting
that the diagnosis of MCS has no validity
(Staudenmayer, Selner, & Buhr, 1993). Consistent
with these results, objective medical findings
usually do not exist (Labarge & McCaffery, 2000).
346 forensic neuropsychology
MCS often is associated with various psychiatric
illnesses (Black, 2000; Staudenmayer, 2001),
especially depression (Caccappolo-van Vliet,
Kelly-McNeil, Natelson, et al., 2002) and anxiety.
Experimental data from some laboratories pro-
vided no evidence that people with MCS are any
more sensitive to odors than control subjects
(Dalton & Hummel, 2000; Doty et al., 1988), while
other laboratory challenge studies suggested both
a physiological hypersensitivity and a psychologi-
cal component to the illness (Fiedler, Giardino,
Natelson, et al., 2004; Osterberg, Orbaek, Karlson,
et al., 2003).
A model of MCS involving neurohormonal
sensitization of olfactory-limbic circuits has been
proposed (Bell, Baldwin, & Schwartz, 1998).
According to this model, some individuals can be
sensitized by low doses of chemicals that may not
have been troublesome to them in the past. In this
model, amplification of responses is hypothesized
to occur in the limbic system, including the
mesolimbic dopaminergic (reward) pathway.
Subsequent activation of sensitized pathways is
purported to lead to impaired function of behav-
ioral, immune, and other systems.
MCS can be caused by classical conditioning.
Limited pairings of a conditioned stimulus of a
noxious odor and an unconditioned stimulus of
air rich in carbon dioxide led to the conditioning
of both somatic symptoms and altered respiratory
responses in humans in reaction to just the condi-
tioned stimulus of the odor (Van den Bergh et al.,
2001). Importantly, conscious awareness of the
relationship between the odor and the symptoms
induced by carbon dioxide was not necessary for
the effects to occur. Symptomatic reactions gener-
alized not only to new, noxious odors but also
to situations in which participants imagined
situations where the symptoms had occurred.
There were individual differences in the effect.
Participants who had higher scores on a measure
of negative affectivity (neuroticism) or who suf-
fered from nonorganic illnesses had more learned
symptoms and more easily generalized the illness
response to new odors. Extinction was demon-
strated with sufficient exposure to just the condi-
tioned stimulus. This work has been replicated by
the same group and by another lab (Sorg, Tschirgi,
Swindell, et al., 2001; Van den Bergh et al., 2001;
Winters, Devriese, Van Diest, et al., 2003).
Experimental work on the interaction of
health expectancy and the pleasantness of odors
also shows a psychological influence on symp-
tomatology (Dalton, 1999). Participants exposed
to a solvent-like alcohol scent (butanol), a winter-
green scent, and a balsam scent reported more
symptoms when they were warned of solvent
exposure than when they were told they would be
exposed to a natural extract with a relaxing effect.
The odors and self-reported chemical intolerance
also had significant effects on symptoms. There
are a variety of cognitive influences related to
sensory and somatic responses to chemical stimu-
lation (Dalton & Hummel, 2000). In one classical
conditioning study there was no effect on somatic
symptoms without a warning about harmful
consequences (Winters et al., 2003).
The few available neuropsychological studies
of MCS show little or no evidence of neurocogni-
tive impairment in controlled investigations
(Bolla, 2000; Caccappolo-van Vliet et al., 2002;
Labarge & McCaffrey, 2000; Simon, Daniell,
Stockbridge, et al., 1993). Bolla emphasized the
lack of specificity of neuropsychological testing
in persons with symptoms of MCS because of the
lack of a biological marker of MCS and the
absence of evidence of neurocognitive problems
among people with MCS symptoms, including
cognitive tests thought to be especially sensitive to
limbic system dysfunction (Brown-DeGagne &
McGlone, 1999). Expectancy appears to play a
role in neuropsychological problems thought to
be associated with MCS. In a placebo-controlled
study, people with MCS had lowered neuro-
psychological performance when they perceived
that they were exposed to substances that they
considered “chemical,” but there were no perfor-
mance decrements associated with the actual
substances to which they were exposed (Smith &
Sullivan, 2003). In summary, there is no credible
evidence of neuropsychological impairment
caused by MCS.
TOX I C M O L D A N D S I C K
BUILDING SYNDROME
A guideline of the American College of
Occupational and Environmental Medicine
(Hardin et al., 2003) summarized the state of
knowledge regarding toxic mold and human
health. Some fungi produce beneficial metabolites
known as mycotoxins that can be converted into
antibiotics such as penicillin and cyclosporine.
“Mold” is the commonplace term for multicellular
fungi that grow in a mat. The growth of molds
in indoor environments has been cited as the
explanation for a variety of nonspecific symp-
toms. However, the reality is that fungi and
molds are ubiquitous and exposure is unavoidable
 Forensic Assessment of Medically Unexplained Symptoms
unless draconian isolation measures are utilized.
Essential for the decomposition of organic mate-
rial, many species live on the surface of the
human body.
Fungi can harm human health through allergy,
infection, and toxicity. Allergic responses occur in
roughly 5% of the population and usually are
experienced as allergic asthma or rhinitis, the
latter commonly known as “hay fever.” Uncommon
allergy syndromes include allergic bronchopul-
monary aspergillosis and allergic fungal sinusitis.
Ingestion of foods with sufficient quantity of cer-
tain molds can cause illnesses known as myco-
toxicoses. Superficial fungal infections such as
tinea pedia, commonly known as “athletes foot”
and tinea cruris, commonly known as “jock itch”
are common in humans. Of much greater concern
are infections in persons who are immunocom-
promised, including patients on immunosuppres-
sant medications and persons with AIDS and
severe diabetes. Previously healthy persons are
subject to rare, serious fungal infections caused by
fungi including Cryptococcus and Histoplasma or
to hypersensitivity pneumonitis, an exaggerated
immune system response after inhalation of large
quantities of protein such as fungal proteins.
“Organic dust toxic syndrome” has been described
after inhalation exposure of agricultural workers
to spoiled grain products. These illnesses are asso-
ciated with thick clouds of dust, and not with
musty odor from wood with dry rot. The concen-
tration of fungi in grain silos is far in excess of the
concentration in normal indoor environments
(Lees-Haley, 2004).
Ergotism, in one form, is a neurological dis-
ease resulting from consumption of the alkaloids
derived from the Claviceps purpurea fungus,
found in rye and other grains. A neurovascular
gangrenous form of the disease also occurs.
Disease outbreaks throughout history probably
were more commonly associated with rye wheat
consumption because the dark fungus is more dif-
ficult to see in dark rye flour than in lighter col-
ored flours. Outbreaks of this disease were
common until the 19th century in Europe. Out-
breaks continue, particularly in less-developed
countries. Neurological symptoms include par-
esthesias, muscle contractions, seizures, psycho-
sis, and signs of peripheral neuropathy (Pryse-
Phillips, 2003; Walton, 1985).
Coccidioides immitis, a mold found in the soil
in the southwestern United States, can be inhaled
and lead to a pulmonary infection, followed some-
times by disseminated diseases such as vasculitis
347
and cerebral infarctions. Subarachnoid hemor-
rhage is a rare complication (Erly, Labadie,
Williams, et al., 1999).
Toxic-mold-related illnesses resulting from
breathing air in buildings allegedly contaminated
by mold are a different matter than well-defined,
serious diseases such as ergotism, which is caused
by eating mold-infected grain, or disseminated
coccidioidomycosis. To be sure, mold can be
found in buildings. However, mycotoxins are not
significantly volatile; they do not off-gas into the
environment or pass through solid substances
such as walls. The musty odor associated with
mold is not caused by mycotoxins.
Sick building syndrome is a poorly defined set
of symptoms attributed to occupancy of an alleg-
edly contaminated building. Usually, no specific
cause is found for the complaints. In some cases a
mycotoxin-producing mold, Stachybotrys char-
tarum, is identified in the building, but generally,
there is no scientific evidence of a causal relation-
ship between indoor air exposure to Stachybotrys
chartarum and human illnesses. Hardin et al.
(2003) concluded that fungi rarely are significant
human pathogens, except through ingestion of
contaminated foods and that current scientific
evidence does not support the proposition that
human health has been adversely affected by
inhaled mycotoxins. Similar views have been
expressed by others (Burge, 2001; Kuhn &
Ghannoum, 2003; Robbins et al., 2000).
Hodgson (2000) suggested that sick building
syndrome could be caused by problems associ-
ated with humidification and ventilation systems.
He also noted that individuals varied in their sus-
ceptibility to the two most common building-
related problems, namely, mucosal problems in
either the nasal passages or eyes.
Some relevant neuropsychological data on
sick building syndrome have been published. In
one study, there were no differences between
exposed persons and controls (Hodgson et al.,
1998). An experimental acute exposure study of
respiratory irritants, including volatile organic
compounds and ozone, showed no neuropsycho-
logical effect (Fiedler et al., 2005).
Some authors have claimed that their data
supported a link between inhalation of toxic mold
in buildings and neuropsychological deficits, but
these studies, as reviewed in more detail elsewhere
(McCaffrey & Yantz, 2007), are badly flawed. For
example, Gordon, Johanning, and Haddad (1999),
in a clinical study that was not peer reviewed,
reported neurocognitive impairment, but there
348 forensic neuropsychology
were no control subjects and the participants were
self-selected after claiming cognitive impairment
caused by inhalation of toxic mold. When patients
are self-selected there could be many reasons for
their symptoms other than the cause that they
allege. Other authors have claimed that there were
neuropsychological effects from exposure (Baldo,
Ahmad, & Ruff, 2002). Critiques of the Baldo
et al. study (Lees-Haley, 2004; McCaffrey & Yantz,
2005) pointed out several methodological flaws.
Among the errors were lack of any reasonable
control group, lack of information about the type
and intensity of exposure, and the self-selected
nature of the patient/litigants in the study.
Neuropsychological abnormalities in this popula-
tion sometimes can be explained by suboptimal
motivation rather than by actual cognitive impair-
ment (Stone, Boone, Back-Madruga, et al., 2006).
At the present time, there is no credible scien-
tific evidence that inhalation of toxic mold such as
stachybotrys in the concentrations typically found
in residences and workplaces causes encephalopa-
thy (Lees-Haley, 2003; 2004; McCaffrey & Yantz,
2007; Terr, 2005). Respiratory, systemic, and cog-
nitive complaints are common in patients alleging
injury from toxic molds, but transient irritation,
unrelated and preexisting diseases, and psycho-
genic problems explain the complaints (Khalili &
Bardana, 2005). There is no specific pathophy-
siological mechanism to explain the complaints of
patients alleging building-related inhalational
mold toxicity (Khalili & Bardana, 2005). The con-
dition has been characterized as litigation-induced
(Lees-Haley, 2003; 2004; Terr, 2005) and as a
pseudoillness (Terr, 2005).
PSYCHOLOGICAL STRES S
AND DISEASE
Human and infrahuman studies indicate that
stressors can cause pathological changes in func-
tioning in the immune and endocrine systems
and disease (McEwen, 2002). Individuals differ
in their biological susceptibility to stressors, pos-
sibly because of psychological traits (Kirschbaum
et al., 1995). Animal models have shown that
early stressors cause chronic alterations in hypo-
thalamic-pituitary-adrenal axis function, chroni-
cally negative emotions, and easily elicited alarm
reactions in juvenile monkeys, changes that
persist into adulthood (Barlow, 2000). In veterans
of World War II and Vietnam the stress of combat
experience was associated with an increased
risk of physical decline and death (Boscarino,
2008; Elder, Shanahan, & Clipp, 1997). In humans,
depression is associated with large changes in
immune system functioning, for example, lower
natural killer-cell activity and change in white
blood cell counts (Herbert & Cohen, 1993).
Suppression of immune system function persists
in persons with PTSD (Boscarino, 2008) and in
persons with past history of PTSD but with no
current psychiatric disorder (Kawamura, Kim, &
Asukai, 2001). Cytokine-induced immune system
activation temporarily produces memory impair-
ment (Reichenberg, Yirmiya, Schuld, et al., 2001).
PTSD among Vietnam veterans was associated
with self-reported diagnoses of circulatory, diges-
tive, musculoskeletal, nervous system, respiratory,
and infectious diseases (Boscarino, 1997) and
more than two-fold increase in mortality
(Boscarino, 2008).
A neuroanatomical model of panic (Gorman,
Kent, Sullivan, & Coplan, 2000) was based on
animal studies of conditioned fear due to the
behavioral and physiologic similarities between
panic and conditioned fear. Gorman et al.
described a fear network with the amygdala inter-
acting with the hippocampus and prefrontal
cortex. The amygdala receives the sensation
of a conditioned stimulus and coordinates auto-
nomic, sympathetic, and behavioral responses
to the conditioned stimulus. Projections from
the amygdala to the periaquadactal gray causes
postural freezing. The fear network could be
inappropriately activated if bodily cues were pro-
cessed defectively. As noted above, early stressors
also cause changes in neuroendocrine function-
ing in the hypothalamic-pituitary-adrenal axis.
Davidson (2000) reviewed further relation-
ships between emotions, psychopathology, and
neurophysiology. People have baseline electro-
physiological differences that are stable and that
predict individual differences in reactivity to emo-
tionally eliciting events. Davidson characterized
these differences as forming a neurophysiological
vulnerability to the elicitation of both positive and
negative emotions. The intensity of negative affect
is related to these neurophysiological differences
as well as to the immune system functioning and
activity of the autonomic nervous system. In
infrahuman subjects, early environmental manip-
ulations lead to differences in reactivity and brain
circuitry (Barlow, 2000; Davidson, 2000).
PTSD and severe stressors have been asso-
ciated with cognitive abnormalities and structural
brain changes in humans. Excess levels of
glucocorticoids secreted during stress may con-
tribute to neuronal death and atrophy in the
 Forensic Assessment of Medically Unexplained Symptoms
hippocampus in PTSD and major depression
(Lee, Ogle, & Sapolsky, 2002; Sapolsky, 2000).
Hippocampal size was associated with diagnoses
of PTSD and depression (Bremner et al., 1995).
Neuroimaging findings associated with PTSD
have been reviewed (Grossman, Buchsman, &
Yehuda, 2002). The chapter by Andrikopoulos and
Greiffenstein on PTSD in the current volume fur-
ther reviews this literature and studies of possible
cognitive abnormalities associated with PTSD.
Exposure to trauma is associated with the
development of medically unexplained physical
symptoms, PTSD, depression, and substance
abuse (Beckham et al., 1998; Schnurr & Spiro,
1999; Sledjeski, Speisman, & Dierker, 2008; Stein,
Walker, Hazen, & Forde, 1997). As noted above,
trauma exposure in those who survive natural
disasters is associated with pseudoneurological
symptoms (Cardena & Spiegel, 1993; Escobar
et al., 1992). Somatization symptoms are associ-
ated with both PTSD (Andreski, Chilcoat, &
Breslau, 1998) and panic disorder (Simon, Katon,
& Sparks, 1990). Somatization also is associated
with a history of childhood sexual abuse
(Morrison, 1989). Physical and sexual abuse and
other types of trauma also are associated with
nonepileptic seizures (Alper, Devinsky, Perrine,
Vazquez, & Luciano, 1993; Rosenberg, Rosenberg,
Williamson, & Wolford, 2000) and diagnoses of
fibromyalgia (Walker, Keegan, Gardner, Sullivan,
Bernstein, & Katon, 1997).
T H R E AT S T O T H E
A C C U R A C Y O F T H E H I S T O RY
P ROV I D E D B Y T H E
EXAMINEE
Neuropsychological assessment requires differen-
tial diagnosis (Binder, 1997). The patient may be
symptomatic because of depression or other psy-
chiatric problems, pseudoneurological problems,
developmental learning disabilities, medical ill-
ness unrelated to the injury, malingering
(Larrabee, this volume), or chronic pain disorder
(Greve, Bianchini, & Ord, this volume). It is erro-
neous to automatically attribute symptoms to a
traumatic brain injury (Roebuck-Spencer &
Sherer, this volume; Larrabee, this volume),
alleged neurotoxic exposure (Bolla, this volume),
or other events without performing a differential
diagnosis. In order to make an accurate differen-
tial diagnosis it is essential to obtain accurate
historical information. The purpose of this sec-
tion is to discuss the barriers to obtaining an
accurate history and some other confounds in the
349
interpretation of assessment results as well as the
possible impact on health of some forms of
inaccurate self-disclosure.
ACCURACY OF
SELF-DISCLOSURE AND
I M PA C T O N H E A LT H
In this section, literature will be reviewed showing
that the level of accuracy of people who are pro-
viding their medical and psychiatric histories or
in reporting current psychological distress is less
than may generally be assumed by health care
professionals. People often are inaccurate in
reporting easily defined medical events (Harlow
& Linet, 1989). For example, acute medical ill-
nesses and the use of sick leave were not accurately
reported a relatively short time later (Rogler,
Malgady, & Tryon, 1992). Recall of acute illnesses
occurred in only 42% of cases only a month later,
and recall of medical events was 70% accurate
after one month but only 26% accurate 9–12
months later (Rogler et al., 1992). Patients with
medically unexplained neurological symptoms
tend to overpathologize their medical histories
(Schrag, Brown, & Trimble, 2004).
People also often are inaccurate reporters of
childhood events of potential psychological
significance. For example, a longitudinal study
found that participants at age 18 often had recol-
lections discrepant from more contemporaneous
data, including reports by their mothers of family
conflict at various ages, earlier self-reports of
hyperactivity, and earlier self-reports of depres-
sion (Henry, Moffit, Caspi, Langley, & Silva, 1994).
A 30-year follow-up of ex-child guidance clinic
patients, using methodology similar to Henry
et al., examined interview agreement with
events previously recorded (Robins et al., 1985).
Agreement ranged from low to high, depending
on the event. For example, after 30 years 91%
correctly recalled not always living with their
parents, but only 47% were cognizant of their
family receiving welfare assistance and only 56%
remembered living with relatives.
Traumatic events sometimes are underre-
ported or otherwise distorted. Adults who were
sexually abused or otherwise traumatized during
childhood or early in adulthood, according to
childhood records contemporaneous with the
reported abuse, often failed to report this history
when directly asked many years later (Widom &
Morris, 1997). A longitudinal study of Persian
Gulf War veterans found that participants were, in
general, more likely to report specific traumatic
350 forensic neuropsychology
events two years after their return from the
Persian Gulf than one month after their return,
and that the increase in traumatic memories was
associated with increased symptoms of PTSD
(Southwick, Morgan, Nicolaou, & Charney, 1997).
These authors felt that exaggeration was the most
likely reason for the increase in self-reported
exposure to traumatic events. A competing hypo-
thesis not ruled out by the authors was that the
initial reports minimized meaningful events that
later, after reflection, were more fully recalled.
Another longitudinal study of Gulf War veterans
showed that participants who reported high
combat stress were more likely to believe that they
had been exposed to chemical or biological weap-
ons (Stuart, Ursano, Fullerton, & Wessely, 2008).
Although exposure to stressors may be exag-
gerated, mental health history generally is mini-
mized (Simon & VonKorff, 1995). In one study,
depression was studied by structured interview,
and a year later in follow-up the subjects com-
pleted a self-report instrument measuring depres-
sion (Coyne, Thompson, & Racioppo, 2001).
There was no significant overlap between the ini-
tial structured interview and self-report after a
year, a finding the authors found “disheartening”
(Coyne et al., 2001, p. 167). Premorbid somatic
and mental symptoms often associated with post-
concussive syndrome also were minimized in a
longitudinal study of athletes, some of whom sus-
tained concussions while participating in inter-
collegiate athletics (Ferguson et al., 1999).
Ferguson et al., who characterized this observa-
tion as the “good old days” phenomenon, repli-
cated some of the findings of other researchers
(Hilsabeck, Gouvier & Bolter, 1998; Mittenberg
et al., 1992). Symptomatic patients after mild TBI
reported fewer premorbid symptoms than did
normal controls (Gunstad & Suhr, 2001;
Mittenberg et al., 1992). The same observation
was made of people in litigation claiming head-
injury symptoms (Lees-Haley, Williams, &
English, 1996). Denial of well-documented preex-
isting problems has been documented in striking
fashion in patients after motor vehicle accidents
(MVAs) with axial pain complaints (Carragee,
2008). The accuracy of past medical, psychologi-
cal, and substance abuse histories provided by
335 patients from five spine specialist clinics
was compared with pre-MVA records (Don &
Carragee, 2009). About 50% of the patients over-
all who denied pre-MVA axial pain problems
actually had preexisting axial pain documented in
medical records. Although denial of documented
preexisting problems occurred in patients who
judged the MVA to either be their fault or no one’s
fault, the rate of denial of preexisting pain was
twice as high in patients who blamed the MVA on
another party. In this study, substance abuse,
psychological problems, and drug and alcohol
abuse were considered relevant comorbid condi-
tions; about 75% of the participants had comorbid
conditions documented in preexisting records
that they denied when providing past medical
histories after the MVAs. In summary, patients,
litigants, and people in a position to become
litigants are poor historians and minimize the
reports of premorbid problems.
Not only is past mental health and medical
history incorrectly reported in, on the average, a
minimizing direction, but current mental health
problems sometimes are denied. In one investiga-
tion, volunteer participants completed self-report
ratings of psychiatric symptoms and were rated by
an expert on mental health through use of the
Early Memory Test (Shedler, Mayman, & Manis,
1993). This test was blindly scored by the expert
based on qualitative factors such as self-represen-
tation, affective tone, coherence of narrative, and
presence of internal contradictions. Some partici-
pants were classified as reporting illusory mental
health because they were abnormal on the Early
Memory Test and normal on self-report (Shedler
et al., 1993).
Cognitive behavioral theorists have provided
partial explanation for the phenomenon of illu-
sory mental health. Anxiety is conceptualized as
comprising three loosely coupled response sys-
tems of overt behavior, verbal report, and physio-
logical activation (Lang & Cuthbert, 1984). People
often experience stressors physiologically or
respond behaviorally without reporting or experi-
encing a cognitive component of the anxiety; they
feel anxious but are unable to verbalize what is
making them anxious (Barlow, 2000). Many
patients with medically unexplained symptoms
deny psychopathology, but often the medically
unexplained somatic or neurological symptoms
coexist with emotional complaints (Cragar et al.,
2002; Henningsen et al., 2003; Rief & Broadbent,
2007).
LY I N G A N D E X A G G E R AT I O N
The preceding section discussed inaccurate
reporting of mental health and medical history
without respect to the intentionality of the inac-
curate reporting. This section considers lying,
the intentional distortion of information, and
 Forensic Assessment of Medically Unexplained Symptoms
exaggeration of history. Mental health experts
generally are not permitted to testify in court
regarding the credibility of people whom they
have examined, an issue that is determined only
by the trier of fact. Despite this evidentiary restric-
tion, experts may choose how much weight to
give to reports by examinees regarding pre-injury
and post-injury history, including educational
and occupational attainments, medical history,
symptoms, and limitations. An expert should give
less weight to improbable statements by an exam-
inee, and statements that cannot be verified are
less probable if they are given by a person who is
known to have been inaccurate or deceptive about
other aspects of her/his history. Therefore,
attention should be paid to inconsistencies and
misstatements, some of which could be lies.
Some people, usually males, exaggerate ath-
letic or military exploits. Some well-publicized
incidents of resume padding by public figures
provide examples. An Oregon Congressman, Wes
Cooley, lost his seat in the U.S. House of Repre-
sentatives in the 1990s after it was discovered that
his claim of military service in the Korean War
was false. Cooley also made false claims about
motorcycle racing success. A manager of the
Toronto Blue Jays baseball team, Tim Johnson,
was fired after falsely claiming combat experience
in Vietnam; and a University of Notre Dame foot-
ball head coach, George O’Leary, was terminated
when it was discovered that he exaggerated his
football playing experience and education.
Patients also occasionally exaggerate past
experiences. A woman undergoing intensive EEG
monitoring for diagnosis of medically intractable
seizures reported onset of the seizures while serv-
ing in an intelligence unit in Vietnam when her
jeep struck a land mine, overturning her jeep and
causing a cerebral concussion. She was applying
for VA benefits for an alleged disability. Her
service record indicated that she had not served
in Vietnam, and the EEG monitoring led to a
diagnosis of nonepileptic seizures. A book has
been written about exaggeration of Vietnam War
combat exploits (Burkett & Whitley, 1998). One
examinee made grandiose claims about his base-
ball playing prowess despite an obvious physical
deformity to his throwing arm that he reported
occurred in an accident during adolescence.
Another examinee with cerebral palsy reported
that he had been a high school football star. People
who are untruthful about their past may not be
truthful about their symptoms, time of onset, or
symptoms in relation to a potentially financially
351
compensable incident such as an accident, or their
past medical history.
Level of education is related to premorbid and
post-injury neuropsychological performance.
Whenever possible, self-reported educational
attainment should be checked in forensic cases.
If transcripts are not available, they should be
requested. If one cannot obtain a transcript, some
colleges (Johnson-Greene & Binder, 1995) and
high schools may verify by telephone attendance
and attainment of degrees and diplomas. One
nonforensic patient reported that he had received
a degree from the Illinois Institute of Technology.
A phone call to this university revealed no record
of his attendance. When asked why he made a
false report, he replied, “Because it’s a good
school.” The same patient with cerebral palsy who
reported that he was a football star also claimed
that he had graduated from college. The univer-
sity in question had no record of his attendance.
Grades obtained in high school sometimes are
exaggerated in forensic cases (Greiffenstein, Baker,
& Johnson-Greene, 2002), underscoring the
need to review school records rather than rely on
self-report.
Medical history sometimes is underreported
to such an extreme that one must question if
the underreporting is deliberate. Whether mini-
mization of relevant prior problems was inten-
tional or not was not directly assessed in the axial
pain study summarized above (Don & Carragee,
2009), but I would infer that many of the partici-
pants were lying. Patients who felt the MVA was
another party’s fault often did not report history
of axial pain problems even when they had
received spinal imaging, pain injections, and, in a
few cases, invasive procedures for pain. As an
example from my practice, a woman with chronic
pain had not received any treatment for an alleged
injury at work until 20 days had elapsed, when she
made a single emergency department visit and
then received no additional treatment for another
five months. Her work-related disability began
seven months after her alleged injury. Her degree
of disability was disproportionate to the degree of
injury and the medical findings. She failed to
provide details to multiple examiners about two
separate, similar, financially compensable injuries
within the past ten years.
Psychotherapy notes of treatment prior to a
mild head injury, when they are available, some-
times reveal many more sessions of treatment and
much more serious psychopathology than
reported by the examinee. Such distortions may
352 forensic neuropsychology
be deliberate attempts to maximize the financial
recovery from litigation, but they also could result
from a general tendency to distort past episodes
of emotional problems (Coyne et al., 2001).
I M PA C T O F D I S T O R T I O N
O F M E D I C A L H I S T O RY
Data suggest that people who deny psychological
problems, that is, people whose psychological
defenses do not allow them to recognize their
problems, are at risk for medical illnesses because
their defenses are associated with increased auto-
nomic reactivity. Shedler et al. (1993) found that
participants classified in the illusory mental health
group showed greater coronary maximal and
mean reactivity than participants in either the
subjectively distressed or genuinely healthy
groups. Furthermore, in the group with illusory
mental health, the lower the self-rating of psy-
chological problems, the greater the coronary
reactivity.
There is limited experimental evidence that
people with medically unexplained disorders also
can be classified as experiencing illusory mental
health. In one study, fibromyalgia patients were
experimentally presented with emotionally pro-
vocative images. These patients reacted more
physiologically while acknowledging less affective
change than control subjects (Brosschot & Aarsse,
2001). In this study the fibromyalgia patients were
both highly anxious and highly defensive, and
tended to attribute their physiological responses
to somatic rather than psychological causes.
In a series of studies, Pennebaker and col-
leagues showed that inhibition of thoughts and
emotions was associated with increased auto-
nomic nervous system activity in the short term
and that inhibition of emotions in the long term
served as a cumulative stressor that increased the
probability of psychosomatic disease. Their data
also indicated that not discussing an emotional
trauma was a harmful form of inhibition. Adults
who reported in a questionnaire that they had
been subjected to childhood trauma or who
suffered recent trauma were more likely to have
suffered health problems within the past year
(Pennebaker & Susman, 1988). Another survey
examined the health effects of a recent, sudden
death of a spouse. The more respondents talked
about the death of a spouse, the fewer health prob-
lems they suffered in the following year. However,
the more they simply ruminated about the death
without talking about it, the more health prob-
lems they suffered (Pennebaker & Susman, 1988).
Undergraduates who had the opportunity to
write about past emotional trauma experienced a
significant drop in visits to the student health
center, even when compared with students who
wrote about the facts of the trauma without
writing about the associated emotions (Smyth,
1998). In a similar study of the effect of trauma
writing, sexual offenders incarcerated for treat-
ment decreased health care visits after a trauma
writing exercise (Richards, Beal, Seagal, &
Pennebaker, 2000). Writing about emotions led to
a beneficial effect in short-term measures of
immune system functioning, including circulat-
ing total lymphocytes and CD4 (helper) T lym-
phocyte levels. Thought suppression was harmful
for short-term immune system functioning as
measured by CD3 T lymphocyte levels (Petrie,
Booth, & Pennebaker, 1998). Difficulty expressing
feelings was associated with increased somatic
complaints (Kirmayer & Robbins, 1993).
Studies summarized in the preceding sections
demonstrate that people tend to underreport past
events including stressors, episodes of medical
and mental problems, and treatment for those
problems. Traumatic events, whether encountered
during childhood or during adulthood, can cause
serious medical and mental health problems.
These events also can mediate effects which lead
to social disruptions and somatic or psychological
problems. The medical and mental effects of
trauma can be reduced through disclosure and
emotional processing, but disclosure and emo-
tional processing frequently do not occur. In the
next section the implications of these findings for
the assessment of medically unexplained disor-
ders is discussed.
AS SES SMENT OF
M E D I C A L LY U N E X P L A I N E D
S Y M P TO M S
Conversion disorder in the form of nonepileptic
seizures is an excellent model of a pseudoneuro-
logical condition often associated with inaccurate
self-report of psychiatric symptoms and history.
Intensive EEG monitoring and neuroimaging
data rule out or make unlikely a diagnosis of
epilepsy or other neurological explanations for
the seizures. Data reviewed above indicate that
patients with nonepileptic seizures generally have
neuropsychological abnormalities.
There are two observations about patients
with nonepileptic seizures relevant to the present
discussion. First, even after careful evaluation,
the majority of these patients do not receive any
 Forensic Assessment of Medically Unexplained Symptoms
psychiatric diagnosis other than conversion
disorder (Alper, Devinsky, Perrine, Vazquez, &
Luciano, 1995). This observation is extraordinary.
Despite high levels of disability, despite frequently
having a poor prognosis (Ettinger, Devinsky,
Weisbrot, Ramakrishna, & Goyal, 1999), and
despite the truly bizarre nature of their symptoms,
many of these patients neither demonstrate nor
report any psychopathology other than their
seizures. The extreme nature of the symptom of
nonepileptic seizures surely indicates underlying
psychopathology, but this psychopathology often
cannot be detected because it is not acknowl-
edged. Anecdotally, some of these patients deny
existing, clear-cut psychiatric history, including
hospitalizations and suicide attempts.
Second, consistent with the fact that some of
these patients receive a psychiatric diagnosis only
of conversion disorder, the mean MMPI-2 profiles
of this population show a Conversion V (Binder
et al., 1994; Brown et al., 1991; Wilkus et al., 1984).
The highest MMPI-2 elevations in the mean pro-
file, by a wide margin, are on scales HS and HY.
The mean profile is less severely elevated on scales
measuring symptoms of depression and anxiety.
The conventional interpretation of a MMPI-2
Conversion V profile (Greene, 2000) is that the
person uses physical symptoms as a form of psy-
chological defense against the experience and
source of psychological distress. Graham (1990, p.
90) described this profile as indicating persons
who “present themselves as normal, responsible,
and without fault. . . . They prefer medical expla-
nations for their symptoms, and they lack insight
into psychological factors underlying their prob-
lems . . . they do not show appropriate concern
about their symptoms and problems.”
It is likely that the lessons of nonepileptic sei-
zure patients with conversion disorders apply, at
least in some cases, to other types of medically
unexplained disorders. Some studies of people
with fibromyalgia and CFS and other similar con-
ditions show increased rate of psychiatric prob-
lems, especially anxiety and mood disorders, prior
to the onset of their illness (Black, 2000; Walker,
Keegan, Gardner, Sullivan, Katon, & Bernstein,
1997). Furthermore, many people with medically
unexplained somatic symptoms concurrently
have psychiatric complaints (Rief & Broadbent,
2007). However, many people with these condi-
tions do not report either mental health treatment
or significant episodes of psychiatric disorder
prior to the onset of their illnesses, and they do
not necessarily report unusual psychological
353
traumas during childhood or adulthood
(Staudenmayer, 1996). There also is evidence that
some people with these disorders both overreact
to stressors and deny their anxiety (Brosschot &
Aarsse, 2001), that is, they lack insight into their
current psychological experience.
It is hypothesized that denial and lack of
insight about past and present psychological
stressors and current problems occurs commonly
in people with medically unexplained disorders
(Staudenmayer, 1996). What many people
with medically unexplained symptoms do not
know, or what they do not report to health care
professionals, are the very things that might be
hurting them. This hypothesis is consistent with
the evidence reviewed above and is testable
through large scale, longitudinal investigations.
For example, people with documented history of
childhood abuse (Widom & Morris, 1997) or
other social upheavals (Henry et al., 1994) could
be assessed for relatively common conditions such
as fibromyalgia and chronic fatigue. It is hypoth-
esized that participants subjected to childhood
traumas will suffer a higher lifetime prevalence of
medically unexplained disorders, especially if
they do not disclose or have not emotionally
processed the childhood traumatic events that
were reported earlier. The psychological or psy-
chophysiological pathogen may be less severe
than a history of childhood sexual or physical
abuse, for example, a neurophysiological predis-
position towards intolerance of ordinary stressors,
a trait that can be measured (Barlow, 2000;
Davidson, 2000). People with this trait could be
followed longitudinally and their prevalence of
medically unexplained symptoms could be com-
pared with the prevalence in people without a
high degree of neurophysiological reactivity to
ordinary stressors.
Patients with medically unexplained disorders
also are heterogeneous with respect to reports of
emotional problems and often report depression
or anxiety (Rief & Broadbent, 2007), with similar
findings among patients with psychogenic
seizures (Cragar, Berry, Fakhoury, et al., 2002).
Patients with emotional complaints can be
expected to be more likely to seek mental health
treatment.
I M P L I C AT I O N S F O R
FORENSIC PRACTICE
Mental health professionals, including neuro-
psychologists, can perform the most accurate
assessment when they have access to mental
354 forensic neuropsychology
health and medical records from the past
(Coyne et al., 2001). Denial of past mental illness
may not be accurate. Moreover, the life events that
may have been most damaging to the mental
health of the patient being examined may be the
very events not reported to the clinician, despite
careful inquiry. Records sometimes reveal that the
same stressful life events that were denied to
the current examiner were acknowledged to pre-
vious examiners. Anecdotal evidence suggests
that childhood traumatic events sometimes are
initially denied and later acknowledged to the
same clinician. Asking about a history of psycho-
logical traumas in multiple ways or waiting
until the examinee is more at ease may increase
the probability that the patient will provide accu-
rate information. People with medically unex-
plained symptoms should be asked about history
of possible childhood and adulthood stressors
and traumas, according to the International
Consensus Group on Depression and Anxiety
(Ballenger, Davidson, Lecrubier, et al., 2004).
Although actual childhood abuse may be denied
in adulthood (Widom & Morris, 1997), such his-
tory may not be obtained unless the clinician asks.
History of childhood abuse is not inevitably asso-
ciated with medically unexplained symptoms,
however (Raphael, Widom, & Lange, 2001). The
effect of childhood trauma on adult mental and
physical health is variable. Stressors in adulthood
may be poorly tolerated in people with history of
adverse childhood experiences only if they also
have a history of more recent adult stressors
(Stewart, Petrie, Balfour, et al., 2004).
Studies reviewed here also have implications
specifically for neuropsychological practice. Many
people with these disorders have mild neuropsy-
chological abnormalities (Binder et al., 2001;
DiPino & Kane, 1996; Grace et al., 1999, Hart
et al., 2000; Tiersky et al., 1997) that do not neces-
sarily signify the presence of neurological disease,
at least not the way neurological disease currently
is defined. Evidence reviewed above clearly indi-
cates that brain chemistry can be altered by psy-
chological traumas. There also is some support for
the hypothesis that brain structures may be altered
by psychological traumas. These findings blur the
distinctions between “organic” and “psychiatric”
illnesses.
Cognitive abnormalities are nonspecific.
Their presence does not necessarily signify the
presence of neurological disease or injury (Bolla,
2000). Cognitive abnormalities may be caused
by the considerable natural variability in human
performance (Binder, Iverson, & Brooks, 2009).
In a neuropsychological test battery, the average
normal person will have a few abnormal scores.
Low scores also are caused by developmental learn-
ing disabilities (O’Donnell, Kurtz, & Ramanaiah,
1983; Selz & Reitan, 1979), or by attention deficit
disorder (Fischer, Barkley, Edelbrock, & Smallish,
1990). Neuropsychological impairments are asso-
ciated with certain personality disorders, depres-
sion, substance abuse (Gonzalez, Vassileva, &
Scott, 2009; Rourke & Grant, 2009), and other psy-
chiatric disorders (Johnson & Magaro, 1987; Judd
& Ruff, 1993; O’Leary, Brouwers, Gardner, &
Cowdry, 1991). As reviewed elsewhere in this
volume, neuropsychological testing must include
assessment of effort because suboptimal motiva-
tion in some samples of patients with medically
unexplained symptoms is common (Gervais et al.,
2001; Suhr, 2003), including some cases with no
identified external incentives (Kemp, Coughlan,
Rowbottom, et al., 2008).
Assuming that cognitive abnormalities
resulted from a valid examination of mental abili-
ties, the neuropsychologist can assist the patient
in various ways, such as documenting the find-
ings, measuring the extent of the cognitive prob-
lem, suggesting means of coping with the deficits,
and recommending and implementing therapy.
However, when evaluating patients with medi-
cally unexplained disorders such as fibromyalgia,
MCS, toxic mold syndrome, or chronic fatigue
syndrome, it should not be assumed that the
presence of cognitive abnormalities signifies the
presence of a traditionally defined neurological
disease affecting the brain.
A history of medically unexplained symptoms
or illness provides an explanation for mild
cognitive deficits that may be more compelling
than a potentially compensable condition such
as mild head injury or alleged toxic exposure.
The cognitive deficits in information processing
speed, attention, and memory associated with
illnesses such as chronic fatigue and fibromyalgia
are strikingly similar to the deficits that some
authors ascribe to late post-concussive syndrome
(Larrabee, this volume) and neurotoxicity (Bolla,
this volume).
Sensible treatment recommendations can
be made despite some uncertainty about the
possible multifactorial etiology of these condi-
tions. Cognitive behavioral therapy, sometimes in
combination with exercise, has been effective for
fibromyalgia (Burckhardt, 2002), chronic fatigue
syndrome (Afari & Buchwald, 2003; Friedberg &
 Forensic Assessment of Medically Unexplained Symptoms
Jason, 2001; Raine, Haines, Sensky, et al., 2002),
multiple chemical sensitivities (Staudenmayer,
1996), Gulf War illnesses (Donta, Clauw, Engel,
et al., 2003), and health anxiety (Taylor &
Asmundson, 2004). Clinicians should recom-
mend exercise in some form. Clearly, negative
expectancies play a role for many people with
these ill-defined conditions (Dalton, 1999; Deary
et al., 2007; Moss-Morris et al., 1995; Taylor &
Asmundson, 2004). The classically conditioned
responses of multiple chemical sensitivities may
be treated with extinction, that is, repeated
presentation of the odor without illness (Van den
Bergh et al., 2001). This behavior therapy proba-
bly requires medical input.
The presence of a medically unexplained
disorder, coupled with subjective cognitive
complaints, provides a rationale for a neuro-
psychological evaluation. The evaluation should
include an in-depth psychological assessment.
The not-always-attainable goal of such an
assessment is to provide a psychological explana-
tion for the physical symptoms, and to determine
what treatment might be helpful. Among the
psychological assessment questions that should
be answered, whenever possible, are the follow-
ing: Is a mood disorder present? Is an anxiety
disorder present? Has there been sufficient
emotional trauma to cause PTSD or post-
traumatic stress symptoms? Is post-traumatic
stress present? Is there secondary gain or illness
behavior in the form of financial incentives or
social/familial attention? If one of these condi-
tions is identified, how should it be treated?
Psychological problems in the absence of clear
physical disease or injury are often the most par-
simonious explanations for neuropsychological
symptoms.
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 14
Something to Talk About?
The Status of Post-traumatic Stress Disorder
in Clinical Neuropsychology
J I M A N D R I K O P O U L O S A N D M A N F R E D F. G R E I F F E N S T E I N
“No diagnosis in the history of American
psychiatry has had a more dramatic and perva-
sive impact on law and social justice than post-
traumatic stress disorder” (Stone, 1993, p. 23).
Clinical and forensic neuropsychologists may
react with puzzlement to a new but more frequent
referral question: “Patient/claimant states they
cannot work because of post-traumatic stress
disorder. Please conduct neuropsychological
testing to verify diagnosis.” The perplexed response
is understandable, for the question contains tacit
assumptions at odds with the traditional role of
neuropsychology. First, neuropsychologists typi-
cally evaluate prospects for cognitive and func-
tional residuals of confirmed brain dysfunction
(e.g., definite stroke) or strongly suspected
dysfunction (e.g., dementia). The referral ques-
tion, however, implies a neurological basis, either
structural or physiological, that is reliably associ-
ated with post-traumatic stress disorder (PTSD).
Second, neuropsychologists evaluate patients
whose leading features are cognitive in nature,
even if there is no prior evidence to suspect
clinical brain damage. PTSD’s cardinal signs,
however, involve lingering and irrational fear
reactivity, not core cognitive complaints. Third,
the question assumes neuropsychological testing
has incremental validity, that it has attained
greater accuracy in diagnosis of PTSD than tradi-
tional psychometric and clinical methods.
However, most of the literature on PTSD diagno-
sis and research relies on history, interview, obser-
vation, and personality tests.
The begging of multiple questions leads back
to the unanswered one: Does professional and
scientific clinical neuropsychology have a basis to
inform PTSD diagnosis, treatment, theory, and
research in a manner that justifies a specific
neuropsychology referral? Or does neuropsy-
chological assessment only inform cognate issues
and not central ones? These questions give prece-
dence to the title for this chapter: “Something to
Talk About?”
Neuropsychology delving into PTSD might
presumably contribute something to the dialogue
of what has been a controversial clinical entity
from the start. The PTSD controversy has had a
greater impact upon the mental health field than
the mild head injury (MHI) controversy has had
in clinical neuropsychology.
G E N E R A L C O N S I D E R AT I O N S
There are some self-imposed limitations to the
scope of this chapter. First, the discussion will be
limited to adults. Second, the focus is on civilian
PTSD, with a cursory discussion of combat
PTSD to help illustrate some points and explain
the history of the disorder. Because a large por-
tion of the PTSD literature comes from the
veteran population, it deserves more space then
available in this chapter, but a distinction must be
made to illustrate the poor generalization from
military to civilian patients. In their meta-analysis
of PTSD risk factors, Brewin, Andrews, and
Valentine (2000, p. 729) summarize the literature:
“This distinction represents the single largest and
most important division in the literature on the
prediction of PTSD, and it accounted [sic] for
the greatest number of significant moderator
variables.”
There are many factors that severely limit
generalization from a military sample to civilian
allegations of PTSD (Horner & Hamner, 2002).
First, female gender is a risk for civilian PTSD
(Brewin et al., 2000), but the veteran PTSD
366 forensic neuropsychology
population is overwhelmingly male. Second, the
medicolegal aspects of PTSD within the
Department of Veteran Affairs (VA) compensa-
tion system also differ in that the burden of
proof is lower than in civil litigation. Per a recent
directive, the VA is “amending its adjudication
regulations regarding service connection for
PTSD by eliminating the requirement of evidence
corroborating occurrence of the claimed in-
service stressor in claims in which PTSD is diag-
nosed in service” (Department of Veterans Affairs,
2008, p. 64208). Third, medical and psychiatric
conditions that arise out of military service are
compensable for the remainder of the veteran’s
life; consequently a noncompensation PTSD
sample cannot be formed within the VA, which
makes it difficult to validate symptom validity
tests (SVTs) to use in civilian studies.
There are other methodological issues the
reader should be aware of in examining the neuro-
psychology and PTSD literature. Studies in which
patients are recruited via newspapers, advertise-
ments, or similar means (e.g., undergraduate
students reporting “traumas”) and diagnosed with
PTSD are not easily generalizable. As an example,
Stein, Kennedy, and Twamley (2002) adminis-
tered a broad range of common neuropsycholo-
gical tests in addition to a well-validated structured
interview for PTSD. They reported no cognitive
group effects between trauma-exposed patients
with PTSD, without PTSD, and normal controls
on tests of verbal memory, but significant differ-
ences in nonverbal cognitive tasks. Stein et al.’s
(2002) findings are the reverse of what most
researchers report in military studies. Bottom
line: The study differs because the sample was
recruited via posted advertisements and personal
contacts among treatment centers specializing
in domestic violence. It was not a consecutive
clinical sample of treatment-seekers.
Our discussion recognizes there is a near
absence of PTSD known-groups studies (com-
pensable versus noncompensable patient groups
in which malingering is operationally defined),
unlike the MHI literature in which MHI litigants
are compared to more severely head-injured
nonlitigants. While there is no shortage of epide-
miological and clinical studies of civilian PTSD
arising from rape, terrorism, and other traumas,
finding a large sample of civilians claiming PTSD
with detailed psychological and SVT assessment
as well as known litigation status is rare. Most psy-
chologists, let alone neuropsychologists, do not
have access to both litigating and nonlitigating
PTSD samples, which are important for
developing classification studies of legitimate
versus invalid presentations of PTSD. Instead,
simulation groups are used. In the present chap-
ter, we only review a few simulation studies in any
detail, as the results of these types of investiga-
tions may not be generalizable to clinical practice.
For example, in a “Cry for Help” MMPI-2 analog
investigation, all ten basic clinical scales were
elevated when the psychiatric outpatient sample
was asked to take the test a second time under
Cry for Help instructions (Berry et al., 1996). It is
uncommon for a patient exaggerating psychiatric
symptoms to have elevations on all ten scales.
To remedy the absence of known-groups
studies, we offer as an alternative the application
of a concept borrowed from the forensic neuro-
psychology literature. One procedure for the
detection of malingered cognitive dysfunction is
the level of impairment method. This is also
referred to as the floor effect strategy (Backhaus,
Fichtenberg, & Hanks, 2004), or the dose response
relationship method (Bianchini, Curtis, & Greve,
2006). This procedure involves a comparison of a
person’s score on a cognitive test to the average
score of individuals who are markedly impaired
as established by unequivocal medical evidence
of a brain injury (i.e., coma, abnormal imaging
studies, or neurological examination), or those
who have a more severe injury as reflected in a
worse Glasgow Coma Scale (GCS). This level of
impairment method can also be applied to psy-
chological tests. In our proposed operationaliza-
tion the severity of PTSD as measured by
standardized tests or interviews arising from a
minor motor vehicle accident (MVA) should not
be at the same level or exceed that of a person
who might be the victim of rape. Until more
civilian malingering studies using a known-
groups design appear in the PTSD literature, the
level of impairment method remains one of
the easiest, most intuitive (especially to a jury),
and straightforward methods for assessing malin-
gered PTSD. Most neuropsychologists that are
assessment focused are more likely to be exposed
to PTSD patients within an independent medical
evaluation (IME) context. Although not ideal,
the level of impairment method can be applied
within one’s own practice-specific sample of
litigants. Those with operationally defined severe
stressors or traumas (e.g., traumatic amputation,
demonstrable bodily injury or witnessing a death,
etc.) can be compared to those with everyday
stressors.

PTSD DEFINED
“Saving PTSD from itself in DSM-V” (Spitzer,
First, & Wakefield, 2007, p. 233).
Posttraumatic stress disorder is widely viewed
as a persistent anxiety disorder temporally linked
with a life-threatening event. It is also widely
agreed that the core features are re-experiencing
the trauma (in nightmares, flashbacks, or exces-
sive rumination), and numbing (emotional under-
reactivity). Depending on what definition is used,
other symptoms used in PTSD diagnosis are
nonspecific, meaning they overlap with other
anxiety disorders or conditions. These nonspecific
features include avoidance (also seen in phobia,
generalized anxiety disorder, and personality dis-
orders), insomnia, poor concentration, restricted
range of affect (depression, normal reactivity
style, and medications), proto-emotions such as
irritability, and hypervigilance (paranoid features
and general anxiety, antisocial and narcissistic
personality disorders).
Table 14.1 summarizes the Diagnostic and
Statistical Manual-IV-Text Revision (DSM-
IV-TR) criteria for PTSD (American Psychiatric
Association, 2000). There are three important
points about the DSM-IV-TR criteria. First, the
status of Criterion A as a “gatekeeper” is critical:
Both prongs (A-1 and A-2) must be met confi-
dently before even applying the symptom criteria
(B-D). A person involved in a potentially life-
threatening event (e.g., high speed car accident)
who acts calmly (by self-report and/or ER records)
does not meet Criterion A-2 and hence cannot be
diagnosed with PTSD. Conversely, a person who
reacts with horror and panic to a single harsh crit-
icism at work (possibly meets A-2 by self-report)
cannot meet A-1 (life-threatening event). Second,
a common mistake is to make a “presumptive
PTSD diagnosis” based on the mere fact of an
accident, assault, crime, or other event (meets
only A-1). The base rates for PTSD (to be dis-
cussed in depth below) make clear that posttrau-
matic resiliency is the rule and PTSD is the
exception in traumas where the only incentive is
primary gain (reducing distress). Third, individual
symptoms must be linked to the trauma and not
merely present. Complaining of hypervigilance is
insufficient to meet D-4. Hypervigilance for a spe-
cific situation naturally resembling the trauma
must be present.
The current criteria contain two controversies,
relevant to the clinical neuropsychologist, that
Something to Talk About? 367
were introduced in previous editions of the DSM.
The first was the inclusion in DSM-III of “delayed”
PTSD, whereby symptoms can appear six months
or more after the trauma (American Psychiatric
Association, 1980). This is relevant because neu-
ropsychologists first see such patients long after
traumas. The concept of delayed PTSD is a nullifi-
cation of the principle that trauma, physical or
psychological, should have a statute of limitations;
it should appear within a reasonable time proxi-
mate to the event. The second controversy con-
cerned expanding the definition of trauma. In
DSM-III events outside the experience of the
majority of people such as combat, rape, torture,
and similar traumas were required. In DSM-III-R
this gatekeeper threshold was loosened to include
more commonplace events (American Psychiatric
Association, 1987). Both of these controversies
will be discussed later.
H I S T O R I C A L C O N T E X T,
THE DSM, AND THE
C O N T ROV E R S I E S
“The concept of PTSD took off like a rocket,
and in ways that had not initially been antici-
pated” (Andreasen, 2004, p. 1322).
An older and experienced clinician may dis-
cover that they have to contend with disorders
that were infrequent at the time of their training.
The appearance of new psychological disorders
can indicate an advance in clinical science, new
adaptive challenges from an altered environment,
or an environmental sociopolitical change. If,
however, a disorder exists at time A, disappears
from the nomenclature at time B, only to reappear
under a different name at time C, one would at the
very least have to consider the validity of the diag-
nosis. If the same societal circumstance dictated
its emergence and re-emergence at times A and C
respectively, it is reasonable to weigh the role of
political factors in diagnostic validity.
In 1952, the first Diagnostic & Statistical
Manual (DSM) posited the diagnostic category of
“Gross Stress Reaction” in which the stressor was
to be coded as either due to combat or a civilian
catastrophe (e.g., fire, earthquake, explosion)
(American Psychiatric Association, 1952).
Of particular note is the statement, “If the reac-
tion persists, this term is to be regarded as a tem-
porary diagnosis to be used only until a more
definitive diagnosis is established,” (p. 40). There
are two implications to this statement that came
368 forensic neuropsychology

TABLE 14.1 * DSMIVTR CRITERIA FOR POSTTRAUMATIC STRESS DISORDER

A. The person has been exposed to a traumatic event in which both of the following were present:
1) the person experienced, witnessed, or was confronted with an event or events that involved actual or
threatened death or serious injury, or a threat to the physical integrity of self or others
2) the person’s response involved intense fear, helplessness, or horror
B. The traumatic event is persistently reexperienced in one (or more) of the following ways:
1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions
2) recurrent distressing dreams of the event
3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience,
illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or
when intoxicated)
4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an
aspect of the traumatic event
5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of
the traumatic event
C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present
before the trauma), as indicated by three (or more) of the following:
1) efforts to avoid thoughts, feelings, or conversations associated with the trauma
2) efforts to avoid activities, places, or people that arouse recollections of the trauma
3) inability to recall an important aspect of the trauma
4) markedly diminished interest or participation in significant activities
5) feeling of detachment or estrangement from others
6) restricted range of affect (e.g., unable to have loving feelings)
7) sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal
life span)
D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the
following:
1) difficulty falling or staying asleep
2) irritability or outbursts of anger
3) difficulty concentrating
4) hypervigilance
5) exaggerated startle response
E. Duration of the disturbance (symptoms in Criteria B, C, and D) is more than 1 month.
F. The disturbance causes clinically significant distress or impairment in social, occupational, or other important
areas of functioning.
Specify if:
Acute: if duration of symptoms is less than 3 months
Chronic: if duration of symptoms is 3 months or more
With Delayed Onset: if onset of symptoms is at least 6 months after the stressor

* modified from the DSM-IV-TR

to dominate the future debate on PTSD: First, a
chronic form of this condition was not reliably
observed in the years after World War II combat
operations ended, and second, in the event
that symptoms persisted, alternative diagnostic
categories within DSM were more likely to
capture their nature. There was no basis for creat-
ing a new diagnostic category. Nancy Andreasen,
the “midwife at the birth of PTSD” recounts the
history (Andreasen, 2004). For unknown reasons,
gross stress reaction was dropped in DSM-II
(American Psychiatric Association, 1968).

Andreasen, a psychiatrist studying the psychiatric
consequences of severe burns in the early 1970s
was called upon by Robert Spitzer, the Chairperson
of the DSM Task Force for the upcoming DSM-III
to assist in addressing the psychological conse-
quences of the returning Vietnam veteran
(American Psychiatric Association, 1980). At the
time, an active group of Vietnam veterans and
academicians vigorously lobbied to have the diag-
nosis of “post-Vietnam syndrome” included in the
DSM-III. Realizing this would exclude noncom-
bat trauma, they instead coined the term “post-
traumatic stress disorder” for which Andreasen
wrote the entire text description based on her
work with burn victims.
Forensic neuropsychologists should not only
be aware of the medicolegal DSM-related implica-
tions of PTSD, but also the controversies outside
the legal context. The reader is referred to two
texts. Young (1995) in his book The Harmony of
Illusions: Inventing Post-traumatic Stress Disorder
outlines this controversial history. While PTSD is
real, the facts that surround its invention are the
topic of his book. It was the anti-war mental health
professionals, the most prominent of which were
Robert Jay Lifton and Sarah Haley, who helped to
push the newly coined construct into the psychi-
atric nomenclature. In a second, more clinically
oriented text, PTSD researcher Brewin (2003)
addresses the “malady or myth” of PTSD. The
arguments of the “skeptics” are that PTSD need-
lessly medicalizes normal human reaction to
trauma, is not clearly distinct from existing
psychiatric disorders, and its invention has no
historical parallel.
EPIDEMIOLOGICAL STUDIES
“The full syndrome as defined by the DSM-III
was common only in veterans wounded in
Vietnam” (Helzer, Robins, & McEvoy, 1987,
p. 1630).
Here we consider the prevalence of PTSD via
a review of the best clinical studies using popula-
tions that have been through horrific events. Four
well-done epidemiological studies about truly
traumatic events are remarkably consistent in
their conclusions on the prevalence of PTSD.
Approximately 30% of individuals experiencing
events rarely seen by most people will develop
PTSD: 34.9% of Ugandan and Congolese child
soldiers (Bayer, Klasen, & Adam, 2007), 31% of
victims in the Paris terrorist bombings of the mid
Something to Talk About? 369
1990s (Verger et al., 2004), 34.3% of the victims of
the Oklahoma City bombing (North et al., 1999),
and 24.8% of survivors of the Rwanda genocide
(Pham, Weinstein, & Longman, 2004). These are
individuals with direct experience of the trau-
matic event. For individuals that might circu-
itously be affected by an act, the prevalence of
PTSD is cut by a third. The prevalence of probable
PTSD following the attacks of September 11 in
the New York metropolitan area was 11.2% in the
two months following the attacks (Schlenger
et al., 2002). This could be an overestimate as the
method used was a self-report measure of PTSD
versus a clinical interview. This includes persons
claiming PTSD from having watched the attacks
on television. Some remain understandably skep-
tical about the possibility of developing PTSD
from watching television: “virtual PTSD”
(McNally & Breslau, 2008). Using a DSM-based
interview module, the rate is closer to 7.5% one
month after the attacks and 0.6% at six months
(Galea et al., 2003). Using the level of impairment
method, the psychological consequences of the
above traumatic events can now be compared
against more commonplace events such as a
minor MVA that the patient reports resulted in
PTSD.
A second group of epidemiological studies
that need to be reviewed are the population-based
studies along with the conceptual arguments for
modification of the A criteria. These arguments
provided the rationale and background for remov-
ing the DSM-III requirement that the stressor or
event be outside the realm of normal human
experience. This criterion was weakened but still
present in DSM-III-R, and omitted completely in
DSM-IV (American Psychiatric Association,
1994). This has served to broaden the types of
events that could potentially lead to a diagnosis of
PTSD. Not unexpectedly, it is the view of some
that the decision to broaden Criterion A needs to
be reconsidered (Andreasen, 2004). We share this
view.
Shortly before the “outside the realm of usual
human experience” criterion was removed from
the DSM-IV, two prominent PTSD researchers
made some observations that arguably make a
case for the weakening of the stressor criterion
including a) defining “unusualness” in regard to
the event is difficult as it varies based on the sub-
jective perspective of not only the patient, but the
clinician; b) events still within the experience of
most persons can be distressing and cause the
syndrome (citing divorce and job loss); c) since
370 forensic neuropsychology
even the most extreme levels of stress may not
always lead to PTSD, it must be something in or
about the person’s perception of the stressor that
may be relevant (Davidson & Foa, 1991). The
step-wise process of expanding PTSD beyond the
Vietnam veteran (for whom it was intended) was
termed “conceptual bracket creep” by Harvard
psychologist Richard McNally (2003). This means
that Criterion A, requiring that the event be out-
side the realm of everyday experience, became
increasingly diluted and captured more patients
with each edition of DSM.
An early paper by PTSD epidemiologist Naomi
Breslau convincingly argues that there was very
little empirical evidence for the validity of PTSD
as a distinct clinical entity in DSM-III (Breslau &
Davis, 1987). There is no literature to support the
view that a discrete class of stressors increases the
probability of developing a psychiatric disorder.
They concluded:
Extraordinary stressors are like more ordinary
stressful events with respect to their complex
differential effects upon individuals. Personal
characteristics and the nature of the social
environment modify the likelihood and form
of the response of individuals to all types of
stressors. (p. 255).
Breslau followed this with an epidemiological
study of young adults from the Detroit, Michigan
area. The lifetime prevalence of exposure to trau-
matic events was 39.1%. The rate of PTSD in those
who were exposed was 23.6%, yielding lifetime
prevalence in the sample of 9.2% (Breslau, Davis,
Andreski, & Peterson, 1991). This set the stage for
the argument that “traumatic events” are not
uncommon in the general population and can
produce PTSD. This viewpoint was codified in the
most often cited PTSD epidemiological study, the
National Comorbidity Survey, which was the first
nationally representative mental health survey in
the United States to use a fully structured DSM-
III-R diagnostic interview (Kessler, Somnega,
Bromet, Hughes, & Nelson, 1995). They con-
cluded that PTSD is more prevalent than previ-
ously believed, and that “virtually all qualifying
events for PTSD are quite common, and that none
is such that virtually everyone exposed to it devel-
ops PTSD” (p. 1057). Breslau and Kessler (2001)
were to later investigate the stressor criterion.
Nineteen events were used to operationalize the
A-1 criterion resulting in a 59% increase in the
number of events that can be used to diagnose
PTSD. With this loosening of the criteria, “almost
everyone has experienced a PTSD-level event”
(p. 703).
We conclude with a discussion of demographic
risk factors associated with the development of
PTSD. Two meta-analytic studies have identified
these factors. In the first, Brewin et al. (2000)
identified 14 risk factors. Trauma severity, lack of
social support, and life stress conveyed the largest
risk of developing PTSD. This is followed by:
adverse childhood events, low intelligence, low
SES, childhood abuse, female gender, family and
personal psychiatric history, a previous trauma,
lack of education, younger age, and minority
status. When excluding military studies, low intel-
ligence and younger age at onset were no longer
risk factors. What merits mention, and perhaps is
not coincidental, is that many of these variables
can be viewed as predictors of litigation. In a later
meta-analysis, a different approach was used
(Ozer, Best, Lipsey, & Weiss, 2008). Trauma sever-
ity was not studied as a predictor because, by
definition, a stressor is required for the diagnosis.
They found that peritraumatic dissociation and
emotional responses, perceived support, and
perceived life threat were the highest predictors
while prior trauma, prior adjustment, and family
psychiatric history were all equal predictors.
THE NEUROBIOLOGY
OF PTSD
“Now we know much about the neurobiology
of PTSD: So what?” (Figley, 2010).
A fundamental question is “Does stress cause
brain damage?” A brief review of structural imag-
ing literature may provide answers. The integrity
of the human hippocampus plays a major role in
clinical neuropsychology and in recent PTSD
scholarship as well. The role of the hippocampus
in recent memory is so well established that it
does not need review in this chapter, but its role
in stress physiology does require review. It is
generally accepted that stress hormones, such as
corticosteroids, are transiently suppressive of
hippocampal function (McEwen, 1999). These
facts lead naturally to the question whether PTSD
is associated with structural changes in the hip-
pocampus, and much literature arose around the
question.
Bremner et al. (1995) conducted the first study
to analyze hippocampal volume in persons with
PTSD. Twenty-six Vietnam PTSD-disordered and

22 nondisordered veterans, matched for demo-
graphic characteristics, underwent MRI, and right
hippocampal volume was significantly smaller by
8% relative to controls. There was no difference in
the volume of other brain regions. Surprisingly,
Wechsler Memory Scale verbal subtest scores
were correlated with smaller right hippocampal
volume in PTSD patients only. This study trig-
gered many follow-up studies, and fed a prema-
ture belief that PTSD was an organic brain
syndrome.
Subsequent neuroimaging studies showed
widely varied and contradictory results, and none
replicated Bremner et al.’s (1995) findings. Gurvits,
Shenton, Hokama, and Ohta (1996) used MRI
with a small PTSD sample (seven with PTSD and
eight without PTSD), and reported both left and
right hippocampi were significantly smaller in the
combat PTSD group, and hippocampal volume
was directly correlated with self-reported combat
exposure. Bonne et al. (2001) conducted a pro-
spective study of hippocampus volume in recent
trauma survivors who developed PTSD (N = 37).
The patients with PTSD did not differ from trauma
survivors without PTSD in hippocampal volume,
right or left, at one-week and half-year follow-ups,
and there was no volume reduction over time.
Villareal et al. (2002) assessed both hippocampal
and whole brain volume in civilian PTSD, finding
lower left hippocampal volume and lower white
matter/intracranial volume ratios, consistent with
generalized white matter atrophy. Hedges et al.
(2003), in a pilot study with only four examinees,
showed bilateral hippocampal volumes were sig-
nificantly smaller in post-traumatic stress disor-
der subjects. Vermetten, Vythilingam, Southwick,
Charney, and Bremner (2003) found smaller hip-
pocampi that normalized after treatment with
paroxetine. Jatzko et al. (2006) looked for long
term changes fifteen years post-trauma in chronic
PTSD patients: Neither conventional volumetry
nor morphometry detected any differences in
hippocampus volume or structure. Weniger,
Lange, Sachsse, and Irle (2008) examined the
caudality of hippocampal volume. They found
significantly smaller posterior hippocampi in
PTSD, with no difference in the volumes of
anterior hippocampus or subiculum. There were
also no volume differences between PTSD result-
ing from prolonged childhood abuse compared to
single adult-trauma exposure.
Correlation does not equal causation, and
some investigators examined prospects that hip-
pocampal volume differences predated trauma
Something to Talk About? 371
exposure. Gilberston et al. (2002) examined sev-
enteen monozygotic twins discordant for
Vietnam-era combat exposure. Hippocampal
MRI data showed smaller hippocampal volume in
combat-experienced twins with more severe
PTSD symptoms, but the noncombat probands
also exhibited smaller hippocampal volume. The
data supported the notion that smaller hip-
pocampi in PTSD represented a preexisting con-
dition.
Pitman et al. (2006) also studied twins; the
index cases were PTSD and the probands unex-
posed to combat. Both index cases and probands
showed increased neurological soft signs, dimin-
ished hippocampal volume, and presence of
abnormal cavum septum pellucidum.
A more exhaustive review of the neurobiology
of PTSD is beyond the scope of this chapter. Three
chapters in the edited text by Vasterling and
Brewin (2005), devoted to the biology of PTSD,
are recommended. The neurobiology of PTSD is
discussed throughout the current chapter when
clinically applicable, and more specifically as it
might apply to the forensic arena. The work of
McNally (2006) is especially insightful.
Part of the reluctance in avoiding an extensive
basic science discussion has to do with how this
might be translated into clinical practice. The
impasse facing the field of translational research is
that much of what is learned in the laboratory
does not always transfer to the clinic in a way that
is clinically meaningful (Figley, 2010). For exam-
ple, in a PTSD study of MVA patients with and
without PTSD, EEG asymmetry was demon-
strated. Activation of the right anterior and poste-
rior regions during exposure to trauma-related
pictures was seen. After treatment, there was a
reduction of right-sided anterior activation (Rabe,
Beauducel, Zoolner, Maercker, & Karl, 2006). The
common method for measuring psychophysio-
logical reactivity related to PTSD has been the
script-imagery paradigm (McNally, 2006). The
physiologic reactivity of the patient being rem-
inded of the event is said to provide indirect proof
of PTSD. Keane et al. (1998) conducted the largest
study on the physiological concomitants of PTSD.
Vietnam veterans were exposed to audiovisual
presentations of combat. The results of heart rate,
skin conductance, and EMG findings identified
75% of veterans with and without PTSD. Abnormal
physiological reactivity has been shown in patients
with PTSD following MVA in the Albany Motor
Vehicle Project (Blanchard et al., 1996a). Such
a differential response between the PTSD and
372 forensic neuropsychology
non-PTSD patients would indirectly suggest the
presence of the disorder independent of patient
self-report.
Does this biological response support the
diagnosis of PTSD? In an imaginative experiment,
skin conductance, heart rate, and EMG response
of the left lateral frontalis were measured in
persons claiming to be abducted by aliens. Those
reporting the most negative alien experiences
(versus those with neutral or positive experiences)
had the greatest reactivity on all three physio-
logical measures (McNally et al., 2004). The reac-
tivity reactions of these subjects to the audio
recordings of their abduction were at least as great
as the findings in the Keane study. According
to McNally (2006), “Reactivity, however, is not
specific for PTSD; rather, it is specific for emo-
tionally evocative memories, whether true or
false” (p. 273).
T H E M OTO R V E H I C L E
ACCIDENT & PTSD
“Giving the same diagnosis to death camp
survivors and someone who has been in a
motor vehicle accident diminishes the magni-
tude of the stressor and the significance of
PTSD” (Andreasen, 2004, 1321).
Can a MVA in which no serious injury is sus-
tained cause PTSD? Unless “severe motor auto-
mobile accidents” are experienced, as noted in the
DSM-IV-TR, developing PTSD is improbable.
Furthermore, if the DSM-III requirement that the
event be outside the realm of everyday human
experience is considered, many MVAs would not
qualify. The best literature employs a prospective
cohort methodology. Using this methodology,
PTSD is rare following a MVA. The studies below
are chosen because they represent the best epide-
miological investigations; they are prospective,
assess consecutively admitted hospital patients,
and use structured clinical interviews.
In one early study, 107 patients were examined
an average of 28 months after an accident. Only
one patient had PTSD (Malt, 1988). In another
series (N=106) comprised exclusively of patients
sustaining severe life-threatening injuries (60%
from MVA), 1.9% had PTSD at one year (Schnyder,
Moergeli, Trentz, Klaghofer, & Buddeberg, 2001).
Of 100 consecutive MVA admissions to an inten-
sive care unit, 8% had PTSD four to six weeks
post-injury (Matsuoka et al., 2008). At one year,
only 2.5% (N=208) had PTSD in another study
(Wrenger, Lange, Langer, Heuft, & Burgmer,
2008). Presumably, the likelihood of PTSD would
be higher if a person were to witness an injury of
a family member in that same accident. In a study
addressing PTSD in 68 children, no father had
PTSD one year following the accident and 5.7% of
the mothers did (Landolt, Vollrath, Timm,
Gnhem, & Sennhouser, 2005).
Deviation from sound study design can result
in gross overestimates of PTSD and affect the
validity of clinical beliefs. The earliest and largest
body of work on the psychological consequences
of MVA is the Albany Motor Vehicle Accident
Project, summarized in the book After the Crash,
by Blanchard and Hickling (2004). The problem
in their approach was the use of a self-selected
sample. Participants comprised a combination
of paid volunteers recruited via newspapers
ads and treatment seekers; over half were in
litigation. The subjects (N=161) were seen an
average of 11 months following their MVA.
Of these, 68% had PTSD and a mean Clinician
Administered PTSD Scale (CAPS) (Weathers
et al., 2004) in the severe range (mean score of
72). Given the obvious external incentive of their
patient sample, the long post-accident duration,
and the high severity of symptom report in a
majority, one would think that symptom validity
should require some minimum level of scrutiny,
which is a basic tenet of forensic psychology.
Blanchard and Hickling, however, dismissed any
prospect that malingering could corrupt the data.
They state, a) “We made no effort to check the
veracity of participants’ reports but found no
obvious reason to doubt them…We had no
instances for which we felt we had been misled”
(p. 197); b) “In our larger sample of more than 400
participants, only two participants had been iden-
tified as having faked or exaggerated their symp-
toms” (p. 243); c) “We do not routinely use the
MMPI-2 or other tests that might add validity
measures or tests of malingering to the assess-
ment” (p. 246); d) “We did not collect medical
records on our patients” (p. 247); e) “Initially,
participants were asked if they contacted a
lawyer; if they answered affirmatively, they were
scored as involved in litigation” (p.186). This last
point requires elaboration, as it is an overlooked
issue in malingering research.
When forming compensation- and noncom-
pensation-seeking samples, the statement of the
patient that they have not retained an attorney
does not define compensation status or potential
compensability. If, for example, a patient waiting

at a stop sign is rear-ended, their claim of not
being involved in litigation at the time of evalua-
tion is no guarantee that this will not occur in the
future. It is naïve to accept at face value the
patient’s denial of litigation if the circumstances of
the injury clearly indicate that it is compensable.
Litigation status should be defined by whether the
injury is compensable (someone can be held
accountable) versus noncompensable (e.g.,
occurred in one’s home, single car accidents, car
accidents where the patient is at fault, or sports
injuries), and not by the involvement of an attor-
ney. Consequently, when a study describes a clini-
cally referred, symptomatic, noncompensable
MHI sample, one has to question how that group
was formed. In the experience of the authors, such
clinical referrals are very rare (Andrikopoulos,
2001; Greiffenstein, Baker, & Gola, 1994).
A second large series of studies comes from
Bryant and colleagues from the University of New
South Wales in Australia. While their methodol-
ogy is sounder than the Albany studies, the PTSD
prevalence rates in their two earliest prospective
studies are unexpectedly high and remarkably
consistent with approximately 25% of patients
suffering from PTSD (Bryant & Harvey, 1998;
Harvey & Bryant, 1998). One of these studies
involved an MHI sample suffering from PTSD
(a topic that will be discussed more in depth
below). Notable by its absence in these two studies
is any discussion of the possibility that litigation
may play some role. Even within the Bryant and
Albany MVA Project studies, in the infrequent
instances where litigation was a variable of inter-
est, it predicted PTSD status (Blanchard et al.,
1996b; Blanchard et al., 1998; Bryant & Harvey,
1995; Bryant & Harvey, 2003). Finally, using the
level of impairment method outlined above, the
PTSD prevalence rate in the Bryant studies
exceeds that of patients with more serious MVA
(Schnyder et al., 2001; Matsuoka et al, 2008), and
equals or approaches the PTSD rates of the child
soldier and Rwanda studies (Bayer et al., 2007;
Pham et al., 2004).
A third group of studies comes from the
University of Oxford and provides lower base
rates. The earliest and best of these studies assessed
188 consecutive patients and found that 11% met
the DSM-III criteria for PTSD one-year post-
injury (Mayou, Bryant, & Duthie, 1993). Litigation
status was not addressed. Ehlers, Mayou, and
Bryant (1998) assessed a larger consecutive series
(N=781) using a PTSD questionnaire (versus a
semi-structured interview) and found a higher
Something to Talk About? 373
prevalence rate of 16.5% at one year. In this study
they did find that PTSD was three times more
common in litigants (24.6%) versus nonlitigants
(8.1%).
H E A D I N J U RY A N D P T S D
“Late-appearing dual diagnosis is a litigation
phenomenon so intertwined with secondary
gain as to be a byproduct of it” (Greiffenstein &
Baker, 2008, p. 565).
The medicolegal implications of MHI and
PTSD are well known. It goes without saying
that the synergistic effect of combining both dis-
orders in one patient can appear, at least on the
surface, a challenging assessment to perform. The
task has been made more seemingly onerous of
late by the emergence of two developments. The
first of these is the concern over the cognitive
effects of blast injury, the so called “signature
wound” of the Iraq and Afghanistan conflicts
(Bhattacharjee, 2008). The MHI and cognitive
impairment that is said to result from the blast is
coupled with the traumatic events of combat that
can also lead to PTSD (Hoge et al., 2008). A dis-
cussion of blast injury is beyond the scope of this
chapter. The reader is referred to the mild head
injury chapter by Larrabee in this text.
Suffice it to say that if blast injury alone
(without consideration of more traditional indi-
cators such as the GCS and post-traumatic amne-
sia) were accepted as a mechanism of action for
head injury, our conceptualization of head injury
and how it has been studied for decades would
have to change. We believe that there is no evi-
dence that this mechanism of injury provides any
incremental clinical information above and
beyond the traditional measures that predict
head injury outcome (primarily the GCS). This
development has served to popularize an impres-
sion that untangling the effects of a head injury
from the symptoms of PTSD can be difficult
(Bryant, 2008). This is a misrepresentation. A
post-concussive syndrome and PTSD are two
wholly separate clinical entities. The core features
that define each can and should be partitioned.
While one can argue that head-injured and PTSD
patients both have memory, attention, and emo-
tional problems, one can also point to schizo-
phrenics who also have such problems. A clinician
would not confuse the core symptoms of schi-
zophrenia with the post-concussive symptoms
of MHI.
374 forensic neuropsychology
In tandem with these developments is the
concern over the effects of sports concussion, with
some suggesting that repeated traumas can
result in an encephalopathy (Omalu et al., 2005).
The best evidence from the sport concussion
literature shows that following a single concus-
sion, cognitive function returns to baseline in a
week (McCrea et al., 2003). The evidence that
repeated concussions can produce an encephal-
opathy came initially from a handful of neuro-
pathological case studies in which there is an
absence of clinical data to corroborate the neuro-
pathology (Omalu et al., 2005, 2006). The con-
cepts of chronic traumatic encephalopathy and
blast injury have served to promulgate and extend
a debate in the absence of any data. These issues
are further discussed in the chapter on MHI in
the current volume.
Applying the same methodology (prospective,
consecutively examined hospital admissions,
knowledge of litigation status, and a standardized
DSM PTSD diagnosis) that we applied to the
examination of the prevalence of PTSD following
MVA to the co-occurrence of PTSD and MHI, we
find that the two conditions infrequently occur
simultaneously. The largest MHI/PTSD data set
produced to date comes from a recent publication
of Bryant et al. (2009). Using the American
Congress of Rehabilitation Medicine (1993) defi-
nition of MHI, they examined 425 patients with
MHI and 532 without MHI at three months post-
injury, using the CAPS. At follow-up, 11.8% of the
MHI group had PTSD, and 7.5% of the non-MHI
group had PTSD. Once the severity of the injury
was controlled for, they concluded that PTSD is
more likely to occur in those with MHI. The MHI
group also had a higher CAPS severity score at
follow-up (19.83 for MHI and 16.9 for the non-
MHI group). The advantage of the study is that it
provides a reasonable prevalence rate and CAPS
data on a group of moderately physically injured
patients (mean of 12 days in hospital) upon which
the clinician can rely to apply the level of impair-
ment method. The CAPS score of the whole
sample falls into the lowest CAPS severity range
of minimal symptoms. No neuropsychological
testing was conducted to confirm that those iden-
tified as having had a MHI actually had one that
resulted in any impairment, although impairment
at three months post uncomplicated MHI is
unlikely (see Larrabee chapter in the present
volume). Longer post-traumatic amnesia (PTA)
was associated with less severe intrusive memo-
ries at the acute assessment, suggesting that
PTA appears to be protective against selected
re-experiencing symptoms.
A prospective study by Dikmen and colleagues
of head injuries of varying severity yielded
a similar prevalence rate of as many as 11%
(N=125) meeting symptom criteria at any
point during the six months following the
injury, with only 5.6% meeting the full criteria at
six months (Bombardier et al., 2006). Another
prospective study (N=69) revealed 13% prevalence
at three months post injury (Levin et al., 2001). A
similar prevalence rate of 14% (N=122) was
observed at six months (Gil, Caspi, Ben-Ari,
Koren, & Klein, 2005). None of the above studies
relied on SVT or reported on litigation status.
In the one study that reported litigation status,
Koren, Arnon, and Klein (1999) noted that 100%
of the PTSD group was in litigation and 97% of
the non-PTSD group, because all Israeli citizens
are entitled to compensation. The implication is
that even when the trauma is compensable, the
co-occurrence of mild brain injury and PTSD is
uncommon.
Notwithstanding the well-done epidemiologi-
cal study of Bryant et al. (2009), the debate regard-
ing the relationship between MHI and PTSD
arose primarily from earlier studies by Bryant and
colleagues that addressed both conditions in the
same patient. Again, similar to the Bryant studies
which addressed only PTSD, the prevalence of
PTSD in head-injury patients was similarly high
(about 25%) and litigation status is not mentioned
(Bryant & Harvey, 1999; Bryant, Marosszeky,
Crooks, & Gurka, 2000), including in literature
reviews (Bryant, 2001).
In the studies mentioned above, for those that
address the presence of a comorbid MHI in the
context of PTSD, none take into account the base
rate of malingering following MHI (Mittenberg,
Patton, Canyock, & Condit, 2002), which averages
around 40% (see chapter 5 this volume). The topic
of malingering, which occupies the largest share
of current neuropsychological research, is over-
looked (Sweet, King, Malina, Bergman, &
Simmons, 2002). While some of the well-designed
studies above answer important epidemiological
questions with regard to PTSD and head injury,
only in clinical samples can the issue of litigation
and malingering be addressed, provided that the
question is asked.
A final issue regarding the relationship
between head injury and PTSD merits mention. It
has been debated whether one can develop PTSD
in the context of a head injury that results in a loss

of consciousness and/or post-traumatic amnesia,
since there is no “witnessing” of the traumatic
event. The earliest study to address this issue
within a medicolegal context convincingly
argues that the two disorders do not coexist
(Sbordone & Liter, 1995). The method employed
to detect PTSD may not be acceptable from
a clinical/research standpoint, but within a medi-
colegal context it represents sound clinical
reasoning. Sbordone and Liter asked MHI and
PTSD litigants to volunteer their symptoms rather
than giving a PTSD interview or self-report
measure. The MHI group, 85% of whom reported
a loss of consciousness, did not volunteer any
of the symptoms that are specific to PTSD (e.g.,
nightmares, hypervigilance, avoidance, intrusive
recollections, etc.). This mostly theoretical
issue of the relationship between PTSD and
loss of consciousness is partially unnecessary
since the real issues are if cognitive impairment
can arise from a single uncomplicated head
injury, and if PTSD can be seen following a minor
MVA. In the event that a patient reports amnesia
from a MHI and post-traumatic symptoms,
what is the likelihood that malingering will be
present?
Greiffenstein and Baker (2008) examined the
coexistence of PTSD symptoms and MHI in
litigants. They formed a dual diagnosis group
(N = 95) composed of patients claiming both
amnesia secondary to the head injury and re-
experiencing symptoms of PTSD, and a sub-
syndromal group (N=228) consisting of those
with avoidance and hyperarousal without the re-
experiencing symptoms. The remaining patients
(N=476) had no PTSD symptoms and were desig-
nated as the late post-concussive syndrome
group. The validity measures employed included
finger tapping, grip strength, the Test of Memory
Malingering (TOMM), MMPI-2 Symptom Validity
Scale (FBS) raw score and F T-score, and Reliable
Digit Span. Using two separate cutoffs based on
previous research to designate probable invalidity
(bottom tenth percentile) and definite invalidity
(≤1 percentile) they found a very high rate of non-
credible performance. The dual diagnosis group
failure rate ranged from 88% for the MMPI-2 FBS
to 25% for grip strength using the probable inva-
lidity rule. The definite rule failure rate was 49.5%
for the FBS to 1.1 percentile, respectively for grip
strength. The major finding is that those claiming
re-experiencing symptoms with amnesia have
incrementally higher failure rates on validity
indicators.
Something to Talk About? 375
“ D E L AY E D ” P T S D
“…PTSD—which advocates say can manifest
itself twenty years after the triggering inci-
dents—is political, not scientific” (Burkett &
Whitley, 1998, p. 232).
According to the DSM-IV-TR, delayed PTSD
refers to the presentation of PTSD after six months
have elapsed since the time of the traumatic event.
To understand the inherently illogical premise of
delayed PTSD, one needs only to draw a parallel
with the delayed symptom presentation often seen
in MHI litigants, even those seen clinically. The
first 100 MHI patients referred by 11 different
neurologists to the first author were seen approxi-
mately one year after the injury. These presumably
neurologically mediated symptoms may appear
closer to the trial or hearing date than to the actual
accident based on a medical record review. This
time lag is consistent with the MHI litigation lit-
erature. The decision to sue may occur to some-
one at some point after the accident. They are now
left with the difficult circumstance of having to
complain of symptoms that they had not reported
before. As the symptoms they are now complain-
ing of may be severe and presumably due to a
sudden neurological event, one is hard pressed to
explain why they have never reported these symp-
toms before. It would be analogous to seeing a
neurologist for the first time to report loss of sen-
sation for a stroke that occurred months or years
before. Such a sequence of events would make
little “neurological sense.” In the case of a MHI,
when the patient is eventually sent to the neurop-
sychologist, they understand that this person
assesses cognitive abilities and not physical
symptoms, which may be the only thing they
complained about since the injury. When the neu-
ropsychologist inquires about cognitive symp-
toms, the patient is put in a situation of deciding
whether to report such symptoms. Delayed PTSD
should be characterized in the same way.
The delayed onset subtype was introduced
as a by-product of the Vietnam War. The main
argument for the introduction of the term in
DSM-III was that the syndrome could emerge
long after the trauma. The initial intent of the
delayed onset type, at least as conceptualized by
Andreasen (2004), was that PTSD may not mani-
fest until the veteran returned home, since a stress
reaction in the course of combat is not adaptive.
What was not anticipated is that veterans may
file a PTSD claim at any time, often years after the
376 forensic neuropsychology
precipitating event. An early population-based
epidemiological study, done shortly after the
DSM-III was published, revealed that the delayed
PTSD was found only among Vietnam veterans
(Helzer et al., 1987). The preponderance of the evi-
dence since then indicates that PTSD symptoms
develop within hours or days of the trauma. For
those individual cases that are reported to have
had a delayed onset, it usually involves delayed
help-seeking or subsyndromic symptoms. A sys-
tematic review of the evidence has suggested that
the delayed onset of PTSD in the absence of previ-
ously unrecognized symptoms is rare (Andrews,
Brewin, Philpott, & Stewart, 2007). Not withstand-
ing any flawed literature that might support the
contention of delayed PTSD, it only stands to
reason that there would be no rational explanation
for why a person experiencing a truly horrific
event would be completely asymptomatic follow-
ing the event but symptomatic six months later.
MALINGERED PTSD
“It is rare to find a psychiatric diagnosis that
anyone wants to have, but PTSD seems to be
one of them” (Andreasen, 1995, p. 963).
Concerns about the ease with which PTSD
could be malingered began at the conclusion of
the Vietnam War. The earliest published report on
malingered combat PTSD in Vietnam veterans
came from Sparr and Pankratz (1983). Loren
Pankratz, a VA psychologist, arguably introduced
the forced choice method for the detection of
malingering to clinical psychology (Pankratz,
Fausti, & Peed, 1975). More has been written
about malingered combat PTSD than the civilian
variety. The compensable nature of the disorder
within the VA makes it a desirable diagnosis.
Prevalence of PTSD Malingering
According to the influential National Vietnam
Veterans Readjustment Study (NVVRS), 30.9% of
men (over 960,000) and 26.9% of women (over
1,900) have had PTSD at some point in their lives
(Kulka et al., 1990). When you include the
lifetime prevalence of partial PTSD, an additional
22.5% of male veterans and 21.2% of female
veterans have some symptoms of PTSD. This
would mean that 53.4% of the men and 48.1% of
the women have had clinically significant stress
reaction symptoms, out of 1.7 million veterans.
A more accurate but less influential study pre-
dated the publication of the NVVRS. The Vietnam
Experience Study indicated 2.2% of Vietnam
veterans had PTSD in the month preceding the
examination (Centers for Disease Control, 1988).
The cultural climate of the times dictated this
PTSD prevalence rate to be too low and the study
was disregarded. A partial vindication came from
a more accurate (but still high) reanalysis of the
NVVRS data presented in the journal Science,
putting the lifetime prevalence at 18.7% and cur-
rent PTSD at 9.1% (Dohrenwend et al., 2006). The
authors used military records to construct a
combat exposure measure and to cross-check that
with the diagnoses assigned to 260 veterans.
Burkett and Whitley (1998), in their often
cited book Stolen Valor, argue against such a high
prevalence of PTSD in the NVVRS. They estimate
that 75% of those receiving compensation for
PTSD do not have the disorder. The limitation of
the book, in scientific terms, is that Burkett and
Whitley selected cases already suspicious for
symptom over-statement; theirs is not a represen-
tative sample. To cure this, Frueh et al. (2005)
used the Freedom of Information Act to draw a
random sample of 100 files for veterans receiving
benefits for combat PTSD. Only 41% had clearly
been in combat. Assuming not all combat veter-
ans develop PTSD, a malingering base rate
of >41% is implied. Frueh et al. further reported
no statistical difference in the CAPS scores of the
combat (76) and no combat (79) groups, but the
unclear combat group had a statistically higher
score (94) than the other two groups. Scores in the
70s suggest severe PTSD and the 90s extreme
PTSD. The absence of combat exposure in concert
with the difficult-to-reconcile CAPS scores sug-
gests malingering. Test-specific methods are
needed to diagnose malingered PTSD. For now,
the methods that do exist are the same as those
found in the forensic neuropsychology literature.
PTSD-specific SVT is in its infancy.
Two observations regarding malingered PTSD
merit mention. First, the brief review above indi-
cates the literature on malingered PTSD is limited.
Second, the opening sentence of one malingering
review declares, “PTSD is easy to fake” (Knoll &
Resnick, 2006). There are few forensic reviews in
which this statement is not repeated. The cumula-
tive effect of these two observations might cause
one to conclude that the detection of malingered
PTSD is difficult. This is purportedly illustrated
by a simulation study in which 94% of naïve sub-
jects correctly identified PTSD symptoms on a
self-report measure (Burges & McMillan, 2001).
This nihilistic conclusion from the abstract does

not tell the whole story. Only one subject out of
134 was able to correctly volunteer enough
symptoms to meet the DSM criteria for PTSD.
When a second group of subjects were asked to
complete the same self-report measure, 16 non-
PTSD symptoms were added to the 17 PTSD
symptoms, and 5 of the 16 non-PTSD symptoms
were identified as PTSD symptoms by over 50% of
simulators. The purpose of the next section is to
dissuade the reader from the notion that PTSD is
easy to feign.
The MENT
Morel (1998) developed the only stand-alone
forced-choice test to assess malingered PTSD: the
Morel Emotional Numbing Test (MENT). This
test consists of three sets of 60 items in which the
patient is asked to match a facial expression (e.g.,
sad, happy, etc.) with the word that best describes
the face. The subject is told that the test measures
the ability to identify facial expressions and that in
some individuals with PTSD this ability is
impaired. In this initial validation study, Morel
reports an overall malingering hit rate of 95.6% in
a veteran population. In a second small veteran
study the MENT had a hit rate of 75.7% (Morel,
2008a). It appears, however, that these were neu-
ropsychological and not PTSD referrals. One
MENT validation study (Morel, 2008b) reported
on an eight-question response bias test, the Quick
Test for Posttraumatic Stress Disorder (Q-PTSD).
The Q-PTSD classified 81% of a veteran disability
claimant group as being credible or not credible
based on their MENT performance.
The first civilian study using the MENT in
conjunction with the Structured Inventory of
Malingered Symptomatology (Widows & Smith,
2005) and Word Memory Test (WMT) (Green,
2003) in 61 civilian PTSD claimants revealed that
40% failed the MENT, 51% the SIMS and WMT,
with 25% failing all three (Merten, Thies,
Schneider, & Stevens, 2009). In one other study
that included patients claiming recovered memo-
ries of childhood abuse, patients did no worse on
the MENT than those without such memories. All
participants scored beyond the cutoff for malin-
gering on the MENT. While all patients denied
litigation, it is not known who had PTSD, as this
was not assessed (Geraerts, Jelicic, & Mereckelbach,
2006).
The MENT requires further validation by
other researchers in civilians, using a known-
groups design. Two additional concerns are the
rationale behind the MENT and the test instruc-
Something to Talk About? 377
tions. The test relies solely on the forced choice
method with no clear rationale of why PTSD
patients should fail to recognize emotional
expressions; psychic numbing refers to an internal
poverty of emotions, not a failure to recognize
emotions in others. The MENT may be effective
only because of the response set induced in
the patient, that the test is sensitive to PTSD.
A further difficulty is methodological: A different
set of instructions was given to the PTSD patient
group (Morel, 1998). As for the Q-PTSD, no
information or other studies are available other
than the study cited above. There are equally lim-
ited data on other PTSD specific SVT measures.
DA P S
The Detailed Assessment of Posttraumatic
Stress (DAPS) is a 104-item self-report PTSD
instrument (Briere, 2001). An apparent advantage
of the DAPS, compared to other self-report mea-
sures, is the presence of a validity scale, the
Negative Bias Scale (NBS), to capture feigned
PTSD. The face validity of the items suggests
insensitivity to malingering. For example, it seems
improbable that a patient feigning PTSD would
endorse wanting to take their clothes off in public.
Demakis, Gervais, and Rohling (2008) studied
301 consecutively referred litigants seen for psy-
chological assessment that included the DAPS,
and both cognitive and psychological SVTs:
Computerized Assessment of Response Bias
(Allen, Conder, Green, & Cox, 1997), the WMT,
and trial 2 of the TOMM (Tombaugh, 1996). The
failure rates for the many SVTs ranged from 35%
(MMPI-FBS) to 4% (MMPI-F), with the DAPS
NBS failed by 25%. In all, 29% failed at least one
cognitive validity measure, and 49% failed at least
one psychological validity measure. A concern is
the heterogeneous sample of persons claiming
different forms of psychological disability, not just
PTSD. Further, the significance of different failure
rates for different SVTs is unclear, because the
litigating group was so mixed as to etiology.
No conclusions can be drawn about comparative
sensitivity of these measures.
TSI
One additional self-report instrument, the Trauma
Symptom Inventory (TSI) merits brief mention
for two reasons (Briere, 1995). First, it is the most
popular self-report instrument among self-desig-
nated “traumatologists” (Elhai, Gray, Kashdan, &
Franklin, 2005a) and has a response bias measure,
the Atypical Response (ATR) scale. The first ATR
378 forensic neuropsychology
validation study compared an outpatient sample
believed to show genuine PTSD (N=47) with 63
undergraduates simulators. The ATR classifica-
tion rate of 59% (Elhai et al., 2005b), was barely
above the sample base rate of 55% malingering
(only 4% incremental hits). Another study used
just simulation groups and found an overall hit
rate of 83% (Edens, Otto, Dwyer, 1998). A subse-
quent simulation study suggested that the ATR
cut score produced a high false positive rate
(Rosen et al., 2006). A PTSD combat study identi-
fied 19% of the TSI profiles as invalid based on the
recommended ATR cutoff. Only one profile was
identified based on the Inconsistent Response
scale of the TSI (Nye, Qualls, & Katzman, 2006).
Given, however, that the base rate for malingered
combat-PTSD may be over 50% (see earlier dis-
cussion of Frueh et al., 2005), the TSI appears
insufficiently sensitive when used in isolation.
In a final study an outpatient PTSD sample, a
remitted-trauma simulation group that was
coached to feign PTSD and an uncoached remit-
ted-trauma simulation group were compared
(Efendov, Sellbom, & Bagby 2008). Although the
ATR and FBS discriminated the uncoached simu-
lators from the outpatient PTSD sample, there
was no difference on the ATR between the coached
simulators and patient PTSD group. This implies
the ATR is better able to detect naïve fakers, but
not ones with better education in PTSD symp-
toms. The Infrequency scales of the MMPI-2
(F, FB and FP) were better than the FBS and ATR in
distinguishing coached from PTSD patients under
treatment. The limitation of the study was that the
PTSD patient group was workers’ compensation
claimants, some of whom may have been exagger-
ating despite best efforts to exclude malingerers, a
shortcoming acknowledged by the authors. The
reliance on financially motivated ex-workers as a
“genuine” PTSD group is a recurrent problem in
this literature (see also Bury & Bagby, 2002), espe-
cially given the vague nature of the industrial
traumas and the unchanged symptoms reported
years later. On the basis of these mixed findings
being derived from various samples and method-
ologies, and in the absence of known-groups stud-
ies, the TSI cannot be recommended. At most, the
above studies tell us the mean ATR scores of a
clinical sample (61.60 in Elhai et al. 2005b) and a
litigant sample (64.85 in Efendov et al. 2008)
“screened” for malingering are very similar, indi-
cating either the insensitivity of the ATR to magni-
fication, or the influence of secondary gain in a
putative “genuine” PTSD group. Elhai et al. (2005b)
summarized their views on the insensitivity of
the ATR: It is a general validity scale that is not
designed to detect malingered PTSD, and the TSI
is not tied to the DSM criteria.
Other Scales
The Miller-Forensic Assessment of Symptoms
(Miller, 2001) and the Structured Interview of
Reported Symptoms (SIRS) (Rogers, Bagby, &
Dickens, 1992) are two structured interviews
developed for the detection of malingering. There
are no known-groups studies using these instru-
ments in civilian PTSD litigants. However, one
PTSD veteran study suggested a 53% malingering
incidence rate, with a mean SIRS score of 89 and a
CAPS score of 87 (Freeman, Powell, & Kimbrell,
2008). In a recent simulation study, the SIRS was
administered to an inpatient “severe trauma”
sample (not necessarily with PTSD) under stan-
dard conditions and a volunteer group of feigners
(Rogers, Payne, Correa, Gillard, & Ross, 2009).
The SIRS false positive rate was unacceptably
high, but Rogers et al. developed a post hoc
Trauma Index from three SIRS scales, and this
reduced false positives.
T H E F O R E N S I C E VA L UAT I O N
“If mental illnesses were rated on the New York
Stock Exchange, PTSD would be a growth
stock to watch” (Lees-Haley, 1986, p. 17).
Unlike most other psychiatric diagnoses,
PTSD is “incident specific.” Valid diagnosis of
PTSD requires a concrete incident that presum-
ably precipitated the disorder. This makes PTSD a
“litigation friendly” diagnosis, because other
mental illnesses have multifactorial etiologies.
Because of the simplistic post hoc ergo propter hoc
nature of the diagnosis, the forensic examiner
must reach to other factors to better distinguish
between legitimate versus feigned PTSD, and
between PTSD and other non-PTSD psychiatric
disorders.
The Practice Guidelines from the International
Society for Traumatic Stress Studies (ISTSS)
provide some assessment recommendations that
go beyond the simple “after, therefore because
of ” reasoning (Foa, Keane, Friedman, & Cohen,
2008). The recommendations that appear most
practical in the forensic context are excerpted.
First and foremost, multiple measures and meth-
ods should be employed in assessing the PTSD
patient. A semi-structured interview should be

used. With generally unlimited time constraints
for an IME, the use of the CAPS is recommended.
DSM-IV-TR linked PTSD self-report measures
should complement the personality testing. The
MMPI-2 and Personality Assessment Inventory
(PAI) are offered as possibilities, and can be help-
ful in the differential diagnosis of non-PTSD psy-
chiatric disorders. Finally, malingering should be
assessed routinely in all clinical and research con-
texts and where the potential for malingering is
high, malingering-specific instruments should be
considered. While this may seem self-evident, the
assessment of malingering was not addressed in
the earlier ISTSS guideline (Foa, Keane, &
Friedman, 2000). The description of the forensic
evaluation is presented in the order of suggested
administration: cognitive and SVT, personality
testing, patient interview, self-report-instruments,
and the informant interview if the opportunity
presents itself.
Cognitive Function in PTSD
Issues regarding the neuropsychological etiology
or consequences of PTSD aside, PTSD, like any
other major psychiatric disorder, is frequently
accompanied by cognitive complaints. The typical
examination can be short (approximately 2½
hours) and include some neuropsychological
tests. This can be comprised of two tests per cog-
nitive domain, abbreviated intelligence testing,
and three or four SVT procedures that include the
embedded indicators and the preferred personal-
ity test. Some cognitive testing is justified for three
reasons. First, patients with PTSD may present
with subjective cognitive impairment, especially
concentration and attention problems associated
with putative heightened arousal. Second, objec-
tive cognitive measures are necessary to substan-
tiate these complaints, or assess any functional
impact of emotionality. Finally, cognitive testing
provides an opportunity to administer SVTs and
embedded measures of response bias (covered in
chapter 5 of this text). One might not expect
malingered cognitive impairment in PTSD claim-
ants, but persons who feign PTSD must also feign
functional disability. As an example, between 37%
and 60% of disability-seeking pain patients will
fail the TOMM, even though cognitive dysfunc-
tion is not at the core of pain complaints (Greve,
Etherton, Ord, Bianchini, & Curtis, 2009).
The literature on the cognitive correlates of
PTSD shares the same limitation as the MMPI-2
literature: The overwhelming majority of the
research is on veterans. In an article entitled
Something to Talk About? 379
“Questioning the link between PTSD and cogni-
tive dysfunction,” Danckwerts and Leathem
(2003) review the PTSD literature. Of the 15
studies they cite, only five are from civilian
populations, and two of those are from the same
sample. The authors warn about the generalizabil-
ity of the veteran data to the general population,
and conclude by arguing that a more sophisticated
neuropsychological approach that includes
imaging might answer the question. Although we
agree on the limitations of generalizability from
military samples and the utility of some neurop-
sychological measures, we are doubtful that
neuroimaging will add incremental validity.
Also, there is no reason to believe that neuropsy-
chological testing in PTSD (or any psychiatric
disorder) would serve the purpose of lesion local-
ization, because there is no “lesion” in PTSD.
Neuropsychological testing serves no other pur-
pose than to document the presence and severity
of functional cognitive impairment associated
with either an emotional disturbance or baseline
(pre-trauma) limitations.
Misguided attempts to “neurologize” psychia-
try have been encouraged by the advent of
advanced neuroimaging techniques. Early in the
era of functional imaging an interesting paper
titled “Frontal Lobology: Psychiatry’s New
Pseudoscience” illustrates this point (David,
1992). Many psychiatric disorders have been sub-
jected to the scanner. The modal conclusion for
most psychiatric disorders is that there is either
hypo- or hypermetabolism in the frontal lobes, or
in the cortical and subcortical connections with
occasional abnormality in the hippocampus.
There is virtually no psychiatric population (or
neurobehavioral disorder) in which the frontal
lobes have somehow not been implicated, and
PTSD is no exception (Francati, Vermetten, &
Bremner, 2007). In neuropsychology the measur-
ing of frontal lobe function can be viewed as a
second “g factor.” It is a ubiquitous phenomenon
applicable to all patients, the clinical implications
of which are sometimes unknown.
Next follows a brief review on the cognitive
correlates of PTSD diagnoses. Studies included
are those addressing the cognitive performance
of adults with civilian PTSD who are seeking
treatment, or who are prospectively enrolled. For
the review to be clinically meaningful, and in
order to apply the level of impairment method,
only studies employing commonly used neuro-
psychological tests with means and standard devi-
ations reported are included. Some of the studies
380 forensic neuropsychology
cited below contain a normal control group. Two
additional caveats are that some studies include
non-English-speaking patients, and that not all
studies used a reliable structured interview to
identify PTSD.
When a strict level of impairment analysis is
applied, the results of neuropsychologically based
studies support broad conclusions of nonspecific
differences between civilian groups with and
without PTSD. Findings include: PTSD patients
do worse than trauma patients without PTSD
(Jenkins, Langlais, Delis, & Cohen, 2000; Kivling-
boden & Sundbom, 2003; Yehuda, Golier,
Halligan, & Harvey, 2004); PTSD patients do
worse than trauma patients without PTSD on a
plurality to half of the tests (Johnsen,
Kanagaratnam, & Asbjørsen, 2008; LaGarde,
Doyon, & Brunet, 2010; Matsuo et al., 2003);
trauma patients without PTSD do not differ from
normal controls (Jenkins et al., 2000; Yehuda
et al., 2004); PTSD patients do worse than normal
controls (Bremner et al., 1995; Gil, Calev,
Greenberg, Kugelmass, & Lerer, 1990; LaGarde
et al., 2010; Yehuda et al., 2004); those with more
PTSD symptoms do worse than those with fewer
symptoms (Brandes et., 2002); and PTSD patients
do not differ from non-PTSD psychiatric patients
(Gil et al., 1990). Further, this general impairment
is relatively mild with low-average mean group
performances at worst.
Pattern analysis (comparison of cognitive
domains) shows the most commonly reported
relative weakness is on verbal memory and timed
attention measures (Vasterling & Brailey, 2005).
Other studies showed mixed results for visual
memory and visuocognitive function, and lower
IQ. But there has been no demonstration of speci-
ficity on neuropsychological measures in common
use: Despite the evidence suggesting greater cog-
nitive impairment in PTSD patients, overall gen-
eral impairment appears to be no greater than
other patients with mood and anxiety disorders.
The difference between PTSD and non-PTSD
groups is a statistical difference versus a clinically
meaningful difference. The implication is that
outright defective scores (greater than would be
seen by chance alone or falling two standard devi-
ations below the mean) should raise suspicion of
malingered impairment. While the suggested
level of impairment method is to compare the
PTSD claimant’s scores with those of the samples
above, another approach would be to use a well-
defined moderately to severely head-injured
group as the comparator (Dikmen, Machamer,
Winn, & Temkin, 1995). In other words, why
would a psychological trauma cause more severe
impairment than seen in patients with prolonged
coma and radiologically demonstrated structural
abnormalities in the brain?
We conclude this section with a discussion of
the most interesting cognitive finding that is of
heuristic and clinical value: premorbid cognitive
function as a predictor of PTSD. As clearly stated
by Vasterling and Brailey (2005), there is no good
reason to jump to the conclusion that psycholo-
gical trauma is the cause of mild cognitive deficits.
It is reasonable to consider that baseline cognitive
weaknesses are a risk factor for emotional distur-
bance. Some well-designed studies examined this
issue. A Vietnam Twin Registry study (2386 twins)
found a significant dose-response relationship
between precombat cognitive ability and risk for
PTSD (Kremen et al., 2007). After controlling for
confounders, veterans at the 75th percentile in
terms of cognitive ability had almost a 50% lower
risk of developing PTSD than those at the 25th
percentile. Twins without PTSD had the highest
cognitive scores, those twins where both had
PTSD had the lowest cognitive scores, and PTSD-
discordant pairs had intermediate scores.
Differences in precombat cognitive ability were
only evident in the dizygotic pairs discordant for
PTSD; the monozygotic pairs discordant for
PTSD did not differ on precombat cognitive abil-
ity. The authors concluded that pre-exposure cog-
nitive ability is a risk or a protective factor for
PTSD, and that the variance in PTSD explained
by pre-exposure cognitive ability is accounted for
entirely by common genetic factors.
Another informative Vietnam twin study
questions the conclusion that cognitive deficits
are attributable to PTSD (Gilbertson et al., 2006).
The study included monozygotic twin pairs in
which one brother served in combat (exposed)
and their twin brother did not (unexposed). Four
groups were formed: 19 veterans exposed to
combat with PTSD and their noncombat twin
without PTSD; 24 veterans exposed to combat
who did not develop PTSD and their noncombat
twin without PTSD. The main finding was no
difference in IQ between twin pairs regardless of
combat exposure, and that PTSD-diagnosed
combat veterans had lower IQ and cognitive
scores than non-PTSD veterans on verbal memory
and attention, but did not differ on visual memory
or spatial perception measures. The two implica-
tions are: (1) Cognitive capacity, as a familial trait,
influences risk for developing PTSD, and (2) none

of the cognitive impairments within the groups
rose to a level that might be considered clinically
significant. The only exception was perseverative
errors on the Wisconsin Card Sorting Test in
combat veterans with PTSD, but they did not
differ from their unexposed twins.
The Gilbertson et al. (2006) findings are
supported by a large epidemiological civilian
study following disastrous brush fires (Parslow &
Jorm, 2007). Through a fortunate coincidence, the
baseline cognitive abilities of all subjects had
already been assessed twice pre-disaster, as part of
a longitudinal study on cognition and mental ill-
ness. Those with higher PTSD symptoms showed
lower baseline scores on immediate and delayed
memory from the California Verbal Learning
Test, digit backwards, Symbol Digit Modalities,
and an estimate of verbal intelligence (Spot-the-
Word-Test). Additionally, while subjects showed
the expected improvement in cognitive function
from baseline to the second testing as a result of
practice effects, those reporting the most PTSD
symptoms showed significantly less improvement
on the California Verbal Learning Test during the
third wave of testing which occurred after the
fires. There is an inverse relationship between
premorbid cognitive function as measured three
years before the fires and the presence of PTSD
symptoms: The lower the premorbid cognitive
ability, the higher the risk for PTSD symptom
reporting. The finding of lower attention, process-
ing speed and verbal memory as a predictors
of PTSD is in line with the Brewin et al. (2000)
meta-analysis.
Minnesota Multiphasic Personality
Inventory-2
The gold standard for personality assessment in
forensic matters is the MMPI-2. It has the most
research, can show distinctive litigant profiles,
and has validity scales. Among litigants exagger-
ating neurological symptoms, the “somatic malin-
gering” profile, consisting of marked elevations in
the Hypocondriasis and Hysteria scales, has been
the most robust finding among the clinical scales
(Larrabee, 1998), while the FBS has been the best
measure of malingering among the validity scales
(Nelson, Hoelzle, Sweet, Arbisi, & Demakis,
2010). We will focus only on the MMPI-2. At the
time of this writing there are no published PTSD
studies on the MMPI-2-RF (Ben-Porath &
Tellegen, 2008).
The MMPI-2 PTSD literature contains a
number of limitations. The first is that there are
Something to Talk About? 381
few MMPI-2 studies on civilian PTSD, and much
less on PTSD litigants. In a literature review of the
original MMPI in PTSD patients, out of
21 studies, only three involved civilian popula-
tions; two involved patients in motor vehicle
accidents, some of who may have been litigants.
The 8–2 profile was the most common two-point
code (62%), but only in half of the studies did this
code-type differentiate the PTSD sample from
the non-PTSD psychiatric sample (Wise, 1996).
A second limitation is that the very robust somatic
malingering profile was meant to identify
pseudoneurological and not pseudopsychiatric
symptoms. In line with this argument, the FBS
cut-off for identifying neurological malingering is
much lower than for identifying psychiatric
malingering (see Greiffenstein, Fox, & Lees-Haley,
2007, for further discussion of the moderating
effects of psychiatric disturbance on the FBS).
Lees-Haley (1992) compared a “pseudo-PTSD”
sample (N=55) to a control group (N=64) who
were also litigants claiming to be psychologically
disabled. The main finding was that original FBS
cutoff proposed by the author of 20 was raised to
24 for men and 26 for women in the case of psy-
chological injury claims (Lees-Haley, English, &
Glenn, 1991). While the absence of a nonlitiga-
tion PTSD sample is problematic, the study illus-
trates the importance of adjusting the FBS to fit
the claimed injury. For example, an FBS score as
low as 21 may differentiate MHI litigants from
severely head-injured non-litigants (Larrabee,
2003; Ross, Millis, Krukowski, Putnam, & Adams,
2004). In contrast, the mean FBS score for 61
DSM diagnosed PTSD work injury claimants
all of whom were seeking or receiving workers’
compensation benefits was 26.31 (Bury & Bagby,
2002).
A third limitation is that many PTSD MMPI-2
studies are simulation studies. The limitations of
studies that employ this method (e.g., Bury &
Bagby, 2002) have been addressed (Greiffenstein
et al., 2004). Greiffenstein et al. (2004) formed a
probable post-traumatic stress group (Prob-PTS)
that was clinically referred, and an improbable
post-traumatic stress group (Imp-PTS) of liti-
gants. For the Prob-PTS group, their event was
outside the realm of usual human experience.
They were seen within five months of the event
rather than the “delayed PTSD” of the Imp-PTS
group seen two years post-event. This contrast
between groups is the strength of the study.
A third group consisted of litigants with old but
major traumas (Lit-MPTS). The mean FBS scores
382 forensic neuropsychology
of the Prob-PTS, Imp-PTS, and the Lit-MPTS
groups are 20, 28, and 24, respectively. A score of
30 or greater suggests a high probability of malin-
gering regardless of the base-rate level. The
F-family of scales was not sensitive (F, F(p), and
F-K) in differentiating the groups. A limitation
acknowledged by the authors is that the majority
of the Prob-PTS group sustained their injury in
the workplace, making it compensable despite the
denial of litigation. The absence of a structured
PTSD interview or self-report instrument is also a
limitation. It is not known which patients actually
met criteria for PTSD.
Aside from FBS, a general validity measure, a
PTSD-specific malingering scale has been identi-
fied. The Infrequency-Posttraumatic Stress
Disorder (Fptsd) scale was developed to identify
malingered PTSD (Elhai et al., 2002). The disad-
vantage of the scale is that it was initially devel-
oped on Vietnam veterans. The results are mixed
as to their applicability in civilian PTSD. In the
Elhai et al. (2004) study the Fptsd possessed incre-
mental validity beyond the traditional F-related
validity scales in discriminating malingered from
genuine PTSD. In a simulation study using college
students simulating PTSD and sexual abuse vic-
tims, the Fptsd demonstrated some incremental
validity over F but not over Fp. The authors con-
cluded that the Fptsd might be more appropriate
for combat PTSD
In addition to identifying malingered PTSD,
the MMPI-2 has been employed in identifying
PTSD. The 49-item MMPI PK scale was devel-
oped with Vietnam era veterans to identify PTSD
(Keane, Malloy, & Fairbank, 1984). The scale was
modified in the MMPI-2 by the elimination of
three items that were repeated in the original scale
but are now presented only once (Lyons & Keane,
1992). This resulted in a new recommended cutoff
for combat veterans of 28 instead of 30. The first
attempt to validate the PK scale in a civilian
sample compared two small PTSD samples: the
validation (N=18) and a cross-validation sample
(N=15) with a control sample of psychiatric
patients representative of a typical outpatient
practice (N=35). A cut score of 19 resulted in an
87% and 88% hit rate in the validation and cross-
validation samples, respectively (Koretzky & Peck,
1990). The scale correctly classified 80% of bat-
tered women with and without PTSD using a
cutoff of 22 (Perrin, Van Hasselt, & Hersen, 1997).
In a large study of outpatient treatment seeking
civilians, the PK scale did not identify acute PTSD
(hit rate 18%), was only moderately successful in
identifying chronic PTSD (42%), and identified
83% of panic disorder patients as true negatives
(Gaston, Brunet, Koszycki, & Bradwejn, 1996). Of
note is that the authors contend that no patient
was involved in litigation. The authors conclude
that clinical and forensic evaluations of PTSD
patients should not employ assessment proce-
dures that have been validated on Vietnam veter-
ans.
In a follow-up to the latter study, the same
group using the same sample subjected all the
MMPI items for analysis in an effort to create a
new scale that might identify acute and chronic
PTSD (Gaston, Brunet, Koszycki, & Bradwejn,
1998). A 32-item MMPI acute PTSD scale and a
41-item chronic PTSD scale were developed that
had a hit rate of 83% and 75% respectively in com-
parison to the panic disorder sample. The authors
listed the corresponding MMPI-2 items that make
up both scales. Of note was that only seven of the
items from the PK scale overlapped with the
chronic PTSD scale, and four items for the acute
PTSD scale, clearly supporting the earlier conten-
tion of the authors that combat PTSD is not gen-
eralizable to civilian PTSD (Gaston et al., 1996).
There appears to have been no attempt to replicate
these promising findings. In another civilian study
the PK scale failed to detect those with and with-
out PTSD. Unfortunately, the sample was seen in
the context of work-related psychological injuries
(Scheibe, Bagby, Miller, & Dorian, 2001). A review
by Lyons and Wheeler-Cox (1999), however, sug-
gests that while the MMPI-2 may be helpful in
distinguishing PTSD from those without a psy-
chiatric disorder, it does not do well in distin-
guishing PTSD from other psychiatric disorders.
The above mixed results would suggest that the
PK scale has limited value in ruling in PTSD due
to poor specificity; on the other hand, nonelevated
scores may be useful as one indicator of the
absence of PTSD.
In addition to the MMPI-2, the PAI has also
been recommended by the ISTSS guidelines. No
known-group designs using the PAI or the Millon
Clinical Multiaxial Personality Inventory-III
exist.
In summary, the FBS has most promise in
identifying malingered PTSD symptoms. Whether
the PK scale has any ability in identifying civilian
PTSD from non-PTSD conditions remains an
open question. Since the accepted standard pro-
cedure for identifying PTSD remains the inter-
view, the use of any MMPI-2 scale in the
identification of PTSD may very well be a moot

point, although absence of evidence for signifi-
cant problems with anxiety and depression on the
MMPI-2 could provide data contradicting the
presence of PTSD.
T H E PAT I E N T I N T E RV I E W
The semi-structured interview is the cornerstone
of the PTSD evaluation. Before discussing the
mechanics of the interview, two prerequisite
points need to be emphasized. First, there is the
patently obvious caution regarding self-report:
“Self-report is problematic because it communi-
cates a personal experience that is not falsifiable”
(Greiffenstein & Baker, 2008, p. 566). Falsifiability
is the essence of science and is also a requirement
in deciding what constitutes admissible expert
testimony in some legal venues (i.e., Daubert).
Subjective evidence under the control of the
respondent does not provide sufficient evidence
to declare a person impaired or disabled. It is a
tenuous contention at best to say “with a reason-
able degree of medical certainty” that a patient
has a psychiatric disorder when the sole basis is
the patient’s self-report. The prerequisite second
point concerns how the subjectivity of the patient
interview can be overcome. As in medicine,
the most critical part of any clinical evaluation
(including neuropsychological) is the clinical
interview and history of the illness. While test
administration requires only literacy, arriving at a
diagnosis via the interview implies knowledge of
syndromes. It is exceedingly common to find
recorded in the majority of neuropsychological
evaluations a list of symptoms the patient reported
without any effort by the interviewer to char-
acterize these symptoms in a manner that would
result in a diagnosis independent of any other
information, namely the actual testing. This
phenomenon has been referred to as the “bean
counting” of symptoms (Bielauskas, 1999).
In order for patients involved in litigation to
be compensated for an injury they must report
symptoms that produce impairment. In the neu-
ropsychological evaluation, the patient may man-
ifest this impairment via cognitive and personality
testing. Should a patient decide to feign testing,
knowing what to feign is difficult. It requires
knowledge of what the tests measure, and what
pattern and level of performance one might see
depending on the disorder under consideration.
Additionally, an examinee may be aware that
SVTs are administered. Consequently, from the
perspective of the examinee, a cautious approach
to the evaluation would be to not malinger the
Something to Talk About? 383
objective testing, especially the cognitive testing
in the case of PTSD. Should they decide not to
feign the testing, they are now put in a catch-22
situation whereby they must somehow communi-
cate disability and/or impairment. These patients
convey their impairment via the interview only.
It is a rare situation that a patient feigns impair-
ment on formal testing and does not communi-
cate this impairment via the interview. Symptoms
that suggest disability (and malingering when
present in an exaggerated or atypical nature) are
virtually always communicated in the interview,
but not always on the testing. Once the patient
conveys their symptoms, a good interviewer
takes control of the interview and examines each
symptom to determine its origin. For example,
the most common movement disorder is tremor.
No competent neurologist will simply record
the tremor as absent or present without charac-
terizing it and reaching a diagnosis. A final
caveat about the recommended interview format
described below is that unlike objective testing
there is, by definition, some variability among cli-
nicians in how to approach the interview. It is
hoped that the reader will find the suggestions
herein useful.
While there may be advantages to doing the
patient interview first for purposes of building
rapport, particularly if the interview begins with
a discussion of the traumatic event, four reasons
are offered for conducting the PTSD interview at
the completion of the testing. If the intent is to
malinger, the more information the examiner has
ahead of the interview (both medical records
and testing) works to the disadvantage of the
claimant. Second, if the testing is malingered
outright, the clinical interview can be shortened if
time is an issue, unless there is independent
medical record evidence supporting presence of
PTSD (e.g., ER evidence of significant post-
accident emotional distress requiring sedation in
a litigant who then malingers, but also may have
PTSD). Third, the IME context provides for the
collection of extensive records where the basic
medical, social, psychiatric, and injury history is
already available. Finally, at the conclusion of a
well-done interview, the patient who malingers
the interview may sense that they did not provide
a believable constellation of symptoms. If the
interview were done at the onset, and with the
patient feeling they may not have provided a
reasonable narrative, they might take a more
conservative approach to the upcoming testing.
This may result in less sensitivity in detecting
384 forensic neuropsychology
malingering, when present, on the objective psy-
chological testing.
The examiner should begin with a neurop-
sychological interview similar to the one typi-
cally done when assessing for the presence of a
neurobehavioral disorder. Since a portion of the
PTSD evaluation will involve cognitive testing,
the results of the testing need to be corroborated
by a neuropsychological interview. One suggested
format is for the interview to begin by asking the
patient to volunteer the symptoms they are expe-
riencing or in what ways they act or behave differ-
ently, without necessarily mentioning the trauma.
Here it is important for the patient to volunteer an
exhaustive list. At this point it is not necessary for
them to give examples of the symptoms or elabo-
rate on them; this should be reserved for the direct
symptom inquiry phase of the interview. The vol-
unteering of these symptoms results in a bi-modal
distribution. There are a few patients who come
prepared with an exhaustive list. In contrast, there
are those that volunteer few symptoms, yet the
symptoms volunteered initially can mushroom
during the direct symptom inquiry. Volunteering
the symptoms of a disorder one does not have is
difficult. It is made easy for the patient by intro-
ducing the purpose of the interview (as instructed
by the CAPS interview module), and volunteering
the symptoms for the patient so they could admit
or deny them. Volunteering symptoms, direct
symptom inquiry, and self-report instruments
(administered in that order) can result in an
increasing number of reported symptoms with
each successive method in litigants with question-
ably valid PTSD claims.
Following the volunteering of all symptoms,
the structured symptom inquiry portion of the
interview begins with the neuropsychological
interview. This involves posing direct questions
regarding cognitive, motor/sensory, and non-
PTSD psychiatric symptoms. The patient is asked
if they have the symptom, the onset, and if the
symptom has gotten better, worse, or the same
since the onset. Randomly mixed in with the
motor and sensory symptoms, the examiner
should inquire about all of the symptoms that
make up panic disorder. Mixing in physical symp-
toms of an anxiety disorder in the midst of basic
neurological symptoms disguises the intent. The
physiological concomitants of PTSD symptoms
are addressed in the CAPS interview where the
intent of the interview is more obvious. There is
no reason why the examiner cannot inquire
about the same symptom more than once. At the
conclusion of the neuropsychological interview
the patient is asked to describe, in detail, the
PTSD-causing event without any prompting or
questioning from the examiner.
Before the CAPS interview begins the exam-
iner has some idea from the neuropsychological
interview as to the presence of PTSD. Did the
patient volunteer symptoms of PTSD when asked
to list their symptoms? Were there any signs of
distress as they were describing the PTSD-causing
event? Did the patient endorse symptoms of major
depression or general anxiety? A lifetime history
of at least one other psychiatric disorder is found
in roughly 80% of PTSD patients (Kessler et al.,
1995). Were symptoms consistent with panic
attack or generalized anxiety disorder endorsed?
Was the neuropsychological interview malin-
gered?
Some patients prepared for a PTSD interview
are perplexed by questions regarding cognitive,
motor, and sensory symptoms they had not
planned on answering or rehearsed. As an exam-
ple, a patient who experienced a significant trau-
matic event asked two or three times during the
neuropsychological interview why he was not
being asked about his accident; not something
one suffering from PTSD would normally insist
on discussing. They must now decide on the spot
if these are symptoms they should endorse. Since
it is not likely that they have endorsed non-PTSD
symptoms before, providing the onset and course
of these symptoms, much less examples, becomes
problematic, resulting in a stilted and awkward
narrative. There is some evidence that unexpected
questions increase the ability of the interviewer to
detect malingering (Vrij et al., 2009).
Elhai et al. (2005a) surveyed members of the
ISTSS on the instruments they most commonly
use to assess traumatic events. The “gold standard”
for interview-based PTSD assessment is the
CAPS. This is by far the most commonly used
instrument by both researchers and clinicians.
The CAPS is the only PTSD interview that assesses
both frequency and severity of symptoms. The
Structured Clinical Interview for DSM- IV (SCID)
is the second most common, though three times
the number of traumatologists preferred the
CAPS to the SCID (First, Spitzer, Gibbon, &
Williams, 1997). However, one disadvantage to
the CAPS is that it takes longer to give (as long as
an hour) when you include the initial prompts
and follow-up questions. Aside from the time it
takes to give, some amount of practice and
training to become comfortable with the test is

required. The extensive research on the CAPS has
been summarized (Weathers, Kean, & Davidson,
2001). We recommend the CAPS as the preferred
structured interview in forensic evaluations. It is
beyond the scope of this chapter to cover the
CAPS in detail. We will focus only on how the
administration should be tailored for the IME.
The interview portion of the PTSD evaluation
needs to be carefully tailored and planned to the
circumstances of the claimant’s history (namely
medical records since the trauma), is labor inten-
sive, detailed, and can possibly last well over an
hour. It goes without saying that in an IME each
test is not introduced to the patient in a manner
that makes it clear what the test is measuring.
Similarly, one does not preface a PTSD interview
in such a fashion so as to make its purpose obvi-
ous. Per the CAPS manual, the interview is intro-
duced by telling the patient that they are going to
be asked about potentially traumatic events, and
to identify the one that is the most stressful, which
then becomes the focus of the CAPS interview. In
the IME context, this introduction is not neces-
sary since the PTSD causing event is known.
When asked to describe the PTSD-causing event
at the conclusion of the neuropsychological inter-
view, did the patient volunteer symptoms of fear,
helplessness, or horror? If yes, Criterion A-2 has
been met. If they do not volunteer these symp-
toms, per the CAPS instructions, they are asked
how they responded emotionally to the event, and
finally asked directly about A-2 symptoms. As to
Criterion A-1, whether the trauma is of sufficient
severity to cause PTSD, the examiner should
accept it as meeting A-1 criteria no matter how
trivial. While we are of the belief that the event
should be outside the realm of everyday human
experience, in the discussion section of the IME
report the reader should be made aware of the
controversy surrounding the stressor criterion.
The trier of fact can decide if the event is of suffi-
cient severity to produce PTSD. The examiner
should then go through the CAPS interview
making sure to cover all the questions. Item 22 of
the CAPS requires the examiner to estimate the
overall validity of the interview, but provides no
direction on how to do this in some objective
reproducible manner. CAPS items that were
denied in the previous interviews are skipped and
those previously reported are elaborated on via
the prompts outlined in the CAPS booklet. The
CAPS is then scored in order to obtain a severity
score, and the level of impairment method is
applied by comparing the patient’s CAPS score to
Something to Talk About? 385
that of well-defined PTSD groups from published
studies.
With regard to PTSD symptoms it is critical
that the patient be asked to provide concrete exam-
ples of their symptoms. For the patient who is
malingering, the examiner will appreciate the pro-
longed pauses, vague examples, no examples, lack
of detail, the contradictory answers, “I don’t know”
answers, or even nonresponsive answers that might
suggest that the patient does not have PTSD. The
patient attempting to feign PTSD may have some
awareness in the second or third hour of the inter-
view that their narrative may not be believable. It is
then not uncommon for revealing statements such
as “to tell you the truth, doc,” “to be honest, doc,”
“this is difficult to explain,” or “I know this is not
making sense” may be volunteered.
Two PTSD symptoms merit special attention:
flashbacks and nightmares. Both of these symp-
toms should be treated with scrutiny as they are
portrayed in the popular media as symptoms of
PTSD. The onset, course, frequency, and nature of
these symptoms should be fully explored includ-
ing detailed examples. In a recent PTSD IME, the
whole of the patient’s PTSD consisted of flash-
backs and nightmares. The PTSD criteria were
not even met on the PTSD self-report instrument.
The patient reported the dream as always being an
exact replication of the event. This is improbable.
As reported by McNally (2004), the majority of
patients asked to prospectively record their night-
mares dream about events related to the trauma
instead of “instant replays” of the trauma (p.7). As
for flashbacks, it is commonly overlooked that
these were described as rare in DSM-III when
they were introduced, and have continued to be
considered rare in the current DSM-IV-TR. PTSD
historians have offered a plausible explanation for
this rarity. They have convincingly argued that
flashbacks were rarely described in wars preced-
ing the Vietnam War (Jones et al. 2003). The flash-
back was actually a metaphor borrowed from the
film industry and blended into the newly coined
PTSD construct (Frankel, 1994; Lembcke, 1998).
Brewin (2003) summarized the argument of the
skeptics (versus “saviors”) that inventing the term
PTSD was not necessary since the symptoms of
the PTSD patient can be found in already existing
diagnostic categories; flashbacks are the only
symptom unique to PTSD.
There are additional observations that may
suggest malingered PTSD. As currently defined,
almost all persons have had at least one event that
can meet A-1 criteria as being life threatening.
386 forensic neuropsychology
The CAPS and some self-report instruments
provide an opportunity to identify stressful events
aside from the one that is the focus of the IME.
There may be instances where past events that are
normally outside the realm of usual human expe-
rience did not produce PTSD, but the trivial one,
which is the subject of the IME, did. In one
instance, a patient developed delayed PTSD fol-
lowing an electrical injury, but suffered no such
symptoms when during his teenage years he wit-
nessed the traumatic amputation of his father’s
leg, which was followed by a 20-minute attempt to
rescue him. That noncompensable event produced
no PTSD symptoms. In one case that went to trial,
a Vietnam veteran denied any symptoms of PTSD
from his combat experience, none following a
MVA that was litigated in which he sustained
some injuries, but did report PTSD following a
second MVA in which he sustained no demon-
strable injury.
It stands to reason that any person experienc-
ing a truly horrific event has a goal of forgetting
that event and moving on with their lives, while
for the litigating patient the maintenance of symp-
toms is necessary. It is important to remember
that the natural course of any sudden traumatic
event, be it neurological (e.g., stroke or head
injury) or psychological is recovery. Even in the
most common of civilian traumatic events such as
rape, recovery is the rule. While over 90% may be
diagnosed with PTSD within two weeks after the
rape, by week 12 less than half (47%) have PTSD
(Rothbaum, Foa, Riggs, Murdoch, & Walsh,
1992). Similarly, DSM-IV-TR reports that half of
the cases of PTSD show full recovery within three
months (American Psychiatric Association, 2000).
As already noted, PTSD in its original form, gross
stress reaction, was viewed as a temporary condi-
tion. Even for litigants who experience terrible
events, the need to forget them may outweigh the
need to be compensated.
By chance, in the course of a single week, three
separate PTSD IMEs were conducted by J. A. in
three cities within one state. In the first instance, a
driver of a compact car, in a successful suicide
attempt, rammed his car head-on into the semi-
truck of the patient. The driver of the car died, and
the patient and his wife barely escaped from the
cab of the semi-truck before it was engulfed in
flames. In the second incident, a driver employed
by the city accidentally hit and killed a pedestrian.
Both men had immediate PTSD symptoms, sought
immediate help, including two inpatient treat-
ments for the patient that killed the pedestrian
(he had a prior psychiatric history). Both men
were examined two years and one year after their
traumas. Neither met the criteria for PTSD by
their own report. In the third IME, a women who
sustained a laceration of her finger at work did not
report any PTSD symptoms until six months after
the injury, and, after aggressive treatment, had a
CAPS score of 63 (severe PTSD) 17 months after
the injury. The only similarity is that all three
patients claimed to have experienced significant
peritraumatic stress at the time of the trauma
based on a self-report PTSD instrument, with the
two male patients understandably reporting
higher elevations. Of note, medical records con-
temporaneous with the accidents documented
typical PTSD symptoms in the two men, but did
not support the presence of these symptoms in the
woman until six months post-trauma. Moreover,
only in the female patient did the symptoms per-
sist. Any nonimprovement and/or worsening of
symptoms should be viewed with skepticism.
Nonimprovement in symptoms is sometimes seen
in the face of treatment that has gone way beyond
the proven time-limited therapy that is recom-
mended for PTSD. In the case of rape, prospective
treatment studies show that after 6 weeks of treat-
ment there is a marked improvement in CAPS
scores (Resick, Nishith, Weaver, Astin & Feuer,
2002). In addition, one may find that the CAPS
score of the litigant receiving longer treatment
exceeds the mean CAPS score of rape victims who
have received one course of time-limited treat-
ment, followed by recovery.
The interview of a family member or an infor-
mant may or may not be needed, depending on
the situation, or may not be possible. In some
instances the informant might refuse the inter-
view or the attorney representing the patient may
deny access to a family member. In an IME con-
text the informant interview serves three pur-
poses. First, failure to conduct such an interview
is sometimes raised in deposition, or trial testi-
mony as reflecting a shortcoming of the IME.
Family members are frequently included in the
legal process by the plaintiff ’s side to convey how
the patient has been affected by the injury or
event. A defense expert might want to avail him
or herself of the same opportunity so as to avoid
the accusation that they have ignored important
collateral information. For some examiners the
informant interview may serve this latter purpose
versus gathering any information that would add
to the evaluation from a diagnostic and treatment
standpoint. If it is determined that the patient is

malingering, the interview of the informant would
add little as it does not negate the fact that the
patient is malingering. The exception would be a
case in which malingering is present, but there is
also evidence of legitimate PTSD. Second, the
informant can provide useful information about
the psychological reaction of the patient to a gen-
uine trauma. Informant interviews, whether clini-
cal or within a medicolegal context, should always
be done in the absence of the patient.
In conclusion, there are some points regarding
the PTSD interview that need to be emphasized.
First, regardless of the fact that some forensic
neuropsychologists might not rank the clinical
interview as a high priority in the IME process, it
is nevertheless the method by which PTSD is
diagnosed. The interview needs to be planned and
carefully executed proceeding from open-ended
to more structured questioning. Second, when
malingering is present, the results of the interview
need to be conveyed in the report in a way that
communicates the high likelihood of malinger-
ing, regardless of the formal testing. The interview
of the patient and informant should stand on their
own. Points arguing the case for a malingered
interview should be numbered and lettered for
the purposes of allowing the reader to easily iden-
tify the exact reasons that argue for the opinions
expressed in the report. An interview is easier to
explain to a referral source or a jury than is a test.
Regrettably, there is more to say about the clinical
interview that cannot be conveyed in this chapter
due to space limitations.
PTSD Self-Report Measures
While easily malingered, a self-report instrument
has the advantage of quantifying what the patient
reports, as opposed to the interview, which may
be argued is more subjectively interpreted. The
self-report instrument should not be viewed by
the examiner with skepticism, but instead as pro-
viding the patient with an opportunity to either
accurately report or over-report symptoms in
the easiest and clearest way. This then allows for
the implementation of the level of impairment
method, provided that there has been sufficient
research on the instrument in well-defined PTSD
clinical samples. PTSD self-report measures that
are tied to the DSM criteria are recommended by
the ISTSS treatment guidelines (Foa et al., 2008).
The need to use a DSM-linked measure effectively
rules out the most popular trauma scale, the TSI.
Giving these self-report instruments after
the interview prevents “indirect coaching”
Something to Talk About? 387
(i.e., suggesting symptoms that are later presented
during the interview). For this reason, these are
the only tests that are given at the completion of
the interview. The incidence of PTSD can vary by
two-fold depending on whether a self-report
checklist is used versus the standard interview,
especially if litigation is present (Sumpter &
McMillan, 2005). Completion of these instruments
allows for the evaluation of discordant informa-
tion between personality testing, the patient, and
informant interviews. In one example, a patient
was asked in an open-ended format to describe her
emotional response to the accident; intense fear,
helplessness, and horror were not mentioned
(including in the medical records). Even when
asked directly in the CAPS interview she denied
them. It was only after the interview when this
question was asked on a self-report instrument
that she admitted to experiencing these emotions.
Immediately recognizing the contradiction, she
stated, “This is going to contradict some of the
things we talked about now that I read them.”
Choosing among PTSD self-report instruments
is not as straightforward as the use of the CAPS.
Excluding measures designed for combat PTSD,
there are two instruments from the top ten that
are preferred by ISTSS members (Elhai et al.,
2005a): the PTSD Checklist (PCL) (Weathers, Litz,
Herman, Huska, & Keane (1993), and the Posttrau-
matic Stress Diagnostic Scale (PDS) (Foa, 1995).
Both are used by 16% of society members. The PCL
takes less time to give. It has 17 items (versus 49 for
the PDS), is free, and has a Spanish version (Miles,
Marshall, & Schell, 2008). The PDS has the advan-
tage of assessing all symptoms of PTSD, not just the
17 core DSM symptoms, and can be computer or
hand scored. The DAPS ranks third (9% of mem-
bers). The DAPS, like the PDS, assesses both DSM
and non-DSM symptoms. A possible advantage of
the DAPS over the PDS is the presence of a response
bias scale. As the DAPS is a relatively new scale,
there is little published research, which makes it a
major drawback. This precludes the use of the level
of impairment method. One seemingly attractive
feature of the DAPS and PDS is the normative data
provided in the test manuals.
However, as Rosen (2004) has tirelessly
emphasized, one has to assume that every PTSD
database is at least partially contaminated by
malingering. As an example, the normative data
for the PDS is comprised of 242 subjects with
mixed traumas, 27.8% of whom are combat veter-
ans. The employment status of the normative
sample suggests the possibility of secondary gain:
388 forensic neuropsychology
36.8% were unemployed and 15.4% disabled.
When the PDS was published 15 years ago, trau-
matologists rarely addressed malingered PTSD in
published studies. Even less is known about the
DAPS normative data, and it appears to be less
generalizable than the PDS norms. The PDS
normative sample was recruited through clinical
and research centers while the DAPS sample
was recruited through mailed advertisements,
after which the questionnaires were mailed
out. The sample included 70 university students.
Additionally, the PDS has two other advantages
over the DAPS: it measures impairment in func-
tioning and has more research behind it. This
arguably makes the PDS the preferable self-report
instrument.
Self-report instruments of depression and
anxiety should also be administered. The Patient
Health Questionniare-9 (Kroenke, Spitzer, &
Williams, 2001) and Generalized Anxiety
Disorder-7 (Spitzer, Kroenke, Williams, & Löwe,
2006) are recommended. These brief measures are
publicly available, and assess not only the severity
of these conditions, but also whether the DSM-
IV-TR criteria for either condition are met. This
will also assess the presence of comorbid condi-
tions that may or may not have been reported in
the neuropsychological interview.
I AT R O G E N I C
P T S D , T R E AT M E N T
R E C O M M E N D AT I O N S ,
A N D C A S E C O N S U LTAT I O N
“It was later during unrelated activity that
I bumped into a description of posttraumatic
stress disorder and thought to myself ‘Whoa,
this guy has a lot of these symptoms’” (Stein,
2002, p. 1514).
Competent consultation may go a long way in
correcting any misconceptions about the case and
directing the referral source to the proper health
care professional or resource, recommending
treatment, or an IME if necessary. The recom-
mendations below derive from evidence-based
approaches to the treatment of PTSD and our
suggestions where no guidelines exist.
It is in the ethics code, and hopefully in the
nature of every health care professional to want to
help their patient. The first step in that process is a
correct diagnosis from which proper treatment
follows. The frontline health care professional,
making most diagnoses, is the primary care
physician. When the patient is inaccurately diag-
nosed with PTSD this may perpetuate a sequence
of iatrogenic consequences that are set in motion
not necessarily by the PTSD claimant seeking
compensation, but by a doctor only trying to help.
The pitfalls in the diagnosis of PTSD are ubiqui-
tous errors made by presumably knowledgeable
mental health care professionals. It goes without
saying that a clinician who does not specialize
in psychiatric disorders cannot begin to consider
the complexities involved in making a diagnosis
of PTSD. The near constant coverage by the
media of the psychological effects of the Middle
East conflicts serves to make health care profes-
sionals “PTSD hypervigilant” so as to not miss the
diagnosis.
Two cases illustrate this iatrogenic hypervigi-
lance. In the first instance the patient was involved
in a MVA resulting in no injury, except for feeling
somewhat “skittish” when he drives. He relayed
this skittishness to his internist, an army reserve
officer just returning from the Middle East who
indicated, “We see a lot of this over in Iraq,” and
diagnosed him with PTSD. Once the diagnosis
found its way into the medical record, the insur-
ance company balked at offering treatment. The
patient was not sure what to do, and the case
dragged on for two years until the IME was com-
pleted. When the patient was told he did not have
PTSD, he was relieved. In another example, a
patient with a preexisting chronic and severe his-
tory of depression was involved in a MVA in
which she sustained no injury. The case took a
sudden turn when her family doctor, who had
seen her many times before and since her acci-
dent, saw that she was not getting better. In the
second year post injury he added PTSD to her
depression diagnosis. Unlike depression, the
PTSD incident-specific diagnosis changed the
direction of her litigation in the mind of her attor-
ney. This prompted an IME at the request of the
defense, which resulted in a diagnosis of malin-
gering, and in the trial the jury found for the
defense. The malingering unnecessarily arose
when the patient was indirectly called upon by the
diagnosis of her physician to now present with
symptoms of PTSD, which she never had, and
which she could not successfully malinger.
These two instances of well-intentioned
doctors may appear to be exceptions, but in fact,
physician gatekeepers are forever called upon to
be cognizant of every possible malady that might
ail the patient, including PTSD. It is one thing to
recognize and refer, but mere recognition is not

the sole precondition for competency. The above
quote from Stein (2002) comes from a Journal of
the American Medical Association article. The
Clinical Crossroads feature of the journal offers
teaching points via clinical vignettes. In this arti-
cle a primary care physician made a diagnosis of
PTSD after “stumbling upon” the diagnosis in the
course of some “unrelated activity.” The recom-
mendation of the article is for the primary care
physician to actively tackle this diagnosis. As for
litigation, the article acknowledged, “. . . misuse of
the diagnosis for monetary gain may occur on
occasion . . .” (Stein, 2002, p. 1517). The case dis-
cussant predicted a good outcome for the patient,
Mr. M., with no treatment recommended (neither
pharmacological or psychotherapy). In an update
to this case, two years later, we find Mr. M. par-
tially symptomatic and seeing a therapist who was
initially consulted because of the accident (Ship,
2004). Could this case have been managed differ-
ently? We will first begin with the evidenced
based-treatment recommendations followed by a
discussion on how to assist a referral source in
managing the PTSD claim. Unlike the treatment
recommendations, our forensic case consultation
suggestions are based primarily on experience.
In making treatment recommendations, we
decided to draw from as many different official
guidelines and sources as possible in an effort to
provide cumulative evidence for a certain recom-
mendation. While treatment recommendations
typically are not sought in forensic evaluations of
civil litigants or private disability claimants, such
recommendations are not uncommon in workers’
compensation cases. Additionally, not all recom-
mendations are uniform and we find some recom-
mendations more useful and user friendly than
others. Our recommendations have to be tem-
pered, and thus modified by the fact that they are
being made within a medicolegal and not a clinical
context. The recommendations we include come
from the ISTSS (Foa et al., 2008), the practice
guidelines of the American Psychiatric Association
(Benedek, Friedman, Zatzick, & Ursano, 2009),
the Cochrane Reviews (Bisson & Andrew, 2007;
Stein, Ipser, & Seedat, 2006) the Australian Center
for Posttraumatic Mental Health (Forbes,
Wolfgang, & Cooper, 2009), and the guidelines
published by the National Institute for Health and
Clinical Excellence (NICE) in Britain, which we
highly recommend (National Institute for Health
and Clinical Excellence, 2005).
The simplest of recommendations to make
comes from the Federal Drug Administration
Something to Talk About? 389
(FDA) as they are the gatekeeper for drug approval
in the United States. In order for the FDA to
approve a medication they require at least two
randomized, double-blind, placebo-controlled
trials. The only FDA-approved medications for
the treatment of PTSD are Paxil (paroxetine) and
Zoloft (sertraline). A Cochrane meta-analysis has
demonstrated the efficacy of the selective sero-
tonin reuptake inhibitors, the most often studied
of the medications used to treat PTSD (Stein,
Ipser, & Sedat, 2006). Per the NICE (2005) guide-
lines, pharmacotherapy should not be offered as
first-line treatment over psychotherapy unless,
per the Australian guidelines a) psychotherapy
has proved ineffective; b) the patient refuses ther-
apy; c) it is used to stabilize the patient before
therapy is begun in severe cases; d) it is used to
lessen the symptoms that might be exacerbated by
psychotherapy (Forbes, et al., 2009). Concomitant
short-term pharmacological treatment should
also be considered for any sleep problems, and
should be continued for 12 months before gradual
withdrawal. Before it is determined whether
psychotherapy or medication is needed, “watchful
waiting” is recommended in the first month
during the acute stress disorder phase. A follow-
up at one month is suggested at which time treat-
ment is considered. The Cochrane review by
Bisson and Andrew (2007) recommends trauma-
focused cognitive behavioral therapy (TFCBT),
eye movement desensitization and reprocessing
(EMDR), and stress management. There is some
indication that TFCBT and EMDR are superior to
stress management.
While EMDR is recognized as a treatment for
PTSD, it is not without controversy. The contro-
versy is partially due to some early, arguably
unfounded claims regarding its efficacy, atheoreti-
cal nature, and current lack of empirical support
for treating certain populations (children and
combat PTSD) and multitrauma PTSD (Rubin,
2003). As TFBCT has more data and is grounded
in cognitive behavior therapy, it might be a prefer-
able treatment modality. Clinicians with experi-
ence in the treatment of PTSD, and who have
been trained in these techniques should conduct
these therapies. TFCBT should be 8 to 12 sessions
in length, conducted once a week. Consideration
can be given to extending the 12 sessions if there
are comorbid or other psychosocial problems that
are contributing. The focus of therapy should be
primarily on the trauma.
Since symptoms of PTSD generally improve
with time, when a patient does not respond to
390 forensic neuropsychology

treatment it generally means one of three things:
the diagnosis is not accurate and the patient is
being treated for the wrong thing, the patient’s
symptoms are refractory to treatment and/or the
patient is not getting better because they are not
truly having the symptoms, or they are not as
severe as the patient reports.
The above recommendations presume a clini-
cal context in which the goal of the patient is to
get better. The absence of improvement, the wors-
ening of symptoms, having not returned to work,
or consulting with an attorney usually invites con-
sultation and recommendations that are more
fitting with what is now a medicolegal context.
Table 14.2 offers an approach to managing the
PTSD claim within a medicolegal context that is
based on nothing more than personal experience.
Frequently, it is the absence of improvement in
symptoms that call for case consultation or an
IME. If the patient has not improved on medica-
tion, treatment should be transferred to a psychia-
trist for more aggressive management. While the
insurer, employer, or workers’ compensation
nurse might be accustomed to choosing a certain
doctor in the case of surgery or other common-
place medical procedure, the patient should be
allowed to choose a psychotherapist, preferably a
doctoral-level psychologist familiar with the treat-
ment of PTSD and TFCBT. This is not to say that
a non-doctoral-level therapist cannot benefit the
patient, but all things being equal, it is hard to
argue against having a person with a terminal
degree treat the patient. While one cannot predict
how long treatment might take, requesting a time-
line from the therapist does two things. First, a
therapist agreeing to at least a tentative timeline is
a tacit understanding on the part of the therapist
and patient that the treatment of choice for PTSD
is time limited and trauma focused. Second, a
timeline creates an expectation that the patient
will improve, and puts the burden on both the
patient and therapist to work toward that end. The
patient should have only one psychotherapist in
addition to the physician providing the medica-
tion. The patient’s attorney may insist on another
or second therapist but this should be resisted
unless it is the patient’s wish. It is possible that a
new therapist is justified if the patient has not
reached a level of comfort with the therapist that
will allow therapy to progress in a successful
manner. A second therapist request should signal
the need for an IME before treatment with the
new therapist begins.
It is not uncommon, in the case of a physical
injury or after surgery, for the insurer to ask for an
impairment rating from the treating physician.
This should never be asked of the therapist as this
creates an irreconcilable conflict for them, which

TABLE 14.2 PTSD CASE CONSULTATION

What to recommend regarding treatment:

If no improvement medication management should be transferred to a psychiatrist
The patient should choose mental health treater, preferably a psychologist
Request from provider approximate timeline for treatment
Evaluate the necessity, reasons and need to switch therapists at the patient’s request
Multiple providers should not treat the PTSD
Do not ask the treater to do an impairment rating
Do not ask the treater if the patient is malingering
Recommend additional cycle of TFCBT when malingering is present following a truly
traumatic event
When to recommend an IME:
The trauma is trivial or commonplace event
The PTSD evaluation of the treater is incomplete
A forensic psychologist should be recommended over a psychiatrist
The PTSD symptoms appear in medical records after a delay (> 1 month)
The patient is not compliant with treatment
One course of TCCBT has failed
The patient is not improving with TFCBT or pharmacotherapy
Treater is unwilling to commit to a treatment timeline
Treater assuming the role of expert witness

will be discussed in more detail below. By the
same token, asking the therapist if the patient is
malingering puts them in an awkward position.
First, it is rare for a therapist to ever suggest, much
less document, malingering. Second, the lack of
improvement that will eventually require an IME
will address the issue of malingering. The prob-
lematic moment comes when there is malingering
present in the face of a clearly serious injury (e.g.,
traumatic amputation). In this circumstance, all
parties are informed of the malingering diagnosis,
and a brief eight-session course of additional
TFCBT can be recommended after which point
treatment should end. The purpose of this is to
demonstrate a good faith attempt to try to help
the patient, given the severity of the injury, despite
the presence of malingering. Here the case may be
complicated by the possibility that the patient may
have PTSD despite the malingering diagnosis.
Additionally, they may have had PTSD at one
point, recovered, yet still report symptoms that
they no longer have, making the detection of
malingering more challenging since they do not
have to feign symptoms but maintain them.
Table 14.2 outlines when an IME should be
recommended. Here we start at the beginning: the
event that presumably produced the PTSD. More
in line with DSM-III, the event should be outside
the realm of everyday human experience. If the
event is trivial, including any MVA that does not
result in serious injury, one should consider an
IME before treatment is instituted. It is the rule
rather than the exception that the PTSD evalua-
tion of the treater is often incomplete. In all fair-
ness to the treater, the scrutiny and thoroughness
with which one approaches a clinical evaluation is
not at the level of a forensic evaluation. For exam-
ple, in routine clinical care, depression is diag-
nosed without any clear evidence that the patient
was asked about all the symptoms that make up
the disorder. Keane, Buckley, and Miller (2003)
outline the common errors made in the forensic
assessment of PTSD. While these errors should
not occur in an IME context, they are ubiquitous
in the routine clinical evaluation of PTSD. They
include a) relying solely on patient self-report for
the diagnosis to the exclusion of corroborative
information; b) the clinical criteria for PTSD
are not fulfilled either because the clinician did
not ask, or failed to record the symptoms; c) fail-
ure to provide examples or characterize the symp-
toms (here we sometimes find the criteria are
listed, sometimes verbatim from the DSM, but no
examples of the symptoms are provided); and
Something to Talk About? 391
d) assuming an advocacy versus a scientific role.
The consultant should make the referral source
aware of any limitation of the evaluation of the
treater. This might require an IME or some
obligation on the part of the treater to account for
these diagnostic lapses.
With psychological testing at our disposal,
and a vast malingering literature to rely on, a psy-
chologist (versus psychiatrist) should do the IME.
The advantage psychologists hold is indirectly
acknowledged by psychiatry. It is not uncommon
for psychiatrists to call upon psychologists to do
personality testing on their behalf in order to
supplement their interview. On the other hand, as
already argued above, this recommendation is
negated by the suggestion that a good interview
may be all that is needed. The medical records
should establish the reporting of emotional symp-
toms within weeks of the trauma. Delayed symp-
tom onset should be considered the paradoxical
unequivocal Babinski sign indicating the absence
of PTSD. While delayed PTSD signals the need
for an IME in the mind of the forensic psycholo-
gist, it is usually the lack of improvement, failed
treatment and/or failure to return to work that
result in the referral source initiating an IME.
Based on a review of the last half dozen PTSD
evaluations conducted by the first author, in which
malingering was diagnosed, the average amount
of time between the trauma and the IME is
approximately 22 months. With the exception of
one case in which medical records were equivocal
as to the onset of symptoms, all presented with
delayed PTSD. The last circumstance that might
call for the intervention of an expert is when the
treating clinician assumes, often unknowingly,
the role of an expert witness. It should be the duty
of every consultant to educate all parties on the
critical distinction between the role of a treater
versus an expert (see chapter 2, Greiffenstein
and Kaufmann, in the present volume, for further
discussion of this issue).
Invariably, the patient’s attorney will often call
upon the patient’s mental health treaters to make
some statement about the patient’s condition and/
or rebut the statements of an expert witness.
A treater consenting to provide medicolegal opin-
ions regarding their patient is problematic. First,
the type and amount of data gathered as part of a
clinical referral are not adequate to form a proper
foundation to determine causation for medicole-
gal purposes. Secondly, treaters who provide testi-
mony as expert witnesses create an irreconcilable
ethical conflict between their therapeutic role as a
392 forensic neuropsychology
treater (or fact witness, which is what treaters are
considered) and the role of an expert witness,
which is the role the treater would be enacting
when making a causal inference between the
symptoms the patient reports, and the most prob-
able cause. Treaters should limit their activity to
treating the patient, providing testimony as a fact
witness if necessary, and testifying only to the
opinions contained in their original report only.
They should not act as post-hoc experts. Two arti-
cles that address this issue are highly recom-
mended (Greenberg & Shuman, 1997; Strasburger,
Gutheil, & Brodsky, 1997). This advice runs con-
trary to the recommendation provided by the
JAMA article in regard to Mr. M. as discussed
above: “Although it can be a burden, physicians
who care for traumatically injured patients should
be willing to complete necessary paperwork and/
or testify on the status of their patients when
required, or risk further imperiling the patients’
recovery” (Stein, 2002, p. 1517).
FINAL THOUGHTS
“I don’t know about this PTSD, but they did
bomb symptom validity testing.” (Anonymous
Forensic Neuropsychologist)
We would like to end by revisiting the ratio-
nale for the title of this chapter: “Something to
Talk About?” The title is meant to convey the
humility with which clinical neuropsychology
should approach a topic that some could right-
fully argue does not fall under its purview. It is
because this is a forensic neuropsychology text
that PTSD is included. While clinical neuro-
psychology is identified as a specialty requiring
a certain skill set, assessing PTSD requires no
prerequisite training per se.
Our answer is that we have nothing to talk
about if the issue is lesion localization. The totality
of the neuropsychological, neurophysiologic and
cognitive literature, applied both clinically and
empirically, has shown there is no definitive neu-
rological basis to PTSD that is widely accepted
(Vasterling & Brewin, 2005). The hot streak of
hippocampal size research ended with futility:
The right, left, or both hippocampuses showed
association with PTSD, but hippocampal differ-
ences were also shown to predate trauma.
Importantly, hippocampal size varies within time
within individuals.
First, the main contribution of neuropsy-
chologists is to address the role of intelligence and
select measures of attention, processing speed
and verbal memory in diagnosis and prognosis.
Empirical literature supports the notion that
intelligence level is a risk factor for development
of PTSD: Lower intelligence is associated with
greater reporting of PTSD symptoms, and higher
intelligence supports resilience or better progno-
sis. Measures of attention, processing speed, and
verbal memory play a similar role, with evidence
suggesting utility of certain measures of executive
dysfunction such as the Wisconsin Card Sorting
Test, and measures of visual memory function.
The practice implication is there is no need for a
lengthy neuropsychological test battery beyond
an acceptable measure of IQ, and well-validated
measures of attention, processing speed and
verbal and visual memory, in addition to standard
history-gathering and personality testing and
administration of SVTs, if the only claim is PTSD
(note that in many cases, a PTSD claim may be
accompanied by a brain injury claim, in which
case a comprehensive neuropsychological battery
would be justified).
Second, it follows that neuropsychologists
should not market their services as superior in
quality or diagnostic accuracy to that of psycholo-
gists who are not neuropsychologists, regarding
claims of PTSD alone. This assumes equality of
clinical psychology training and experience. But it
does not mean we should refuse such referrals.
Third, our Ethics Code reminds us to be aware
of the boundaries of our competence (American
Psychological Association, 2002). The forte of the
clinical neuropsychologist is that the forensic lit-
erature at their disposal dwarfs the literature of all
other disciplines. The “traumatologists” lack this
literature, and have only recently formally
recognized the importance of assessing response
bias in clinical and research assessments of PTSD
(Foa et al., 2008).
Fourth, our greatest strength is the assessment
of response bias. Although non-neuropsycholo-
gists receive some training in this important area,
neuropsychologists have been on the forefront of
deception and malingering research for at least
two decades. A problem one finds in the PTSD
civilian literature is the dissociation between what
a forensic neuropsychologist may be interested in
and what those who study and treat the disorder
focus on. Traumatologists assess PTSD and not
malingering, and neuropsychologists interested
in forensic assessment of PTSD assess malinger-
ing, but have little to say about the PTSD. While
our PTSD colleagues might benefit from our

malingering research, if all we have to talk about
is the binomial theorem we are not likely to
engender confidence. There appears to be an
inverse relationship between the enthusiasm an
individual has for SVT and their knowledge of the
syndrome they are trying to refute with the SVT.
When there is diagnostic uncertainty about a case,
the rapidity with which the neuropsychologist
asks the obligatory “What were their SVT scores?”
can be embarrassing at times. One has to question
if SVT has led to the “dumbing down” of clinical
neuropsychology. In medicine, advances in
technology (e.g., MRI) put fewer intellectual
burdens on the physician to identify the syndrome
based solely on the history and physical. If foren-
sic neuropsychology is to make a contribution in
the assessment of PTSD, they have an obligation
to acquire clinical competency in PTSD. The
accusation once leveled against the informally
trained weekend workshop neuropsychologist,
“the weekend wonder,” is a condemnation that
may be rightfully leveled at us by our PTSD
colleagues who devote more than just weekends
to a serious and complex disorder.
In closing, we revisit the question posed in the
introduction to this chapter regarding the incre-
mental validity of neuropsychological testing in
the assessment of PTSD. The neuropsychologist is
in a good position to address the medicolegal impli-
cations of the PTSD diagnosis, but not in a unique
position. Our future success hinges on acquiring a
comparable clinical and research PTSD knowledge
base on the accurate diagnosis of PTSD when it is
present, and being able to generate malingering
PTSD literature using a known-groups design for
detection of malingering when it is present.
AC K N OW L E D G M E N T
The authors wish to thank Ryanne Skalberg for
her editorial assistance.
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 15
Assessing Civil Competencies in
Older Adults with Dementia1
Consent Capacity, Financial Capacity, and Testamentary Capacity
D A N I E L C . M A R S O N , K AT I N A H E B E R T , A N D
ANDREA C. SOLOMON
INTRODUCTION
In the five years that have passed since the first
publication of Forensic Neuropsychology, issues of
competency assessment in the elderly have
received increasing attention both in terms of
scholarship and public recognition (American
Bar Association Commission on Law and Aging
& American Psychological Association, 2005;
American Bar Association/American Psycho-
logical Association Assessment of Capacity in
Older Adults Project Working Group, 2006, 2008;
Fackelmann, 2008). A major reason for this is the
demographic dynamics of our aging society.
Unfortunately, with the graying of America has
also come the dementing of America (Marson &
Zebley, 2001). Prevalent neurodegenerative dis-
eases in later life, such as Alzheimer’s disease (AD)
and Parkinson’s disease (PD), cause dementias
that progressively erode cognition and everyday
functioning (Griffith et al., 2003; McKhann et al.,
1984). As the first Baby Boomers approach retire-
ment age, the prevalence of dementia in the US
is expected to rise dramatically (Alzheimer’s
Association, 2008). Some estimates project that
by 2030 there will be approximately 72 million
adults over the age of 65 in the US, representing
an increase from 12% (in 2003) to 20% of the U.S.
population (Wan, Sengupta, Velkoff, & Debarros,
2005). Moreover, the oldest-old (persons aged 85
and older) population in the US is expected to
reach 9.6 million by 2030 and 20.9 million by 2050
(Wan et al., 2005). Although the majority of older
adults do not have dementia, advancing age is a
major risk factor for cognitive impairment, and
the prevalence of AD in persons aged 65 and older
is estimated to reach 7.7 million by 2030 and 11 to
16 million by 2050 (Alzheimer’s Association,
2008). Put differently, currently every 72 seconds
a person develops Alzheimer’s disease in our
country; by 2050, without effective treatments,
that rate will increase to a new case every 33
seconds (Alzheimer’s Association, 2008). In the
context of these figures, the growing societal
impact of dementia on decisional capacities in
the elderly is alarmingly apparent.1
Impairment of competency, or decision-
making capacity (Appelbaum & Gutheil, 1991), is
an inevitable consequence of neurodegenerative
dementias like Alzheimer’s disease (AD) and
Parkinson’s disease (PD) (Dymek, Atchison,
Harrell, & Marson, 2001a; Marson, Ingram, Cody,
& Harrell, 1995c; Marson, Schmitt, Ingram, &
Harrell, 1994a). As capacities for memory, judg-
ment, reasoning, and planning erode, AD patients
eventually lose decision-making capacity in every
sphere of life. Specific competencies that are lost
include the capacity to make medical decisions
(Marson, Hawkins, McInturff, & Harrell, 1997a;
Marson et al., 1995c), to consent to research (Kim,
Caine, Currier, Leibovici, & Ryan, 2001), to
manage financial affairs (Marson, 2001a; Marson
et al., 2000), to execute a will (Spar & Garb, 1992;
Walsh, Brown, Kaye, & Grigsby, 1997), to drive
(Drachman, Swearer, & Group, 1993; Hunt et al.,
1997), to manage medications (Barberger-Gateau,
Dartigues, & Letenneur, 1993), to live indepen-
dently, and ultimately to handle even the most
basic activities of daily life. Patients with
Parkinson’s disease and dementia have demon-
strated deficits in medical decision-making
capacity (Dymek et al., 2001a; Griffith, Dymek,
Atchison, Harrell, & Marson, 2005; Martin et al.,
402 forensic neuropsychology
2008) and are likely to be impaired in other higher
order capacities such as financial management.
Loss of competency in dementia has important
consequences for patients and their families, for
health care and legal professionals, and for society
as a whole (Marson et al., 1994a).
As noted above, since the first edition of this
book, there have been important developments in
the field of civil competency assessment in the
elderly. Befitting the continuing growth of this
area, there has been a notable increase in peer-
reviewed publications, particularly in the areas of
consent to treatment and research, as reflected by
several recent review articles (Dunn, Nowrangi,
Palmer, Jeste, & Saks, 2006; Karlawish, 2008; Lai
& Karlawish, 2007; Palmer & Savla, 2007). There
has been new attention paid to the competency of
patients in the prodromal stages of dementia,
commonly referred to as mild cognitive impair-
ment (MCI) (Jefferson et al., 2008; Okonkwo
et al., 2007; Okonkwo et al., 2008a). Perhaps of
greatest significance, however, is a series of three
handbooks on competency assessment in older
adults that have been jointly published by the
American Bar Association (ABA) and American
Psychological Association (APA) (American Bar
Association Commission on Law and Aging &
American Psychological Association, 2005;
American Bar Association/American Psycho-
logical Association Assessment of Capacity in
Older Adults Project Working Group, 2006, 2008).
These three handbooks, which respectively
address assessment of diminished capacity by
attorneys, by probate court judges in guardian-
ship proceedings, and by psychologists, are the
products of an interdisciplinary group of attor-
neys and psychologists called the ABA-APA
Working Group for Assessment of Competency
in Older Adults. The handbooks represent a suc-
cessful bridging of science and practice in the field
of competency assessment; each volume incorpo-
rates a guiding conceptual framework along with
pragmatic content areas and appendices that pro-
vide clear direction to professionals within the
discipline. Taken together, the body of new work
since the first edition of Forensic Neuropsychology
underscores the clear emergence of civil compe-
tency assessment as a distinct and expanding field
of clinical, ethical, and medical-legal research
(Karlawish & Schmitt, 2000; Marson & Ingram,
1996; Moye & Marson, 2007).
In keeping with the prior edition, this chapter
presents conceptual and clinical approaches to
assessing different civil competencies in older
patients with cognitive impairment and demen-
tia. At the same time, we seek to incorporate new
studies and findings within the different chapter
sections. We begin by outlining basic theoretical
concepts that provide a general context for under-
standing competency assessment and research.
We then focus on conceptual and empirical aspects
of three specific civil competencies: medical deci-
sion-making capacity (treatment consent capac-
ity), financial capacity, and testamentary capacity
(capacity to execute a will). In the area of treat-
ment consent, we consider a cognitive model of
consent capacity, and then review psychometric
and neuropsychological studies of this compe-
tency in patients with AD, PD with dementia, and
MCI. In the area of financial capacity, we present a
clinically based conceptual model, and then
review psychometric and other studies of this
competency in patients with AD and MCI. In the
area of testamentary capacity, we present the legal
elements of this capacity, and emphasize the con-
tinuing need for conceptual and empirical research
regarding this important civil competency. We
describe two approaches to clinical assessment of
testamentary capacity: contemporaneous and ret-
rospective, and note recent contributions by the
ABA-APA working group to this area.
Finally, in a chapter epilogue, we note strengths
and limitations of competency research in older
adults with MCI and dementia, and suggest direc-
tions for future research in the field.
C O N C E P T UA L I S S U E S I N
COMPETENCY AS SES SMENT
Competency is an elusive and frequently misun-
derstood medical-legal construct (Marson,
2001b). Sound clinical assessment and empirical
research in the area of competency requires iden-
tification and clarification of terminology and
basic concepts (Marson, Schmitt, Ingram, &
Harrell, 1994b). In this section, we highlight a
number of key terms and principles related to
competency.
Key Terms and Principles
What is “Competency”?
Competency refers to an individual’s legal
capacity to make certain decisions and to perform
certain acts (Appelbaum & Gutheil, 1991). In the
U.S. legal system, adults are presumed to have the
capacity to exercise choices and make decisions
for themselves until proven otherwise (Appelbaum
& Roth, 1981). However, neurological or psychi-
atric illness may impair one’s ability to make
 Assessing Civil Competencies in Older Adults with Dementia
rational decisions. In addition, some individuals
with developmental or acquired disabilities in
childhood will never, even as adults, possess the
competency to make certain decisions. Under
these circumstances, the state, through exercise of
its protective parens patriae power, may deem
these persons incompetent and appoint substitute
decision makers (Kapp, 1992). Accordingly, com-
petency may be usefully defined as “a threshold
requirement for an individual to retain the power
to make decisions for themselves” (Appelbaum &
Gutheil, 1991) (p. 218). Since a legal declaration
of incompetency entails deprivation of rights
and autonomy, competency evaluations and
determinations are serious matters (Appelbaum
& Gutheil, 1991; Marson et al., 1994b).
Capacity versus Competency
The terms capacity and competency are often used
interchangeably (Marson, 2001b). This can be
misleading, as the terms, although related, repre-
sent distinct concepts (Kapp, 1992). Capacity
denotes a clinical status as judged by a health care
professional, whereas competency denotes a legal
status as determined by a legal professional (i.e., a
judge). A capacity evaluation involves a clinical
assessment and judgment based on a patient’s his-
tory, presentation, and test performance. A judge
may consider such clinical capacity findings as
part of his/her competency decision-making pro-
cess, but will also consider other sources of
authority, such as statutes, case law precedent, and
principles of equity and justice. It is important
and useful to be mindful of the capacity/compe-
tency distinction, although for reasons of conve-
nience the terms are often used interchangeably
(Marson, 2001b).
It should be noted that recently judges and
other legal professionals have begun to favor the
use of the term capacity in referencing matters of
legal competency, in response to concerns that
the term competency carries with it historically
pejorative and archaic connotations. This change
of usage can present some difficulties in maintain-
ing the capacity-competency distinction discussed
above. Perhaps the best current solution is simply
to distinguish between matters of “clinical
capacity” and “legal capacity” (American Bar
Association Commission on Law and Aging &
American Psychological Association, 2005;
American Bar Association/American Psycholo-
gical Association Assessment of Capacity in Older
Adults Project Working Group, 2006, 2008). For
purposes of this chapter, use of the terms capacity
403
or competency will refer to their clinical meaning,
unless otherwise indicated.
Multiple Competencies: Competency
to do What?
The term competency is commonly used in an
undifferentiated way to describe a variety of
capacities (Marson et al., 1994b). Competency,
however, is not a unitary construct; rather, there
are multiple specific competencies. The typical
adult possesses a number of distinct competen-
cies, including the capacity to make a will; to
drive; to consent to medical treatment; to manage
financial affairs; and ultimately, to manage all of
his or her personal affairs. Each competency
involves a distinct combination of functional
abilities and skills that distinguish it from other
competencies (Grisso, 1986). For instance, the
cognitive and physical abilities requisite for
driving (knowledge of road signs, visual scanning
abilities, reaction time, gross motor skills) are
arguably quite distinct from those involved in
making a medical decision (e.g., understanding
medical concepts, short-term memory for medi-
cal symptoms and treatment options, rational
weighing of risks and benefits) (Marson, 2001b).
In addition, each competency tends to operate
within a specific and somewhat individualized
context (Grisso, 1986). For example, issues related
to competency to consent to treatment almost
invariably arise in a hospital or medical setting.
The reality of multiple competencies suggests that
rather than asking “Is the individual competent?”
one should ask “Is the individual competent to do
X in Y context?” (Marson et al., 1994b).
Specific versus General Competency
One useful distinction for analyzing different
competencies is that of “specific” versus “general”
competency (Appelbaum & Gutheil, 1991).
General competence is defined as the capacity to
manage “all one’s affairs in an adequate manner”
(Appelbaum & Gutheil, 1991) (p. 219), and is the
focus of most state statutes in the U.S. governing
guardianship. Specific competency, in contrast,
concerns the capacity to perform a specific act or
set of specific actions (Appelbaum & Gutheil,
1991). As suggested above, there are many specific
competencies recognized by the law (Marson,
2001b), including the capacity to manage finan-
cial affairs, make a will, be a parent (adoption and
custody), stand trial, and consent to medical treat-
ment. In the authors’ experience, each specific
competency must be approached and analyzed
404 forensic neuropsychology
discretely, as each taps distinct underlying func-
tional abilities.
Limited Competency
Because competency determination by its nature
results in a categorical assignment (i.e., competent
vs. incompetent), competency outcomes have
historically been treated as dichotomous proposi-
tions (Appelbaum & Gutheil, 1991). Limited
competency refers to the fact that, within a gen-
eral or specific competency, an individual may
have the ability to perform some actions but not
others. For instance, a patient with mild dementia
of the AD type may be unable to engage in
complex investment and financial decisions, but
may retain the ability to write checks and manage
small daily sums of money (American Bar
Association/American Psychological Association
Assessment of Capacity in Older Adults Project
Working Group, 2008; Marson, 2001b). As such,
this individual could be characterized as having
limited competency to manage his or her financial
affairs. The legal system has recognized the impor-
tance of limited competency through its use of
limited guardianships and conservatorships
(American Bar Association/American Psycholo-
gical Association Assessment of Capacity in Older
Adults Project Working Group, 2006).
Intermittent Competency and
Restoration of Competency
It is important to recognize that competency
status may change over time (Marson, 2001b). For
instance, fluctuations in chronic psychiatric
illness may periodically compromise an individu-
al’s ability to give consent to receive medication or
to manage his or her personal affairs. In situations
of intermittent competency, periodic re-evalua-
tions are indicated. In some cases, the underlying
neurological or psychiatric condition compromis-
ing an individual’s competency may resolve, result-
ing in the individual regaining decision-making
abilities. In such cases, legal competency may be
restorable through a formal court hearing and
decision (American Bar Association/American
Psychological Association Assessment of Capacity
in Older Adults Project Working Group, 2006).
Diagnosis Does Not Constitute
Incompetence
A diagnosis of dementia or other neurological or
psychiatric disorder is not synonymous with
incompetence (Marson, 2001b). A patient who
meets the National Institute of Neurological
and Communicative Disorders and Stroke–
Alzheimer’s Disease and Related Disorders Asso-
ciation (NINCDS-ADRDA) criteria for probable
AD (McKhann et al., 1984) may nonetheless be
competent to consent to medical treatment or
research or to perform other activities such as
driving or managing financial affairs. A key point
here is that in making determinations of compe-
tency, the examiner must perform a functional
analysis; that is, the examiner must consider
whether the individual possesses the skills and
abilities integral to performing a specific act in its
context. Certainly, diagnosis is a relevant factor in
evaluating competency. However, because diag-
nosis conveys no specific functional information,
it cannot by itself be dispositive of the competency
question (Marson et al., 1994b).
Mental Status Impairment Does Not
Constitute Incompetence
For similar reasons, mental status and neurop-
sychological impairment cannot, in isolation,
decide issues of competency (Marson, 2001b).
Such evaluations are important for diagnosing
dementia and for measuring level of cognitive
impairment, and they are clearly highly relevant
to a competency evaluation. However, like diag-
nosis, they cannot by themselves be dispositive of
the competency issue (Grisso, 1986; High, 1992).
As noted by Grisso, decision makers must go fur-
ther and “present the logic that links these clinical
observations [i.e., test results] to the capacities
with which the law is concerned” (Grisso, 1986,
p. 8). For example, neuropsychological impair-
ments in attention, auditory verbal comprehen-
sion, and abstractive capacity become relevant to
a competency determination only when they are
meaningfully related to competency-specific
functional impairments (e.g., the inability to
express a treatment preference, or to rationally
explain the treatment choice) (Marson, Chatterjee,
Ingram, & Harrell, 1996; Marson, Cody, Ingram,
& Harrell, 1995a; Marson et al., 1997a).
Individual Values and Preferences
An individual’s lifelong personal values and
preferences, and historical patterns of decision
making, are important facts to consider in
conducting a competency evaluation. The consis-
tency of an older adult’s current choices with his/
her historical values and preferences is often a
critical factor in a clinician deciding between
competency and incompetency. Knowledge of
an individual’s core values can play a particularly
 Assessing Civil Competencies in Older Adults with Dementia
significant role in guardianship cases, as it can
guide a court’s candidate selection and assign-
ment of a guardian, and can (and should) shape
the guardian’s own activities on behalf of the
protected individual (American Bar Association/
American Psychological Association Assessment
of Capacity in Older Adults Project Working
Group, 2006).
C A PA C I T Y T O C O N S E N T T O
M E D I C A L T R E AT M E N T
The capacity to consent to medical treatment
(treatment consent capacity) is a fundamental
aspect of personal autonomy, as it concerns inti-
mate decisions regarding the care of a person’s
body and mind (Marson, 2001b). Consent capac-
ity refers to a patient’s cognitive and emotional
capacity to accept a proposed treatment, to refuse
treatment, or to select among treatment alterna-
tives (Grisso, 1986; Tepper & Elwork, 1984). In
the US, consent capacity is the cornerstone of the
medical-legal doctrine of informed consent,
which requires that a valid consent to treatment
be informed, voluntary, and competent (Kapp,
1992; Marson, Ingram, Cody, & Harrell, 1995b).
From a functional standpoint, consent capacity
may be viewed as an “advanced activity of daily
life” (ADL) (Wolinsky & Johnson, 1991) and
an important aspect of functional health and
independent living skills in both younger and
older adults.
As a competency, consent capacity is distinc-
tive for several reasons: (1) it arises in a medical
rather than legal setting; (2) it generally involves
a physician, psychologist, or other health care
professional, rather than a legal professional, as
decision maker; and (3) these judgments are
rarely subject to judicial review (Grisso, 1986). As
discussed above, clinicians are not deciding
competency in a formal legal sense. However,
their decisions can have the same effect as a
courtroom determination insofar as the patient
will often yield decision-making power to others
(Appelbaum & Gutheil, 1991).
As discussed below, in dementia and more
specifically in Alzheimer’s disease, consent capac-
ity becomes increasingly impaired as the disease
progresses (Marson et al., 1995a). As cognitive
skills such as memory, reasoning, judgment, and
planning decline, patients lose the ability to
encode and process medical information and to
make coherent treatment decisions. Because it is
often unclear at what point cognitive decline
translates into loss of competency, the question
405
of whether a dementia patient is competent to
consent to treatment is of considerable interest to
health care providers (Farnsworth, 1990; Marson
et al., 1994b; Sherlock, 1984).
Cognitive Model for Consent Capacity
Consent capacity may be conceptualized as con-
sisting of three core cognitive tasks: comprehen-
sion and encoding of treatment information;
information processing and internally arriving at
a treatment decision; and communication of the
treatment decision to a clinical professional
(Alexander, 1988; Marson, 2001b; Marson &
Harrell, 1999). These core cognitive tasks occur in
a specific context: a patient’s dialogue with a phy-
sician, psychologist, or other health care profes-
sional about a medical condition and potential
treatments (Marson et al., 1995a). The compre-
hension/encoding task involves oral and written
comprehension and encoding of novel and often
complex medical information presented verbally
to the patient by the treating clinician. The infor-
mation processing/decision-making task involves
the patient processing (at different levels depend-
ing on the complexity of the information and
treatment options) the consent and other infor-
mation presented, integrating this information
with established declarative and episodic knowl-
edge (including personal values and risk prefer-
ences), rationally weighing this information, and
arriving internally at a treatment decision. The
decision communication task involves the patient
communicating his/her treatment decision to the
clinician in some understandable form (e.g., oral,
written, and/or gestural expression of consent/
nonconsent).
This model affords a basis for understanding
the cognitive structure of consent capacity deci-
sions, and also loss of competency in neurodegen-
erative disorders (Marson, 2001b). For example,
short-term memory ability is relevant to consent
capacity because impaired learning and short-
term recall will limit the amount of encoded
medical information available for further proce-
ssing. Similarly, receptive language skills are
relevant to consent capacity because they afford
comprehension of treatment-related information.
Conceptualization and executive functions are
important to consent capacity because they are
necessary for organized processing of treatment
information. Judgment and reasoning abilities
are equally important as they make possible a
patient’s rational weighing of all this information
and his/her internal determination of a treatment
406 forensic neuropsychology
choice. Expressive language skills, in turn, may be
important because of their relevance to effective
communication of the treatment choice in the
patient-clinician dialogue. In this regard, it should
be noted that treatment consent capacity is a
highly verbally mediated competency (the only
pragmatic arguably is the signature on the form)
and thus verbal measures are likely to load highly
on it (Marson & Harrell, 1999).
Psychometric Assessment of
Consent Capacity
In recent years a number of investigators have
developed instruments for assessment of consent
capacity in different patient populations (Cea &
Fisher, 2003; Dunn et al., 2006; Edelstein, Nygren,
Northrop, Staats, & Pool, 1993; Grisso &
Appelbaum, 1991, 1995; Grisso, Appelbaum,
Mulvey, & Fletcher, 1995; Janofsky, McCarthy, &
Folstein, 1992; Marson, Earnst, Jamil, Bartolucci,
& Harrell, 2000; Marson et al., 1995c; Marson,
McInturff, Hawkins, Bartolucci, & Harrell, 1997b;
Vellinga, Smit, van Leeuwen, van Tilburg, &
Jonker, 2004). These instruments represent a fun-
damental advance in the competency field, as they
have brought psychometric rigor, in the form of
standardized content and administration, and
quantitative scoring and norming, to an area in
which previously subjective clinical interviews
were the standard.
Our group has developed an instrument for
empirically assessing the capacity of dementia
patients to consent to medical treatment under
different legal standards (Capacity to Consent to
Treatment Instrument, CCTI; Marson et al.,
1995c). Specifically, we developed two clinical
vignettes (i.e., neoplasm vignette and cardiac
vignette) designed to test competency under
five distinct standards of consent capacity. Each
vignette presents a hypothetical medical problem
and symptoms, and two treatment alternatives
with associated risks and benefits. The medical
content of each vignette was reviewed by a neu-
rologist with expertise with the elderly and
dementia. The vignettes, which are presented
orally and in writing in an uninterrupted disclo-
sure format (Grisso & Appelbaum, 1991), were
written at a fifth- to sixth-grade reading level
(Flesch, 1974) with low syntactic complexity
and a moderate information load. The adminis-
tration format for each vignette approximates
an informed consent dialogue and requires the
subject to consider two different treatment
options with associated risks and benefits.
Administration involves the individual
simultaneously reading and listening to an oral
presentation of the vignette information.
The individual then answers questions designed
to test consent capacity under five different
legal thresholds or standards. These standards
or thresholds have been drawn from case law
and the psychiatric literature (Appelbaum &
Grisso, 1988; Roth, Meisel, & Lidz, 1977). They
are set forth below in order of increasing difficulty
for patients with AD type dementia (Marson et al.,
1995c):
S1: capacity simply to “evidence” a treatment
choice;
S3: capacity to “appreciate” the consequences
of a treatment choice;
S4: capacity to reason about treatment/
provide “rational reasons” for a treatment
choice; and
S5: capacity to “understand” the treatment
situation and treatment choices.
The above standards represent different
thresholds for evaluating capacity to consent
(Marson et al., 1994b). For example, S1 (evidenc-
ing a choice) requires nothing more for compe-
tency than an individual’s communication of a
treatment choice. S3 (appreciating consequences)
is of moderate difficulty and requires patients to
appreciate how a treatment choice will affect
them personally. S4 (rational reasons) bases
competency upon an individual’s ability to supply
rational reasons for the treatment choice. S5 is a
comprehension standard and requires a patient
to demonstrate conceptual and factual knowledge
concerning the medical condition, symptoms,
and treatment choices and their respective
risks/benefits. It should be noted that these
four standards can be readily applied to other
competencies to consent, such as capacity to
consent to research, and to decisional capacity
generally.
In addition to these four standards, there is an
additional consent-related ability described as
making the “reasonable” treatment choice (when
the alternative is manifestly unreasonable) (Roth
et al., 1977). This ability, which we reference as
[S2], emphasizes outcome rather than the mere
fact of a decision or how it has been reached. The
patient who fails to make a decision that is roughly
congruent with the decision that a “reasonable”
person in like circumstances would make is
 Assessing Civil Competencies in Older Adults with Dementia
viewed as incompetent. [S2] is not an accepted
legal standard for judging consent capacity
because of concerns about arbitrariness in deter-
mining what constitutes a “reasonable choice”
(Tepper & Elwork, 1984). Accordingly, [S2] is
referenced in brackets to distinguish it from the
other four established Ss. However, [S2] remains
useful as a means of understanding treatment
preferences of patients with neurocognitive
disorders (Dymek, Atchison, Harrell, & Marson,
2001b).
The CCTI has a detailed and well-operational-
ized scoring system for each vignette according to
the specific legal standards outlined above. In
prior work with AD patients, three trained raters
achieved high inter-rater reliability for standards
with both interval (r > . 83, p < .0001) (LS3-LS5)
and categorical scales (>96% agreement) (S1,
[S2]) (Marson et al., 1995c). The CCTI scoring
system permits evaluation of both an individual’s
competency performance and competency
impairment status on each standard. By “compe-
tency performance,” we refer to the quantitative
score that an individual achieves on a particular
standard as determined by the CCTI scoring
system. By “competency impairment status,” we
refer to the level of impairment and assigned cat-
egorical outcome (competent, marginally compe-
tent, or incompetent) of an individual on a
standard, based on use of psychometric cutoff
scores derived from normal control performance
(Marson et al., 1995c). It should be emphasized
that these impairment outcomes are useful
research classifications, but do not represent
actual clinical or legal judgments of capacity or
competency.
TABLE 15.1 PERFORMANCE ON CCTI CAPACIT Y STANDARDS BY
GROUP 2
N LS1 [LS2]*
0–4 0–1
Older Controls 15 4.0 (0.0) .93
Mild AD 15 3.9 (0.4) 1.00
Moderate AD 14 3.6 (0.9) .79
* No group differences emerged on [LS2] (X2 = 4.2, p = .12)
a
Normal mean differs significantly from moderate AD mean (p < .001)
b
(p < .0001)
c
Normal mean differs significantly from mild AD mean (p < .01)
d
(p < .0001)
e
Mild AD mean differs significantly from moderate AD mean (p < .01)
407
Consent Capacity in Patients with
Alzheimer’s Disease
Capacity Performance and Impairment
Outcomes in AD
In an initial study, we used the CCTI to investi-
gate loss of competency in patients with mild
Alzheimer’s disease (n = 15), patients with mod-
erate AD (n = 14), and older controls (n = 15).
Performance on the five CCTI standards was
compared across groups. As shown below in
Table 15.1, the CCTI discriminated the perfor-
mance of the normal controls, the mild AD group,
and the moderate AD group on three of the five
standards. While the three groups performed
equivalently on minimal standards requiring
merely a treatment choice (S1) or the reasonable
treatment choice [S2], mild AD patients per-
formed significantly below controls on more
difficult standards requiring rational reasons (S4)
and understanding treatment information (S5).
Moderate AD patients performed significantly
below controls on appreciation of consequences
(S3), rational reasons (S4), and understanding
treatment (S5), and significantly below mild AD
patients on S4 and S5 (Marson et al., 1995c).
In addition to capacity performance, the
impairment outcome of AD patients on the
standards was classified as capable, marginally
capable, or incapable using psychometric cutoff
scores referenced to control group performance
on each S. As shown in Table 15.2, assignment of
capacity status resulted in a consistent pattern of
compromise (marginally capable and incapable
outcomes) among AD patients that related
both to dementia stage and stringency of stan-
dard. Mild AD patients demonstrated substantial
LS3 LS4 LS5
0–10 0–12 0–70
8.7a (1.2) 10.3b, c (3.8) 58.3b, d (6.6)
7.1 (2.0) 6.1e (3.4) 27.3e (9.6)
5.9 (2.7) 2.3 (2.4) 17.9 (10.6)
408 forensic neuropsychology

TABLE 15.2 EXPERIMENTAL OUTCOMES BY CCTI

CAPACIT Y STANDARD AND GROUP 3
Standard/Group Capable Marginally Capable Incapable
S1 Evidencing Choice
Controls 15 (100%) 0 (0%) 0 (0%)
Mild AD 13 (87%) 2 (13%) 0 (0%)
Moderate AD 11 (79%) 1 (7%) 2 (14%)
[S2] Reasonable Choice
Controls 14 (93%) 1 (7%)
Mild AD 15 (100%) 0 (0%)
Moderate AD 11 (79%) 3 (21%)
S3 Appreciate Consequences
Controls 14 (93%) 1 (7%) 0 (0%)
Mild AD 10 (67%) 2 (14%) 3 (20%)
Moderate AD 5 (36%) 2 (14%) 7 (50%)
S4 Reasoning
Controls 14 (93%) 1 (7%) 0 (0%)
Mild AD 7 (47%) 5 (33%) 3 (20%)
Moderate AD 1 (7%) 3 (22%) 10 (71%)
S5 Understand Treatment
Controls 15 (100%) 0 (0%) 0 (0%)
Mild AD 0 (0%) 1 (7%) 14 (93%)
Moderate AD 0 (0%) 0 (0%) 14 (100%)

*Control (N=15); Mild AD (N=15); Moderate AD (N=14)

compromise on S4 (53%) and S5 (100%), the two
most stringent and clinically relevant CCTI stan-
dards. Moderate AD patients demonstrated sig-
nificant compromise on the three more complex
and clinically relevant standards S3 (64%), S4
(93%), and S5 (100%). The results raised the con-
cern that, depending on circumstances such as
the complexity of intervention, the level of treat-
ment risk, and the standard to be applied, a major-
ity of moderate AD patients and many patients
with mild AD may lack consent capacity (Marson,
2001b; Marson et al., 1995c).
Longitudinal Decline in Consent
Capacity in Mild AD Patients
More recently, our group has investigated consent
capacity longitudinally in patients with mild AD
(Huthwaite et al., 2006). We conducted a two-year
study comparing healthy older adults (n=15) and
mild AD patients (n=20) using the CCTI. At base-
line, mild AD patients performed equivalently
with controls on simple standards of evidencing a
choice (S1) and making the reasonable choice
([S2]), but significantly below controls on com-
plex standards of appreciation, reasoning, and
understanding (S3, S4, S5) (p < .02). Control
performance was stable over time on all capacity
standards. At one-year follow-up, the mild AD
group did not show significant decline from
baseline on any capacity standard. However, at
two-year follow-up, the mild AD group showed
significant declines from baseline on the three
complex standards (S3, S4, S5) (p < .02), and a
trend on one of the simple standards (S1). The
findings replicated the prior finding that mild
AD patients have impaired consent capacity
at baseline and extended prior work by showing
that individuals with mild AD experience
significant decline on complex consent abilities of
appreciation, reasoning, and understanding over a
two-year period. The findings highlight the value
of early assessment and regular monitoring at
two-year intervals of decisional capacity in
patients with mild AD (Huthwaite et al., 2006).
 Assessing Civil Competencies in Older Adults with Dementia
Cognitive Predictors of Consent
Capacity in AD Patients
In addition to providing a standardized basis for
evaluating competency performance and out-
come, instruments like the CCTI also provide a
psychometric criterion for investigating neuro-
cognitive changes associated with loss of consent
capacity in neurodegenerative disorders such as
AD. We used the CCTI and a neuropsychological
test battery sensitive to dementia in the above
sample to identify cognitive predictors of declin-
ing competency performance in AD patients
under the four standards (Marson et al., 1996;
Marson et al., 1995a). Table 15.3 presents stepwise
multiple regression results for the combined AD
group for these standards.
Findings from these psychometric studies
suggest that multiple cognitive functions are asso-
ciated with loss of consent capacity in patients
with Alzheimer’s disease, as measured by the
CCTI standards (Marson et al., 1996; Marson
et al., 1995a). Deficits in conceptualization,
semantic memory, and probably verbal recall
appear to be associated with impaired capacity in
both mild and moderate AD patients to under-
stand a treatment situation and choices (S5).
Deficits in simple executive function (word flu-
ency) appear linked to the impaired capacity of
both mild and moderate AD patients to provide
rational reasons for a treatment choice (S4), and
to the impaired capacity of moderate AD patients
to identify the consequences of a treatment choice
(S3). Finally, receptive aphasia and semantic
memory loss (severe dysnomia) may be associ-
ated with the impaired ability of advanced AD
patients to evidence a simple treatment choice
(S1). The results offer insight into the relationship
between different legal thresholds of competency
TABLE 15.3 MULTIVARIATE COGNITIVE PREDICTORS * OF CAPACIT Y
PERFORMANCE IN THE AD GROUP N=29 4
S1 S3
(Evidencing Choice) (Appreciating Consequences)
R2 p R2
SAC .44 .0001 CFL 58
* No measures achieved univariate or multivariate significance for the control group. CFL=Controlled Oral Word Association Test (Benton &
Hamsher, 1978); BNT= Boston Naming Test (Kaplan, Goodglass, & Weintraub, 1983); DRS CON= Dementia Rating Scale Conceptualization
subscale (Mattis, 1976); DRS IP= Dementia Rating Scale Initiation/Perseveration subscale (Mattis, 1976); SAC= Simple Auditory Comprehension
Screen (Eisenson, 1954)
409
and the progressive cognitive changes character-
istic of AD, and represent an initial step toward a
neurologic model of competency (Marson et al.,
1996; Marson et al., 1995a).
Since these initial studies, a number of other
investigators have begun to examine the relation-
ship of specific neuropsychological abilities to
decisional capacity (Moye, Karel, Gurrera, & Azar,
2006; Palmer & Jeste, 2006). An excellent review
of work in this area has recently been published
by Palmer and colleagues (Palmer & Savla, 2007),
who note that “this line of [neuropsychological]
research may foster the development of better
consent procedures, as well as aid in refining the
construct of decisional capacity toward a form
that better reflects the underlying neurocognitive
processes” (Palmer & Savla, 2007) (p. 1047). In
the sections that follow, we reference some of
these new studies that seek to identify the cogni-
tive underpinnings of consent capacity deficits in
different neurocognitive disorders.
Consent Capacity in Individuals with
Mild Cognitive Impairment (MCI)
Treatment Consent Capacity in
Patients with MCI
Mild cognitive impairment (MCI) is a transitional
phase between normal cognitive aging and AD
and other dementias (Morris et al., 2001; Petersen
et al., 2001). Individuals with MCI may present
with memory or other cognitive deficits, and the
amnestic form of MCI (aMCI) represents the sub-
type most likely to progress to AD (Palmer,
Backman, Winblad, & Fratiglioni, 2008; Tabert
et al., 2006; Yaffe, Petersen, Lindquist, Kramer, &
Miller, 2006). Although intact functional status
was originally considered a key diagnostic feature
distinguishing MCI from AD (Petersen et al.,
S4 S5
(Reasoning) (Understanding
Treatment)
p R2 p R2 p
.0001 DRS IP .36 .0008 DRS CON .70 .0001
BNT .11 .001
410 forensic neuropsychology
1999), it is increasingly recognized that MCI
involves subtle declines in higher order func-
tional abilities (Artero, Touchon, & Ritchie, 2001;
Griffith et al., 2003; Okonkwo et al., 2007;
Okonkwo et al., 2008a; Ritchie, Artero, & Touchon,
2001; Touchon & Ritchie, 1999), including medi-
cal decision-making capacity (Okonkwo et al.,
2007; Okonkwo et al., 2008a; Okonkwo et al.,
2008b). As discussed below, several recent studies
have shown that declines in treatment consent
capacity occur in individuals with MCI prior to
the emergence of a frank dementia.
Our group recently examined medical deci-
sion-making capacity in 56 older controls, 60 indi-
viduals with aMCI, and 31 patients with mild AD
(Okonkwo et al., 2007). Results from this study
showed that individuals diagnosed with aMCI
exhibit impaired medical decision-making capac-
ity relative to older controls. The MCI participants
in our study performed more poorly than controls
on cognitively complex consent standards of
understanding treatment, reasoning about treat-
ment, and appreciating consequences of treat-
ment. Interestingly, the individuals with aMCI
performed better than patients with mild AD on
standards of reasoning and understanding. These
findings suggest that consent capacity is also com-
promised in MCI but to a lesser degree than in a
frank AD-type dementia.
We have also investigated longitudinal decline
in medical decision-making capacity in a group of
healthy older controls (n = 88) and individuals
with aMCI (n = 116) over a period of one to three
years (mean = 1.7 years). Results from this study
(Okonkwo et al., 2008a) showed that declines in
medical decision-making capacity are detectable
in individuals with aMCI over a three-year period.
Specifically, individuals with aMCI exhibited pro-
gressive decline in their ability to understand con-
sent information and a similar trend emerged for
decline in ability to reason about treatment. The
data also indicated that individuals with aMCI
exhibit a marked drop in their ability to under-
stand consent information at the time of conver-
sion to AD, and that the rate of decline on this
ability accelerates after conversion.
Cognitive Predictors of Consent
Capacity in MCI
We have also developed cognitive models of med-
ical decision-making capacity in healthy and
cognitively impaired older adults (Okonkwo et al.,
2008b). In a study of 56 older controls, 60 indi-
viduals with aMCI, and 31 patients with mild AD,
we found that verbal memory was the primary
predictor of medical decision-making capacity for
three of the four CCTI standards (understanding,
reasoning, appreciation), and executive function
was a secondary predictor. The cognitive models
were generally robust in the aMCI group, with
overall R2 values of .53 and .30 for understanding
and reasoning, respectively. The overall R2 value
for the appreciation model was comparatively
small at .16; this finding was consistent with prior
data suggesting that appreciation is a dimension of
consent capacity more difficult to cognitively
model (Dymek et al., 2001a; Gurrera, Moye, Karel,
Azar, & Armesto, 2006). Overall, the findings
clearly indicate that medical decision-making
capacity is mediated primarily by short-term
verbal memory in MCI, a finding highly consistent
with the amnestic deficits characteristic of MCI.
Research Consent Capacity in
Patients with MCI
Consent capacity is relevant not only in a medical
treatment decision-making context, but also in
the context of decisional capacity to participate in
research (Jefferson et al., 2008; Karlawish et al.,
2008). Jefferson and colleagues (2008) recently
examined cognitive correlates of decisional capac-
ity in a sample of individuals with MCI (n=40)
and 40 cognitively intact older adults. The authors
assessed capacity to give informed consent for a
hypothetical clinical trial, as well as examined
neurocognitive functioning across a variety of
cognitive domains. Results from this study indi-
cate that individuals with MCI perform more
poorly than controls on measures of decisional
capacity, particularly understanding and reason-
ing. The data also indicate that executive dysfunc-
tion is associated with impaired decisional
capacity in MCI. This finding contrasted with our
group’s prior observation that verbal memory is
preeminent as the predictor in MCI. Overall, this
study’s findings indicate that decisional capacity
declines in MCI occur in both research and
clinical settings, and suggest that consent capacity
be carefully evaluated in potential research
participants with MCI.
Consent Capacity in Patients with
Parkinson’s Disease
Over the past decade, most medical decision-
making capacity research involving older adult
dementia populations has focused on AD
(Karlawish et al., 2008; Kim et al., 2001; Marson,
Earnst, Jamil, Bartolucci, & Harrell, 2000; Marson
 Assessing Civil Competencies in Older Adults with Dementia 411

et al., 1997b; Marson et al., 1994b), with relatively
little attention paid to consent capacity in patients
with Parkinson’s disease. PD is one of the most
prevalent and disabling of neurologic disorders
(Jacobs, Stern, & Mayeux, 1997); over time, patients
become extremely incapacitated by their progres-
sive motor, cognitive, and neuropsychiatric impair-
ments (Marson & Dymek, 2004). Impairment of
medical decision-making capacity in PD and its
dementia syndrome is likely to differ in important
ways from that in AD, as these two dementias have
differing neuropathology and neurologic sub-
strates, and cognitive, psychiatric, and motor fea-
tures (Farlow & Cummings, 2008; Griffith et al.,
2008; Heindel, Salmon, Shults, Walicke, & Butters,
1989; Mahler & Cummings, 1990; Stern, Richards,
Sano, & Mayeux, 1993). The prominence of motor
dysfunction in PD has tended to obscure the con-
tributions of cognitive impairment and dementia
to patients’ functional decline. In this regard, con-
sent capacity is a competency that is particularly
suitable for study in PD, as it is primarily a verbally
based construct (Marson & Dymek, 2004).
Capacity Performance and Impairment
Outcomes in Patients with PD
and Dementia
Our research group has conducted several studies
of consent capacity and cognitive performance in
individuals with PD. In 2001, we published find-
ings from a study of medical decision-making
capacity in 20 older adults with idiopathic PD and
cognitive impairment (Dymek et al., 2001b).
Although a formal dementia diagnosis using
DSM-IV criteria (American Psychiatric Association,
1994) was not used in the study, most if not all of
the PD patients were demented, as reported by
the study neurologist and as reflected by the mean
DRS Total Score of 117 (sd=14.5) (Dymek et al.,
2001b). Thus, the PD patient group in this study
probably closely approximated how a formally
diagnosed group of patients with Parkinson’s dis-
ease dementia syndrome (PDDS) would perform.
Accordingly, we reference the PD group as PDDS
to reflect its probable dementia status.
Results from this study revealed that the PDDS
group performed worse than the control group on
the four core CCTI consent abilities: evidencing a
choice, appreciating consequences, reasoning about
treatment (rational reasons), and understanding
treatment (S1, S3-S5). In contrast, PDDS patients
performed equivalently with controls on the
experimental consent ability of reasonable choice
([S2]) (Dymek et al., 2001b) (Table 15.4).
Impairment outcome status of PDDS patients
on the standards was classified as capable, mar-
ginally capable, or incapable using psychometric
cutoff scores referenced to control group perfor-
mance (Marson et al., 1995c) (Table 15.5). Similar
to AD patients (see above), PD patients demon-
strated a pattern of capacity compromise (defined
as the combination of marginally capable and
incapable outcomes) that related to stringency of
the standard: [S2] (5%), S1 (30%), S3 (45%), S4
(55%), and S5 (80%).
These data suggest that medical decision-
making capacity is impaired in individuals with
PDDS. In addition, findings from this study
indicate that patients with PDDS may have more
difficulty with complex and clinically challenging
aspects of medical decision making (i.e., reason-
ing and understanding). Similar to findings in

TABLE 15.4 GROUP COMPARISONS ON DEMOGRAPHIC, DEMENTIA SCREEN, AND

CCTI CONSENT STANDARD VARIABLES 5
Older Controls PDDS Patients
Variable (n = 20) (n = 20) F p
Mean sd Range Mean sd Range
Age 68.1 (5.8) [60–79] 75.0 (7.5) [63–86] 10.4 .003
Education 14.8 (2.3) [9–18] 14.3 (3.1) [9–20] 0.34 .56
DRS Total Score 141.2 (3.1) [138–144] 117.3 (14.5) [72–129] 51.8 .0001
S1-Evidencing Choice 4.0 (0.0) [4] 3.6 (.8) [1–4] 5.9 .020
[S2]-Reasonable Choice 0.95 (0.2) [0–1] 0.95 (0.2) [0–1] — —
S3-Appreciate Consequences 8.9 (1.2) [6–10] 7.5 (2.5) [1–10] 5.7 .022
S4-Reasoning about Treatment 10.9 (3.7) [6–21] 5.1 (3.2) [1–11] 27.9 .000
S5-Understanding Treatment 59.0 (6.0) [51–68] 36.8 (13.0) [1–60] 47.8 .000
412 forensic neuropsychology

TABLE 15.5 EXPERIMENTAL CAPACIT Y OUTCOMES BY

CCTI STANDARD AND PATIENT GROUP 6
Capable Marginally Incapable
Capable
S1 Evidencing Choice
Controls 20 (100%) 0 (0%) 0 (0%)
PDDS Patients 14 (70%) 5 (25%) 1 (5%)
[S2] Reasonable Choice
Controls 19 (95%) — 1 (5%)
PDDS Patients 19 (95%) — 1 (5%)
S3 Appreciate Consequences
Controls 17 (85%) 3 (15%) 0 (0%)
PDDS Patients 11 (55%) 5 (25%) 4 (20%)
S4 Reasoning about Treatment
Controls 20 (100%) 0 (0%) 0 (0%)
PDDS Patients 9 (45%) 10 (50%) 1 (5%)
S5 Understanding Treatment
Controls 20 (100%) 0 (0%) 0 (0%)
PDDS Patients 4 (20%) 3 (15%) 13 (65%)

Capable: For S3-S5, scores falling at or above 1½ SDs below the control group mean on the S.
For S1, a score of 4. For [S2], a score of 1. Marginally Capable: For S3-S5, scores falling between
1½ and 2½ SDs below the control group mean on the S. For S1, a score of 3. No marginally capable
outcomes are possible on [S2]. Incapable: For S3-S5, scores falling below 2½ or more SDs below
the control group mean on the S. For S1, a score of 0–2. For [S2], a score of 0.

studies with AD patients (Marson et al., 1995c), it
appears that the four CCTI standards may be
hierarchical in difficulty for PDDS patients, with
standards tapping reasoning (S4) and medical
treatment information comprehension (S5) as
being the most difficult and requiring a level of
information retention and processing that may be
beyond the capacity of many PDDS patients.
Cognitive Predictors of Consent
Capacity in PD patients
with Dementia
We also examined cognitive predictors of PDDS
patient performance and outcome on the CCTI
capacity standards. Tables 15.6 and 15.7 present
the univariate correlates and also the multivariate
predictors of PDDS patient performance and
capacity outcome on three of the standards. No
cognitive measures correlated significantly with
S3 or [S2] on the univariate level (Dymek et al.,
2001b), and thus these two standards were
excluded from subsequent multivariate analyses
and no predictor models are reflected in the two
tables (Dymek et al., 2001b).
These findings suggest that declines in execu-
tive functions, and to a lesser extent memory, are
key neurocognitive changes associated with com-
petency loss in patients with PD (Dymek et al.,
2001b). Executive dysfunction was closely associ-
ated with PDDS patient performance on S5
(understanding treatment) and also S4 (reasoning
about treatment). Specifically, simple measures of
executive function (i.e., EXIT 25; Royall, Mahurin,
& Gray, 1992) and memory (i.e., DRS Memory
subscale; Mattis, 1976) predicted S5 performance,
together accounting for 68% of score variance.
Using the EXIT 25, a nonparametric discriminant
function analysis (DFA), showed a very high
classification rate of S5 impairment outcomes
(90%), which increased to 95% when both the
EXIT 25 and DRS Memory were used. The EXIT
25 is a bedside test of simple executive abilities,
including verbal and spatial fluency, inhibition,
primitive reflexes, and set flexibility (Royall et al.,
 Assessing Civil Competencies in Older Adults with Dementia 413

TABLE 15.6 COGNITIVE PREDICTORS OF CAPACIT Y STANDARD

PERFORMANCE FOR PDDS PATIENTS N=20 7

Standard Variable(s) Predictor Univariate Correlation Stepwise Regression

r p cumR2 p

S1: Evidencing Choice DRS Memory .73 .000 .55 .000 STEP 1
WAIS-R .67 .002
Comprehension
DRS Attention .58 .008
EXIT 25 −.53 .02
S4: Rational Reasons EXIT 25 −.67 .002 .45 .002 STEP 1
Trails B −.60 .005
DRS Attention .58 .008
WMS-LM II .48 .04
S5: Understanding Treatment EXIT 25 −.75 .000 .56 .000 STEP 1
DRS Memory .71 .000 .68 .000 STEP 2
WAIS-R .70 .001
Comprehension
WMS-R LM II .65 .002

1992). DRS Memory is a composite measure of
memory, consisting of short-term verbal recall
items, orientation items, and verbal and visual
recognition items (Mattis, 1976). Thus, basic exec-
utive, and to a lesser extent memory, functions
appear to mediate PDDS patients’ capacity to com-
prehend a treatment situation and choices. This
finding was consistent with the task demands of
S5, which require conceptual organization as well
as recall of factually complex material (Dymek
et al., 2001b; Dymek, Marson, & Harrell, 1999).
Executive dysfunction was also associated
with PDDS patient performance on S4 (reason-
ing). The EXIT 25 was the key predictor of S4
performance, accounting for 45% of score vari-
ance. Using the EXIT 25, nonparametric DFA
showed a very high classification rate of S4 impair-
ment outcomes (90%), which increased to 95%

TABLE 15.7 NEUROPSYCHOLOGICAL PREDICTORS OF

EXPERIMENTAL CAPACIT Y STANDARD OUTCOMES IN THE
PDDS GROUP 8
Standard Predictor Variable (s) Classification
Accuracy Rate*
S1: Evidencing Choice DRS Memory 70%
DRS Memory/WAIS-R Comprehension 100%
S4: Rational Reasons EXIT 25 90%
EXIT 25/Trails B 95%
S5: Understanding Treatment EXIT 25 90%
EXIT 25/DRS Memory 95%

* Percentage of capacity outcomes on each standard that were accurately classified by the respective neuro-
psychological predictor variable(s). As there are three outcomes (capable, marginally capable, incapable), a chance
classification rate would be 33%.
414 forensic neuropsychology
when using both EXIT 25 and Part B of the Trail
Making Test (Trails B) (Reitan, 1958). Trails B is a
measure of visuomotor sequencing and set flexi-
bility that is strongly associated with executive
ability (Reitan, 1958). Thus, basic executive func-
tions also appear to mediate PDDS patients’
capacity to provide rational reasons for a choice of
medical treatment. This finding was consistent
with the task demands of S4, which require an
individual to integrate information regarding two
treatment choices and their risk/benefit profiles,
and to provide logical reasons (pro and con) for
his/her treatment choice.
Simple memory and comprehension/
judgment abilities were associated with PDDS
patient performance on S1. As discussed above,
S1 is a minimal standard requiring only commu-
nication of a treatment choice. DRS Memory
emerged as the only multivariate predictor of
PDDS patients’ S1 scores, accounting for 55% of
the variance and correctly classifying 70%
of patient impairment outcomes. When DRS
Memory was coupled with WAIS-R Compre-
hension, they together correctly classified 100% of
S1 competency outcomes. These findings suggest
that simple memory and comprehension/
judgment deficits underlie PD patients’ declining
capacity for simply communicating a treatment
choice (S1).
The findings from this study are consistent
with our current understanding of PD as a disor-
der of fronto-striatal circuitry with associated
executive dysfunction (Lichter, 2001; Mahurin,
Feher, Nance, Levy, & Pirozzolo, 1993; White, Au,
Durso, & Moss, 1992). The most problematic
CCTI standards for the PD patients were the rea-
soning and comprehension standards (S4 and S5)
that are the most cognitively complex (Dymek
et al., 1999; Marson et al., 1995c). Previous
research has shown that PD patients perform well
on simple cognitive tasks; however, as task com-
plexity increases, performance deteriorates, likely
a result of impaired higher order executive
control of cognitive processes (Filoteo, Maddox,
Ing, & Song, 2007; Girotti et al., 1986; Gotham,
Brown, & Marsden, 1988; Lichter, 2001; Troster,
2008). The findings are also consistent with
research on patients with frontal lobe dementia
and significant executive dysfunction who show
impaired decision making capacity despite intact
language, memory, perception, and the absence of
apraxia and agnosia (Schindler, Rachmandi,
Matthews, & Podell, 1995). As such, these data
suggest a link between fronto-striatal dysfunc-
tion, cognitive impairment (particularly executive
dysfunction), and competency loss in PD (Dymek
et al., 2001a; Marson & Dymek, 2004).
Consent Capacity in Patients with
PD Without Dementia
Consent capacity is also compromised in
individuals with PD who exhibit cognitive impair-
ment but do not meet criteria for dementia. In a
recent study (Martin et al., 2008b) of 16 patients
with PD and cognitive impairment without
dementia (PD-CIND), 16 patients with PD
dementia (PDD), and 22 healthy older adults, we
examined medical decision-making capacity with
the CCTI. We assessed capacity performance on
the five different consent standards and assigned
impairment outcomes (capable, marginally capa-
ble, or incapable) on the standards for the two
patient groups.
The findings from this study revealed that,
relative to controls, PD-CIND patients demon-
strated significant impairment on the understand-
ing treatment consent standard, clinically the
most stringent CCTI standard. Relative to con-
trols and PD-CIND patients, PDD patients were
impaired on the three clinical standards of under-
standing, reasoning, and appreciation. These
results suggest that impairment in decisional
capacity is already present in cognitively impaired
patients with PD without dementia and worsens
as these patients progress to the point of demen-
tia. As such, these finding indicate that clinicians
and researchers should carefully assess decisional
capacity in all patients with PD with cognitive
impairment.
Consent Capacity in Patients
with PD Dementia versus
Patients with AD
An important area of future competency research
involves comparisons of capacity performance
across neurocognitive disorders. Such studies can
reveal how different neuropathologies can give
rise to differing patterns of cognitive impairment
that in turn can result in different forms of capac-
ity impairment. We conducted an initial study of
this type by comparing the CCTI performance of
older controls (n=18), patients with PD and
dementia (PDDS) (n=17), and patients with mild
AD (n=22) (Griffith et al., 2005). The PDDS
group and mild AD group had similar levels of
cognitive impairment as measured by Dementia
 Assessing Civil Competencies in Older Adults with Dementia
Rating Scale Total Score (Mattis, 1988). While
both the PDDS and AD groups performed below
controls on the cognitively complex understand-
ing, reasoning, and appreciation standards, we
found important dissociations between the two
dementia groups on the understanding (S5) and
evidencing choice (S1) standards. The PDDS
group performed better than the AD group on the
understanding standard, a finding consistent with
the more intact episodic memory found in PD
versus AD. In contrast, PDDS patients performed
below AD patients on the basic evidencing choice
standard, a finding that may reflect the inatten-
tiveness, distractability, and bradyphrenia charac-
teristic of PD (Griffith et al., 2005). We believe
that this small study shows the future promise of
cross-dementia and cross-disorder studies of
competency.
C A PA C I T Y T O M A N A G E
F I N A N C I A L A F FA I R S
Background
The capacity to manage financial affairs (i.e.,
financial capacity) comprises a broad range of
conceptual, pragmatic, and judgment abilities
(utilized across a range of everyday settings) that
are critical to the independent functioning of
adults in our society (Marson, 2001a; Marson
et al., 2000). As such, it differs in many respects
from medical decision-making capacity, which is
almost exclusively a verbally mediated capacity
arising in a medical setting.
Epidemiological studies in the elderly have
suggested that financial capacity is an “advanced”
or instrumental activity of daily living (IADL)
(Marson et al., 2000; Wolinsky & Johnson, 1991).
The advanced ADLs are mediated by higher cog-
nitive functions and can be distinguished from
“household” ADLs (e.g., meal preparation, shop-
ping, housekeeping) and “basic” ADLs (e.g., bath-
ing, dressing, walking) (Wolinsky & Johnson,
1991). Financial capacity entails a complex set of
abilities, ranging from basic skills of identifying
and counting coins/currency, to conducting cash
transactions, to managing a checkbook and bank
statement, to higher level abilities of making
investment decisions. As might be expected, such
abilities can vary enormously across individuals,
depending on a person’s socioeconomic status,
occupational attainment, and overall financial
experience (Marson, 2001a; Marson et al., 2000).
Along with medical decision-making, driving,
415
and mobility, financial capacity is a core aspect of
individual autonomy in our society.
Definitions of Financial Capacity
From a legal standpoint, financial capacity repre-
sents the financial skills sufficient for handling
one’s estate and financial affairs, and is the basis
for determinations of conservatorship of the estate
(or guardianship of the estate, depending on the
state legal jurisdiction) (American Bar
Association/American Psychological Association
Assessment of Capacity in Older Adults Project
Working Group, 2008). Broadly construed, finan-
cial capacity also conceptually encompasses more
specific legal capacities such as contractual capac-
ity, donative capacity, and testamentary capacity.
Thus, financial capacity is an important area of
assessment in the civil legal system (Marson &
Hebert, 2008a).
Historically, the legal standard for financial
capacity in conservatorship statutes was generally
(and vaguely) cast as the capacity to manage “in a
reasonable manner all of one’s financial affairs”
(American Bar Association/American Psycho-
logical Association Assessment of Capacity in
Older Adults Project Working Group, 2008). A
more modern and specific standard is set forth in
Section 410(2) of the Uniform Guardianship and
Protective Proceedings Act (UGPPA), which
states that a court may appoint a conservator if
the court determines that “the individual is unable
to manage property and business affairs because
of an impairment in the ability to receive and
evaluate information or make decisions, even
with the use of appropriate technological assis-
tance”; and the individual has property that will
be wasted or dissipated unless management is
provided, or funds are needed for the support of
the individual or of others entitled to the individ-
ual’s support (American Bar Association/
American Psychological Association Assessment
of Capacity in Older Adults Project Working
Group, 2008).
There is not yet a widely accepted clinical defi-
nition for financial capacity. However, Marson
has recently proposed the following: “the capacity
to manage money and financial assets in ways that
meet a person’s needs and which are consistent with
his/her values and self-interest.” (see Widera,
Steenpaas, Marson, and Sudore, 2011) (p. 698).
This working definition seeks to incorporate
the performance and judgment aspects character-
istic of financial capacity (described in more
416 forensic neuropsychology
detail below), as well as consideration of a person’s
longstanding values.
Performance and Judgment Aspects
of Financial Capacity
Financial capacity can be understood to have
both a performance aspect and a judgment aspect.
In order to have financial capacity, a person must
be able to perform a variety of financial tasks and
skills in order to meet his/her needs. Such tasks
and skills include understanding basic financial
concepts, possessing basic monetary skills, carry-
ing out cash transactions in a grocery store, and
paying bills. However, in order to have financial
capacity, an individual must also be able to
exercise judgment and act in ways that protect and
enhance financial self-interest. Thus, in addition
to performance skills, the individual must be
able to carry out financial activities in ways that
promote and protect his/her self-interest.
These performance and judgment dimensions
of financial capacity are distinct. By way of
example, a patient with schizophrenia may have a
number of intact financial performance skills
(count coins/currency, carry out cash transac-
tions, use a money order or checkbook), but due
to concurrent mental illness and substance abuse
problems, is unable to exercise good judgment
and utilize the skills in ways that meet basic
needs and protect his/her self-interests. Such a
patient may impulsively spend his/her disability
entitlement check within a few days of receipt,
resulting in disruption of his/her medication
regimen and nutrition, and threatening continu-
ity of housing such that he/she may become
homeless.
Consequences of Loss of
Financial Capacity
Loss of financial capacity (FC) has a number of
important consequences for dementia patients
and families, and implications for health care and
legal professionals (Marson, 2001a; Marson et al.,
2000). First, loss of FC can have economic and
household consequences. People suffering from
dementia such as Alzheimer’s disease often have
difficulty paying their bills and carrying out basic
financial tasks (Overman & Stoudemire, 1988).
They are continually at risk for making decisions
that endanger assets needed for their own long-
term care or intended for testamentary distribu-
tion to family members. Second, there are also
important psychological consequences to finan-
cial capacity loss. Much like loss of the car keys,
loss of control over one’s own funds and
checkbook implicates a core aspect of personal
independence in our society and can lead to
depression and other significant psychological
consequences (Moye, 1996). Third, loss of FC has
clinical significance to health care professionals.
Impairments in higher order financial skills
and judgment are often early functional changes
demonstrated by dementia patients (Marson et al.,
2000) and by some patients with mild cognitive
impairment (Griffith et al., 2003; Triebel, Martin,
Griffith et al., 2009). As discussed below, research
has shown that patients suffering from mild
Alzheimer’s disease demonstrate significant
impairments in most financial activities and in
many specific financial abilities (Marson et al.,
2000). Fourth, declining financial capacity is
closely linked to legal issues of elder abuse
(Marson et al., 2000). Financial exploitation is an
all-too-common form of elder abuse commonly
associated with victims’ diminished or impaired
mental capacities (Nerenberg, 1996). There are
daily media accounts of older adults victimized in
consumer fraud and other scams (Walton, 2002;
“Woman out $5,300 in two cons,” 1996). Older
adults can also be more covert victims of undue
influence exercised by family members, profes-
sionals, and third parties (Marson, Huthwaite, &
Hebert, 2004; Spar & Garb, 1992).
Finally, loss of FC can trigger important legal
issues of guardianship and conservatorship
(Grisso, 1986; Marson et al., 2000). Dispropor-
tionately high numbers of older adults are subjects
each year of conservatorship proceedings (pro-
bate court proceedings concerning control and
management of an individual’s assets and estate),
due to the high incidence of dementias and other
mental and medical illnesses affecting financial
competency in this age group (Grisso, 1986).
In addition, an individual’s financial skills are
also considered as part of a guardianship proceed-
ing (American Bar Association/American Psycho-
logical Association Assessment of Capacity in
Older Adults Project Working Group, 2006).
These two legal proceedings involve significant
time and expense for families (Marson, 2001a).
Clinical Conceptual Model of
Financial Capacity
Despite its clear relationship to everyday living
and independence, there has been a surprising
lack of conceptual and empirical study of finan-
cial capacity. Early work in the area of IADLs
offered elementary and unsatisfactory schema
 Assessing Civil Competencies in Older Adults with Dementia
such as ‘financial management skills,’ without
providing needed conceptual structure or detail.
We present below a clinically based conceptual
model of financial capacity in older adults
(Marson & Zebley, 2001; Marson et al., 2000;
Martin et al., 2008a). This model has been the
basis for instrument development and for ongo-
ing studies of financial capacity in MCI, AD, and
other clinical populations.
Because financial capacity represents a broad
continuum of activities and specific skills, it may
be best conceptualized as a series of domains of
activity that each have specific clinical relevance
(Griffith et al., 2003; Marson, 2001a; Marson et al.,
2000). Examples of these domains include: basic
monetary skills, carrying out cash transactions,
managing a checkbook, managing a bank state-
ment, and exercising financial judgment. This
domain-based approach is clinically oriented and
is consistent with the presumed multidimension-
ality of FC and its variability across individuals.
It is also consistent with the previously discussed
legal doctrine of limited financial competency
adopted within most state legal jurisdictions,
which recognizes that an individual may be
competent to carry out some financial activities
and not others (Grisso, 1986; Marson, 2001a;
Marson et al., 2000).
In addition to domains of activity, our model
identifies specific financial abilities, or tasks
(Marson, 2001a; Marson et al., 2000). Tasks reflect
more basic financial skills that comprise domain-
level capacities. For example, the domain of
‘financial conceptual knowledge’ might draw
upon specific abilities, such as understanding
simple concepts (e.g., a loan or savings) and prag-
matically applying such concepts in everyday life
(e.g., selecting interest rates, identifying a medical
deductible, and making simple tax computations).
The domain of financial judgment might consist
of tasks related to detection/awareness of financial
fraud, or of making informed investment choices.
Therefore, tasks represent basic abilities that when
combined constitute broader, clinically relevant
domains of financial activity. We have defined
tasks as being simple or complex, depending on
the level of cognitive resources they appear to
require (Marson, 2001a; Marson et al., 2000).
Our model also considers FC at the global
level (Griffith et al., 2003; Marson & Zebley, 2001).
Competency is ultimately an overall categorical
judgment or classification made by a clinician or
legal professional. Thus, the conceptual model of
financial capacity currently has three levels
417
(Griffith et al., 2003): (1) specific financial abilities
or tasks, each of which is relevant to a particular
domain of financial activity; (2) general domains
of financial activity, which each have clinical rele-
vance to the independent functioning of commu-
nity dwelling older adults; and (3) overall financial
capacity, which reflects a global measure of capac-
ity based on the summation of domain- and task-
level performance. Our conceptual model of FC
currently comprises 9 domains, 18 tasks, and 2
global levels (Griffith et al., 2003; Martin et al.,
2008a). It is presented below in Table 15.8.
Psychometric Studies of Financial
Capacity in Alzheimer’s Disease
Financial Capacity in Mild and
Moderate AD
Using this conceptual model, our laboratory
has conducted studies seeking to investigate FC
in cognitively impaired populations such as
Alzheimer’s disease (Marson, 2001a; Marson et al.,
2000). The Financial Capacity Instrument (FCI) is
a psychometric instrument designed by our group
to assess performance of older adults at the task,
domain, and global levels of the conceptual model.
The original FCI (FCI-6) assessed six domains
and 14 tasks (Marson et al., 2000) (the global level
was introduced in later versions of the FCI—see
below). In an initial study, a sample of 23 older
controls and 53 AD patients (30 with mild demen-
tia, and 23 with moderate dementia), were admin-
istered the FCI-6 (Marson et al., 2000). As shown
in Table 15.9, we found that mild AD patients per-
formed equivalently with control participants on
Domain 1 (basic monetary skills), but significantly
below controls on the other five domains.
Moderate AD patients performed significantly
below controls and mild AD patients on all
domains. On the FCI tasks, mild AD patients per-
formed equivalently with controls on simple tasks
such as naming coins/currency, counting coins/
currency, understanding parts of a checkbook,
and detecting risk of mail fraud. Mild AD patients
performed significantly below controls on more
complex tasks such as defining and applying
financial concepts, obtaining change for vending
machine use, using a checkbook, understanding
and using a bank statement, and making an invest-
ment decision. Moderate AD patients performed
significantly below controls and mild AD patients
on all tasks (Marson, 2001a; Marson et al., 2000).
Using a cut-score method derived from the
performance of the control group (Marson,
2001a; Marson et al., 2000), we translated the
418 forensic neuropsychology

TABLE 15.8 REVISED CONCEPTUAL MODEL OF FINANCIAL CAPACIT Y * :

18 TASKS, 9 DOMAINS, 2 GLOBAL SCORES 9
Task Description Task
Difficulty
Domain 1 Basic Monetary Skills
Task 1a Naming coins/currency Identify specific coins and currency Simple
Task 1b Coin/currency relationships Indicate relative monetary values of coins/currency Simple
Task 1c Counting coins/currency Accurately count groups of coins and currency Simple
Domain 2 Financial Conceptual Knowledge
Task 2a Define financial concepts Define a variety of simple financial concepts Complex
Task 2b Apply financial concepts Practical application/computation using concepts Complex
Domain 3 Cash Transactions
Task 3a 1 item grocery purchase Enter into simulated 1 item transaction; verify change Simple
Task 3b 3 item grocery purchase Enter into simulated 3 item transaction; verify change Complex
Task 3c Change/vending machine Obtain change for vending machine use; verify change Complex
Task 3d Tipping Understand tipping convention; calculate/identify tips Complex
Domain 4 Checkbook Management
Task 4a Understand checkbook Identify and explain parts of check and check register Simple
Task 4b Use checkbook/register Enter into simulated transaction; pay by check Complex
Domain 5 Bank Statement Management
Task 5a Understand bank statement Identify and explain parts of a bank statement Complex
Task 5b Use bank statement Identify specific transactions on bank statement Complex
Domain 6 Financial Judgment
Task 6a Detect mail fraud risk Detect and explain risks in mail fraud solicitation Simple
Task 6c Detect telephone fraud risk Detect and explain risks in telephone fraud solicitation Simple
Domain 7 Bill Payment
Task 7a Understand bills Explain meaning and purpose of bills Simple
Task 7b Prioritize bills Identify overdue utility bill Simple
Task 7c Prepare bills for mailing Prepare simulated bills, checks, envelopes for mailing Complex
Domain 8 Knowledge of Assets/Estate Indicate/verify asset ownership, estate arrangements Simple
Domain 9 Investment Decision-Making Understand options; determine returns; make decision Complex
Global 1 Sum of Domains 1–7 Overall functioning across tasks and domains Complex
Global 2 Sum of Domains 1–8 Overall functioning across tasks and domains Complex

quantitative performance of the AD patients into
categorical impairment outcomes (capable,
marginally capable, incapable) on each domain.
Table 15.10 presents capacity outcomes for the
mild and moderate AD subgroups on the FCI-6
domains. In the context of a prototype instrument
and small control sample, these outcomes should
be interpreted cautiously. However, mild AD
patients demonstrated an interesting pattern of
capacity loss across the domains. While approxi-
mately 50% of mild AD patients were found capa-
ble on Domains 1, 2, and 3, less than 30% were
found capable on Domains 4 and 5 (checkbook
management, bank statement management), and
less than 15% were found capable on Domain 6
(financial judgment). These findings suggest that
the FCI domains may form a general hierarchy of
difficulty for patients with mild AD. Moderate AD
patients, in turn, demonstrated very high rates of
incapable outcomes on all FCI domains (range
90–100%). The relationship of the AD patients’
dementia level to their capacity outcomes was sta-
tistically robust for all domains (Table 15.10)
(Marson et al., 2000).
 Assessing Civil Competencies in Older Adults with Dementia 419

TABLE 15.9 FCI6 DOMAIN AND TASK PERFORMANCE BY GROUP 10

Score Controls Mild AD Moderate AD

Range [n = 23] [n = 30] [n = 20]
Domain 1 Basic Monetary Skills 0–79 77.9a (1.9) 75.5c (3.5) 57.9 (16.3)
Task 1a Naming Coins/Currency 0–30 30.0a (0.0) 30.0c (0.0) 26.7 (4.7)
Task 1b Coin/Currency Relationships 0–37 36.0a (1.8) 34.0c (3.0) 22.7 (9.2)
Task 1c Counting Coins/Currency 0–12 11.9a (0.3) 11.5c (0.8) 8.6 (3.8)
Domain 2 Financial Concepts 0–41 35.5a,b (2.7) 29.6c (5.4) 19.1 (6.3)
Task 2a Defining Concepts 0–16 13.0a,b (1.9) 9.7c (2.9) 7.1 (2.7)
Task 2b Applying Concepts 0–25 22.5a,b (1.4) 19.9c (3.6) 12.0 (4.6)
Domain 3 Cash Transactions 0–48 46.2a,b (2.7) 38.6c (8.5) 22.2 (10.1)
Task 3a 1 Item Purchase 0–16 15.3a (2.5) 14.4c (3.2) 8.6 (4.9)
Task 3b 3 Item Purchase 0–16 15.2a,b (1.3) 10.7c (5.0) 4.6 (3.3)
Task 3c Change/Vending Machine 0–16 15.7a,b (0.6) 13.6c (2.8) 9.0 (4.1)
Domain 4 Checkbook/Register 0–62 60.2a,b (2.1) 50.7c (8.0) 33.3 (16.1)
Task 4a Understanding Checkbook 0–32 30.7a (1.5) 27.9c (3.1) 20.6 (7.6)
Task 4b Using Checkbook 0–30 29.5a,b (1.5) 22.8c (6.1) 12.2 (9.1)
Domain 5 Bank Statement 0–40 37.4a,b (2.2) 28.6c (7.6) 14.9 (7.2)
Task 5a Understanding Bank 0–22 19.7a,b (2.1) 15.0c (4.1) 8.0 (3.6)
Statement
Task 5b Using Bank Statement 0–18 17.7a, b (0.9) 13.6c (4.3) 6.9 (4.1)
a,b c
Domain 6 Financial Judgment 0–37 30.0 (3.0) 20.8 (5.4) 10.7 (5.1)
Task 6a Detecting Fraud Risk 0–10 8.6a (2.0) 7.8c (2.2) 6.9 (2.8)
Task 6b Investment Decision 0–27 21.4a,b (2.1) 13.0c (4.4) 5.3 (3.5)
a
Normal control mean differs from moderate AD mean using LSD post hoc test (p < .01)
b
Normal control mean differs from mild AD mean (p <.01)
c
Mild AD mean differs from moderate AD mean (p < .01)

This study represented the first empirical effort
to investigate loss of financial capacity in patients
with AD (Marson, 2001a). The findings suggest
that significant impairment of financial capacity
occurs in AD, even in the early stage of the disease.
Mild AD patients appear to experience deficits in
complex financial abilities (tasks), and some level
of impairment in almost all financial activities
(domains). Moderate AD patients appear to expe-
rience loss of both simple and complex financial
abilities, and severe impairment across all finan-
cial activities. Based on these initial findings, we
proposed two preliminary clinical guidelines for
assessment of financial capacity in patients with
mild and moderate AD (Marson et al., 2000):
(1) Mild AD patients are at significant risk for
impairment in most financial activities, in
particular complex activities like checkbook
and bank statement management. Areas of
preserved autonomous financial activity should
be carefully evaluated and monitored.
(2) Moderate AD patients are at great risk
for loss of all financial activities. Although each
AD patient must be considered individually,
it is likely that most moderate AD patients
will be unable to manage their financial affairs
(p. 883).
Declining Financial Capacity
in Patients with Mild AD
In another study in our laboratory, we showed
that financial capacity declines in mild AD over
the course of just one year (Martin et al., 2008a).
In a sample of 55 individuals with mild AD and 63
healthy older adults, we examined financial capac-
ity on two occasions with the FCI-9. Results from
this study replicated our prior cross-sectional
findings and indicated that patients with mild AD
exhibit global financial capacity deficits relative to
420 forensic neuropsychology

TABLE 15.10 CAPACIT Y OUTCOMES ON FCI6 DOMAINS ACROSS AD

PATIENT SUBGROUPS 11
Capable Marginally Incapable p*
Capable
Domain 1 Basic Monetary Skills .0002
Mild AD Patients 53% (16/30) 17% (5/30) 30% (9/30)
Moderate AD Patients 10% (2/20) 0% (0/20) 90% (18/20)
Domain 2 Financial Concepts .002
Mild AD Patients 47% (14/30) 13% (4/30) 40% (12/30)
Moderate AD Patients 5% (1/20) 5% (1/20) 90% (18/20)
Domain 3 Cash Transactions .0002
Mild AD Patients 47% (14/30) 10% (3/30) 43% (13/30)
Moderate AD Patients 0% (0/20) 0% (0/20) 100% (20/20)
Domain 4 Checkbook/Register .02
Mild AD Patients 27% (8/30) 13% (4/30) 60% (18/30)
Moderate AD Patients 0% (0/20) 5% (1/20) 95% (19/20)
Domain 5 Bank Statement .003
Mild AD Patients 27% (8/30) 16% (5/30) 57% (17/30)
Moderate AD Patients 0% (0/20) 0% (0/20) 100% (20/20)
Domain 6 Financial Judgment .007
Mild AD Patients 13% (4/30) 37% (11/30) 50% (15/30)
Moderate AD Patients 0% (0/18) 6% (1/18) 94% (17/18)

* Significance of difference in capacity outcomes across dementia stage (mild v. moderate AD) using chi square

same-aged cognitively intact peers at baseline.
At one-year follow up, participants in the mild
AD group exhibited marked declines in overall
financial capacity and on the majority of financial
capacity domains. In contrast, the healthy older
adults exhibited stable financial capacity over the
course of the study. Overall, the AD group exhib-
ited relatively rapid change, with an overall 10%
decline over the course of one year—from approx-
imately 80% of the control group’s performance
level at the baseline assessment to 70% of the
control group’s performance level at follow-up.
Psychometric Study of Financial
Capacity in Mild Cognitive Impairment
Financial Capacity in Patients with MCI
Our group has also examined financial capacity in
patients with mild cognitive impairment (MCI).
As noted above, MCI represents a transitional
phase between normal cognitive aging and
dementia (Morris et al., 2001; Petersen et al.,
2001), with less cognitive and in particular func-
tional impairment than is characteristic of demen-
tia but nevertheless with emerging declines in
instrumental activities of daily living (Daly
et al., 2000; Morris, 2002; Ritchie et al., 2001;
Griffith et. al 2003).
In an initial study using an expanded FCI
(FCI-9), we examined financial capacity in a
cross-sectional sample of 21 older controls, 21
patients with amnestic MCI, and 22 patients with
mild AD (Griffith et al., 2003). We found that, at
the domain level, controls performed significantly
better than mild AD subjects on all domains with
the exception of Domain 8 (Knowledge of Assets/
Estate). Controls performed significantly better
than the MCI group on Domains 2 (Financial
Concepts), 4 (Checkbook Management), 5 (Bank
Statement Management), 6 (Financial Judgment),
and 7 (Bill Payment). There were no domains on
which the MCI group performed better than con-
trols. In turn, the MCI group performed signifi-
cantly better than mild AD patients on all domains
except Financial Judgment and Knowledge of
Assets/Estate.
At the task level, controls performed signifi-
cantly better than the mild AD group on most
abilities, with the exception of simple tasks of
 Assessing Civil Competencies in Older Adults with Dementia
basic monetary skills, cash transactions, and tele-
phone fraud. Controls performed significantly
better than the MCI group on tasks of applying
financial concepts, understanding and using a
bank statement, understanding bills, and prepar-
ing bills for mailing. The MCI group, in turn,
demonstrated significantly higher scores than the
AD group on tasks of understanding and applying
financial concepts, using a vending machine,
understanding and using a checkbook, under-
standing and using a bank statement, prioritizing
bills, and preparing bills for mailing. There were
no tasks on which the MCI group performed
better than controls.
For overall financial capacity (Domains 1–7),
control participants performed significantly
better than MCI and AD participants, and MCI
participants performed significantly better than
AD participants. On an experimental measure of
overall financial capacity that included knowledge
of assets and estate arrangements (Domains 1–8),
smaller samples of control and MCI subjects
performed significantly better than AD patients
but did not differ significantly from each other.
This study represents one of the first published
reports of psychometric evidence for higher order
functional decline and capacity loss in MCI
(Griffith et al., 2003). Using a direct assessment
approach, we found that patients with amnestic
MCI demonstrated significant, albeit mild, defi-
cits on some (but not all) financial abilities com-
pared to age, education, gender, and racially
matched healthy controls. MCI patients showed a
decline in overall financial capacity (Domains
1–7) of 1.74 SD units compared to control partici-
pants (Table 15.11). These results suggest that
initial declines in more complex financial abilities
begin in MCI prior to the development of a frank
dementia.
Cognitive Predictors of Financial
Capacity in MCI and Mild AD
We recently identified cognitive predictors of
FC in a sample of healthy older controls (n=85),
aMCI patients (n=113), and mild AD patients
(n=43) (Sherod et al., 2009). Our goal was to
develop and compare multivariate cognitive
421
models of FC across the continuum from normal
aging to dementia. As reflected below in
Table 15.12, robust cognitive models of FC
emerged for each group. Written arithmetic skill
(WRAT-3 Arithmetic) was the primary predictor
of FC across all three models, accounting for
27% (control model), 46% (mild AD model),
and 55% (aMCI model) of variance. Visuomotor
tracking/executive function was a secondary
cognitive predictor of FC across the two patient
models. Short-term verbal memory and visuomo-
tor tracking/executive function were secondary
predictors for the normal aging group. The find-
ings strongly implicate written arithmetic skills
as a critical cognitive function supporting FC
in both cognitive aging and neurodegenerative
disease.
Summary of Financial
Capacity Research
In summary, this line of research supports our
conceptual model of FC and suggests the utility of
psychometric instruments for direct assessment
of financial capacity in patients with neurodegen-
erative disease. The FCI represents a potential
advance in functional assessment in dementia
(Moye, 2003). It is specific to the construct of
financial capacity, and is based on a model con-
ceptualizing financial capacity as a series of
discrete spheres of activity (domains) linked to
independent community functioning. The FCI
operationalizes these domains with tests of
specific financial abilities (tasks), which are objec-
tive and behaviorally anchored. It also provides
global estimates of financial capacity useful to cli-
nicians. In addition, the FCI has demonstrated
construct validity by discriminating the financial
performance and capacity outcomes of controls,
mild AD patients, and moderate AD patients
(Marson et al., 2000), and the performance of
controls, amnestic MCI patients, and mild AD
patients (Griffith et al., 2003). Finally, neurocog-
nitive modeling of financial capacity has yielded
promising results, with findings suggesting that
written arithmetic skills are strongly associated
with FC performance in both cognitive aging and
prodromal and clinical AD (Sherod et al., 2009).
 TABLE 15.11 COMPARISONS OF GROUP PERFORMANCE ON THE FCI9 12
Score Controls MCI AD Patients P Post-hoc
Range (n = 21) Patients (n =22) (2-tailed) p <.05
X (SD) (n = 21) X (SD)
X (SD)
Domain 1/Basic Monetary Skills 0–48 45.2 (3.5) 44.3 (3.7) 41.0 (6.3) .011 C M>A
Naming Coins/Currency 0–8 7.9 (0.3) 7.8 (0.4) 7.6 (0.7) .050 C>A
Coins/Currency Relationships 0–28 24.9 (3.4) 24.8 (3.5) 22.0 (5.5) .044 —
Counting Coins/Money 0–12 12.0 (0.2) 11.7 (0.5) 11.5 (1.2) .119 —
Domain 2/Financial Concepts 0–40 36.9 (3.2) 33.1 (4.7) 27.6 (7.5) .001 C> M > A
Understanding Concepts 0–15 13.8 (1.2) 12.9 (1.8) 11.2 (2.6) .001 C M> A
Applying Concepts 0–25 23.1 (2.4) 20.2 (3.6) 16.4 (5.3) .001 C >M > A
Domain 3/Cash Transactions 0–30 27.0 (3.4) 24.8 (3.6) 20.6 (5.9) .001 C M>A
One Item Transaction 0–6 6.0 (0.0) 5.8 (0.6) 5.5 (1.1) .044 C>A
Multi-Item Transaction 0–7 6.1 (1.9) 5.7 (1.8) 4.5 (2.4) .037 C>A
Vending Machine 0–9 8.6 (0.9) 8.0 (1.4) 5.6 (1.9) .001 C M> A
Tipping 0–8 6.3 (1.7) 5.4 (1.5) 5.1 (2.1) .068 —
Domain 4/Checkbook 0–54 53.2 (1.5) 50.6 (2.9) 42.9 (8.0) .001 C M >A
Management
Understanding Checkbook 0–24 23.5 (0.8) 22.8 (1.5) 21.2 (2.5) .001 C M >A
Using Checkbook 0–30 29.6 (1.4) 27.9 (2.2) 21.7 (6.0) .001 C M >A
Domain 5/Bank Statement 0–38 35.2 (2.7) 29.9 (5.6) 23.3 (8.3) .001 C> M> A
Management
Understanding Bank Statement 0–18 16.2 (1.6) 13.4 (2.7) 10.6 (3.9) .001 C> M> A
Using Bank Statement 0–20 19.1 (1.5) 16.5 (4.0) 12.7 (4.9) .001 C> M> A
Domain 6/Financial Judgment 0–26 25.6 (1.2) 23.2 (3.7) 23.5 (3.5) .029 C> M A
Mail Fraud 0–8 8.0 (0.0) 7.3 (1.3) 7.1 (1.6) .045 C> A
Telephone Fraud 0–18 17.6 (1.2) 15.9 (3.0) 16.4 (2.3) .051 —
Domain 7/Bill Payment 0–46 43.7 (3.3) 38.4 (6.2) 28. 3 (9.6) .001 C> M> A
Understanding Bills 0–6 5.9 (0.4) 5.1 (1.2) 4. 7 (1.6) .006 C> M A
Identifying/Prioritizing Bills 0–13 12.6 (0.6) 12.3 (1.1) 10. 9 (1.7) .001 C M> A
Preparing Bills for Mailing 0–27 25.1 (3.3) 20.4 (6.1) 12. 7 (8.4) .001 C> M> A
Domain 8/Assets & Estate 0–20 18.1 (1.6) 17.4 (2.6) 16. 2 (2.8) .068 —
Arrangementsa
Domain 9/Investment Decision 0–17 13.9 (2.9) 12.4 (2.3) 9. 2 (3.5) .001 C M> A
Makingb
FCI Total Score (Domains 1–7) 0–282 266.8 (13.2) 243.8 (21.7) 207.2 (38.0) .001 C >M >A
FCI Total Score (Domains 1–8)a 0–302 282.1 (14.1) 264.0 (17.8) 223.8 (39.9) .001 C M >A
a
control = 15, MCI = 13, AD = 21
b
control = 21, MCI = 19, AD = 18
C>A = control mean is greater than AD mean C>M>A = control mean is greater than MCI mean and AD mean, and MCI mean is greater
than AD mean
C>MA = control mean is greater than MCI and AD means CM>A = control and MCI means are greater than AD mean

422
 Assessing Civil Competencies in Older Adults with Dementia 423

TABLE 15.12 MULTIVARIATE COGNITIVE PREDICTOR MODELS a OF FCI TOTAL

SCORE DOMAINS 17 ACROSS GROUPS 13

Control Predictor Model MCI Predictor Model Mild AD Predictor Model

(n = 85) (n = 113) (n = 43)
Measure r Cum R2 Measure r Cum R2 Measure r Cum R2

Step 1 Arithmetic .54 .27 ‡ Arithmetic .74 .55‡ Arithmetic .67 .46‡
Step 2 Log Mem II .35 .35 † Trails B −.73 .66‡ Trails A .60 −.0.56†
Step 3 Trails A −.29 .38* Race −.55 .69‡ Log Mem I .63 65†
Digits Forward .34 Dig Symbol .59
Trails B −.31 Vis Rep I .54

* p < .05
† p < .01
‡ p < .001
a
Tasks in bold entered into the multivariate predictor models, while non-bolded tasks did not enter into the model.
Arithmetic = Wide Range Achievement Test-Third Edition (Arithmetic subtest)
Log Mem I = Logical Memory I (immediate recall) subtest from the Wechsler Memory Scale-Revised
Log Mem II = Logical Memory II (delayed recall) subtest from the Wechsler Memory Scale-Revised
Digits Forward = Digit Span subtest (digits forward portion) from the Wechsler Memory Scale-Third Edition
Dig Symbol = Digit Symbol from the Wechsler Adult Intelligence Scale-Third Edition
Spat Back Raw = Spatial Span Backwards subtest from the Wechsler Memory Scale-Third Edition
Vis Rep I = Visual Reproduction I (immediate recall) subtest from the Wechsler Memory Scale-Third Edition

T E S TA M E N TA RY fact appear to be increasing in number (Nedd,

C A PA C I T Y
Background
In this section we discuss conceptual and clinical
aspects of a third civil competency: capacity to
make a will (testamentary capacity). The freedom
to choose how one’s property and other posses-
sions will be disposed of following death—known
as the right of testation—is a fundamental right
under Anglo-American law (Frolik, 2001; Marson
et al., 2004). A key requirement of the law of
testation is that a testator (person making the will)
have testamentary capacity or competency (TC):
“that measure of mental ability recognized in law
as sufficient for the making of a will” (Black, 1968).
If testamentary capacity is lacking at the time of
execution of the will, the will is invalid and void in
effect (Perr, 1991). The legal requirement of testa-
mentary capacity exists across all state jurisdic-
tions, and Anglo-American law has strongly
supported testation over intestacy (Frolik, 2001;
Marson et al., 2004). Public policy and legal prec-
edent have clearly favored allowing individuals to
choose how their property will be distributed after
death rather than leaving such decisions to state
laws governing intestacy. However, despite the
legal system’s tendency to favor the rights of the
testator, cases challenging the validity of wills and
specifically the testamentary capacity and/or inde-
pendent volition of testators are common and in
1998). This increase in will contest litigation reflects
a number of factors, in particular our aging society
and increasing numbers of older adults with neu-
rologic, psychiatric, and medical impairments that
impair mental capacity (Marson et al., 2004). Other
factors include the breakdown of the nuclear family
and increase in blended families with conflicting
agendas, and the enormous transfer of wealth
currently ongoing between the World War II and
baby boomer generations (Nedd, 1998).
The legal concept of testamentary capacity
should be distinguished from that of undue
influence. In order to make a valid will, the law
also requires, in addition to testamentary
capacity, that the testator be free from undue
influence by another individual who may profit
from a new will or a legal amendment of an
existing will (codicil) (Spar, Hankin, & Stodden,
1995). Thus, even when a testator has sufficient
testamentary capacity, the will may be voided
by the court if the court or jury deems that the
volition of the testator was supplanted by an indi-
vidual exercising undue influence over him/
her. The doctrine of undue influence, which also
exists in various forms across state jurisdictions, is
thus analytically distinct from testamentary
capacity—it applies in cases in which the testator
possesses some level of testamentary capacity
that is subverted through a relationship with the
influencer (American Bar Association/American
424 forensic neuropsychology
Psychological Association Assessment of Capacity
in Older Adults Project Working Group, 2008;
Frolik, 2001). As discussed further below, these
two legal issues very frequently co-occur and
intertwine in will contests.
Legal Elements of Testamentary Capacity
The current legal requirements for testamentary
capacity in the United States vary to some degree
from state to state. In many states (although
not all) four specific criteria or elements are
recognized (Marson et al., 2004; Spar & Garb,
1992). A testator must:
(1) understand the nature of the testa-
mentary act (i.e., know what a will is);
(2) understand and recollect the nature and
situation of his or her property;
(3) have knowledge of the persons who are the
natural objects of his or her bounty; and
(4) know the manner in which the
disposition of the property is to occur.
The way in which these elements are weighed
by courts in determining the validity of a will
varies across states (Frolik, 2001; Spar et al., 1995).
Some states require that the testator meet only
one or two of the criteria for a will to be valid.
Other states may require additional criteria;
for example, that the testator understand a will,
demonstrate memory of all property and poten-
tial heirs, and ‘hold this information in mind’
while developing a plan for disposition of assets
(Spar & Garb, 1992; Walsh et al., 1997).
In addition to the elements mentioned above,
many states also require that the testator at the
time the will is executed not exhibit delusions
and/or hallucinations that may result in a will that
excludes or favors potential heirs based on false
beliefs and/or is uncharacteristic of the testator’s
preferences in the absence of delusions and
hallucinations (Spar & Garb, 1992; Walsh et al.,
1997). However, a will may be ruled valid if
delusions and hallucinations are discrete, unasso-
ciated with the testator’s property and potential
heirs, and/or have seemingly little or no impact
on testator’s plan for the disposition of assets
(Marson et al., 2004; Walsh et al., 1997).
Conceptual Models of
Testamentary Capacity
There continues to be a need for useful conceptual
models of testamentary capacity that can inform
clinical and forensic assessment. Initial studies in
this area by Spar and Garb focused on developing
practical approaches to clinical assessment as
opposed to model building (Spar & Garb, 1992).
One useful approach to conceptual model building
involves direct analysis of the component legal ele-
ments of testamentary capacity. Using the model for
analyzing legal capacities developed by Grisso
(Grisso, 2003), this approach begins by identifying
the specific legal standard for testamentary capacity
(the legal elements of testamentary capacity) and
next involves identification of the ‘functional’
requirements of these legal elements. What cogni-
tive, emotional, and pragmatic abilities (functional
requirements) are required to understand the nature
of a will, know the nature and extent of one’s prop-
erty, know the natural objects of one’s bounty
(potential heirs), and know general plan of property
disposition? Systematic conceptualization of the
functional requirements will allow clinical evalua-
tors to better determine in individual cases whether
or not the testator has testamentary capacity, which
in turn will assist judges who must make the ulti-
mate legal determination of testamentary capacity.
This approach to the issue naturally leads to
questions regarding (1) the neuropsychological
abilities that underlie each of the component legal
elements, and whether they can be conceptual-
ized and measured, and (2) more generally, how
to operationalize the legal elements of testamen-
tary capacity for purposes of assessment instru-
ment development.
Preliminary Neuropsychological
Model of Testamentary Capacity
Some initial ideas for development of a neuropsy-
chological model of testamentary capacity can be
found in the legal and psychological literature.
Walsh and colleagues, in conjunction with the
American Bar Association, identified several fac-
tors required for the determination of testamen-
tary capacity as defined in medical terms (Walsh
et al., 1997). These are functional autonomy, work-
ing memory, orientation, attention, and calcula-
tion (Walsh et al., 1997). Likewise, research on
medical decision-making and financial capacity
has found correlations between these civil compe-
tencies and performance on neuropsychological
measures of conceptualization, calculation, seman-
tic memory, verbal recall, and executive function,
particularly word fluency (Marson, Sawrie, Stalvey,
McInturff, & Harrell, 1998; Marson et al., 1996;
Marson et al., 1995a). A very recent study has
identified written arithmetic ability as the primary
predictor of financial capacity in cognitively
normal controls, patients with amnestic MCI, and
 Assessing Civil Competencies in Older Adults with Dementia
patients with mild AD (Sherod et al., 2009). It is
likely that arithmetic ability may also play a role in
the element of testamentary capacity relating to
understanding the nature and extent of property,
and possibly also to disposition of assets.
What is currently needed, however, are empir-
ical studies that specifically correlate performance
on neuropsychological test measures with mea-
sures of testamentary capacity. The literature is
silent here with the exception of one recent brief
report (Roked & Patel, 2008). This study from
England found that two screening measures (the
MMSE and CAMDEX-R) were each able to pre-
dict 87% of independent rater judgments of testa-
mentary capacity in a sample of 74 patients with
mild to moderate AD. The language domain of
the CAMDEX-R was the strongest cognitive
domain predictor, while short-term memory and
concentration domains were not predictors.
Testamentary capacity was also associated with
dementia severity, with 62.5% of mild AD patients
rated as capable, versus 35% of moderate AD
patients and 2.5% of severe AD patients. Insofar as
its major conclusion is that global mental status is
associated with testamentary capacity in AD,
knowledge provided by this study is limited. In
addition, the study did not provide needed infor-
mation regarding the relationship of cognitive per-
formance to the respective legal elements of
testamentary capacity. Nonetheless, the study rep-
resents a first step in what hopefully will be a grow-
ing focus of forensic neuropsychological research.
Although empirical data are presently lacking,
a theoretical neuropsychological model of testa-
mentary capacity continues to have heuristic value.
Our capacity research group has previously
described the following hypothesized cognitive
constructs for the four legal elements of testamen-
tary capacity described above (Marson et al., 2004).
A discussion of the material below can also be
found in the ABA/APA capacity handbook for psy-
chologists (American Bar Association/American
Psychological Association Assessment of Capacity
in Older Adults Project Working Group, 2008).
1. Cognitive Functions Related to
Understanding the Nature of a Will: This
element requires a testator to understand
the nature, purposes and consequences of a
will, and to express these verbally or in
some other adequate form to an attorney or
judge. Possible cognitive functions involved
may include semantic memory regarding
terms such as death, property, and
inheritance, verbal abstraction and
425
comprehension abilities, and sufficient
language abilities to express the testator’s
understanding (borne out by the recent
language domain findings referenced above
in the recent paper by Roked and Patel;
Roked & Patel, 2008). Recognition items
may assist a testator with expressive
language problems. A reply of ‘yes’ or ‘no’ to
an attorney’s queries regarding the nature of
a will is unlikely to be satisfactory in this
regard, as such responses do not clearly
support the testator’s independent
understanding of the element. Similarly, a
testator’s signature on a legal document by
itself does not demonstrate understanding,
as a signature is an automatic procedural
behavior not dependent upon higher level
cognition (Greiffenstein, 1996).
2. Cognitive Functions Related to Knowing
the Nature and Extent of Property: The
second legal element of testamentary
capacity requires that the testator
remember the nature and extent of his or
her property to be disposed. As reported
earlier, some states differ in their
interpretation of this (§2.04 Variation in
Requirements, pp. 2–13) (Walsh et al.,
1997). Possible cognitive functions
involved here would include semantic
memory concerning assets and ownership,
historical memory and short-term memory
enabling recall of both long-term and more
recently acquired assets and property, and
knowledge and comprehension of the value
tied to different assets and property. If the
testator has recently purchased new
possessions prior to his or her execution of
a will, then impairment in short-term
memory (the hallmark sign of early AD)
can significantly impact his or her recall of
these items. Testators also must be able to
form working estimates of value for key
pieces of property that reasonably
approximate their true value; it is likely that
executive function abilities play a role here.
(Marson et al., 2004; American Bar
Association/American Psychological
Association Assessment of Capacity in
Older Adults Project Working Group, 2008)
3. Cognitive Functions Related to Knowing the
Objects of One’s Bounty: This legal element
requires that the testator be cognizant of
those individuals who represent his natural
heirs, or other heirs who can place a
426 forensic neuropsychology
reasonable claim on the estate. Historical
and also short term episodic personal
memory of these individuals, and of the
nature of their relationships with the
testator, would appear to be prominent
cognitive abilities associated with this
element. As dementias like AD progress,
testators may be increasingly unable to
recall family members and acquaintances,
leading ultimately to failure to recognize
these individuals in photographs or even
when presenting in person (Marson et al.,
2004; American Bar Association/
American Psychological Association
Assessment of Capacity in Older Adults
Project Working Group, 2008).
4. Cognitive Functions Related to a Plan for
Distribution of Assets: This final legal element
of testamentary capacity requires that the
testator be able to express a basic plan for
distributing his or her assets to the intended
heirs. Insofar as this element integrates the
first three elements in a supraordinate
fashion, the proposed cognitive basis for this
element arguably represents an integration
of the cognitive abilities underlying the other
three elements. Accordingly, higher order
executive function abilities are implied as the
testator must demonstrate a projective
understanding of how future dispositions of
specific property to specific heirs will occur,
and the rationale for these dispositions
(Marson et al., 2004; American Bar
Association/American Psychological
Association Assessment of Capacity in Older
Adults Project Working Group, 2008).
The preliminary theoretical neuropsychologi-
cal model of testamentary capacity proposed
above represents a step towards conceptual model
building in this area. The model currently focuses
on proposed cognitive demands of the legal
elements, and does not address the emotional/
psychiatric aspects of the capacity. Such a model
would require empirical verification in an older
adult sample through use of a relevant testamen-
tary capacity instrument and neuropsychological
test measures. As discussed below, there is cur-
rently a lack of psychological assessment instru-
ments and associated empirical research specific
to this domain of forensic practice (but in the legal
sphere, refer to The Legal Capacity Questionnaire
[§ 1.10, pp. 1–17 to 1–22]; Walsh et al., 1997).
As testamentary capacity matures as an area of
civil competency practice and research, one can
anticipate the emergence of conceptually based
assessment instruments.
Empirical Studies of
Testamentary Capacity
There is currently little published empirical
research on testamentary capacity (Marson et al.,
2004). In part this reflects the still early develop-
mental stage of the field of capacity assessment
generally. With the exception of treatment con-
sent capacity, for which there is now a reasonable
body of research (Appelbaum & Grisso, 1995;
Dunn et al., 2006; Grisso & Appelbaum, 1995;
Grisso et al., 1995; Karlawish, 2008; Kim et al.,
2001; Marson et al., 1995c; Palmer & Savla, 2007),
relatively little conceptual and empirical research
has been conducted thus far regarding other
important civil competencies such as financial
capacity (Marson, 2001a; Marson et al., 2000;
Martin et al., 2008a; Sherod et al. 2009). However,
this point notwithstanding, the area of testamen-
tary capacity seems to have been particularly
neglected. Although there is a growing literature
providing general clinical guidelines for assess-
ment of testamentary capacity (American Bar
Association/American Psychological Association
Assessment of Capacity in Older Adults Project
Working Group, 2008; Marson et al., 2004; Spar &
Garb, 1992) there is currently no body of empiri-
cal research that can inform and advance the field.
Given the prevalence and societal importance of
inheritance by will, this remains a key knowledge
gap in neuropsychological forensic science as it
relates to civil competencies and the elderly.
Prototype Psychometric Instrument for
Assessing Testamentary Capacity
As discussed above, no standardized psychologi-
cal measures of testamentary capacity currently
exist in everyday practice. However, a prototype
psychometric instrument, called the Testamentary
Capacity Instrument (TCI), has recently been
developed and field tested by the lead author and
a co-author (K.H.) (Hebert, Scogin, & Marson, in
preparation). The TCI is a structured, psychomet-
ric measure for assessing and differentiating the
testamentary capacity of cognitively-intact versus
cognitively-impaired older adults.
The TCI measures capacity using the four legal
elements of testamentary capacity discussed above.
Performance on each element is based on the indi-
vidual’s ability to recall or recollect information
pertinent to the execution of a will. The degree to
 Assessing Civil Competencies in Older Adults with Dementia
which memory for relevant information is required
by law varies (Walsh et al., 1997). For this reason,
the four elements are measured using free recall
and recognition items (multiple-choice and also
forced-choice). An individual who may not be
able to freely recall information pertinent to a legal
element may still be able to accurately identify this
information in a recognition or forced-choice
(Yes-No/True-False) format. All items are admin-
istered orally or in writing and are quantitatively
scored. Within a legal element, item scores are
summed, giving rise to an overall performance
score. These performance scores, in turn, can sup-
port judgment outcomes (capable, marginally
capable, or incapable), for the individual element,
and also for overall testamentary capacity.
Although if necessary the TCI is designed to be
a stand alone assessment, its administration to an
older adult testator should ideally co-occur with a
comprehensive neuropsychological evaluation. The
standardized and objective cognitive and emotional
test data will provide an important overall context
for the evaluation, and can help inform findings
regarding the specific legal elements, as well as
guide the clinician’s overall judgment of capacity.
Standardized assessment of testamentary capac-
ity involves certain methodological challenges that
require attention. Unlike knowledge of a will
(Element 1), information concerning a testator’s
assets/property, his/her natural heirs, and his/her
plan of distribution (Elements 2–4) is individual
specific and not as readily amenable to standardized
inquiry across patients/clients. Accordingly, it is
very important to obtain accurate information
regarding the testator’s property and heirs from reli-
able collateral sources, in order to evaluate and verify
the testator’s own responses to questions tapping
these three legal elements (Spar & Garb, 1992). Thus,
the TCI explicitly seeks collateral information for all
four legal elements. However, collateral sources
sometimes may have limited or inaccurate informa-
tion regarding the testator’s assets and/or relation-
ships with potential heirs (Marson et al., 2004). In
addition, collateral sources may have potential con-
flicts of interest insofar they are often also prospec-
tive heirs of the testator. Such conflicts of interest
may thus bias responses of collateral sources to
inquiries regarding the testator’s assets and heirs,
as well as regarding the testator’s general cognitive
function, psychiatric health, and quality of rela-
tionships with other prospective heirs. These
issues obviously require application of clinical
judgment by the examiner in selecting collateral
sources and using the TCI and related instruments.
427
Initial Empirical Study of Testamentary
Capacity in Dementia
Using the TCI, a member of our group (K.H.,
co-author) has conducted an initial empirical
study of testamentary capacity in a small sample
of cognitively healthy older controls and patients
with mild to moderate AD (Hebert et al., in prep-
aration). This paper is currently in preparation for
publication and thus formal specific findings will
not be reported here. However, it appears that
impairment in testamentary capacity is already
evident in the early stages of AD, with all four ele-
ments of testamentary capacity showing compro-
mise. In addition, distinct forms of cognitive
impairment are associated with the elements of
testamentary capacity, and with overall testamen-
tary capacity, in AD (Hebert et al., in preparation).
The results appear very promising and support
the feasibility of psychometrically measuring
testamentary capacity constructs and of pursuing
empirical studies of testamentary capacity in
cognitively impaired older adults.
Clinical Assessment of
Testamentary Capacity
Current clinical practice in cases of testamentary
capacity can be divided into two major areas:
(1) prospective clinical assessments of testamen-
tary capacity involving living testators and family
members, usually completed contemporaneously
with a will execution (American Bar Association/
American Psychological Association Assessment
of Capacity in Older Adults Project Working
Group, 2008; Marson et al., 2004; Spar & Garb,
1992); and (2) retrospective analyses of testamen-
tary capacity and undue influence in cases involv-
ing a now deceased or incompetent testator
(American Bar Association/American Psycholo-
gical Association Assessment of Capacity in Older
Adults Project Working Group, 2008; Greiffenstein,
1996; Marson et al., 2004; Spar & Garb, 1992). In
each of these areas, current practice patterns vary
quite widely in approach and quality, in large part
due to uneven conceptual understanding among
many practitioners of capacity assessment gener-
ally (Marson & Ingram, 1996; Marson, 2001b),
and of the legal requirements of testamentary
capacity and undue influence specifically.
Contemporaneous Assessment of
Testamentary Capacity
In certain circumstances, an attorney, judge, or
family member may request that a mental health
professional assess the capacity of a living testator
428 forensic neuropsychology
prior to or contemporaneously with his/her execu-
tion of a will. Two common scenarios underlie
such a referral. The attorney or judge may have
concerns about the testamentary capacity of the
proposed testator, and therefore will seek clinical
expertise and input on the issue before proceeding
further. Alternatively, in cases of ongoing or antic-
ipated family conflict, the foresighted attorney
may seek to preempt a future will contest by having
his client undergo a capacity assessment prior to
or contemporaneous with will execution (Marson
et al., 2004; American Bar Association/American
Psychological Association Assessment of Capacity
in Older Adults Project Working Group, 2008).
Spar and colleagues have written cogently on
the topic of contemporaneous clinical assessment
of testamentary capacity and undue influence
(Spar & Garb, 1992; Spar et al., 1995). Their clini-
cal interview guidelines for testamentary capacity
published in 1992 continue to represent a key con-
tribution to forensic practice in this area. The key
aspects of the interview are to ‘assess the legal ele-
ments of testamentary capacity, identify any fea-
tures of the testator’s personality and mental status
that could affect susceptibility to undue influence,
and determine the nature, extent, and general
functional consequences of mental illness, if any’
(pp. 171–172) (Spar & Garb, 1992). The authors
highlight the importance of conducting the clini-
cal interview in close proximity to the moment the
testamentary document is executed (Marson &
Hebert, 2008b). Interviews conducted in close
proximity to the time of testamentary document
execution are more likely to be influential in court
than those conducted at more distant time peri-
ods. This consideration is important as courts gen-
erally place great emphasis on the testator’s mental
functioning at the time in question and recognize
that individuals’ mental functioning can vary at
different time points (Spar et al., 1995).
A second and perhaps more difficult challenge
for the clinical examiner is to obtain as much
information as possible about the testator’s
property (Element 2) and names and relationships
of potential heirs (Element 3). As noted above,
this can be a difficult task when the testator’s
informants are limited to family members who
may also serve to profit from the examiner’s testi-
mony. An objective independent source of infor-
mation regarding a testator’s potential heirs and
possessions is strongly recommended but may
not always be practical. A private interview
with only the testator is recommended to limit
outside influences. A videotaped recording of the
interview with the testator may prove beneficial
for illustrating both testamentary capacity and the
lack of outside influences; however, this should
first be discussed and cleared with the testator’s
attorneys.
As part of the evaluation, an assessment of the
testator’s lifelong values about money, personal
property, and finances can be very useful. As dis-
cussed above, for reasons of public policy, courts
invoke a low legal threshold for upholding wills
and permitting legal transfer of property after
death. Thus, the personal values and interests of
the testator may be given considerable weight by
courts (American Bar Association/American
Psychological Association Assessment of Capacity
in Older Adults Project Working Group, 2008). In
this regard, important information can be ascer-
tained by reviewing prior wills of a testator, which
will presumably reflect the prior application of
his/her values to the assignment of property to
designated heirs. A testator’s radical departure
from prior testamentary value patterns in a new
will, known legally as an ‘unnatural will,’ may lead
a court to consider whether a testator is suffering
from diminished capacity or from coercion
through the effects of undue influence (American
Bar Association/American Psychological
Association Assessment of Capacity in Older
Adults Project Working Group, 2008). Issues of
continuity of a testator’s values are also important
in both contemporaneous and retrospective
assessments of testamentary capacity (see below).
Retrospective Assessment of
Testamentary Capacity
Although contemporaneous evaluations of
testamentary capacity are highly desirable and
useful, they probably do not represent the major-
ity of forensic evaluations in this area. More fre-
quently, neuropsychologists and other mental
health professionals are called upon by attorneys,
by the probate court, or by interested family mem-
bers, to render retrospective opinions regarding
the existence of testamentary capacity (and some-
times undue influence) at a previous point in time.
Retrospective evaluations of testamentary capac-
ity usually arise after the death (or sometimes the
incompetency) of a testator, when heirs and/or
other interested parties contest a will on grounds
that the decedent lacked testamentary capacity at
the earlier time of will execution. Although recog-
nized and used by the courts, no clear rules for
conducting such evaluations have been estab-
lished (Spar & Garb, 1992). However, there is
 Assessing Civil Competencies in Older Adults with Dementia
increasing academic attention to the issue
(American Bar Association/American Psycholo-
gical Association Assessment of Capacity in Older
Adults Project Working Group, 2008; Marson
et al., 2004; Marson & Hebert, 2008b; Shulman,
Cohen, & Hull, 2005).
The process of retrospective evaluation has
sometimes been described as a ‘neuropsycholo-
gical autopsy’ (Greiffenstein, 1996), and neurop-
sychological methods and knowledge can be
particularly useful for these purposes (Marson,
2002). Greiffenstein proposed several steps for
determining testamentary capacity retrospec-
tively (Greiffenstein, 1996). First, the clinician
should consider whether the legal issue at hand
pertains to testamentary capacity or undue influ-
ence, or both. Next, the date of the legal transac-
tion should be identified, as this date will help
determine the relevance of contemporaneous
mental status, medical, and lay testimony evi-
dence. This is typically the date in which the will
was signed. The clinician must also identify the
type of neurologic or psychiatric disorder that the
testator had and determine which, if any, cogni-
tive abilities were impacted. This is done by
gathering evidence of normal and abnormal cog-
nitive and emotional behavior occurring as close
as possible to the date of will execution.
A more comprehensive and detailed approach
to retrospective assessment of testamentary
capacity is presented in the recent ABA–APA
capacity assessment handbook for psychologists
(American Bar Association/American Psycholo-
gical Association Assessment of Capacity in Older
Adults Project Working Group, 2008). As part of
the handbook, a set of recommended steps are
presented for the evaluator. A slightly modified
and expanded version of these steps is set forth
below (reprinted by permission of the ABA-APA)
(pp. 86–87).
Recommended Steps in Conducting
a Retrospective Evaluation of
Testamentary Capacity
1. Identify the operative legal standard for
testamentary capacity in your state
jurisdiction.
2. Organize medical, legal, and other
records relevant to the capacity issue.
Creating a chronological timeline
reflecting important medical and lay
events and contacts, and relevant legal
transactions, is essential to organizing
information for the assessment.
429
3. Where possible and as appropriate,
contact and speak with individuals who
knew the decedent testator and can offer
informed lay and professional judgments
about mental status and capacity at the
time of will execution.
4. Obtain information about the attorneys
involved in the prior will execution. Who
was the attorney and what history did he
or she have with the client? What was the
series of professional interactions leading
up to the will execution?
5. Assess for the presence and severity of a
mental disorder at the time of will
execution. With older adults, the most
often disputed wills are often those that
were made or modified when an
individual had a memory disorder or a
diagnosed dementia. Is there evidence,
through medical or other records, of a
mental disorder that might affect cognitive
and emotional abilities related to the
elements of testamentary capacity? In
some cases, there may be specific cognitive
or neuropsychological test information
that will shed light on mental abilities
relevant to testamentary capacity.
6. In cases of dementia, if possible seek to
determine the stage of dementia at the
time of will execution, as it can
significantly inform the clinical judgment
of testamentary capacity. The Clinical
Dementia Rating (CDR) and the Global
Deterioration Scale (GDS) (Morris, 1993;
Reisberg, Ferris, deLeon, & Crook, 1982)
represent dementia staging tools for cases
of Alzheimer’s disease. Dementia stage
when properly determined can be an
evidentiary source that clinicians and
probate courts can both use in making
retrospective capacity determinations.
7. Keep in mind that the presence of a
dementia or other mental disorder is not
sufficient in itself to decide the
retrospective capacity issue. Because the
legal threshold for testamentary capacity is
low, some individuals with mild dementia
may still be capable of making a new will,
whereas patients with more advanced
dementia increasingly will not be.
However, every capacity matter is
individual specific and irrespective of
430 forensic neuropsychology
diagnosis, cognitive impairment, and/or
dementia stage requires an analysis of the
individual’s mental status and condition in
relation to the particular jurisdictional
elements for testamentary capacity.
8. Assess testamentary capacity by
determining whether there is clinical and
other evidence in the record supporting
the critical legal elements of this capacity.
In some cases it may not be possible to
render such a judgment, if there is
insufficient evidence of the testator’s
cognitive, emotional, and everyday
functional abilities contemporaneous with
the prior will execution.
9. In addition to offering a capacity
judgment, a neuropsychological expert
may in some instances be well-positioned
to offer a retrospective opinion regarding
the possible role of undue influence in will
procurement. Many will contest cases
involve an associated, alternative legal
claim of undue influence, with the
contention that even if the testator
possessed residual testamentary capacity,
it was supplanted by the actions of a
third-party influencer.
There are a number of information sources that
can assist a clinician in making a retrospective
assessment of testamentary capacity (Spar & Garb,
1992). These include the testator’s business records,
checkbook and other financial documents, and
personal documents such as family films, videos,
notebooks, and diaries. Medical records yield par-
ticularly useful information including mental status
and neuropsychological testing, diagnosis, level of
impairment, and behavioral observations. As noted
above, clinicians will find it beneficial to interview
the testator’s family, friends, business associates,
and other involved professionals (i.e., physician,
attorney, accountant, notary public, etc.) regarding
the testator’s cognitive and functional abilities
during the time that the will was executed.
Ultimately, the clinician must assemble all of
the information described above, and make a
judgment as to whether or not the testator had
testamentary capacity at the prior relevant time
points. In some cases it may not be possible to
render such a judgment, if there is insufficient evi-
dence of the testator’s cognitive, emotional, and
functional abilities contemporaneous with the
prior will execution. In such cases, it is likely that
the presumption of competency must stand, inso-
far as there would be insufficient evidence to rebut
the presumption or place it in legal question.
Undue Influence and
Testamentary Capacity
As mentioned above, undue influence is a
separate legal ground for voiding a will which is
related to but also distinct from testamentary
capacity. Undue influence has been defined as ‘any
improper or wrongful constraint, machination, or
urgency of persuasion whereby the will of a person
is overpowered and he is induced to do or forbear
an act which he would not do or would do if left to
act freely’ and also as ‘influence which deprives
person influenced of free agency or destroys free-
dom of his will and renders it more the will of
another than his own’ (Black, 1968, pp. 1697–1698).
In situations of undue influence, the testator retains
some level of capacity but is subjected to direct or
indirect coercion that subverts his/her volition and
thus the validity of the will. The resulting will thus
reflects the preferences of the coercing party rather
than the testator, benefits the coercing party over
other potential heirs, and is inconsistent with what
the testator’s wishes would be in the absence of this
influence (Haldipur & Ward, 1996). Indicators of
undue influence include the active participation of
the coercing party in attaining a will and/or con-
trolling the testamentary act, the role of the coerc-
ing party as an advisor or confidant to the testator
and his or her use of this relationship to influence
the way in which the testator disposes of his or her
assets, and provisions within the will that are incon-
sistent with prior and/or subsequent expressions of
the testator’s intent in executing a will (Frolik, 2001;
Marson et al., 2004).
Older persons with dementia or significant
cognitive decline are usually highly vulnerable to
undue influence. Chronic physical and mental ill-
ness as well as memory loss and cognitive dys-
function associated with dementia increase the
dependency of older adults on others, thereby
increasing their susceptibility to undue influence
(Haldipur & Ward, 1996). However, susceptibility
to undue influence is not restricted to individuals
who have cognitive impairment and/or those that
require assistance in their general care and deci-
sion making. As such, a will may also be ruled
invalid by the courts even in the absence of medi-
cal and/or mental illness if other indicators of
undue influence are present (Walsh et al., 1997).
The topic of undue influence receives
considerable attention in the recent ABA–APA
 Assessing Civil Competencies in Older Adults with Dementia
capacity assessment handbook for psychologists
(American Bar Association/American Psycholo-
gical Association Assessment of Capacity in Older
Adults Project Working Group, 2008). A number
of useful psychological conceptual frameworks
for understanding and analyzing undue influence
are presented there (pp. 114–116). All of these are
relevant to situations of testamentary capacity.
For example, the Brandle/Heisler/Stiegel model
focuses on perpetrator behavior in cases of undue
influence. While the perpetrator’s ultimate goal is
financial exploitation of the testator, this can be
accomplished by a variety of means, including
isolation from others and from information
sources, the creation of fear and feelings of
vulnerability, fostering dependency and a sense of
inadequacy, inducing negative emotions such as
shame, and also rendering intermittent acts of
kindness (American Bar Association/American
Psychological Association Assessment of Capacity
in Older Adults Project Working Group, 2008).
Another useful clinical framework is the ‘SCAM’
model proposed by Bernatz which views undue
influence as an ‘inter-relational concept between
victim and perpetrator’ (p. 114), and which incor-
porates core factors of susceptibility of the victim,
a confidential relationship, active procurement of
financial transactions by the perpetrator, and
resulting financial loss or exploitation (American
Bar Association/American Psychological Asso-
ciation Assessment of Capacity in Older Adults
Project Working Group, 2008).
EPILOGUE: CONCLUSION
A N D S U M M A RY
In this chapter we have examined conceptual,
empirical, and clinical aspects of competency loss
in older adults with dementia by focusing on three
specific civil competencies: treatment consent
capacity, financial capacity, and testamentary capac-
ity. It should be apparent that our group has used
MCI and Alzheimer’s disease, and also Parkinson’s
disease with dementia, as the clinical context for
understanding loss of competency. By virtue of its
relentless progressive nature, AD and its prodrome
MCI continue to be the most useful prism with
which to begin to understand relationships between
abnormal cognition and loss of decisional capacity
in aging. At the same time, the reported study
results may be quite specific to the MCI/AD or PD
context and may not always necessarily generalize
well to other dementias (Dymek et al., 2001a) or to
normal aging. For this reason, it is important to
understand how cognitive changes in other neuro-
431
degenerative diseases, such as Huntington’s disease,
ALS or MS, and in acquired disorders such as trau-
matic brain injury or cerebrovascular accident, may
also affect different competencies (Dymek et al.,
2001a; Marson et al., 2001; Marson et al., 2005). For
example, recent studies have examined medical
decision-making capacity in patients with trau-
matic brain injury (Dreer, De Vivo, Novack,
Krzywanski, & Marson, 2008; Marson et al., 2005),
an acquired neurocognitive disorder with a very
different trajectory of impairment—and recovery—
than neurodegenerative disease.
In addition, normal age-related cognitive
changes may affect higher order functional capac-
ities like consent capacity and financial capacity
(Diehl, Willis, & Schaie, 1995; Park, 1992; Willis,
1996b). Little is known about whether and to what
extent such normative age-related changes may
affect the competency of nondemented older
adults. Thus, studies using different age cohorts of
healthy adults, as well as patient groups with neu-
rodegenerative diseases and dementias other than
AD and PD, are necessary to expand our under-
standing of competency in dementia and in
normal aging. The neurocognitive predictor
model for financial capacity in cognitively normal
older adults (reported above) is instructive in this
regard (Sherod et al., 2009).
Finally, in an exciting development occurring
as the current volume was finalized, the field is
now beginning to use neuroimaging techniques as
a means to better understand the specific changes
in the brain that underlie capacity impairment and
loss in dementia. Using structural MRI, our group
recently found that atrophy in the angular gyrus is
significantly associated with overall financial
capacity (as measured by the FCI) in patients with
amnestic MCI (Griffith et al., 2010). We also found
that written arithmetic was the primary mediator
of this relationship between angular gyrus volume
and financial skill, replicating prior neuropsycho-
logical predictor findings discussed above (Sherod
et al., 2009). Thus, using advanced neuroimaging
techniques, investigators are now poised to develop
a true ‘neuroscience of capacity’ that will advance
both practice and research.
In conclusion, as an investigator who first
began studying competency in older adults more
than 20 years ago, it is gratifying to see the increas-
ing clinical and academic interest in this topic.
Although much work still needs to be done, the
field of civil competency assessment in the elderly
has indisputably emerged as an authentic area of
clinical, academic, and forensic practice, and shows
432 forensic neuropsychology
great future promise as a field of study in our aging
society. It will be exciting to see how this still young
field continues to evolve over the next decade.
N OT E S
1. Supported by grants from the National Institute
on Aging (1P50 AG16582 (Alzheimer’s Disease
Research Center) and R01 AG21927), the National
Institute of Mental Health (R01 MH55427), and the
National Institute of Child Health and Human
Development (R01 HD053074).
2. Adapted from ‘Assessing the competency of
Alzheimer’s disease patients under different legal stan-
dards: A prototype instrument’ by Marson et al. 1995,
Archives of Neurology, 52, p. 952, with permission of
the American Medical Association.
3. Adapted from ‘Assessing the competency of
patients with Alzheimer’s disease under different legal
standards’ by Marson et al. 1995, Archives of Neurology,
52, p. 952, with permission of the American Medical
Association.
4 Adapted from ‘Toward a neurologic model of
competency: Cognitive predictors of capacity to con-
sent to treatment in Alzheimer’s disease using three
legal standards’ by Marson et al. 1996, Neurology, 46,
p. 669, with permission of the American Academy of
Neurology.
5. Adapted from ‘Competency to consent to medi-
cal treatment in cognitively impaired patients with
Parkinson’s disease’ by Dymek et al. 2001. Neurology,
56, p. 19, with permission of AAN Enterprises, Inc.
6. ‘Competency to consent to medical treatment
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 16
Criminal Forensic Neuropsychology
and Assessment of Competency
ROBERT L. DENNEY
Clinical neuropsychologists provide unique
services in a wide variety of settings. Although the
idea of forensic neuropsychological practice may
bring to mind involvement in personal injury and
other civil tort cases, there are a growing number
of clinical neuropsychologists providing services
to participants in criminal forensic proceedings
as well (Denney & Wynkoop, 2000; Giuliano,
Barth, Hawk, & Ryan, 1997; Heilbronner, 2004).
Kaufmann (2008) reported results of a LEXUS
search using the term “neuropsycholo.” This
search reveals the term was used in 3,294 court
cases over the prior 70 years. Approximately 1,775
of those cases occurred in criminal court, with
over two-thirds falling within the last decade. This
trend is understandable given the apparent higher
rates of brain injury among criminal populations
(Barr, 2008; Magaletta, Diamond, McLearen, &
Denney, 2010; Martell, 1992a), but it also reflects
the relevance of neuropsychological expertise to
the criminal judicial system in general.
Borum and Grisso (1995) surveyed test use in
criminal forensic evaluations and found 46–50%
of forensic psychologists indicated they used
some type of neuropsychological assessment in
their pretrial evaluations. Mittenberg, Patton,
Canyock, and Condit (2002) presented results of a
national survey of board-certified neuropsycho-
logists regarding the estimated base rates of
symptom exaggeration and malingering. The 131
survey respondents indicated they completed a
total of 33,531 annual evaluations. Of these evalu-
ations, 34% were considered forensic in nature
(19% personal injury, 11% disability/workers’
compensation, and 4% criminal litigation). This
4% constitutes 1,341 criminally related forensic
evaluations per year for just 131 practitioners.
One could argue this sample is a unique subset of
neuropsychology practitioners; nevertheless, the
information reveals the reality that neuropsy-
chology has something to contribute to criminal
forensic matters (Denney & Sullivan, 2008;
Denney & Wynkoop, 2000; Martell, 1992b).
Clinical neuropsychology’s involvement in the
criminal judicial system is understandable because
the field has much to contribute when issues of
cognition compromising central nervous system
pathologies arise. Neuropsychologists can bring
to the judicial system their understanding of
neuroanatomy, neuropathology, and most impor-
tant, how neuropathological conditions affect
thinking skills and decision-making capacity
(Bigler & Clement, 1997; Lezak, Howieson,
Loring, Hannay, & Fischer, 2004; Ricker, 2003).
No less important is neuropsychology’s ability
to identify when unusual behaviors are not caused
by neuropathological conditions. The obvious
example is feigning of deficits, but nonneuro-
pathological conditions come to play as well, such
as psychopathy, other personality disturbances,
and general psychiatric concerns. Ruling out neu-
rocognitive deficits in non-neurological condi-
tions is just as important as identifying the
presence of potentially disabling neurocognitive
concerns. Further, such evaluations can delineate
neurocognitive functioning when diagnostic
issues other than neuropathology exist, such as
developmental and psychiatric conditions.
Criminal courts need clear understanding
regarding a defendant’s cognitive functioning
when there is concern that it may be compromised.
It has been long held that the U.S. Constitution
requires defendants to have adequate understand-
ing and the ability to aid in their own behalf
when facing criminal proceedings affecting their
“liberty or life” (Youtsey v. United States, 1899).
 Criminal Forensic Neuropsychology and Assessment of Competency
Under the U.S. Constitution, society can
deprive people of their liberty only under two doc-
trines: police power and parens patriae. Parens
patriae refers to the government looking after the
citizen’s welfare in a parental role. An example
includes civil commitment procedures for mental
health treatment. Police power is, of course, the
criminal justice system. The U.S. Constitution
outlines minimal acceptable rights for citizens of
the United States under federal and state laws. States
can always provide more personal rights than
dictated by the U.S. Constitution, but not less.
The aspects of the Constitution most relevant
for practitioners interfacing with the criminal
justice system are the 5th, 6th, and 14th
Amendments. The 5th Amendment includes the
right to be free from self-incrimination. The 6th
Amendment guarantees the right to counsel and
representation. The 14th Amendment establishes
that everyone will have equal protection under
the law. Last, both the 5th and 14th Amendments
declare that no one will lose “life, liberty, or prop-
erty” without due process of the law (Denney &
Sullivan, 2008).
Constitutional guidelines have tremendous
implication for the practice of neuropsychology
in criminal areas. For example, due process
requires a mentally competent defendant. Aside
from mental competency, there are other times
during criminal proceedings when courts can
benefit from neuropsychological expertise, such
as mental state of the defendant at the time of the
crime, mitigating issues and treatment needs to
consider at the time of sentencing, and prerelease
assessment of potential increased dangerousness.
Participants in the criminal judicial system can
benefit from the input of neuropsychology, but
neuropsychologists need to understand the
unique aspects of forensic work in the criminal
setting and have specialized knowledge and tech-
niques for competent practice (Melton, Petrila,
Poythress, & Slobogin, 2007; Denney & Sullivan,
2008).
The goal of this chapter is to provide neurop-
sychological practitioners with an introductory
understanding of issues involved in practicing in
the criminal forensic arena in general and the
assessment of competency to stand trial in par-
ticular. Chapter 17 continues the introduction by
focusing on assessment of criminal responsibility,
diminished capacity and responsibility, danger-
ousness assessment, death penalty, and ethical
and professional development issues.
439
CRIMINAL FORENSICS
A S A S U B S P E C I A LT Y
OF FORENSIC
NEUROPSYCHOLOGY
In the “Petition for the Recognition of Forensic
Psychology as a Specialty in Professional Psycho-
logy,” the American Board of Forensic Psychology
and American Psychology–Law Society jointly
defined forensic psychology in this manner
(Forensic Specialty Council, 2000):
[Forensic psychology is] the professional prac-
tice by psychologists within the areas of clinical
psychology, counseling psychology, neuropsy-
chology, and school psychology, when they are
engaged regularly as experts and represent
themselves as such, in an activity primarily
intended to provide professional psychological
expertise to the judicial system. (p. 6)
Under this definition, forensic neuropsychology
could be viewed as a specialty area within clinical
neuropsychology. Neuropsychologists can pro-
vide expertise to the judicial system in civil as well
as criminal areas. In this regard, the application of
neuropsychological expertise to criminal forensic
matters could be considered a subspecialty of
forensic neuropsychology. Although good clinical
neuropsychological skill and expertise form the
basis of sound practice, forensic neuropsychology,
particularly criminal forensic matters, requires
understanding of a unique knowledge domain
beyond that of sound clinical practice (Denney &
Wynkoop, 2000; Martell, 1992b; Sullivan &
Denney, 2008).
FORENSIC
NEUROPSYCHOLOGY
AS A UNIQUE PRACTICE
SETTING
There are striking differences between neuro-
psychology practice in the general clinical setting
and that of the forensic setting, particularly the
criminal realm. Goals of the two specialties, by
definition, differ greatly. For example, the goal of
clinical evaluation is most often alleviation
of human suffering and improvement of levels of
functioning through evaluation and development
of efficient intervention. With the exception of
treatment recommendations, the goal of forensic
evaluation is most often to determine whether a
defendant’s psychological problems meet a spe-
cific legal standard. These disparate goals create
440 forensic neuropsychology

different assumptions, roles, alliances, and
methods (Denney & Wynkoop, 2000; Goldstein,
2003; Greenberg & Shuman, 1997; Heilbrun,
2001).
Assumptions
In clinical practice, neuropsychologists assume,
for the most part, that patients voluntarily
seek help because they want relief from bother-
some symptoms. There is often a diagnosable
condition that occasions the service, whether
the service is assessment or intervention. Certainly,
within the neurorehabilitation setting, an alliance
is built. The overriding theme is one of colla-
boration, mutual goals, and belief. Criminal
defendants are often not self-referred, or even
voluntary, recipients of services. In many
instances, they may not have a psychological or
neuropsychological complaint. In addition, the
possibility of harsh punishment can create
tremendous motivation to manipulate the evalua-
tor and judicial system (Rogers, 1997). It is coun-
terproductive to assume defendants have
neurocognitive deficits, want help for deficits, or
will present themselves in an honest manner
within such a harsh and potentially punitive
setting. It is no surprise, then, that these differ-
ences in assumptions result in different roles for
neuropsychologists.
Roles
There are striking differences between the roles
of clinical provider and forensic examiner. Heilbrun
(2001) outlined differences between the roles of
forensic examiner and treatment clinician. As can
be seen from Table 16.1, the differences between
the two roles reveal themselves in a variety of
attitudes and behaviors. The clinical provider
maintains a role consistent with helping the
patient. Rather than patient–helper, however, the

TABLE 16.1 DIFFERENCES BET WEEN TREATMENT AND FORENSIC ROLES FOR
MENTAL HEALTH PROFESSIONALS

Dimension Therapeutic Forensic

Purpose Diagnose and treat symptoms of illness Assist decision-maker or attorney

Examiner-examinee Helping role Objective or quasi-objective stance

relationship
Notification of purpose Implicit assumptions about purpose Formal and explicit notification
shared by doctor and patient
Who is being served Individual patient Variable; may be court, attorney, and
patient
Nature of standard being Medical, psychiatric, Medical, psychiatric, neuropsychological,
considered neuropsychological and legal
Data sources Self-report, behavioral observations, Self-report, behavioral observations,
medical diagnostic procedures, medical diagnostic procedures,
and neuropsychological testing. and neuropsychological testing.
Occasional corroborative Nearly always incorporate
information. corroborative and surreptitious
observation by
Response style of Assumed to be predominantly reliable others.
examine Not assumed to be reliable
Clarification of reasoning Optional
and limits of knowledge Very important
Written report Brief, conclusory statement common
Lengthy and detailed, documents findings,
Court testimony Not expected reasoning, and conclusions
Expected

Adapted from Kirk Heilbrun, Principles of Forensic Mental Health Assessment. New York: Springer/Kluwer Academic/Plenum, 2001, p. 9,
Table 1.2. With permission of the author.
 Criminal Forensic Neuropsychology and Assessment of Competency
forensic evaluator maintains a more neutral role, a
role consistent with being a “seeker of truth” and
judicial educator (Greenberg & Shuman, 1997;
Saks, 1990). It can often be a difficult role to main-
tain. The evaluator should realize his or her opin-
ion has the potential to do significant harm,
particularly from a standard psychotherapeutic
mindset. Potential consequences can be great.
Probably the most serious example includes capital
cases, for which the evaluator must provide an
opinion on competence to be executed. A neuro-
psychologist who is uncomfortable with the task of
being an unbiased seeker of truth should avoid
forensic practice.
Alliance
Developing therapeutic alliances with neuro-
rehabilitation patients is required for successful
rehabilitation outcomes. Sohlberg and Mateer
(2001) went so far as to include it as a basic
principle of cognitive rehabilitation. They noted,
“Cognitive rehabilitation requires a sound
therapeutic alliance among the therapist, client,
and family members or care givers” (p. 21).
A therapeutic alliance allows the therapist
to foster motivation and hopefulness on behalf
of the patient (Parenté & Herrmann, 1996).
Forensic evaluations are not therapeutic endeav-
ors. As such, the forensic examiner’s allegiance is
with finding the truth in a thorough, ethical
manner.
It must be remembered who is the recipient of
these services. In general clinical work, the patient
is clearly the recipient. In this manner, the patient
is the client. The client role is less clear in forensic
endeavors. Forensic examiners must realize the
patient is generally not the client. More typically,
the recipient of services, particularly evaluative
services, is the court (and by extension, the jury)
or attorney. Other distinctions between the two
roles are presented in Table 16.1.
Lack of therapeutic alliance in forensic evalu-
ation does not, however, eliminate the need to
develop rapport with the defendant or to treat
him or her with dignity and respect. Rapport
fosters self-disclosure and motivation to perform
during neuropsychological testing. It is possible
to maintain a professional and ethical relationship
while maintaining the strict boundaries of the
forensic evaluation process. The difference in
alliance between clinical and forensic evaluations
is exemplified in the limited confidentiality in
criminal forensic practice. Issues of confidential-
ity within the criminal evaluation are addressed
441
in the Ethical and Professional Issues section of
chapter 17, this volume.
Methodology
Given the different assumptions, roles, and
alliances, it is no surprise competent and ethical
forensic evaluation requires somewhat different
methodology from that of routine clinical prac-
tice. Clinical practice typically incorporates an
interview with the patient, and perhaps an infor-
mant familiar with the patient, and neuropsy-
chological testing to characterize the patient’s
difficulties or to arrive at a diagnosis and make
treatment recommendations. The entire process is
designed to provide assistance to the patient, his
or her caregivers, and medical managers in a
timely fashion. Forensic assessment requires a
broader base of information sources than is
typical of clinical practice.
The evaluator must also place more weight on
objective test results than subjective complaints,
self-report checklists, and behavior during clini-
cal interviews. Systematic assessment of negative
response bias and malingering is a necessity in
the criminal forensic setting. Surreptitious obser-
vation can be invaluable, particularly when signs
of poor motivation or symptom exaggeration
exist (Denney & Wynkoop, 2000; Wynkoop &
Denney, 1999). The evaluator must carry out the
evaluation much like a detective would attempt to
sleuth out the truth. It can take time to locate
and review past medical and educational records
and interview others familiar with the defendant.
Nonetheless, this “search for truth” requires
the forensic psychologist to gather information
from a wide variety of sources aside from the
defendant and to consider more critically the
defendant’s self-report. Along with specialized
knowledge domains, the contrast in methodology
between clinical and forensic practice is a major
difference between specialties. This difference in
theoretical basis necessitates a broader model of
practice.
Denney and Wynkoop (2000) adapted Mrad’s
(1996) multiple data source model (MDSM) to
the practice of criminal forensic neuropsychol-
ogy. The model represents a synthesis of various
authors in forensic psychology (Grisso, 1988;
Melton et al., 2007; Shapiro, 1984, 1991, 1999),
particularly related to the assessment of sanity
(and other past mental states). The model is
represented in Figure 16.1. Although designed to
guide the evaluator in tapping all relevant infor-
mation sources for identifying a defendant’s
442 forensic neuropsychology

Self-report Other Data Sources Opinion

Self-reported symptoms
and behavior when
Present
aware of being observed
Psychological tests
Neuropsychological tests
Present mental
Mental status exam
status and
Behavioral observations
diagnosis
especially unobtrusive
Medical/neurological exam

Defendant’s explanation Arrest reports

of his thoughts, feelings, Investigative records
Time of Mental state,
and behavior prior to, Witness statements
Offense motivation, and Ultimate
during, and following the Video/audio tapes
diagnosis at Issue
offense Physical evidence
time of offense
Confessions
Family/friend reports

Self-reported social history: Hospital/psych. records

Childhood NCIC/FBI record Historical
Education Employment records symptoms,
History Employment/military School records diagnosis, and
Relationships Military records patterns of
Substance abuse Probation officer behavior
Criminal record accounts
Psychiatric treatment Family/friend reports

FIGURE 16.1: Multiple data source model. Reproduced with kind permission of David Mrad, Ph.D.,
ABPP.

mental state at the time of the offense, it is also
helpful as a general model of forensic assessment.
The model ensures the evaluator will acquire
corroborative information rather than relying on
the defendant’s self-report and presentation
during interviews and testing.
The first two columns represent sources of
information (self-report and corroborative) which
when combined can lead to an understanding of
mental state. Each row represents a different point
in time (currently, historically, and a specific time
in the past). There should be reasonable consis-
tency between each of the columns and rows. The
model is discussed more thoroughly as it relates
to sanity in chapter 17, this volume. It can be quite
helpful in the assessment of competency as well
because it facilitates information acquisition from
objective information sources, particularly when
dealing with retrospective competency.
The following case exemplifies the need to
acquire corroborative information about the
defendant’s past behavior. It also demonstrates
how evaluations for competency can lead to
complicated additional judicial inquiries. The case
started out as a reasonably simple evaluation for
competency to be sentenced, but it quickly evolved
into an evaluation of past competency to stand
trial and sanity.
“Where’s the Video?” A Case of
Vital Corroborative Data
A 70-year-old man with diabetes was convicted
by a jury of gambling and money laundering.
After his conviction, defense acquired a mental
health evaluation by a neuropsychiatrist in prepa-
ration for diminished capacity arguments during
sentencing. The neuropsychiatrist found signs of
periventricular white matter changes on magnetic
resonance imaging and concluded the man was
not competent to be sentenced. The court referred
him for inpatient mental health evaluation to
address competency to proceed with sentencing.
During this evaluation, more than one of his
recent attorneys and the defendant’s wife (a code-
fendant also convicted) reported him having
terrible debilitation, particularly at the time of the
recent trial. The case became quite complicated
because new charges were brought against the
man for jury tampering and obstruction of justice
secondary to allegations he contacted and
 Criminal Forensic Neuropsychology and Assessment of Competency
attempted to manipulate a juror during the recent
trial. The judge in charge of the jury tampering/
obstruction case requested a mental health evalu-
ation focused on criminal responsibility. Both
issues were addressed during the same inpatient
evaluation, with reports going to separate courts.
Neuropsychological testing revealed only
minor bilateral motor slowing. All other results,
including measures of attention, concentration,
learning, memory, and abstract reasoning, were in
the range of average to slightly above average given
his age and educational background. Regarding
his current functioning, I considered him compe-
tent to proceed, but the issue was much more
complicated regarding his past mental state.
Regarding the time of the trial, I received a
great deal of information from the defense attor-
ney and very little information from prosecution
beyond basic investigative material, including the
contacted juror statements and the defendant’s
private investigator’s statements. This man assisted
the defendant in acquiring personal information
about the juror. Available information suggested a
combination of uncontrolled insulin-dependent
diabetes mellitus, recent subcortical strokes, stress
of the trial, and depression resulted in some level
of cognitive compromise at the time of the trial.
I provided this opinion regarding his appreciation
of the wrongfulness of contacting a juror (sanity):
There is evidence of mental illness or defect at
the time [of the alleged offense]. . . . Although his
judgment was impacted to a degree, he was not
so incapacitated by illness as to cause him to not
understand what he was doing or what was going
on around him. On the contrary, his behavior as
outlined in the investigative reports suggested he
made comments and acted in a manner consis-
tent with someone who knew their actions were
wrong and/or potentially illegal.
As a result of my opining that the defendant
had “some amount of incapacity at the time,”
defense now claimed he was incompetent during
the past trial, and counsel was ineffective by not
noticing this fact. The first court then requested a
retrospective competency evaluation to deter-
mine if he was, in fact, competent to stand trial
during the jury trial in which he was convicted on
gambling and money laundering.
During this evaluation, striking new informa-
tion came to light. During the lengthy trial
process, the defendant was out of jail on bond
and living at his home. In his free time, he was
443
carrying out real estate transactions, and the other
businessperson with whom he was interacting
described his negotiation and financial analysis
skills as “good as always.”
More striking yet was the fact he was going
through divorce proceedings in a local court
during the same week as the criminal trial. When
he was not in federal court, he was in divorce court.
His divorce attorney was one of the attorneys
claiming how impaired he was during the criminal
trial. The best part was the fact that this particular
divorce court videotaped all its proceedings.
On several videotapes, dated the same week and
interspersed with court appearances in the crimi-
nal trial, the defendant was vigorously questioned
by his attorney regarding real estate property lines
and property values while pointing out boundaries
on a map. He was able to follow rapid-fire ques-
tioning and respond quickly. There were no signs
of cognitive compromise on these tapes.
Last, and even more astounding, was the
acquisition of court transcripts of a postconvic-
tion detention hearing at which the defendant’s
attorney (the very one claiming how incompetent
he was during the trial) was arguing before
the court that the court should release the defen-
dant on bond because his assistance was needed
in preparation for sentencing. The attorney
actually made statements to the effect that he
expected the defendant to continue working on
the case as well as he did during the trial and that
his help had been invaluable; he was like having a
“paralegal.”
All of this new information flew in the face of
my previous opinion that he demonstrated some
cognitive deficits during the trial. My opinion
changed, and I explained in the report how the
new information had an impact on my reasoning.
The defendant was found by the court to have
been competent during the trial. This case dem-
onstrates how easy it is to come to a determina-
tion and only later find out vital information had
not been received. Solid corroborative informa-
tion regarding defendant behavior during exami-
nation of mental state at the time of the offense is
vital in nearly any circumstance, but particularly
when there is documented presence of potentially
debilitating disease.
This case demonstrates the complexity of
neuropsychological assessment in the criminal
forensic setting. Using the multiple data source
model as a template to ensure information from
all relevant areas should increase diagnostic
clarity and provide the needed information to
444 forensic neuropsychology

address forensic questions competently. Even
having the appropriate information, however, will
not facilitate the evaluator making a correct for-
mulation about forensic questions if he or she
does not understand the correct legal standards
relevant to that forensic question. I now turn to
one of the most commonly encountered legal
issues, criminal competency.
CRIMINAL COMPETENCIES
Competency is broadly considered the capacity to
decide or perform certain functions. From a legal
perspective, a large portion of the concept of
competency includes the cognitive construct of
“knowledge.” It implies a person’s understanding
of issues pertaining to participation in a specific
legal proceeding (Reisner & Slobogin, 1990). This
understanding includes some sense of apprecia-
tion for such issues as nature of the procedure,
risks, likelihood of success, available alternative
options and strategies, and relative advantages/
disadvantages of potential courses of action.
The issue of competency can arise during any
phase of the criminal judicial process, from the
first contact a suspect has with law enforcement to
the time of sentencing and even to the point of
execution in capital cases. Table 16.2 presents an
overview of these points, with brief descriptions
(Grisso, 1988).
Threshold to Seek
Competency Evaluation
Competency evaluations are the most commonly
requested mental health studies in criminal
forensics. Defense attorneys typically raise the
issue of a defendant’s competency to proceed;
however, prosecutors and judges (termed sua
sponte) can raise the issue as well. When defense
counsel raises the issue, not uncommonly, it is
over the objection of the defendant, particularly
when psychosis is involved. This event places the
defense attorney in a unique ethical position
between fulfilling the wishes of the client and also
protecting his or her constitutional right to a fair
trial. It also strains the attorney–client relation-
ship (Melton et al., 2007).
Steadman, Monahan, Hartstone, Davis, and
Robbins (1982) found that 6,500 defendants were
adjudicated not competent to stand trial and com-
mitted to public mental institutions for treatment
in 1978. They estimated this result came from
25,000 requested competency evaluations. Hoge
and colleagues (1997) cited a personal communi-
cation from Thomas Grisso regarding information

TABLE 16.2 SPECIFIC COMPETENCIES IN THE CRIMINAL JUSTICE PROCESS

Competency To: General Issue in Question

Confess (or to Waive Understanding and appreciation of rights to silence and legal counsel when the rights
Rights at Pretrial may be waived at the request of law enforcement investigators seeking a self-
Investigations) incriminating statement
Plead Guilty Understanding and appreciation of above, and of the right to a jury trial, the right to
confront one’s accusers, and the consequences of a conviction
Waive Right to Counsel Understanding and appreciation of the dangers of self-representation at trial
Stand Trial Ability to assist an attorney in developing and presenting a defense, and to understand
the nature of the trial and its potential consequences
Be Sentenced Understanding and appreciation of nature of the sentence to be imposed (after trial has
resulted in conviction)
Waive Further Appeal Understanding and appreciation of right for additional appeal and potential
(when facing an consequences of waiving it
execution)
Be Executed Understanding and appreciation of nature and purpose of the punishment, and ability
to assist counsel in any available appeal

Note: The wording of these definitions does not conform to prevailing legal terminology. They are intended only to convey the general issues
raised in each specific competency. Reproduced from Competency to Stand Trial Evaluations, by T. Grisso, 1988, p. 3. with permission of
Professional Resource Press.
 Criminal Forensic Neuropsychology and Assessment of Competency
derived from a 50-state survey (Grisso, Cocozza,
Steadman, Fisher, & Greer, 1994) in which state
forensic directors were asked to estimate the
number evaluations of competency to stand trial
performed. The total estimate was from 24,000 to
39,000 studies. It is not surprising that so many
competency evaluations are done in the United
States, as the threshold to raise concern over
competency is quite low, as revealed by the U.S.
Supreme Court in Pate v. Robinson (1966) and
Drope v. Missouri (1975).
Theodore Robinson was found guilty of
murder and sentenced to life in prison by the
Illinois state court. Although his attorney con-
tended throughout the court proceedings that
Robinson was not competent to proceed and was
insane at the time of the offense and Robinson’s
relatives and family friend testified during the
trial that he was insane, the trial court never
stopped the trial to have him examined for com-
petence. Robinson’s history included significant
childhood traumatic brain injury, subsequent
erratic behavior, and state hospitalization as an
adult for psychotic behavior. It was later argued
that Robinson “deliberately waived the defense of
his competence to stand trial by failing to demand
a [competency] hearing as provided by Illinois
law” (Pate v. Robinson, 1966, p. 821). The U.S.
Supreme Court responded, “It was contradictory
to argue that a defendant may be incompetent,
and yet knowingly or intelligently ‘waive’ his right
to have the court determine his capacity to
stand trial” (p. 821). The High Court concluded
the trial court’s failure to address the competency
issue deprived him of his right to a fair trial.
The Court went on to conclude that a hearing on
competency should occur whenever the evidence
raises a “bona fide doubt” as to the defendant’s
competency.
The U.S. Supreme Court considered this
issue further in the interesting case of Drope
v. Missouri (1975). James Drope was charged
with rape. Prior to trial, the defense had a psychia-
trist evaluate him; the psychiatrist concluded
he needed mental health treatment. The defense
requested a delay in the proceedings for the
defendant to receive psychiatric treatment, but
the trial judge denied the request and proceeded
with trial.
During the trial, the defendant’s wife (the
victim) testified and confirmed his history of
“strange behavior.” On the second day of the
trial, he shot himself in the stomach in an
apparent suicide attempt and was hospitalized.
445
The judge denied a request for mistrial and
continued the trial even without the defendant’s
presence, citing his absence as voluntary. The jury
found him guilty, and he was sentenced to life
in prison. The case eventually came before the
U.S. Supreme Court to determine whether
the trial court erred in not addressing the compe-
tency issue. The Supreme Court concluded there
was certainly enough evidence to meet the bona
fide doubt standard presented in Pate. Trial courts
should consider any evidence coming from
irrational behavior, demeanor at trial, or any prior
medical opinions. Disconcerting information
from even one of these sources may trigger
an inquiry into the defendant’s competency to
proceed.
In the time since these two cases were decided,
it has become clear that courts will rarely refuse a
request for competency evaluation. This very low
threshold for referral results in the fact that most
defendants referred for competency evaluation
are competent to proceed. Consistent with this
belief is the finding that only an estimated 26% of
those competency evaluations mentioned in the
Steadman et al. (1982) survey were considered
not competent by the court.
More recent research from various states
across the United States reveals estimates from
13% to 46% of evaluees were considered not com-
petent to proceed by mental health evaluators
(Cox & Zapf, 2004; Riley, 1998; Rosenfeld &
Wall, 1998; Warren, Rosenfeld, Fitch, & Hawk,
1997). Cochrane, Grisso, and Frederick (2001)
reviewed data for 1,710 criminal defendants
referred by federal courts throughout the US
and found an overall 18% rate of recommended
incompetence in the federal jurisdiction. While
some of these estimates appear high, Melton
and colleagues (2007) suggested “when more
rigorous (i.e., more valid) evaluation standards
and procedures are applied, the percentage found
incompetent is likely to be lower” (p. 142). This
low rate of incompetency occurs for at least
two other reasons beyond a low threshold to
request evaluation. As it will become apparent,
the threshold for competency to stand trial is also
not very high.
Last, many competency referrals occur for
reasons unrelated to mental health concern, such
as attorney ignorance, confusion between sanity
and competency, as an information-seeking ruse,
as a tactical delay, and for strategic planning of
the case (Melton et al., 2007; Roesch & Golding,
1978; Rosenberg & McGarry, 1972).
446 forensic neuropsychology
Competency as a U.S.
Constitutional Right
The concept of not allowing a mentally “defective”
defendant to progress through the criminal
judicial system can be traced to at least the middle
1600s in British Common Law (Melton et al.,
2007). In 1899, the U.S. Court of Appeals for the
6th Circuit determined it was a violation of the
U.S. Constitution’s 14th Amendment right to due
process to allow a mentally incompetent person
to proceed through the criminal judicial process
(Youtsey v. United States, 1899). The circuit court
wrote that it was:
Fundamental that an insane person can neither
plead to an arraignment, be subjected to a trial,
or, after trial, receive judgment, or after judg-
ment, undergo punishment. . . . It is not “due
process of law” to subject an insane person to
trial upon an indictment involving liberty or
life. (pp. 940–941)
In 1899, the term insane was more broadly defined
and often referred to lack of competency, as in
this passage. Youtsey established the constitution-
ality of adjudicative competency, but it was not
until 1960 that the U.S. Supreme Court established
a holding on what constituted the difference
between competency and incompetency (Dusky
v. United States, 1960).
In Dusky, the U.S. Supreme Court identified the
requirement that a person needed a rational as well
as factual understanding for competency to stand
trial. Milton Dusky was arrested in August 1958 for
kidnapping a 15-year-old girl, transporting her from
Kansas to Missouri, and raping her. He was referred
for mental health evaluation, and a psychiatrist tes-
tified Dusky was “unable to properly understand
the proceedings against him and unable to ade-
quately assist counsel in his defense” (p. 402) because
of severe mental illness. He was found competent,
nonetheless, because he was oriented and had some
recollection of the events in question. He was then
convicted of kidnapping. The U.S. Court of Appeals
for the 8th Circuit affirmed the conviction.
The U.S. Supreme Court reviewed the
case, overturned the conviction, and remanded
it back to the trial court for new competency
assessment, indicating the level of competency
was not adequate. They wrote, “It is not enough
for the district judge to find that the defendant
is oriented to time and place and has some
recollection of events” (p. 402). Dusky was to
receive a new trial if he was found competent
under the new standard. The following has
been now termed the “Dusky standard” (Dusky v.
United States, 1960):
[The] test must be whether he has sufficient
present ability to consult with his lawyer with a
reasonable degree of rational understanding—
and whether he has a rational as well as factual
understanding of the proceedings against him.
(p. 402)
The Dusky standard spells out the minimal
level of competency necessary under the U.S.
Constitution for all criminal jurisdictions in the
United States. As such, it has been written into
statute in one form or other in most jurisdictions
in the United States (Grisso, Borum, Edens, Moye,
& Otto, 2003; Marcopulos, Morgan, & Denney,
2008). Although wording varies, each jurisdiction
addresses these two prongs, factual and rational,
at the minimum.
Dusky also made several other key points.
Competency is an issue of current ability as
opposed to mental state at some time in the past
(the exception, of course, is an evaluation of retro-
spective competency, as briefly touched in the
above case example). Implied is the need to remain
competent for the foreseeable near future, at least
as long as the upcoming proceeding.
Occasionally, a defendant’s competency will
vary from week to week in what amounts to a
“moving target.” Under these circumstances,
providing treatment, reevaluation, and guarantee-
ing the defendant a fair trial process can be
difficult work for the judge.
The term ability to consult with his or her
lawyer implies capacity to do so rather than desire
to do so. It is not unusual for criminal defendants
not to want to cooperate with counsel for reasons
not rooted in mental illness. The ability to identify
the motivation for this lack of cooperation is the
task of the forensic evaluator. Further, it is impor-
tant to keep in mind “ability to assist” counsel
does not imply a constitutional right to a “mean-
ingful attorney–client relationship” (Morris v.
Slappy, 1983).
Last, the standard also includes the phrase
reasonable level of understanding, rather than a
perfect level of understanding; a criminal defen-
dant is not expected to have perfect understand-
ing. Although these small components of the
Dusky standard are important, the core issue of
concern remains the nature of “rational as well as
factual understanding.”
 Criminal Forensic Neuropsychology and Assessment of Competency
According to Reisner and Slobogin (1990),
factual understanding comprises a person’s
strict understanding. Examples include a defen-
dant’s ability to repeat information provided,
paraphrasing that information in his or her own
words, and displaying an ability to put the infor-
mation to use. It can be evaluated by observing
how information is used in decision making and
can include such abilities as judgment, compre-
hension, good reality testing, rational weighing of
risks and benefits, and relevance of facts to the
immediate situation. Although there are various
descriptions of specific points within this concept
of competency for various activities, the general
understanding of competency as outlined in
Dusky is the core aspect of competency for any
point in the criminal judicial process.
One issue Dusky does not explicitly address is
the presence of mental abnormality beyond lack
of knowledge. Milton Dusky was considered to
have a severe mental illness, so the issue was in
the record before the U.S. Supreme Court
(Frederick, DeMier, & Towers, 2004). It was
simply not listed in the final Court decision.1
Subsequent case law makes it clear the compe-
tency deficiency must be caused by mental abnor-
mality as opposed simply to ignorance. Individuals
can be unable to assist in their defense for purely
physical reasons, but as it relates to cognitive
functioning, some type of diagnosable mental
condition is required. Most jurisdictions make
this requirement much more clear. An example is
the current federal statute (Title 18, U.S.C., Section
4241a). The statute is very reminiscent of Dusky,
with added emphasis on mental abnormality:
“The defendant, as a result of mental disease or
defect, is unable to understand the nature and
consequences of the proceedings against him or
assist properly in his defense.”
The current federal standard also highlights
another aspect of competency by replacing
“consult” with “assist” regarding working with
counsel. There is no definitive rule as to how much
ability one needs to assist “properly.” The amount
of assistance necessary to give direction to
counsel or rally a defense on one’s own behalf
likely varies depending on the complexity of the
case. In this regard, the standard for competency
to proceed implicates the need to evaluate the
context and situational demands into which the
defendant will likely need to go. Grisso (1986,
1988) provided insight into the need to consider
contextual issues in determining competence to
proceed.
447
Competency as a Contextual Issue
Grisso (1988) presented a conceptual framework
that emphasized the contextual nature of criminal
competency. From this perspective, the likely
demands placed on a defendant must be consid-
ered before determining whether the defendant
can rise to the level of performance required.
Although subsequent U.S. Supreme Court
case law (Godinez v. Moran, 1993) implied
otherwise, it is still a valuable exercise in under-
standing the nature of the interaction between
the defendant’s capabilities and the likely situa-
tional demands. As I will address later in the
chapter, the concern is particularly important for
instances in which otherwise competent
defendants may not be competent to represent
themselves (Indiana v. Edwards, 2008). Viewing
competency as an adaptive function in this
manner makes the process of determining what
neurocognitive deficits likely play a role in the
defendant’s lack of competence and provides
guidance in determining prognosis and treatment
needs. Grisso presented five areas of analysis
relevant for neuropsychologists performing
competency evaluations: functional description
of specific abilities, causal explanations for deficits
in competency abilities, interactive significance
of deficits in competency ability, conclusory
opinions about legal competency and incompe-
tency, and prescriptive remediation for deficits in
competency abilities.
Functional Description of Specific Abilities
The primary objective of a competency evaluation
is not foreign to clinical neuropsychology because
it deals with describing functional strengths and
weaknesses. The difference is in knowing specific
legal standards sufficiently to appreciate the rele-
vance of those deficits to the determination of
competency.
Causal Explanations for Deficits in
Competency Abilities
The logical next step is determining the cause of
those deficiencies, another task well known by
neuropsychologists. The key here is, again, know-
ing the appropriate legal standard and how that
standard is applied. Neuropsychologists are
equipped to communicate neuroanatomical and
neuropathological bases for deficits presented and
to rule out other potential causes of performance
(ignorance, situational influences, cultural
influences, and malingering). Lack of knowledge
pertaining to the law (ignorance) is not grounds
448 forensic neuropsychology
for incompetency. The knowledge and reasoning
skill deficits must be rooted in diagnosable
pathology.
Interactive Significance of Deficits in
Competency Ability
The neuropsychologist should attempt to place
the defendant’s strengths and weaknesses into
context, that is, how the neurocognitive function
interacts with the ecological demands required of
him or her given the specific legal situation.
Although case law suggests the general standard
for competency may not change based on the
complexity of the case, the level of rational and
factual understanding required is not necessarily
interpreted in the same manner for every situa-
tion, particularly when dealing with the issue of a
defendant’s self-representation.
The demands required of the defendant
will vary given the complexity of the case. In
this regard, two defendants with the exact
same neurocognitive deficits could vary in their
competence based on the complexity of the case.
More is required from a defendant in a long,
multiple-count bank fraud trial than for a
single charge of illegal reentry after deportation.
Likewise, pleading guilty will press cognitive
capacity less than a lengthy trial. Before conclud-
ing a defendant’s competency, there must
be a sense of which demands will be placed
on him or her through the particular legal
proceedings. This gray aspect of competency
determination is an excellent example of why it is
important to remember the judge makes the final
decision regarding a defendant’s competency, not
the expert witness.
Conclusory Opinions About
Legal Competency and
Incompetency
Evaluators provide opinions regarding the defen-
dant’s competency. The trier of fact (in this
instance, the judge) will make the actual legal
finding regarding competence. The forensic
neuropsychologist’s role is simply to provide an
expert opinion for the court’s consideration.
Judges consider other salient facts beyond that
provided by the forensic neuropsychologist before
making a legal ruling.
Grisso (1986, 1988) and colleagues (2003)
made the argument that mental health profes-
sionals should refrain from actually providing a
definitive opinion on competency. They suggested
instead that they limit their opinions to clinical
conclusions, particularly in those areas most
relevant to competency, and allow the trier of fact
to make the final legal decision. The final legal
decision before the court is considered the
“ultimate issue.” In competency hearings, the
ultimate issue is whether the defendant is compe-
tent to proceed. Providing an opinion on the
ultimate issue has been debated, particularly
when the expert is providing an opinion before a
jury. There is relatively pervasive case law and
statute limiting mental health experts from
providing ultimate issue opinions on sanity, and
in some jurisdictions, there are formal limits on
providing ultimate issue opinions on competency
as well.
Grisso (1988) pointed out three reasons to
refrain from providing ultimate issue opinion tes-
timony in the area of competence. First, psycholo-
gists are experts in mental health issues, not law.
He argued they are not in a position to know
which demands will be placed on a defendant in
the course of his or her legal actions. In this regard,
clinicians should leave the opinion up to those
who are experts in the judicial process. Second, an
argument has been made that mental health
experts can have too great an influence on the
minds of legal decision makers. Although such
may be the case in jury trials, it is difficult to
fathom that a judge will be unduly swayed to an
opinion of even the best-qualified neuropsycholo-
gist. Third, Grisso suggested no new information
is provided to the judge by mental health profes-
sionals giving their opinions on the ultimate issue
after a description of the neuro/psychopathology
with its functional strengths and weaknesses is
made. In some jurisdictions, however, the expert
is required to provide an opinion on the ultimate
issue regarding competency (Title 18 U.S. Code,
Sections 4241 and 4247). The debate on providing
ultimate issue opinions on competency will likely
continue in academic settings and scholarly writ-
ings whether or not it makes any real difference in
the courtroom.
Prescriptive Remediation for
Deficits in Competency Abilities
If the forensic neuropsychologist believes the
defendant is not competent, it is his or her respon-
sibility to provide prognostic considerations and
outline remedial options from a clinical perspec-
tive, truly the neuropsychologist’s element. The
clinician can educate the court regarding the
nature of the condition, which treatment options
are available, and the likely success potential for
 Criminal Forensic Neuropsychology and Assessment of Competency
each. Grisso (1988) pointed out these issues to
consider:
• Whether the defendant’s deficits are
remediable;
• If so, the treatment that is required for
remediation;
• How long the remediation is likely to
require;
• The local facilities or programs in which
the treatment is available; and
• The conditions of restriction represented
by each of these facilities. (p. 21)
Depending on the nature of the legal case,
courts may have the option to place defendants in
community treatment or rehabilitation programs.
In many instances, the court has little option but
to refer the defendant to forensic hospitals run by
state or federal correctional agencies. For exam-
ple, the federal law dictates that U.S. district judges
are to commit incompetent defendants to the
custody of the U.S. attorney general for inpatient
mental health treatment focused on competency
restoration (Title 18, U.S.C., Section 4241d).
A definite aspect of this commitment is an addi-
tional assessment of competency to proceed.
Customarily, mental health treatment facili-
ties under the department of corrections have
little in the way of neurocognitive remediation
capability. It is important to remember the goal of
treatment is remediation of deficits sufficient to
restore competency. This level of therapeutic
outcome is likely lower than that espoused in
general clinical rehabilitation. The ultimate goal is
the ability to advance successfully through legal
proceedings rather than successful independent
living and community reentry.
More Detailed Considerations
of Competency
Others have attempted to define further the
functional capacities that go into competency as
formulated in Dusky. A previously cited (Grisso,
1986; Melton et al., 2007) example is Florida’s
2002 Title XLVII (Criminal Procedure and
Corrections), Chapter 916.12 (Mentally Deficient
and Mentally Ill Defendants), which spells out the
standard of incompetency in this manner, starting
with paragraph (2):
(2) The experts shall first determine whether
the person is mentally ill and, if so,
449
consider the factors related to the issue of
whether the defendant meets the criteria
for competence to proceed; that is,
whether the defendant has sufficient
present ability to consult with counsel with
a reasonable degree of rational
understanding and whether the defendant
has a rational, as well as factual,
understanding of the pending proceedings.
(3) In considering the issue of competence to
proceed, the examining experts shall first
consider and specifically include in their
report the defendant’s capacity to:
1. Appreciate the charges or allegations
against the defendant;
2. Appreciate the range and nature of
possible penalties, if applicable, that
may be imposed in the proceedings
against the defendant;
3. Understand the adversarial nature of
the legal process;
4. Disclose to counsel facts pertinent to
the proceedings at issue;
5. Manifest appropriate courtroom
behavior; and
6. Testify relevantly; and include in their
report any other factor deemed
relevant by the experts.
(4) If the experts should find that the
defendant is incompetent to proceed, the
experts shall report on any recommended
treatment for the defendant to attain
competence to proceed. In considering the
issues relating to treatment, the examining
experts shall specifically report on:
1. The mental illness causing the
incompetence;
2. The treatment or treatments
appropriate for the mental illness of
the defendant and an explanation of
each of the possible treatment
alternatives in order of choices;
3. The availability of acceptable
treatment and, if treatment is available
in the community, the expert shall so
state in the report; and
4. The likelihood of the defendant’s
attaining competence under the
treatment recommended, an
assessment of the probable duration of
the treatment required to restore
450 forensic neuropsychology

competence, and the probability that elements of competency presented by judges in

the defendant will attain competence
to proceed in the foreseeable future.
There have been clinician/researchers involved
in attempting to operationalize Dusky and pro-
vide evaluators with specific functional abilities.
The Group for the Advancement of Psychiatry
(1974) developed a 21-point list of abilities from
competency assessment instruments available at
the time (Table 16.3). These abilities can assist the
evaluator by providing an outline and road map
for clinical interviewing. Failure in any one or
more points does not necessarily constitute
incompetency, but the points help ensure evalua-
tors identify and consider all relevant issues
before coming to conclusions.
In contrast to the detail that came out of crim-
inal competency research at the hands of behav-
ioral scientists, is the emphasis on the most basic
case law. Wieter v. Settle was an interesting case in
the U.S. District Court for the Western District of
Missouri in 1961. Although Wieter v. Settle is not
a jurisdictionally authoritative decision, meaning
it does not have much power to control other
judicial decisions, it has been presented widely to
better enable mental health professionals to
understand the very basic aspects of “reasonable
understanding” as it relates to mental health com-
petency (Denney & Wynkoop, 2000; Grisso, 1988;
Marcopulos et al., 2008; Stafford, 2003).
Wieter was arrested and charged with a fed-
eral misdemeanor offense after he claimed to
have placed a bomb on a commercial airliner trav-
eling from Seattle, Washington, to Los Angeles,
California. He was found not competent to stand
trial and committed for inpatient mental health
treatment. After 18 months, he filed a habeas
corpus motion seeking relief from mental health

TABLE 16.3 GROUP FOR THE ADVANCEMENT OF PSYCHIATRY 21ITEM

LIST TO ASSIST IN THE EVALUATION OF COMPETENCY

1. Understand current legal situation.

2. Understand current charges.
3. Understand facts relevant to the case.
4. Understand the legal issues and procedures in the case.
5. Understand legal defenses available in the defendant’s behalf.
6. Understand the dispositions, pleas, and penalties possible.
7. Appraise the likely outcomes.
8. Appraise the roles of defense counsel, prosecuting attorney, judge, jury, witnesses, and defendant.
9. Identify and locate witnesses.
10. Relate to defense counsel.
11. Trust and communicate relevantly with counsel.
12. Comprehend instructions and advice.
13. Make decisions after receiving advice.
14. Maintain a collaborative relationship with counsel and help plan legal strategy.
15. Follow testimony for contradictions or errors.
16. Testify relevantly and be cross-examined if necessary.
17. Challenge prosecution witnesses.
18. Tolerate stress at the trial and while awaiting trial.
19. Refrain from irrational and unmanageable behavior during trial.
20. Disclose pertinent facts surrounding the alleged offense.
21. Protect himself by using available legal safeguards.

Reproduced from Misuse of Psychiatry in the Criminal Courts: Competency to Stand Trial (Group for the Advancement of
Psychiatry, Report 89, 1974), Formulated by the Committee on Psychiatry and Law. Reproduced with permission.
 Criminal Forensic Neuropsychology and Assessment of Competency 451

commitment and release because he already Competency to Confess

spent more time in custody than he would have
if convicted of the misdemeanor.
A psychiatrist filed a report indicating Wieter
was still not competent because of mental illness.
The U.S. District Court reheard the case and dis-
agreed with the psychiatric opinion. In considering
the man competent, the court outlined eight mini-
mal abilities required for competency to proceed
(Table 16.4). Subsequent case law substantially
softened the requirement for memory of the events
such that a competent defendant does not necessar-
ily need to recall details of the alleged offense
(Wilson v. United States, 1968). This issue is
addressed further under competency and amnesia.
Competency as Decisional Capacity
Much of the discussion around Dusky has to do
not only with knowledge, but also with the ability
to go through a process. Implied within the
concept of competency to proceed is decisional
capacity, that is, the idea of capacity to make
important legal decisions. Contrasted with deci-
sional capacity is procedural capacity, by which a
person can understand the nature and conse-
quences of proceedings. Criminal defendants
make many decisions in the process of assisting in
their defense, but there are some decisions that
have unique standing because they involve waiv-
ing rights guaranteed under the U.S. Constitution.
Three examples are the right to remain silent, right
to counsel, and right to trial. I address each of
these in turn.
The 5th Amendment of the U.S. Constitution
guarantees the right to be free from self-incrimi-
nation, and the 6th Amendment guarantees the
right to counsel. The U.S. Supreme Court affirmed
these rights in Miranda v. Arizona (1966). As a
result of this famous case, the concept has become
known as the “right to remain silent.” If the sus-
pect waives the right to silence and input from
counsel, any statements given can be used against
him or her. The Court spelled out the need for any
statements given by the suspect to be voluntary,
intelligent, and knowing for them to be admissible
in later criminal proceedings.
Although Miranda appeared to limit law
enforcement deception, later court cases have
outlined that:
As long as the person subjected to interroga-
tion appears to understand the right to remain
silent and the right to counsel subsequent
waiver of those rights will usually be “knowing
and intelligent”; other types of misunderstand-
ings or misimpressions are not relevant to the
admissibility issue. (Melton et al., 2007, p. 169)
Greater emphasis has been placed on the term
“voluntary” in subsequent cases as much of the
concern has revolved around what constitutes
“coercion.”
Coercion was addressed in light of mental
health concerns by the U.S. Supreme Court in
Colorado v. Connelly (1986). Barry Francis

TABLE 16.4 MINIMAL ABILIT Y REQUIREMENTS FOR CRIMINAL COMPETENCY

AS OUTLINED BY THE U.S. DISTRICT COURT IN WIETER V. SETTLE  1961 .
ADAPTED FOR CLARIT Y.

1. Mental capacity to appreciate his/her presence in relation to time, place, and things.
2. Elementary mental processes such that he/she apprehends (i.e., seizes and grasps with what mind he/she has)
that he/she is in a Court of Justice, charged with a criminal offense.
3. Apprehends that there is a judge on the bench.
4. Apprehends that there is a prosecutor present who will try to convict him/her of a criminal charge.
5. Apprehends that he/she has a lawyer (self-employed or court-appointed) who will undertake to defend him/her
against that charge.
6. Apprehends that he/she will be expected to tell his/her lawyer the circumstances, to the best of his/her mental
ability, (whether colored or not by mental aberration) the facts surrounding him/her at the time and place where
the law violation allegedly occurred.
7. Apprehends that there is, or will be, a jury present to pass upon evidence adduced as to his/her guilt or
innocence of such charge.
8. He/she has memory sufficient to relate those things in his/her own personal manner.
452 forensic neuropsychology
Connelly flew from Boston to Denver to confess
to the Denver police about a murder committed
several months earlier in Colorado. Despite
repeated Miranda warnings that he need not talk,
he insisted on giving self-incriminating details of
the murder. Police observed no overt signs of
mental illness. Later testimony presented that the
defendant was “compelled” to confess by com-
mand hallucinations from God.
The U.S. Supreme Court ultimately opined
that the “respondent’s perception of coercion
flowing from the ‘voice of God,’ however impor-
tant or significant such a perception may be in
other disciplines, is a matter to which the United
States Constitution does not speak” (p. 524). There
needed to be police activity amounting to “over-
reaching” to find his confession not voluntary.
The Court confirmed that the waiver of Miranda
rights must be knowing, intelligent, and volun-
tary. Regardless of the Colorado v. Connelly
decision’s emphasis on police overreaching, both
Miranda and Connelly suggest mental health
professionals have a place in evaluating the com-
petency of criminal defendants to confess.
Competency to Plead Guilty and
Waive Counsel
Post-Dusky courts also struggled with the level of
competency required to waive the constitutional
right to counsel and trial. Both of these rights
were addressed and the concepts brought together
in Godinez v. Moran (1993). However, in very
recent U.S. Supreme Court law, the issue of com-
petency to waive counsel was revisited (Indiana v.
Edwards, 2008). I must first lay the groundwork
for these two important cases and then spell out
the current standard in these areas.
In 1966, the U.S. Supreme Court decided
Westbrook v. Arizona, which questioned whether
a general competency hearing addressing Dusky
language was adequate when the defendant chose
to waive right to counsel. Westbrook was initially
found competent to stand trial. He then dismissed
his attorney and chose to act as his own attorney
(termed acting pro se). The High Court eventually
reviewed the case and sent it back to the trial
court, suggesting the need to determine whether
the defendant made an “intelligent and compe-
tent” waiver of his constitutional right to counsel.
This finding suggested a higher standard of
competency to act as one’s own attorney than that
outlined in Dusky.
In a non–mental health, but related, case,
Faretta v. California (1975), the U.S. Supreme
Court concluded that competency to waive the
right to an attorney is not based on a determina-
tion of the defendant’s level of legal knowledge.
Even though it may be bad judgment, competent
defendants can act as their own attorneys
regardless of how ignorant they are in the law and
criminal procedure.
A discussion on the issue of waiving one’s right
to trial by pleading guilty needs to start with a
non–mental health case. In 1970, the U.S. Supreme
Court decided North Carolina v. Alford. Alford
chose to plead guilty in a capital murder case
simply to avoid the possibility of the death pen-
alty. In his statement pleading guilty, he asserted
he did not commit the crime, but was pleading
guilty to avoid the death penalty. The U.S. Supreme
Court reviewed the issue based on the question of
whether Alford was coerced by the gravity of the
situation into waiving his right to a trial. The
Court summarized the issue that defendants must
voluntarily, knowingly, and understandingly waive
a right to trial. They found Alford had made a
“voluntary and intelligent choice among alterna-
tives;” his plea was not compelled merely by the
risk of execution.
The Alford decision set the stage for the 1973
U.S. Court of Appeals for the 6th Circuit decision
in Sieling v. Eyman. In this case, the 9th Circuit
established what appeared to be a higher standard
to waive rights to trial and plead guilty. The court
seemed to propose a standard of a “reasoned
choice among alternatives” in addition to the
general Dusky criteria. The U.S. Supreme Court
encompassed each of these concerns and appeared
to resolve the inconsistencies, for a time, with
their reasoning in Godinez v. Moran (1993).
Richard Moran was charged with murdering a
bartender and bar patron in August 1984. A few
days later, he allegedly murdered his wife and
attempted suicide by shooting himself in the
abdomen. He survived and was handed over to
police in the hospital recovery room. He was
found competent to stand trial and initially
pleaded not guilty. Two and one half months later,
he requested that his defense attorney be dis-
charged, and that he be allowed to plead guilty.
The trial court accepted his waiver of counsel and
trial once assured that he was not pleading guilty
in response to threats or promises, and that he
understood the charges and potential conse-
quences facing him.
In 1985, Moran was sentenced to death. In
1987, he filed a petition for post-conviction relief
claiming he had not been mentally competent to
 Criminal Forensic Neuropsychology and Assessment of Competency
represent himself. The trial court, Nevada Supreme
Court, and U.S. District Court rejected his appeal,
but the U.S. Court of Appeals for the 9th Circuit
reversed the prior decisions, holding the due
process clause of the 14th Amendment required
the court to hold a competency inquiry before
accepting his decision to discharge counsel and
enter a guilty plea. Similar to the reasoning in
Sieling v. Eyman (1973), the Court required
a reasoned-choice-among-alternatives inquiry.
The U.S. Supreme Court took up the question of
whether the competency standard for pleading
guilty or waiving right to counsel was higher than
the competency standard for standing trial. They
rejected the 9th Circuit’s use of reasoned choice
and concluded:
We can conceive of no basis for demanding a
higher level of competence for those defen-
dants who choose to plead guilty . . . nor do we
think that a defendant who waives his right to
the assistance of counsel must be more compe-
tent than a defendant who does not. (p. 332)
Although the Court specifically indicated the
Dusky standard was not increased, they made this
slight enhancement:
A finding that a defendant is competent to
stand trial, however, is not all that is necessary
before he may be permitted to plead guilty or
waive his right to counsel. In addition to deter-
mining that a defendant who seeks to plead
guilty or waive counsel is competent, a trial
court must satisfy itself that the waiver of his
constitutional rights is knowing and voluntary.
(p. 333)
Godinez trumped the reasoning presented
in Westbrook and Sieling by establishing that com-
petency to plead guilty or waive counsel requires
no higher standard than competency to stand
trial. However, the trial court must now specifi-
cally place in the record an inquiry into the defen-
dant’s thought process to verify it is a “knowing”
and “voluntary” decision. Godinez recapitulated
Dusky and spelled out the minimum required
standard for decisional capacity; however, it left
open the unusual possibility that a person could
be competent to stand trial while at the same time
not competent to represent him or herself. This
unusual consideration is exactly the case in the
very recent U.S. Supreme Court case of Indiana v.
Edwards (2008).
453
Ahmad Edwards is a man with schizophrenia
who was caught in the act of trying to steal a pair
of shoes from a department store. While in the
store, he withdrew a handgun and fired it as
security personnel were attempting to detain him,
wounding a bystander. He was charged with
attempted murder, battery with a deadly weapon,
criminal recklessness, and theft. His mental state
was in question during three competency hear-
ings and two self-representation requests. He was
initially found not competent and sent to a foren-
sic hospital for competency restoration treatment.
After 7 months of treatment, the trial court found
him competent to assist his attorneys and stand
trial. Seven months later, defense counsel sought
another competency hearing and presented
additional testimony from a psychiatrist and
neuropsychologist indicating he was not able to
cooperate with his attorney because of delusions.
The court again found him not competent and
returned him to the state hospital. After 8 more
months of treatment, he was found competent
again. Just before the trial, however, he asked the
court for permission represent himself (i.e., waive
his right to counsel) and for an additional delay to
the trial so he could prepare. The court refused
both requests, and the jury convicted him of
criminal recklessness and theft. They could not
reach a verdict on the attempted murder and
battery charges. Approximately 6 months later,
the state retried him on the murder and battery
charges. Again, he requested to represent himself.
Trial court cited his lengthy history of schizophre-
nia, concluded he was competent to stand trial,
but did not find him competent to represent him-
self. Proceeding with assistance of counsel, he was
convicted on both counts.
Edwards took his case to the Indiana appeals
court arguing that the trial court deprived him of
his constitutional right to self–representation
based on Faretta. The appeals court overturned
his conviction and ordered a new trial. The gov-
ernment appealed it to the Indiana Supreme
Court, who agreed with the trial court in many
aspects but, because of Faretta and Godinez, chose
to affirm the appeals court in over-turning the
conviction and requiring the trial court to let him
represent himself. At Indiana’s request, the U.S.
Supreme Court heard the case to consider the
constitutionality of not allowing an otherwise
competent defendant to represent himself.
In considering the case, the U.S. Supreme
Court pointed out that Faretta did not take into
consideration the presence of mental illness
454 forensic neuropsychology
because Faretta was not a mental-health-related
case. Additionally, the Court noted that even the
Faretta decision, as well as later cases, indicated
the right to self-representation was not absolute.
The court noted subtle, but important, distinc-
tions between the Edwards case and Godinez.
Godinez wanted to represent himself in order to
change his not guilty plea to a guilty plea. He did
not seek to represent himself in a trial. In that case
the U.S. Supreme Court only had to answer the
question of his decisional competency, not his
procedural competency to represent himself.
Additionally, in Godinez, the state sought to allow
Moran the right to represent himself. The issue is
confusing because Moran had successfully
obtained the right to waive counsel and plead
guilty. He only filed the appeal after he received a
death sentence, claiming he had actually not been
competent to waive counsel and plead guilty in an
attempt to overturn his conviction. In Edwards,
the issue was whether the state could disallow
the defendant to represent himself during trial
proceedings.
The U.S. Supreme Court concluded that
it could not maintain a single standard of compe-
tency as it pertained to a defendant who is compe-
tent to proceed to trial with aid of counsel
compared to proceeding without aid of counsel.
The court noted the fact that a mentally ill defen-
dant can be competent to proceed with counsel
but not competent to proceed without counsel.
The court also concluded that allowing self-repre-
sentation under such unique circumstances does
not affirm the dignity of the defendant. Last, the
court noted the importance that courts must not
only ensure a fair trial, but they must also ensure
that the trial appears fair to those observing the
proceedings. It is not a long stretch to imagine
the justices reviewing in their minds the debacle
presented when Colin Ferguson represented
himself during the televised New York trial
(Bardwell & Arrigo, 2002). In Edwards, the U.S.
Supreme Court separated the issue of competency
to represent oneself during trial proceedings from
the issues of competency to waive counsel and
plead guilty as outlined in Godinez. Evaluators
must now consider this specific question when
formulating their opinions regarding a criminal
defendant’s competence to stand trial
Burden and Standard of Proof
It is helpful for neuropsychologists to understand
how courts make decisions. Evidence is compared
to sometimes vague legal standards in a manner
remotely analogous to hypothesis testing. As with
science, the court starts out with a default assump-
tion. In the example of criminal conviction, defen-
dants are assumed innocent until shown otherwise.
Enough evidence must be demonstrated on the
record to move the mind of the trier of fact (judge
or jury) to a level “beyond reasonable doubt” to find
the defendant guilty of the crime. In this example,
the prosecution carries the burden of proof, and the
standard of proof is beyond reasonable doubt.
There are three major standards of proof for
issues most relevant to neuropsychologists:
beyond reasonable doubt, clear and convincing,
and preponderance of the evidence. Although
quite artificial, behavioral scientists can use
percentages to communicate better the concept to
such legal terms. In this regard, beyond reason-
able doubt is most similar to 90% to 95% (e.g.,
p < .05), clear and convincing approximates 75%,
and preponderance amounts to just slightly better
than half (51%; Melton et al., 2007, p. 217). Each
of these standards is used during different inqui-
ries in criminal procedure, and there are other
standards used by appellate courts when review-
ing trial court records. I turn to two criminal
competency cases to demonstrate the standard of
proof and who holds the burden of proof in com-
petency determinations.
In 1984, Teofilo Medina stole a gun, held up
four business establishments, murdered three
employees, attempted to rob a fourth, and shot at
two passersby. He was apprehended, tried, and
convicted of three counts of first-degree murder.
Before the trial, defense moved for a hearing on
Medina’s competency to stand trial. He was found
competent, although there was conflicting
expert testimony. After the guilty verdict, Medina
reinstated a previously withdrawn plea of not
guilty by reason of insanity. The jury found him
sane, and he was sentenced to death.
On appeal, it was argued his constitutional
right to due process was violated by placing the
burden of proof on him to establish his incompe-
tence to stand trial. In 1992, the U.S. Supreme
Court heard the case and held (a) the California
statute requiring that the party asserting incom-
petency of the defendant to stand trial had the
burden of proving incompetence did not violate
procedural due process rights of the defendant,
and (b) the statute providing for the presumption
of competency did not violate procedural due
process.
Medina v. California (1992) not only revealed
it is constitutional to place the incompetency
 Criminal Forensic Neuropsychology and Assessment of Competency
burden on the defendant, but also revealed that
the burden is on whoever asserts that the defen-
dant is not competent because defendants are
presumed competent to stand trial. The table
turns after the court has found a defendant not
competent and commits him or her to mental
health treatment for restoration of competency.
At the end of treatment, the burden is now on
whoever asserts the defendant is competent to
proceed because it is assumed the defendant
remains not competent. The issue of who
carries the burden of proof in competency deter-
minations is not particularly critical given the
particular standard of proof involved. The impor-
tance of this standard of proof was addressed
by the U.S. Supreme Court in Cooper v. Oklahoma
(1996).
In Oklahoma at the time Byron Cooper was
charged with murdering an 86-year-old man
during the course of a burglary, defendants in
criminal prosecutions were assumed competent
to stand trial until shown otherwise by clear and
convincing evidence. Questions regarding
Cooper’s competence were raised on five separate
occasions before and after the trial. Initially,
a pretrial judge relied on a psychologist’s opinion
that Cooper was not competent and committed
him to a state hospital for treatment. After 3
months of treatment, however, the trial court
found him competent to proceed. At this point, he
was presumed competent until shown by clear
and convincing evidence not competent. One
week before trial, the lead defense attorney
raised the issue of competence, but the judge
held to his earlier determination that Cooper was
competent.
On the first day of trial, his bizarre behavior
led to a further competency hearing. Additional
expert testimony was heard suggesting Cooper
was incompetent, but there was concern about
malingering. The judge held to his earlier deter-
mination and pushed on with the trial. Cooper
was found guilty. Before sentencing, defense
moved for a mistrial and another competency
hearing, but the motions were denied. Cooper
was sentenced to death. The Oklahoma Court of
Criminal Appeals affirmed the decision.
The Court of Appeals ruling was overturned
by a unanimous decision of the U.S. Supreme
Court. It was concluded Oklahoma’s clear and
convincing evidence rule regarding proof of
incompetence “offends a principle of justice that is
deeply rooted in the traditions and conscience of
our people” (p. 362). By holding to a clear
455
and convincing standard, the state runs too great
a risk of finding an incompetent defendant
competent to proceed and thereby violating his or
her due process rights under the 14th Amendment.
Although Medina provided that it is constitution-
ally sound to place the burden on defendants,
Cooper dictated that the standard of proof in
determining incompetency can be no more strict
than preponderance of the evidence, that is, just
enough to tip the scales.
Competency to Refuse an
Insanity Defense
As demonstrated in Faretta v. California (1975),
competent defendants have the right to make
decisions that may not be in their best interests or
are otherwise demonstrative of poor judgment.
Occasionally, it is difficult to tell whether such
decisions reflect poor judgment. Such is the case
when a mentally ill (but competent) defendant
has a very good case for a successful insanity
defense, but he or she chooses to forgo that
defense. Judge Bazelon of the Court of Appeals for
the District of Columbia wrote these words about
society’s responsibility in this regard (Whalem v.
United States, 1965):
In the courtroom confrontations between the
individual and society the trial judge must
uphold this structural foundation by refusing
to allow the conviction of an obviously men-
tally irresponsible defendant, and when there is
sufficient question as to a defendant’s mental
responsibility at the time of the crime, that issue
must become part of the case. (pp. 818–819)
In Whalem (1965), the appeals court held that
the trial court could impose an insanity defense on
a competent defendant even against the defendant’s
desires. That reasoning was reviewed after the
North Carolina v. Alford (1970) and Faretta (1975)
decisions in another District of Columbia Circuit
Court case, Frendak v. United States (1979).
Paula Frendak’s coworker, Willard Titlow, was
fatally shot on the first floor of their office build-
ing. Frendak traveled out of Washington, D.C., on
a multistate, multicountry trip before she was
apprehended in Abu Dhabi, United Arab Emirates,
for not surrendering her passport. She was found
to possess a pistol and 45 rounds of ammunition.
She was extradited back to the United States and
charged with first-degree murder. She underwent
multiple competency evaluations and was ulti-
mately found competent. Frendak was convicted.
456 forensic neuropsychology
The trial court then overrode her conviction
and found her not guilty by reason of insanity.
She appealed partly to reject the insanity plea. The
District of Columbia Court of Appeals held that
the trial judge may not force an insanity defense
on a defendant found competent to stand trial if
the defendant intelligently and voluntarily decided
to reject the insanity defense. There were several
potentially intelligent rationales for rejecting an
insanity defense (Frendak v. United States, 1979):
1) A defendant may fear that an insanity
acquittal will result in the institution of
commitment proceedings which lead to
confinement in a mental institution for a
period longer than the potential jail
sentence.
2) The defendant may object to quality of
treatment or the type of confinement to
which he or she may be subject in an
institution for the mentally ill.
3) A defendant, with good reason, may
choose to avoid the stigma of insanity.
4) Other collateral consequences of an
insanity acquittal can also follow the
defendant throughout life (e.g., the right
to vote, serve on a federal jury, or even
restrict his or her ability to obtain a
drivers license).
5) A defendant also may oppose the
imposition of an insanity defense because
he or she views the crime as a political or
religious protest which a finding of
insanity would denigrate (pp. 376–378).
It is important for a forensic examiner to be
aware of these potential reasons for wanting to
avoid an insanity defense because the rationale for
choosing a defense goes to competency by way of
“assisting properly” in one’s defense. The evalua-
tor will need to assess the impact of any mental
illness on the defendant’s ability to make an intel-
ligent and voluntary judgment in this regard.
Competency Assessment Tools
There are a number of competency assessment
tools available to assist in the assessment of com-
petency to proceed. Some of these tools are simply
interview outlines; others are structured inter-
views and more formalized tests. They all have
one characteristic in common, however: They do
not determine who is or is not competent to pro-
ceed. As with all competent neuropsychological
evaluations, such tools aid in clinical determina-
tion, but do not replace a thorough integration
of all relevant information as part of a multiple
data source assessment. Several competency
instruments have limited utility at this point and
receive only a brief mention here. I then review
the Competency Assessment Instrument (CAI,
and its revised version R-CAI), Fitness Interview
Test–Revised (FIT-R), Georgia Court Compete-
ncy Test (GCCT, and its revised version GCCT-
MSH), Competency Assessment for Standing
Trial for Defendants With Mental Retardation
(CAST*MR), MacArthur Competency Assess-
ment Tool–Criminal Adjudication (MacCAT-CA),
and the Evaluation of Competency to Stand
Trial–Revised (ECST-R).
The Competency Screening Test (CST;
Laboratory of Community Psychiatry, 1973;
Lipsitt, Lelos, & McGarry, 1971) was developed as
a brief screening test to aid in deciding who
needed more thorough assessment regarding
competency to proceed. It was devised by a group
of psychiatrists, psychologists, and lawyers with a
National Institute of Mental Health grant from
the Center for Studies of Crime and Delinquency.
It is a 22-item sentence-completion test. Each of
the items is scored 0, 1, or 2 and summed for a
total score. Total scores below 21 suggest further
competency assessment is warranted. There has
been criticism of the CST on conceptual, psycho-
metric, and predictive utility grounds. See Grisso
and colleagues (2003) for a more thorough review.
The CST may have value as a general screener for
agencies, but it appears to have limited utility
for neuropsychologists performing competency
evaluations.
The Interdisciplinary Fitness Interview
(Golding, Roesch, & Schreiber, 1984) was devel-
oped as a research tool for Canadian jurisdictions.
The semistructured interview format includes
items on psychopathology as well as legal issues.
The unique aspect of the procedure includes a
joint interview of an attorney with a mental health
professional. No additional research has come out
on the Interdisciplinary Fitness Interview since
Grisso’s detailed review of it in 1986.
The Computer Assisted Determination of
Competency to Proceed (Barnard et al., 1991,
1992) is a computer-administered, 272-item,
18-scale test that addresses social history, psycho-
logical functioning, and legal knowledge. Items
include yes/no, true/false, and multiple choice
formats. It takes over an hour to administer,
and the computer produces a narrative report
 Criminal Forensic Neuropsychology and Assessment of Competency
summary. It was designed to provide organized
and relevant information directly from the defen-
dant for the clinician to review prior to a face-to-
face interview. Preliminary research of the
instrument seemed positive, but there were sig-
nificant concerns about its initial validation. There
has been no published research of the instrument
since 1992, and there is no published manual
(Grisso et al., 2003). Melton and colleagues (2007)
discuss the test only briefly and recommend
against its use clinically.
Competency Assessment Instrument
The CAI (Laboratory of Community Psychiatry,
1973; McGarry, Lelos, & Lipsitt, 1973) was devel-
oped alongside the CST. It is a semistructured
interview that takes about 45 minutes to adminis-
ter. It was originally developed with a scoring
system based on 5-point Likert ratings of 13
competency-related functions. The functional
domains were derived from appellate cases, legal
literature, and experience of the multidisciplinary
development team (Stafford, 2003). There are no
standardized administration rules. Although
clinicians are free to formulate their own ques-
tions to address each knowledge domain, example
questions are provided for each.
The original CAI manual did not specify the
order in which the functions should be addressed,
and many of the questions required only yes or no
answers. It was revised by forensic practitioners
working in the Trial Competency Program at
Atascadero State Hospital in California on three
different occasions over the course of 20 years
(Riley, 1998). The order of questions was changed
to flow more logically during a competency inter-
view. Questions were also added and reworded in
a more open-ended format. An additional domain
was added to deal with capacity to cope with stress
of incarceration prior to trial. Riley stressed
“probing of an area should continue until the
examiner is satisfied that as much as is reasonably
possible is known about [the domain]” (p. 14). He
further pointed out it is not always necessary to
ask every question under each dimension as some
questions are not appropriate given the charge
(e.g., misdemeanor) or current stage of legal
proceedings (e.g., questions about trial when the
defendant is facing sentencing).
Administration of the CAI remains flexible.
A portion of the Revised CAI is shown in
Table 16.5.2 Although the CAI and R-CAI use a
scoring system with cutoffs for incompetency, the
scoring system is generally used solely for research.
457
The instrument is more commonly used as an
interview outline and guide to guarantee impor-
tant areas are not overlooked during the compe-
tency interview process (Denney & Wynkoop,
2000; Stafford, 2003).
The Fitness Interview
Test–Revised
The Fitness Interview Test (FIT; Roesch, Webster,
& Eaves, 1984) was a Canadian adaptation of the
CAI. It included additional items regarding trial
procedures and a separate section addressing gen-
eral defendant mental status. An extensive revi-
sion occurred secondary to Canada’s 1992 revision
of the Criminal Code (Roesch, Zapf, Eaves, &
Webster, 1998). Changes in the FIT were substan-
tial (Grisso et al., 2003). The FIT-R retained the
structured interview format but became more
consistent with United States law. It has now been
published in the United States by Professional
Resource Press as a manual with a CD-ROM
which includes the FIT-R interview for unlimited
printing as well as a number of case law references
and research citations (Roesch, Zapf, & Eaves,
2006). It starts with four introductory questions
(such as “Do you have a lawyer at this point?”)
then moves on to 70 questions grouped in 16
headings under the following three major sections
(which correspond to the Criminal Code of
Canada, Section 2):
Section I: Understanding the Nature or
Object of the Proceedings: Factual
Knowledge of Criminal Procedure
1. Understanding of Arrest Process
2. Understanding of the Nature and
Severity of Current Charges
3. Understanding of the Role of Key
Participants
4. Understanding of the Legal Process
5. Understanding of Pleas
6. Understanding of Court Procedure
Section II: Understanding the Possible
Consequences of the Proceedings:
Appreciation of Personal Involvement in and
Importance of the Proceedings
7. Appreciation of the Range and Nature
of Possible Penalties
8. Appraisal of Available Legal Defenses
9. Appraisal of Likely Outcome
458 forensic neuropsychology

TABLE 16.5 PORTIONS OF THE REVISED CAI.

1. Understanding of Charge(s):
What are you charged with?
Is this a felony or misdemeanor?
Which is more serious?
What would anyone have to do to commit the crime of?
2. Appreciation of Penalties:
If you’re found guilty as charged, what are the possible sentences the Judge could give you?
Where would you serve such a sentence?
What does probation mean?
What are some of the conditions a person must follow on probation?
What happens if a person is found Not Guilty?
Where do they send people found Not Guilty by Reason of Insanity?
3. Appraisal of Available Defenses:
What pleas can a person enter in court?
What does Not Guilty mean?
Guilty?
Not Guilty by Reason of Insanity
4. Appraisal of Functions of Courtroom Participants:
In the courtroom during a trial, what is the job of
a. Public Defender?
b. District Attorney?
c. Judge
d. Jury
e. Defendant
f. Witnesses
5. Understanding the Court Procedures:
Do defendants always have to testify in their own cases?
If you do have to testify, will you have to tell everything that happened?
If you testify, who asks you questions first?
Then who can ask you questions?
What is the district attorney trying to do?
What is the difference between a court trial and a jury trial?

Note: Originally published by NIMH, DHEW Publication No. (ADM) 77–103. Reproduced with permission of Paul
D. Lipsitt. Revised by John A. Riley, PhD, reproduced with permission

Section III: Communicate with Counsel:
Ability to Participant in Defense
10. Capacity to Communicate Facts to
Lawyer
11. Capacity to Relate to Lawyer
12. Capacity to Plan Legal Strategy
13. Capacity to Engage in Own Defense
14. Capacity to Challenge Prosecution
Witnesses
15. Capacity to Testify Relevantly
16. Capacity to Manage Courtroom
Behavior (p. 27)
As with the CAI, responses to questions are rated
0, 1, or 2 for adequacy. Scores are summed to
achieve performance for each section as well as
overall total performance. There are no norms
available. Since it is presented as a 30-minute
screening tool, a poor performance during one of
the three sections would suggest the need for
more in depth assessment.
Viljoen, Roesch, and Zapf (2002) completed a
study regarding inter-rater reliability between
psychologists, physicians, nurses, and graduate
students. The overall intraclass correlation
coefficients based on the full sample of raters
regarding judgment of fitness were quite high,
 Criminal Forensic Neuropsychology and Assessment of Competency
falling from 0.94 to 1.00. Additional research
demonstrated similarly good inter-rater correla-
tions with adolescents (Viljoen, Vincent, &
Roesch, 2006). Viljoen and colleagues (2006) also
demonstrated a three-factor model that corre-
sponded roughly to the requirements of Dusky,
that is, understanding/reasoning about charges
and legal proceedings, appreciation of the conse-
quences of their charges and proceedings, and
ability to communicate with counsel. There is no
research regarding the measures’ susceptibility to
feigned incompetency, nor does it have items
designed to detect feigned incompetence. The
FIT-R is presented as only a screening tool, but it
appears to be a valid and useful measure to assist
neuropsychologists in the assessment of trial-
related competency.
Georgia Court Competency Test
The Georgia Court Competency Test (GCCT)
was developed as an in-house competency screen-
ing tool at Central State Hospital, Milledgeville,
Georgia, to assess competency to proceed in a
relatively rapid manner (Wildman et al., 1980).
In its original form, it was comprised of 17 ques-
tions designed to address knowledge of courtroom
and legal proceedings, current charges and possi-
ble penalties, and relationship with an attorney.
Johnson and Mullett (1988) modified the instru-
ment and raised the number of items to 21 (now
referred to as the GCCT-MSH). Nicholson (1992,
cited in Rogers, Grandjean, Tillbrook, Vitacco, &
Sewell, 2001) reviewed available reliability studies
of the GCCT and concluded the test has moder-
ately high test–retest reliability, high α coefficients,
and excellent interscorer reliability.
Early research suggested the GCCT had a
stable three-factor structure, termed “general legal
knowledge,” “courtroom layout,” and “specific
legal knowledge” (Bagby, Nicholson, Rogers, &
Nussbaum, 1992; Nicholson, Briggs, & Robertson,
1988). Rogers, Ustad, Sewell, and Reinhart (1996)
and Ustad, Rogers, Sewell, and Guarnaccia (1996)
failed to demonstrate this factor structure with
confirmatory factor analysis, but exploratory
factor analysis with mentally ill jail and forensic
hospital samples suggested two factors related to
“legal knowledge.” Research revealed classification
rates of 68% to 78% on the GCCT (Wildman et al.,
1980) and 81.8% on the GCCT-MSH (Nicholson,
Robertson, Johnson, & Jensen, 1988).
Gothard, Rogers, and Sewell (1995) demon-
strated the instrument’s susceptibility to malin-
gering and added an eight-item Atypical
459
Presentation scale. In their subsequent analysis,
the Atypical Presentation scale demonstrated a
90% classification rate for individuals simulating
psychosis.
Although the GCCT-MSH has become
a popular instrument throughout a variety of
jurisdictions (Grisso, 1986), it has been criticized
for only representing the factual knowledge prong
of the Dusky standard (Rogers et al., 2001). The
GCCT-MSH is a helpful tool that only takes about
20 minutes to administer, but clinicians need to
remember it remains a screening instrument
designed to augment more thorough competency
assessment.
Competence Assessment for Standing
Trial for Defendants with
Mental Retardation
The CAST*MR3 was developed by Everington and
Luckasson (1992) to overcome difficulties inher-
ent in using open-ended questions with mentally
retarded defendants. The first 40 items are three
alternative multiple-choice questions dealing with
basic legal concepts and knowledge that would
help the defendant assist in his or her defense. The
last ten items are open-ended questions dealing
with the specific charges and situation of the
defendant. Each of these items is scored as 0, 0.5,
or 1 point based on accuracy and detail. Results
are totaled for each of the three sections (basic
legal concepts, skills to assist defense, and under-
standing case events) as well as a total score.
The procedure takes about 30–40 minutes to
administer. Results are then compared with
performances (mean and standard deviation) of
four groups of criminal defendants: not mentally
retarded (MR); MR but not referred for
evaluation; MR, referred for pre-trial evaluation
and considered competent; and MR, referred
for pretrial evaluation and considered not
competent.
Everington (1990) outlined the development
of the CAST*MR. Cronbach’s α and Kuder-
Richardson 20 coefficients ranged from 0.93 to
0.85 for three groups of older adolescents and
adults with MR from two states. The 2-week,
test–retest Pearson r’s were 0.90 and 0.89.
Subsequent studies using criminal defendants
from Wisconsin, Ohio, Maryland, and New
Mexico were completed. Ten checks of inter-rater
reliability were done, which resulted in 100%
agreement for the multiple choice items and 80%
agreement for open-ended questions. Inter-rater
agreement improved to 86.6% with a larger
460 forensic neuropsychology
number of comparisons (Everington & Dunn,
1995). Competent/not-competent classification
agreement rates with independent forensic
examiners varied from 62.9% to 71.43%, similar
to hit rates of the GCCT and GCCT-MSH.
The CAST*MR appears to be an easy test to
feign, simply by choosing incorrect answers on
items from sections I and II and then claiming
ignorance during section III. Everington, Notario-
Smull, and Horton (2007) demonstrated this fact
in a simulation design study. They incorporated
mildly mentally retarded (MR) individuals and
mentally typical individuals, all of whom had
been involved in the criminal justice system. They
incorporated sections I and II only. Half of each
group was randomly assigned to feign ignorance
and pretend they were on death row seeking to
save their lives, and the other half of each group
was asked to perform their best. MR feigners
performed significantly worse than genuine
MR performance; however, there was no signifi-
cant difference between the MR feigners and
mentally typical feigners. The authors suggested
that performances falling within the random
range on either section I or II should raise the
suspicion for feigning. Last, no literature
exists addressing how brain-injured individuals
perform on the CAST*MR.
MacArthur Competency Assessment
Tool–Criminal Adjudication
The MacCAT-CA (Poythress et al., 1999) is a
trimmed down, clinical version of the broader
research instrument, MacArthur Structured
Assessment of Competencies of Criminal
Defendants (MacSAC-CD; Otto et al., 1998). The
MacCAT-CA is a structured interview consisting
of 22 items organized under three domains:
Understanding, Reasoning, and Appreciation.
Four questions under Understanding and
Reasoning incorporate a brief vignette about two
individuals fighting during a pool game in a bar.
One individual strikes the other with a pool
cue and is charged with a crime. The subject
taking the MacCAT-CA must assume the mindset
of the defendant in the vignette to answer
questions under Understanding and Reasoning
sections. Several questions under Understanding
incorporate brief training after initially inade-
quate responses and follow up with additional
questioning. Items under Reasoning are of
two types. The first requires the test subject to
indicate which of two facts are more important
for the hypothetical defendant to tell his attorney.
The other items require the subject to choose
between two alternative pleading options.
Scoring focuses on the reasoning behind the
choice. The Appreciation items rely on the test
subject’s actual legal situation rather than the
hypothetical vignette. The subject must compare
his or her situation to that of others and decide
whether he or she is “more likely,” “less likely,”
or “just as likely” to have various outcomes.
Summary scores are obtained for each section
(Understanding, Reasoning, and Appreciation).
The MacCAT-CA takes about 45 to 60 minutes to
administer.
Inter-rater reliability was determined with 48
protocols from the norming sample (Otto et al.,
1998; Poythress et al., 1999). Scale score intraclass
correlations were 0.90 (Understanding), 0.85
(Reasoning), and 0.75 (Appreciation). Rogers
(2001) pointed out these scores were likely inflated
because of hierarchical questions that cue raters.
Nevertheless, Rogers et al. (2001) reported results
from Rogers and Grandjean (2000) for 14 subjects
that produced inter-rater correlations from 0.92
to 0.99. There are no published test–retest correla-
tions. Cronbach’s αs were 0.85 (Understanding),
0.81 (Reasoning), and 0.88 (Appreciation) based
on the original studies (Otto et al., 1998).
MacCAT-CA norms are based on 283 adjudi-
cated incompetent defendants, 249 mentally ill
defendants presumed competent, and 197
randomly selected jail inmates also presumed
competent. Subjects came from six states and
ranged in age from 18 to 65 years. Of the sample,
90% were male. Approximately half of the sample
was nonHispanic white defendants (Poythress
et al., 1999). Percentile rank scores are provided
for each of the scales in the MacCAT-CA manual.
There are tables in the back of the manual in order
to make comparisons between a defendant’s score
to the three normative groups on each of the three
domains.
Predictive ability of the MacCAT-CA appears
reasonably strong and as good as the CST and
GCCT-MSH (Stafford, 2003). Each of the scale
scores was correlated with the a priori compe-
tency classifications (Understanding, 0.36; Reas-
oning, 0.42; Appreciation, 0.49). Performance of
incompetent groups was significantly lower than
that of the presumed competent groups.
Zapf, Skeem, and Golding (2005) completed
confirmatory factor analyses on the original
normative sample of 729 individuals. They con-
sidered various theoretically driven models of
criminal competency and found a three-factor
 Criminal Forensic Neuropsychology and Assessment of Competency
structure best fit the data. The three-factor
structure did not exactly fit the three aspects of
the MacCAT-CA (Understanding, Reasoning, &
Appreciation). Results suggested a hierarchical
structure that closely approximated the theoreti-
cal underpinnings of the MacCAT-CA. All items
from Understanding combined with items 14–16
from the Reasoning section comprised the first
factor. The second factor included items 9–13
from Reasoning section, and all items from the
Appreciation section comprised the third factor.
They also completed step-wise regression analy-
ses with MacCAT-CA subscales predicting
Wechsler Adult Intelligence Scale IQ and Brief
Psychiatric Rating Scale total score. As compe-
tency status was a sizeable confound they used a
series of six regression analyses to yield path coef-
ficients. Results revealed a significant indepen-
dent positive relation between MacCAT-CA
scores and IQ and negative relation between
MacCAT-CA performance and increased psy-
chopathology. The authors concluded, “the
MacCAT-CA appears to represent a psychome-
trically sound normative approach to measuring
the generalized aspects of understanding, reason-
ing, and appreciation—as well as an overarching
component—as applied to adjudicative compe-
tence” (p. 443).
The manual includes scale cutoff scores as well
as tables that address sensitivity, specificity, false-
negative rate, and positive and negative predictive
value for every score of each MacCAT-CA scale
(Poythress et al., 1999). Grisso et al. (2003) high-
lighted the fact that, although the MacCAT-CA
authors provided cutoffs, they discouraged users
from taking these indicators as signs of compe-
tency or incompetency. The MacCAT-CA also
does not include an index of subject response set,
and Rogers, Sewell, Grandjean, and Vitacco
(2002) demonstrated the susceptibility of the
MacCAT-CA to malingering.
From a practical perspective, Pinals, Tillbrook,
and Mumley (2006) discussed the instrument’s
utility within an inpatient forensic hospital and
provided anecdotal accounts of its general effec-
tiveness in assisting in competency assessment;
however, they noted malingerers and those con-
sidered not competent both occasionally provided
“I don’t know” responses, and “defendants with
neuropsychological impairments (particularly in
frontal lobe functioning) had difficulty retaining
and manipulating information presented in the
more complex items” (p. 186). They recommended
a defendant-specific approach to choosing to use
461
the instrument rather than an across-the-board
use for all defendants. In my own experience
evaluating neurologically compromised defen-
dants, I have found the MacCAT-CA to perform
well; however, I observed one defendant with a
significant frontal lobe injury who responded
quite concretely to the pool cue assault vignette.
He kept thinking he was going to be charged
with that assault despite my repeated explana-
tions. He appeared competent to proceed in all
other aspects of his performance. This case
appears to be the exception as other frontal-
lobe-injured defendants did not have this specific
trouble, in my experience.
Evaluation of Competency to
Stand Trial–Revised
The ECST-R (Rogers, Tillbrook, & Sewell, 2004) is
a structured interview composed of four main
sections with an additional set of “background”
questions (Rogers et al., 2001, p. 510). It was
developed to measure the two Dusky prongs,
understanding and ability to assist counsel, from
both factual as well as rational perspectives.
The Consult With Counsel scale includes ten
questions to assess the attorney–client relation-
ship. The scale also incorporates five criteria:
“(i) perceptions of the relationship, (ii) defendant’s
expectations of the attorney, (iii) defendant’s
understanding of the attorney’s expectations,
(iv) resolving disagreements, and (v) special
means of communicating with the attorney”
(p. 510). The Factual Understanding scale includes
15 questions regarding courtroom participants.
The Rational Understanding is comprised of ten
questions that measure the defendant’s ability to
make rational decisions. In addition, the ECST-R
includes an Atypical Presentation Scale (ATP) to
assist in identifying feigned incompetency. This
scale has four independent subscales (Realistic,
Psychotic, Nonpsychotic & Impaired) as well as
two composite scales, Both (comprised of
Psychotic and Nonpsychotic subscales) and BI
(comprised of Psychotic, Nonpsychotic [Both
composite], and Impaired subscales). The Realistic
scale serves only as filler items and is not consid-
ered a malingering screen.
Rogers et al. (2001) evaluated the internal and
inter-rater reliabilities of the ECST-R by combin-
ing data from previous studies. The α coefficients
for the combined data were 0.72 (Consult With
Counsel), 0.86 (Rational Understanding), 0.90
(Factual Understanding), and 0.93 (total score).
Inter-rater reliability correlations were 0.97
462 forensic neuropsychology
(Consult With Counsel), 0.99 (Rational
Understanding), 1.00 (Factual Understanding),
and 1.00 (total score).
In this regard, performance of the ECST-R
was commensurate with that for the MacCAT-CA
and somewhat better than for the GCCT-MSH.
Principle axis factoring of the ECST-R revealed a
strong two-factor solution accounting for 43.5%
of the variance. This solution produced 21 sub-
stantial and unique loadings with only two cross
loadings. The two factors corresponded to Factual
Understanding and Rational Understanding
(Ability to Consult With Counsel fell under
Rational Understanding).
Vitacco, Rogers, Gabel, and Munizza (2007)
compared the relative effectiveness of the ECST-R
Atypical Presentation Scale, Miller Forensic
Assessment of Symptoms Test (M-FAST; Miller,
2001), and Structured Inventory of Malingered
Symptomatology (SIMS; Widows & Smith, 2005)
using the Structured Interview of Reported
Symptoms (SIRS; Rogers, Tillbrook, & Sewell,
2004) as the criterion measure among 100 men
who were court ordered to undergo mental health
assessment. All of the malingering subscales
obtain effect sizes that were large to very large.
The Psychotic Scale and Both Scale were most
effective at identifying positive SIRS results,
obtaining a sensitivity rate of 0.95 (missing only
one presumed malingerer). Nonpsychotic and BI
scales demonstrated excellent sensitivity rates as
well (0.90 each). The poorest performer,
Impairment, still demonstrated an impressive
0.81 sensitivity. As these are simply screening
measures, their respective specificity rates were
poor (ranging from 0.77 to 0.52). The respective
negative predictive power scores for the scales
ranged from 0.94 to 0.98 based upon a base rate of
21%. These results suggest the ATP scales were
largely effective at identifying malingerers and
reasonably effective at ruling out malingering of
exaggerated psychiatric presentation.
Applicability of Competency Assessment
Tools to Neuropsychological Evaluations
As competency is a contextual issue, each of the
competency assessment tool authors cautioned
against the use of strict cutoffs and recommended
using their instruments to augment the compe-
tency evaluation by obtaining standardized
information about the defendant’s level of under-
standing and reasoning ability related to legal
issues. It is up to the neuropsychologist to bring
together each defendant’s cognitive strengths and
weaknesses as they relate to issues of competency.
It is possible a defendant may perform well on any
of these competency instruments and yet demon-
strate such severe cognitive deficits as to bring
their competency into serious question. Likewise,
it may very well be possible for a defendant to
perform poorly on a competency assessment tool
for reasons indirectly related to competency.
None of these assessment tools have been
validated with brain-injured or neurological
populations. Anecdotally, I have seen brain-
injured defendants who have been found compe-
tent to proceed have trouble with taking the
perspective of the hypothetical defendant during
the MacCAT-CA, where they have had little trou-
ble with the ECST-R. In contrast, Pinals and
colleagues noted the increased structure of the
MacCAT-CA was helpful with certain individuals
with cognitive impairment. The increased
structure of all these structured interviews would
likely be helpful with most brain-injured defen-
dants as long as the evaluator is mindful of
potential confusion that could arise due to the
MacCAT-CA vignette. One area of potential
concern regarding the use of the ECST-R with
neurocognitively impaired individuals is the focus
of the scoring criteria. It seems to be focused more
on whether or not psychotic mentation is present
rather than lack of understanding or confusion
due to cognitive dysfunction. However, the exam-
iner is freer to include expanded queries and even
paraphrasing compared to the MacCAT-CA,
which ameliorates this concern to some degree.
Regarding the CAST*MR, Stafford (2003)
noted, “This instrument contributes legally rele-
vant data and norms to the assessment of men-
tally retarded or otherwise cognitively impaired
defendants” (p. 369; emphasis added). Empiricism
aside, the CAST*MR does allow comparisons
between a brain-injured defendant’s performance
and that of competent and incompetent individu-
als with mental retardation. This qualitative
comparison can be helpful in evaluating the com-
petence of brain-injured defendants, as results
can help validate perceptions of the defendant’s
basic level of knowledge.
None of the competency assessment tools
include measures of cognitive ability beyond legal
knowledge and decision-making capacity. The
CAST*MR and MacCAT-CA both correlate posi-
tively with IQ (Everington & Dunn, 1995;
Poythress et al., 1999; Zapf et al., 2005). Little is
known regarding the impact neurocognitive
deficits have on competency to proceed. Clearly,
 Criminal Forensic Neuropsychology and Assessment of Competency 463

there is a role for neurocognitive measures in
establishing a criminal defendant’s cognitive
strengths and weaknesses that can help in the
court’s decision.
Nestor, Daggett, Haycock, and Price (1999)
retrospectively studied the neuropsychological
functioning of 181 defendants who underwent
inpatient evaluations at Bridgewater State Hospital
in Massachusetts for competency to stand trial.
The sample consisted of 128 defendants consid-
ered competent to proceed and 53 defendants
considered not competent to proceed. Subjects
were predominantly diagnosed with psychotic
and major mood disorders. There were no com-
parisons of ethnic/racial differences, which sub-
stantially limits the study. Also, sample selection
bias was a concern. Despite these shortcomings,
results suggested competent defendants score
higher in areas of psychometric intelligence,
attention, memory (particularly verbal), episodic
memory (Logical Memory), and verbal and
nonverbal social intelligence (Comprehension and
Picture Arrangement), but not semantic memory
(Vocabulary and Information) or achievement.
See Table 16.6 for specific test scores.
Grandjean (2006) investigated neurocognitive
functioning among 55 defendants who had been
adjudicated incompetent and referred for inpatient
competency restoration treatment. She found com-
petent and incompetent defendants did not differ
in regard to attention, visuospatial, or nonverbal
memory functioning. Competent defendants per-
formed better than incompetent defendants on
measures of verbal comprehension, verbal memory,
social judgment, and executive functions.
Results from Nestor et al. and Grandjean
suggest functional domains of intellect, attention,
verbal learning/memory and social judgment are
important areas of focus. Logic in terms of
what appears important to properly assist in one’s

TABLE 16.6 NEUROPSYCHOLOGICAL TEST SCORES FOR

COMPETENT AND NOT COMPETENT GROUPS.
Measure Competent Not Competent P Effect Size
Intelligence
WAIS-R FIQ 88.25 (15.09) 82.00 (14.44) <0.01 .054
WAIS-R VIQ 88.54 (15.28) 83.06 (15.24) <0.01 .046
WAIS-R PIQ 89.01 (15.50) 82.79 (14.07) <0.01 .043
Memory
WMS-R GMI 88.12 (19.83) 78.25 (18.62) <0.01 .061
WMS-R VerMI 89.26 (17.40) 80.17 (15.87) <0.01 .070
WMS-R VisMI 92.06 (17.69) 84.64 (20.01) <0.05 .039
Attention/Concentration
WMS-R A/CI 87.58 (19.45) 84.00 (21.09) NS
TMT-A sec. 36.70 (17.03) 55.00 (32.19) <0.01 .101
TMT-B sec. 121.29 (92.90) 146.93 (112.74) NS
Executive Function
WCST #Cat. 3.98 (2.06) 3.19 (2.06) NS
Academic Abilities
WRAT-R Read. 81.22 (19.41) 78.88 (23.30) NS
WRAT-R Spell. 77.31 (19.14) 76.71 (22.73) NS
WRAT-R Arith. 79.89 (18.48) 75.05 (22.05) NS

Note: Arith, arithmetic; A/CI, Attention/Concentration Index; Cat., Category Test; FIQ, full-scale IQ; GMI,
General Memory Index; PIQ, performance IQ; Read., reading; Sec., seconds; Pell., spelling; TMT-A, Trail
Making Test-A; TMT-B, Trail Making Test-B; VerMI, Verbal Memory Index; BIQ Verbal IQ; VisMI, Visual
Memory Index; WAIS-R, Wechsler Adult Intelligence Scale-Revised; WCST, Wisconsin Card Sorting Test;
WMS-R, Wechsler Memory Scale-Revised; WRAT-R, Wide-Range Achievement Test-Revised. Adapted from
“Competence to stand trial: A neuropsychological inquiry,” by P.G. Nestor, D. Daggett, J. Haycock, & M. Price,
(1999), Law and Human Behavior, 23, pp. 397–412, with kind permission of Springer.
464 forensic neuropsychology
own defense, particularly when considering the
potential impact of Edwards v. Indiana (2008) and
self-representation, suggest neuropsychological
assessment of competency to stand trial should
thoroughly measure a wide range of functional
abilities. At a minimum, such an assessment
should focus on intelligence, attention and con-
centration, speed of mental processing, verbal
learning and memory, mental flexibility, social
reasoning, and decision-making capacity. More
research needs to occur on the nature and level
of cognitive ability needed for competency to
proceed, and particularly to represent one’s self
without the assistance of counsel.
Last, none of these competency instruments
have indices of cognitive validity. Only the GCCT-
MSH and ECST-R have associated validity indica-
tors, and these are largely directed toward
psychiatric disturbance. All of the competency
assessment tools have substantial face validity as
they are predominantly structured interviews.
They appear easy to fake by defendants simply
claiming ignorance or lack of cognitive ability.
Competency assessment tools are helpful adjunct
procedures, but competency evaluations of trau-
matically brain-injured defendants require a
broader neurocognitive evaluation with a battery
of tests that include measures of negative response
bias specific to neurocognitive functioning.
Amnesia and Competency
to Stand Trial
Claimed amnesia for the alleged criminal activity
is not unusual (Schacter, 1986). Estimates range
from 23% to 65% for homicide (Bradford & Smith,
1979; Guttmacher, 1955; Leitch, 1948; Parwatikar,
Holcomb, & Menninger, 1985). Of 100 cases of
claimed amnesia, 90% pertained to murder or
attempted murder (Hopwood & Snell, 1933). The
rates of claimed amnesia appear much lower for
nonhomicide crimes. Taylor and Kopelman
(1984) found 8% claimed amnesia for 120 cases of
nonhomicide violent crimes, and there were no
claims of amnesia for 47 nonviolent crimes.
Relevant to legal issues, amnesia has been clas-
sified as organic or functional and chronic or lim-
ited. Schacter (1986) provided this summary:
In the large majority of criminal cases that
involve amnesia, the loss of memory either has
a functional origin or concerns only a single
critical event. I have found no cases in the lit-
erature in which a patient afflicted with chronic
organic amnesia has come before the courts on
a serious criminal matter that is related to his
or her memory disorder. Organic factors may
play a role when concussion, alcohol intoxica-
tion, or epileptic seizure occurs during a crime,
with subsequent limited amnesia for the crime
itself, but in these cases memory problems typ-
ically do not exist prior to the crime. (p. 287)
It appears the most common form of organic
amnesia is limited to specific events and is sec-
ondary to alcohol or drug intoxication at the time
of the alleged crime. Criminal defendants occa-
sionally experience a neurological disease severe
enough to hinder recall of events around the time
of the offense or experience a stroke or other neu-
rological event after their arrest, but before trial,
that will raise concern about their competency in
general and their recollection of allegedly crimi-
nal events in particular (Wynkoop & Denney,
1999). It is possible for defendants to experience
the neurological trauma at the time of their arrest
(e.g., gunshot wounds, head trauma from motor
vehicle accidents). In these instances, it is not
unreasonable to suspect some loss of memory for
events directly preceding arrest (retrograde amne-
sia), which can include the crime that occasioned
the arrest. A defendant’s ability to recall events
constituting the alleged offense is an important
issue and one that speaks to their ability to estab-
lish a reasonable defense against criminal prose-
cution.
Amnesia has the capacity to limit competency
to stand trial substantially. For example, the last
criteria put forth by the court in Wieter v. Settle
(1961, Table 4) includes “memory sufficient to
relate those things in his/her own personal
manner.” In 1968, however, the U.S. Court of
Appeals for the District of Columbia addressed
the issue in an interesting manner in Wilson v.
United States. Defendant Wilson incurred a trau-
matic brain injury when his vehicle hit a tree at
the conclusion of a high-speed chase. He was
unconscious at the scene after having ‘fractured
his skull and ruptured several blood vessels in his
brain’ (p. 461). He remained unconscious for 3
weeks. Subsequently, he denied recollection of his
offenses (five counts of assault with a deadly
weapon and robbery). There were no observable
mental difficulties beyond his claimed memory
loss. He was found competent and convicted. The
federal court of appeals concluded that amnesia,
in and of itself, did not necessarily eliminate
competency to stand trial. The court outlined six
criteria for determining the impact amnesia has
 Criminal Forensic Neuropsychology and Assessment of Competency 465

TABLE 16.7 CRITERIA FOR IMPACT OF AMNESIA ON COMPETENCY

1. The extent to which the amnesia affected the defendant’s ability to consult with and assist his lawyer.
2. The extent to which the amnesia affected the defendant’s ability to testify in his own behalf.
3. The extent to which the evidence could be extrinsically reconstructed in view of the defendant’s amnesia. Such
evidence would include evidence relating to the crime itself as well as any reasonably possible alibi.
4. The extent to which the government assisted the defendant and his counsel in that reconstruction.
5. The strength of the prosecution’s case.
6. Any other facts and circumstances that would indicate whether or not the defendant had a fair trial.

Note: Issues set forth in Wilson v. United States (391 F.2d 460, 1968), pp. 463–464, to aid trial courts in determining whether or not amnesia for
the alleged offense substantially impacts the defendant’s competency to stand trial.

on competency (Table 16.7). Note most of these
criteria (3–6) relate to strictly investigative and
prosecutory issues. For example, the court made
this conclusion regarding the strength of the pros-
ecution’s case (Wilson v. United States, 1968):
Most important here will be whether the
Government’s case is such as to negate all rea-
sonable hypotheses of innocence. If there is
any substantial possibility that the accused
could, but for his amnesia, establish an alibi or
other defense, it should be presumed that he
would have been able to do so. (p. 464)
While Wilson is a precedent-setting case, it
has very limited jurisdictional authority. In my
experience dealing with the issue of amnesia in
federal courts within different federal circuits,
trial courts have often relied upon a more recent
United States Circuit Court of Appeals case,
United States v. Rinchack (1987).
In 1980, investigative information clearly con-
nected Louis Rinchack to the smuggling of a large
quantity of marijuana in to the United States from
Jamaica in a twin engine airplane. The Florida
state case was dismissed because the trial court
suppressed most of the state’s evidence, but he was
indicted in federal court in 1985. During the
intervening time, Rinchack had been working on
a vessel in the Pacific Ocean until he was struck
on the head with a steel cable and rendered uncon-
scious for a day and a half. After his federal indict-
ment, he claimed he was not competent to stand
trial due to the work accident “which left him with
memory loss, damage to his cerebellum and brain
stem, vertigo, dizziness, and seizures” (p. 1561).
The trial court found him not competent, based
upon these conclusions:
Rinchack appeared to suffer from memory
loss, confusion, blackouts and catatonic episodes
as a result of the accident. The report also noted
that Rinchack “display[ed] defects that would
suggest organic brain involvement, and . . . these
would undoubtedly interfere with his clarity of
thought, an would make it difficult for him to
properly assist . . . in his own defense when it
would be necessary to recall things, [and] associ-
ate them properly with time and occurrences.”
(p. 1561; quoting from the expert report)
He was committed to treatment at the U.S.
Medical Center for Federal Prisoners for approxi-
mately four months and returned to court for an
additional competency hearing. An expert from
the U.S. Medical Center concluded that “Rinchack
did not appear to be suffering from ‘a true organic-
type amnesia’ and that he was ‘able to remember a
good deal more than he . . . claimed he could.’”
He was found competent to proceed by the mag-
istrate judge and ultimately convicted during a
jury trial. He then appealed with three arguments,
one of which was that his due process rights were
violated by the court “forcing him to go to trial
while he was suffering from severe head trauma
and amnesia.” The United States Court of Appeals
for the 11th Circuit rejected each of his conten-
tions and affirmed the conviction.
The appeals court outlined factors for trial
judges to consider that were similar to that spelled
out in Wilson (1968):
1. The defendant’s ability to take the stand
and testify and otherwise participate in his
defense;
2. Whether the amnesia is temporary or
permanent;
3. Whether the crime and the defendant’s
whereabouts can be properly
reconstructed without the defendant’s
testimony, including any facts giving rise
to a defense;
4. Whether access to government files would
aid in preparing for trial;
466 forensic neuropsychology
5. The strength of the government’s case
against the defendant. (p. 1569)
The appeals court concluded Rinchack’s rights
had not violated after considering each of these
issues. Further, the court addressed the important
issue of potential alibis in this manner:
Finally, while we can never know for sure what
Rinchack might be able to remember if he did not
suffer from amnesia, there does not appear to be
any real possibility the amnesia is “locking in”
exculpatory information. (p. 1570).
In 2006, the 7th Circuit Court of Appeals, in a
case called United States v. Andrews, also addressed
this issue, stood by the same standards, and noted
that its “sister” circuits, including the 11th Circuit,
have agreed similarly in regard to such amnesia
(Davis v. Wyrick, 1985; United States v. Swanson,
1978; United States v. Villegas, 1990). Clearly there
is no “per se” (meaning across the board) rule that
lack of memory for the events constituting the
offense makes a defendant not competent to stand
trial. Each case must be considered based on its
unique merits.
Issues relating to the nature of legal cases,
including the possibility of “exculpatory informa-
tion,” are explicitly non–mental health. The nature
of amnesia and extent to which it affects the defen-
dant’s ability to consult with his or her lawyer and
testify in his or her own behalf, however, are clini-
cal issues. Neuropsychologists have the knowl-
edge and tools to speak directly to these concerns.
Given the issues outlined in the above cases, a
trial court may rule a defendant competent to
proceed even with legitimate amnesia. It should
be clear to the reader that most courts consider a
defendant’s claim of amnesia quite seriously in
terms of their potential competency to proceed. It
is also understandable that courts are concerned
about claimed amnesia and the possibility of
malingering.
Researchers long presented the perspective
that a substantial number of amnestic claims for
criminal events are feigned (Adatto, 1949;
Bradford & Smith, 1979; Hopwood & Snell, 1933;
Lynch & Bradford, 1980; O’Connell, 1960;
Parwatikar, Holcomb, & Menninger, 1985; Power,
1977; Price & Terhune, 1919). There have been a
variety of methods presented to evaluate legiti-
macy of claimed amnesia (see Rubinsky & Brandt,
1986; Schacter, 1986). Symptom validity testing
has been adapted for evaluating the veracity of
criminal defendants claiming partial amnesia for
the alleged offense as well as total retrograde
amnesia, also including the offense (Denney,
1996; Frederick, Carter, & Powel, 1995; Frederick
& Denney, 1998).
Symptom validity testing for remote memory
entails creating, from investigative records (includ-
ing eye witness accounts and prosecutory recon-
structions) and information regarding defendant’s
life history from collateral informants for those
defendants claiming total retrograde amnesia,
two-alternative forced-choice questions based on
information about the alleged criminal activity.
Questions can also be developed to assess recollec-
tion of well-known facts about courtroom partici-
pants and the criminal law process as these areas
can be considered a component of remote memory.
Questions are developed that include the correct
answers and foils that are as reasonably plausible
as the correct alternatives. Developed questions
are presented to the defendant orally. Only those
questions for which the defendant claims no recol-
lection are kept in the analysis. Results are applied
to the binomial theorem to identify below-chance
responding. Significantly worse-than-chance per-
formance (i.e., more frequent choice of foil vs. cor-
rect alternative) provides evidence the defendant
actually knew the correct material but was inten-
tionally choosing the wrong answer to appear
impaired. See Denney (1996) for a thorough
description of the process. Although time con-
suming, the procedure has demonstrated consid-
erable clinical utility (Denney, 1996; Wynkoop &
Denney, 1999) and a sound statistical basis
(Frederick & Denney, 1998).
In an interesting simulation design,
Merckelbach, Hauer, and Rassin (2002) had
undergraduate students perform a mock crime
and feign amnesia for the event afterward. The
researchers then constructed 15 two-alternative,
forced-choice questions as outlined in Frederick
et al. (1995) and Denney (1996). The purpose was
to determine whether or not the presumed poor
sensitivity of forced-choice procedures (Rogers,
Harrell, & Liff, 1993) would be true for this spe-
cific task. Forty percent of the students performed
below chance using a test of very few items. Jelicic,
Merckelback, and van Bergen (2004) completed
another simulation mock crime design but using
a forced-choice of 50 items. Twenty-five items
were related to the mock crime and 25 bogus
items were interspersed between genuine items.
Bogus items were peripherally related to the crime
and included two answers that were equally plau-
sible but unknowable. In this instance, 59% of
participants scored below chance on the genuine
 Criminal Forensic Neuropsychology and Assessment of Competency
items. Generalizing from this study should be
done carefully as it was a simulation study where
87% of the students were female and the crime
entailed stealing a pornographic magazine from a
bar. Nonetheless, the paradigm of interspersing
peripherally related but unknowable items
between genuine items appears promising as a
method to increase the procedure’s sensitivity.
Treatment of the
Incompetent Defendant
The courts have authority to commit incompetent
defendants for mental health treatment involun-
tarily. Jackson v. Indiana (1972), a famous and far-
reaching U.S. Supreme Court case, outlined that
the length of such commitments must have a
“rational relationship” to the nature of the com-
mitment. In other words, it is not constitutional to
hold someone strictly for treatment to restore
competency longer than the person would have
been held if convicted of the crime. Criminal
defendants can be held longer if they are consid-
ered dangerous to themselves or others as a result
of mental illness, however.
Continued commitment for danger to self
requires a change from a criminally established
commitment to a civil commitment procedure.
Most jurisdictions have a process for continued
criminal commitment for those defendants con-
sidered dangerous to others. For example, in the
federal system, 18 U.S.C., § 4246, allows contin-
ued commitment of an incompetent defendant
who is judicially determined to “presently suffer
from a mental disease or defect as a result of which
his release would create a substantial risk of bodily
injury to another person or serious damage to
property of another” but only until a “suitable”
(i.e., safe) state placement is found, or the defen-
dant is no longer dangerous because of mental
illness. Involuntary commitment for treatment
to restore competency to proceed does not neces-
sarily mean treatment with psychiatric medica-
tions, however.
In Riggins v. Nevada (1992), the U.S. Supreme
Court provided vague guidance regarding
medicating incompetent defendants over their
objections. Although the justices indicated
“treatment with antipsychotic medication was
medically appropriate and, considering less
intrusive alternatives, essential for the sake of
[the defendant’s] own safety or the safety of others”
(p. 135), they did not spell out whether involun-
tary treatment simply to restore competency was
appropriate.
467
In an earlier decision (Washington v. Harper,
1990), the court described a balance between state
interests and rights of an incarcerated man by
citing “overriding state interest” as adequate
authority to force medicate. In a similar vein,
courts have found the prosecution of dangerous
defendants a reasonable state interest such that
forced medication for trial competency was
justified (United States v. Charters, 1988; Khiem v.
United States, 1992).
This position appears to be tacitly supported
by the U.S. Supreme Court given the fact they
refused to review the District of Columbia Circuit
Court’s decision to allow forced medication of
Russell Weston, a clearly violent man,4 to restore
his competency to stand trial in a capital case.
The U.S. Supreme Court provided an opinion
regarding involuntary medication for competency
restoration of a nonviolent defendant during June
2003, and the impact of the Sell v. United States
decision has been alarming.
Charles Sell, a St. Louis area dentist, was
originally charged with insurance fraud, Medicare
fraud, and money laundering.5 He had a history of
psychotic mental illness. Dr. Sell was initially
found competent to stand trial, but regressed to a
more clearly psychotic state. He was then found
not competent to stand trial and was committed
for mental health treatment to restore his compe-
tency to proceed. It was recommended he receive
antipsychotic medication, but he would not con-
sent. Over the course of the next 6 years, the
defense argued that he had a right to refuse treat-
ment with antipsychotic medications. The 8th
Circuit Court ruled in favor of forcibly medicat-
ing him, but stayed the order, pending review by
the U.S. Supreme Court. The U.S. Supreme Court
vacated the circuit court order and remanded the
case back to the district court for further consid-
eration. The High Court concluded that the forc-
ible administration of antipsychotic medication
solely to restore competency could be done under
certain circumstances.
First, the Court recommended trial courts
consider such cases based on Washington v.
Harper (1990) grounds (i.e., is the person danger-
ous to self or others grounds). If so, there is no
legal concern. If the defendant is not dangerous to
self or others, then these four issues must be
resolved affirmatively by the trial court in order to
justify forced medication: (a) There are important
government interests; (b) those important
government interests will be significantly furthered
by medication; (c) the medication is necessary
468 forensic neuropsychology
(i.e., there are no less-intrusive alternatives); and
(d) such medicine is medically appropriate.
The impact of the Sell decision has been
striking. At this point in the federal jurisdiction,
criminal defendants committed to inpatient
treatment for purposes of restoration who do not
consent to take antipsychotic medication after
psychiatric recommendation must undergo an
additional hearing (Sell hearing) for the referring
district court to consider first the issue of danger-
ousness, then the four points outlined by the U.S.
Supreme Court. In this manner, the referring
court can authorize forced administration of
antipsychotic medication solely for the restora-
tion of competency. The process is generally more
effective when courts entertain the issue of com-
petency and the proper treatment at the same
time. The difficulty arises when it is determined
after the hearing that involuntary medicine is the
most clinically appropriate method to restore
competency and the defendant then waits in a
forensic hospital to have a second hearing with
the court for this specific purpose. Too many
times, the legal process has been slow to respond
to these defendant’s needs even with repeated
prompting by forensic evaluators. In other
instances, courts have ruled that nonviolent
defendants should not be involuntarily medicated
to seek restoration of competency. In too many of
these instances the defendant will spend months
in a mental health treatment facility in the state of
florid psychosis waiting for the time they will
spontaneously become competent to proceed
with their case. In most of these instances, antip-
sychotic medication could facilitate a return to
competency and allow defendants to effectively
defend themselves in the court of law.
S U M M A RY
This chapter introduced the practice of neuro-
psychology in the criminal forensic arena as a
unique practice opportunity. Neuropsychologists
are more commonly applying principles of brain–
behavior relationships and assessment results to
the specific questions of criminal courts. Although
neuropsychology has a great deal to offer the
courts, practice of neuropsychology in this setting
requires different assumptions and different
methods of evaluation from that of typical clinical
settings. Neuropsychologists must recognize that,
in forensic settings, the client is typically not the
patient. The evaluator’s alliance is with the truth
rather than the patient or referral source. As a
result of this different conceptual standing,
neuropsychologists incorporate slightly different
methodology by including corroborative infor-
mation sources and systematic assessment of
negative response bias and malingering.
The chapter covered the mental health case
law at it relates to criminal competency and how it
applies to various points in criminal proceedings.
Particularly, the Dusky standard and its concep-
tual bases were emphasized. Case law related to
decisional competency, such as pleading guilty,
waiving right to counsel, and refusing an insanity
defense, was addressed. The impact of amnesia on
competency as well as methods to assess its verac-
ity was covered. Last, treatment issues were
addressed as they related to hospitalization and
forced treatment for the sole purpose of restoring
competency.
Chapter 17 furthers the discussion of neurop-
sychological practice in the criminal forensic
arena by expanding on the multiple data source
model and applying it to criminal responsibility
evaluations. The history and current standing of
the insanity defense are covered. Issues around
sentencing are presented, such as diminished
capacity and responsibility, dangerous prediction,
and death penalty. Last, general ethical and pro-
fessional development issues are addressed.
Neuropsychologists have an opportunity to make
substantial contributions to each of these criminal
areas if they have the prerequisite knowledge base
and understand important legal and ethical issues
inherent in criminal forensics.
N OT E S
Opinions expressed in this chapter are those of the
author and do not necessarily represent the position of
the Federal Bureau of Prisons or the U.S. Department
of Justice.
1. Frederick, DeMier, and Towers obtained pri-
mary source documents related to Dusky.
2. Those wishing to obtain the CAI may request
the Competency to Stand Trial and Mental Illness
Packet from Paul Lipsitt, LLB, PhD, at Student Mental
Health Clinic, Boston University, 881 Commonwealth
Avenue, West Entrance, Boston, MA 02215. The
Revised CAI may be obtained from Christine
Mathiesen, PhD, ABPP, Atascadero State Hospital,
Centralized Psychological Assessment Services/
CADM, P.O. Box 7001, Atascadero, California, USA,
93423–7001; telephone: 1–805-468–2000
3. CAST-MR Ordering information: IDS
Publishing, P.O. Box 389, Worthington, OH 43085;
telephone 1–614-885–2323.
4. Weston was charged with a shooting rampage
in the U.S. Capitol building, which resulted in the
 Criminal Forensic Neuropsychology and Assessment of Competency
deaths of two Capitol police. The facts of the case
clearly reveal Weston as the perpetrator.
5. He subsequently was charged with attempted
murder of a federal agent, but the U.S. Supreme Court
made its decision based solely on the facts as if Sell was
considered a nondangerous criminal defendant.
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 17
Criminal Responsibility and Other
Criminal Forensic Issues
ROBERT L. DENNEY
In chapter 16, I presented criminal forensic
neuropsychology as a subspecialty of forensic
psychology. It is a practice area that requires a
unique knowledge base. The forensic role requires
an appreciation of the significantly different
alliance, goals, and methodology. I introduced the
multiple data source model (MDSM) of forensic
assessment. I described mental health case law
regarding competency to proceed and outlined
decisional competency as it relates to confessions,
pleading guilty, waiving one’s right to an attorney,
and refusing an insanity defense. The impact of
amnesia on competency and treatment to restore
competency were also addressed. Each of
these areas establishes a foundation to cover the
more advanced areas of criminal forensics
presented here.
In this chapter, I expand on the forensic assess-
ment model, particularly as it pertains to the
assessment of criminal responsibility. I cover the
historical antecedents of the insanity defense and
its current legal conceptualizations. Sentencing
issues, such as diminished capacity and responsi-
bility, prediction of dangerousness, and death
penalty, are covered. The chapter ends with gen-
eral ethical and professional development issues
for neuropsychologists entertaining the idea of
developing proficiency in criminal forensics.
Part of the unique knowledge base in criminal
forensics is the realization that forensic evaluators
do not share the same goals as general clinical
providers. The client is typically not the patient,
and the evaluator’s alliance is with the truth as
opposed to the patient or referral source. As such,
forensic neuropsychologists utilize a different
methodology that includes extensive use of cor-
roborative information and the systematic assess-
ment of negative response bias and malingering.
The conceptual difference of this approach is best
exemplified, in methodological terms, by the
multiple data source model of assessment.
M U LT I P L E D ATA
SOURCE MODEL
The MDSM is presented in Figure 16.1 (see p.440,
this volume). It represents a synthesis of the works
of various authors in forensic psychology in gen-
eral (Grisso, 1988; Melton, Petrila, Poythress, &
Slobogin, 2007) and Shapiro’s work in criminal
responsibility evaluation in particular (1984,
1991, 1999). The primary aspects of this integrated
model were first presented by Mrad (1996),
adapted and published for use in criminal forensic
neuropsychology (Denney & Wynkoop, 2000),
and later applied to civil forensic work (McLearen,
Pietz, & Denney, 2004).
Figure 16.1 provides an overall picture of how
information sources are classified and integrated
to form reasonable clinical decisions and adequate
support for specific forensic questions, particu-
larly those that involve an opinion about behavior
at some point in the past. Most commonly, the
past opinion will deal with mental state at the time
of a specific crime, but occasionally retrospective
competency evaluations occur as well. Using this
model better ensures that the evaluator considers
relevant information, identifies inconsistencies
between data sources, and comes to a reasonable
conclusion, whether addressing past mental states
or current diagnostic issues.
Figure 16.1 represents a cross-tabulation of
information sources (self-report and corrobora-
tive information) and points on the timeline (cur-
rently, the time of the offense, and life history).
The three rows represent periods of time. The top
row includes information to address current
mental functioning. The lower row refers to life
history. The middle row focuses on mental state,
474 forensic neuropsychology
behavior, and motivation at the time of the alleged
offense (or the row can represent any event in the
past, such as retrospective study of competency to
stand trial, enter a guilty plea, waive right to coun-
sel, understanding Miranda warning, and compe-
tence to confess). The focus on mental state,
behavior, and motivation for that time period has
been referred to as MSO for mental state (at the
time of the) offense (Melton et al., 2007). The left
column of self-report covers the defendant’s
perception and recollection, and the middle
column focuses on information derived from
sources other than the defendant. Self-report and
corroborative information cover each of the three
time periods. The third column refers to the clini-
cian’s opinion about mental state and likely diag-
nosis for each period of time.
There should be a general flow of consistency
between boxes vertically and horizontally. For
example, a defendant’s self-reported history in the
area of mental health symptoms should be rea-
sonably consistent with their current mental state
and MSO given known understanding of the nat-
ural course for that particular mental health con-
cern. The age of onset and symptom manifestation
should make sense. Likewise, medical records,
family reports, and current assessment techniques
should be reasonably consistent from past to
present. The major consistency check, however,
occurs horizontally. Defendant’s report of per-
sonal history should be consistent with educa-
tional records, medical records, family reports,
and so on. This consistency acts as a veracity check
and cannot be ignored. The ultimate focus after
incorporating current and background informa-
tion is the row dealing with MSO. It deserves
special consideration.
Mental State at Offense
Like every other aspect of this model, there should
be reasonable consistency between defendant
self-report regarding thoughts and actions during
and around the time of the offense and that of cor-
roborative sources. It is customary to discuss with
the defendant his or her perception of events lead-
ing up to the alleged offense, behaviors and moti-
vations during the events, and what happened
afterward. Although it is desirable to interview
the defendant about such issues, occasionally the
defendant’s mental illness interferes. The defen-
dant may be unwilling to talk about it or may
indicate that his or her attorney directed him or
her not to speak of events leading up to the alleged
offense. In such cases, coordinating a telephone
conversation between the defendant and his or
her attorney is often helpful. Federal Rule of
Criminal Procedure 12.2(c)(4) provides this pro-
tection for federal defendants:
No statement made by a defendant in the
course of any examination conducted under
this rule (whether conducted with or without
the defendant’s consent), no testimony by the
expert based on the statement, and no other
fruits of the statement may be admitted into
evidence against the defendant in any criminal
proceeding except on an issue regarding mental
condition on which the defendant [has either
introduced mental health evidence or notice of
intent to rely on a mental health defense].
This protection is provided for subjects of court-
ordered evaluations, for which questions of the
defendant’s willingness to cooperate most com-
monly arise. Relatedly, 12.2(d) allows the court to
exclude any expert evidence (even defense evi-
dence) if the defendant does not cooperate with a
court-ordered examination. Reminding defense
counsel of such rules and allowing the defendant
to consult with counsel often resolves the defen-
dant’s concern and allows the evaluation to pro-
ceed as usual. Occasionally, defendants are quite
suspicious of their attorney and will not cooperate
because of paranoid ideation. Typically, these
instances relate to evaluations for competency to
stand trial and are court ordered. The evaluator
will need to progress with the evaluation with
whatever information becomes available and limit
his or her opinions appropriately.
In the federal system, as in most states, intent
to rely on an insanity defense requires notification
to the court by the defense. In this regard, defen-
dants are generally, ostensibly, cooperative because
they have discussed the potential referral for
mental health evaluation with counsel before
making the request to the judge. An insanity-
referred defendant who indicates no desire to use
a mental health defense raises a unique concern.
Because insanity is an “affirmative” defense, mean-
ing the defense must actively seek it and carries
the burden of proof, competent defendants have
the right to refrain from a mental health defense.
Continuing a mental health evaluation on the
issue of sanity is problematic if the defendant does
not want a mental health defense.
Under this circumstance, the issue goes more
to competence to refuse an insanity defense (see
chapter 16). These issues are discussed further
 Criminal Responsibility and Other Criminal Forensic Issues
under Ethical and Professional Issues. The point
here is that most of the time defendants are
willing to provide their perspective of their func-
tioning at MSO if they are seeking a mental health
defense. Occasionally, defendants will be unable
to do so because of acute mental illness or signifi-
cant neurocognitive deficits. Inability to provide
self-report information does not necessarily
eliminate the ability to determine MSO, but it
often limits the opinion to some degree. The
amount of limitation depends on the quality of
corroborative information at MSO.
Acquisition of corroborative information at
MSO is paramount in evaluations of sanity and
past mental states. In this regard, the middle box
under Other Data Sources for MSO is vital under
any circumstance and should be viewed as a king-
pin of the model. Examples of other data sources
dealing with MSO include witness statements,
videotape and audiotape recordings (actual
observed defendant behavior), family reports, and
courtroom transcripts. Each of the surrounding
boxes must be rationally consistent with the infor-
mation from this domain. Synthesizing informa-
tion from each of the other boxes allows the
evaluator to derive a reasoned opinion about the
defendant’s MSO. Once this is done, the evaluator
can consider the ultimate issue, that is, whether
the defendant’s mental health compromised and
altered thinking meets the legal definition in ques-
tion (e.g., insanity, retrospective competency).
It will become apparent under sections deal-
ing with standards for insanity in this chapter that
presence of a mental disease or defect is not
enough by itself to conclude lack of criminal
responsibility. Making such a judgment simply on
presence of mental abnormality, without analyz-
ing defendant’s behavior with corroborative infor-
mation, constitutes what has been referred to as
the “forensic leap of faith” (Denney & Wynkoop,
2000; Mrad, 1996). To the right of the opinion
about MSO box is the ultimate issue box (Figure
16.1, p.440, this volume). The separation of this
box from the opinion box signifies a distinctly
separate analysis that requires comparison of the
MSO opinion to the specific legal standard (e.g.,
insanity) in that criminal jurisdiction. As will
become apparent, insanity standards are not uni-
form across jurisdictions.
CRIMINAL RESPONSIBILITY
A conclusion of criminal responsibility (guilt) for
a criminal offense requires proof, beyond reason-
able doubt, of two elements, actus reus and mens
475
rea. Actus reus refers to the performance of
a prohibited act. Mens rea refers to the mental
state, literally “guilty mind.” Mental health profes-
sionals address mens rea when they provide
opinions on sanity and diminished capacity.
Historical Introduction to Insanity
The concept of evaluating the perpetrator’s mental
state and culpability is as old as documented
history. Mosaic law, written in the 13th century
B.C. (e.g., Numbers 35:22), describes situations in
which “intention” to murder is translated as
“malice aforethought” (Jewish Publication Society,
1982). Suggestions of exculpatory “madness” were
apparent in preclassical Greek writing (Robinson,
1996). Greek moral philosophy clearly addressed
inner will. With the sixth century Justinian Code,
ecclesiastical law influenced secular law by intro-
ducing mens rea more formally. It became clear
that mental illness influenced a defendant’s mens
rea, and courts began wrestling with the defini-
tion of insanity.
Early British legal history recognized the
unjustness of holding persons responsible for acts
stemming from mental aberrations. From 1265
on, legal scholars used terms such as “wild beast,”
“idiots, madmen, [those who] wholly loseth
memory and understanding,” and “infant, brute
or wild beast” (Melton et al., 2007). Some British
courts during the 1700s concentrated more on the
focused issues of an individual’s understanding
between good and evil and right and wrong. In
the 1800s, some British jurisdiction broadened
insanity by using such volitional concepts as
“controlling disease” and “acting power within
which cannot be resisted.” Finally, in 1843 Daniel
M’Naghten was found not guilty by reason of
insanity for shooting the British prime minister’s
personal secretary (Rex v. M’Naghten, 1843).
Ye people of England: exult and be glad, for
ye’re now at the will of the merciless mad . . .
Thomas Campbell (published in several
English papers in response to M’Naghten’s
acquittal, 1843)
Daniel M’Naghten1 had a persecutory delusional
belief that incorporated the Tory Party leader,
Prime Minister Robert Peel. He traveled to
London to ambush Prime Minister Peel, but inad-
vertently shot Peel’s personal secretary, Edward
Drummond. He was acquitted as insane, and
there was immediate outcry in public and Parl-
iament as demonstrated by Thomas Campbell’s
476 forensic neuropsychology

satire (Moran, 1981). After much debate regard-
ing the nature of sanity, the House of Lords called
the judges of the Supreme Court to answer five
specific questions. The answers to these questions
became the M’Naghten rules. A portion of
those rules outlined a strictly right/wrong test
for insanity, which has become known as the
M’Naghten test. Here is the key portion of that
judicial decision:
To establish a defence on the ground of insan-
ity it must be clearly proved that, at the time of
committing of the act, the party accused was
labouring under such a defect of reason, from
disease of the mind, as not to know the nature
and quality of the act he was doing, or, if he did
know it, that he did not know he was doing
what was wrong. (p. 210)
Insanity in the United States
The M’Naghten right/wrong test for insanity
became the standard in the United States as well
as England, although it was criticized for its
rigidity and sole reliance on cognitive under-
standing (Melton et al., 2007). This criticism
gradually led U.S. jurisdictions to loosen the stan-
dard for insanity. The “irresistible impulse” rule
was first adopted in Alabama (Parsons v. State,
1886) and later by a federal jurisdiction (Davis v.
United States, 1895). This rule was a straightfor-
ward volitional controls standard. As described in
Parsons, a defendant would be considered not
responsible if he or she lost the power to choose
between right and wrong and, at the same time,
the criminal behavior was a product of mental
disease solely.
In 1954, the District of Columbia Court of
Appeals carried on similar language when it
adopted a little-known New Hampshire “product
test” (State v. Jones, 1871), in part secondary to
criticisms of rigidity and narrowness of previous
standards (Durham v. United States, 1954).
Also, in response to the growing hope in psycho-
analysis as a method of understanding human
nature, Judge Bazelon opened the doors to psy-
chiatry in the criminal courts by defining insanity
as any action that was a “product of mental dis-
ease or defect” (Durham v. United States, 1954).
This new Durham standard was exceptionally
broad and had occasionally been referred to as the
“but for” test, meaning but for the mental illness,
the crime would have never occurred. The
Durham “product test” was a hopeful experiment
in humanizing the criminal law, but difficulties
inherent in such a broad and poorly defined test
soon appeared.
Several legal decisions over the next 20 years
attempted to tighten the product test for insanity
by more precisely defining mental disease
(McDonald v. United States, 1962) and by limiting
what mental health professionals could say in
front of a jury (Washington v. United States, 1967).
By 1972, nearly every federal jurisdiction in
the United States adopted the American Law
Institute’s (ALI’s) Model Penal Code criteria
(1955),2 which included a two-prong test for
insanity involving cognition and volition (United
States v. Brawner, 1972). Under the ALI standard,
a defendant could be found insane if he or she
lacked substantial capacity, as a result of mental
disease or defect, to appreciate the criminality (or
wrongfulness) of his or her acts or to conform his
or her conduct to the requirements of the law
(Table 17.1). Either one, or both, of these prongs
must be “substantially” impaired as a result of
“mental disease or defect.”
In many respects, the ALI standard combined
the M’Naghten right/wrong knowledge test with

TABLE 17.1 KEY ELEMENTS OF THE AMERICAN LAW

INSTITUTE’S MODEL PENAL CODE
STANDARD FOR INSANIT Y.

The ALI proposed a two-prong test, cognition and volition:

A. Lacks substantial capacity as result of mental disease or defect to:
1. appreciate criminality (optionally, wrongfulness), or
2. conform conduct to requirements of the law.
It contained an optional “caveat paragraph”:
B. Repeated criminal behavior does not constitute a mental disease.

Note: Adapted from American Law Institute (1955).

 Criminal Responsibility and Other Criminal Forensic Issues 477

the irresistible impulse test. Nevertheless, there
were distinct differences that made the ALI
criteria a much more attainable standard. The ALI
replaced M’Naghten’s rigid term, “did not know”
with a more flexible “appreciate” standard. In
addition, the M’Naghten standard suggested an
“all or-nothing” criteria with “did not know” as
opposed to the ALI’s “lacked substantial capacity”
formulation. Many jurisdictions also chose to
adopt the word wrongfulness rather than criminal-
ity. The wrongfulness term references the point
that a person can hold a moral appreciation of
wrongfulness as opposed to simply appreciating
the act was criminal. On the other side of the coin,
however, the ALI formulation contained a second
“optional” paragraph, termed the caveat para-
graph, that effectively eliminated repeated crimi-
nal acts, in and of themselves (i.e., antisocial
personality disorder), as constituting mental dis-
ease. The ALI standard was adopted by a majority
of jurisdictions in the United States and remains a
popular standard today (Melton et al., 2007).
John Hinckley and the Insanity Defense
Reform Act
The ALI standard was in place in 1981 when John
Hinckley shot President Ronald Reagan, Press
Secretary James Brady, and two law enforcement
personnel. Hinckley was believed to have a delu-
sional disorder by which he believed this act
would endear him to a particular Hollywood
actress. He was found not guilty by reason of
insanity under the volitional prong of the ALI
standard. There was an immediate public back-
lash that resulted in the Insanity Defense Reform
Act (IDRA) as part of the broader Crime Control
Act, which became law in 1984. This standard is
currently in place within the federal jurisdiction
and sets the basis for insanity in a majority of state
jurisdictions. Title 18, U.S.C., § 17 contains the
current federal definition of insanity (Table 17.2).
The federal statute effectively eliminated the
volitional prong and required the presence of a
“severe” mental disease or defect. It changed the
burden of proof to keep it on the defense by a clear
and convincing evidence standard rather than
automatically switching the burden over to the
prosecution by beyond reasonable doubt when
the sanity issue is raised (which was the case pre-
viously). This change makes insanity an “affirma-
tive defense.” It retained the ALI standard’s use of
“appreciate” rather than the strict M’Naghten
knowledge test. The U.S. Congress also added
paragraph (b) to Federal Rule of Evidence (FRE)
704, which placed a restriction against mental
health professionals providing an opinion in front
of a jury on the ultimate issue of whether the
defendant is insane or not and, more broadly,
whether the defendant could appreciate the
wrongfulness of his or her behavior. Although
unable to provide that opinion verbally in front of
a jury, professionals are directed to provide their
opinion in written reports [18, U.S.C., § 4247(c)
(4)(B)]. The IDRA also established that once an
individual is acquitted by reason of insanity, he or
she is committed to the U.S. attorney general for
secure hospitalization and is assumed dangerous
until evaluated and judicially determined to be
otherwise (18, USC, § 4243). One can readily see
how IDRA standard represents a synthesis of past
insanity concepts and lessons learned.
Nature, Quality, and Wrongfulness
The exact meanings of nature, quality, and wrong-
fulness have been debated. Melton and colleagues
(2007) considered these words a two-prong stan-
dard of (a) nature and quality and (b) wrongful-
ness (p. 198). They suggested that individuals who
do not meet the first standard will likely not meet
the second. Further, nature and quality are often
ignored altogether as juries focus on wrongful-
ness (Goldstein, 1967, cited in Melton et al., 2007).

TABLE 17.2 CURRENT FEDERAL STANDARD TITLE 18, U.S.C., § 17

(a) Affirmative defense. It is an affirmative defense to a prosecution under any Federal statute that, at the time of
the commission of the acts constituting the offense, the defendant, as a result of a severe mental disease or defect,
was unable to appreciate the nature and quality or the wrongfulness of his acts. Mental disease or defect does not
otherwise constitute a defense.
(b) Burden of proof. The defendant has the burden of proving the defense of insanity by clear and convincing
evidence.
478 forensic neuropsychology
Shapiro (1984, 1991, 1999) described the view
that nature and quality have subtle differences.
Nature is quite basic, such that, “When the defen-
dant picked up the gun, did he know the object
was a gun?” The concept of quality goes more to
consequences. A defendant would not appreciate
the consequences if he beheaded his sleeping
brother thinking it would be funny to see the
brother get up and look for his head in the morn-
ing. Shapiro and colleagues (Goldstein, Morse, &
Shapiro, 2003) considered the terms one basic
concept. In Clark v. Arizona (2006), the U.S.
Supreme Court discussed the issue of nature and
quality in contrast to wrongfulness and suggested
the three terms represent two distinct constructs:
a cognitive capacity (appreciation of nature and
quality) and a moral capacity (appreciation of
wrongfulness). In this same case, the High Court
affirmed Arizona’s elimination of the cognitive
capacity construct altogether in favor of a strictly
right/wrong definition of insanity. Experience has
additionally shown criminal responsibility deci-
sions most often balance on the defendant’s appre-
ciation of wrongfulness.
Is Wrongfulness Moral or Criminal?
The ALI standard included the optional use of the
word “wrongfulness” in place of “criminality”
(Table 17.1). This option reflected the possibility
that a criminal defendant may have appreciated
that his or her act was criminal, but because of
mental illness, believed it was morally justified.
This concept was initially presented in 1915 by
Judge Cordozo in New York, who described “mis-
perceptions” as a result of mental disease that could
cause a defendant to believe his or her act was mor-
ally justified (People v. Schmidt, 1915). In 1970, the
U.S. Court of Appeals for the 9th Circuit (federal
jurisdictions in California, Oregon, Washington,
Arizona, Montana, Idaho, Nevada, Alaska, and
Hawaii) adopted wrongfulness and gave the exam-
ple of a delusion leading to belief in moral justifica-
tion (Wade v. United States, 1970). In a similar case,
the 9th Circuit reiterated the point that the moral
justification must be a result of mental disease
(United States v. Sullivan, 1976). The 9th Circuit
Court went further in 1977 by declaring juries
should be instructed that wrongfulness can be
interpreted as moral rather than criminal only if
there are facts in the case that raise this unique
distinction (United States v. Segna, 1977).
Not only are Wade, Sullivan, and Segna note-
worthy for raising the issue of moral wrongfulness
in the federal jurisdiction and outlining its use,
but also they refer to the ALI standard. In 1988,
the U.S. Court of Appeals for the 8th Circuit
applied this same clarification and procedure
to the post-Hinckley IDRA insanity standard
(United States v. Dubray, 1988). Dubray also
clarified the FRE 704(b) limitation of testimony
on the ultimate issue of sanity by allowing testi-
mony on motivation, mental state, and diagnosis
at the time of the offense. Dubray only governs
federal jurisdictions in the 8th Circuit (North
Dakota, South Dakota, Minnesota, Nebraska,
Iowa, Missouri, and Arkansas), but many other
jurisdiction throughout the country have adopted
this definition of wrongfulness as well.
A Case Study in Wrongfulness
Let us assume a mother3 of a very young child
becomes psychotic with delusions that the only
way to save her child from the fires of hell is to
drown him. She realized she would be arrested
afterward and likely convicted of murder because
she understood it is against the law to kill her
child. Although realizing this fact, she earnestly
believed killing her child was the right thing to do
because, in her psychotic state of understanding,
it was the only possible way for her to truly save
her child.
In this scenario, the woman appreciated the
nature of the act; that is, she realized the act would
terminate the life of her child on earth. She also
appreciated the quality of the act in that the con-
sequences included her son’s death and even the
fact she would be arrested and likely convicted.
The issue of her appreciation of wrongfulness
becomes much more problematic. She clearly
appreciated the criminality of her actions as she
even voiced her awareness of her arrest and likely
conviction. It is reasonable in this instance, given
a jurisdiction that interprets wrongfulness as
moral rather than strictly criminal, to argue she
did not appreciate the moral wrongfulness and
was, therefore, insane. Although criminally
wrong, she believed it was the morally right thing
to do as it was the only way she could save her
child from hell.
This scenario highlights the importance of
understanding the law in the jurisdiction in which
the case is prosecuted. In a strictly criminal juris-
diction, a mental health expert should opine that
she was sane. In a jurisdiction in which wrongful-
ness can mean moral as well as criminal, the
expert should raise the issue of her appreciating
the moral wrongfulness and opine that she was
insane. Not understanding this difference in the
 Criminal Responsibility and Other Criminal Forensic Issues
law can cause otherwise quite competent and
respected mental health experts to come to a
wrong conclusion. The importance in evaluating a
criminal defendant’s sanity is applying our skills
in evaluation and diagnosis to the correct stan-
dard of law.
Current Status of the Insanity Defense
The federal jurisdictions are uniformly IDRA
right or wrong because of statutory authority. As
of 2006, 28 states had adopted the federal stan-
dard in one form or other, 14 states use the ALI
criteria, three use an irresistible impulse test, New
Hampshire continues with the product test, and
Kansas, Idaho, Montana, North Dakota, and Utah
have eliminated the insanity defense but allow
expert testimony on mens rea (e.g., diminished
capacity) (Melton et al., 2007).
About a dozen states have adopted a “guilty
but mentally ill” (GBMI) provision in addition to
an insanity defense as an alternative verdict for
juries to consider. This finding would convict a
defendant of the crime, and thereby guaranteeing
a criminal sentence, but makes it clear he or she is
mentally ill and in need of treatment. The GBMI
provision has been significantly criticized on con-
ceptual grounds and, in most cases, does not
appear to ensure mental health treatment for the
convicted (Melton et al., 2007).
A surprising finding is that, even with these
various formulations, including ALI, IDRA, and
abolition of the insanity defense, research sug-
gests no difference between conviction rates or
rates of hospitalization (Steadman et al., 1993).
Apparently this finding is because every state has
a method of hospitalizing mentally ill persons
convicted of crimes (Favole, 1983), and individu-
als acquitted by reason of insanity appear to spend
the same amount of time securely hospitalized as
they would have been incarcerated if convicted
(Steadman et al., 1993).
Insanity and Traumatic Brain Injury
Changing the insanity standard back to a test of
appreciation for right and wrong would appear to
make it a much more difficult standard to meet
for potentially insane defendants, particularly
when their “mental disease or defect” is caused by
traumatic brain injury (TBI). Contrary to this
appearance, however, the overall incidence of
insanity pleas and their ultimate success rates
seem to have changed little since the reform
(Steadman et al., 1993). Also contrary to public
perception is the finding that insanity defenses are
479
relatively rare, and successful insanity acquittals
are even less common (Silver, Cirincione, &
Steadman, 1994; Steadman et al., 1993). National
data are available that reveal only 2,542 people
were found insane in the entire United States in
1980 (Steadman, Rosenstein, MacAskiel, &
Manderschied, 1988). As said by the legal scholar,
Michael Perlin, successful insanity acquittals are
“rarer than snake bites in Manhattan” (Perlin,
1992).
The incidence of brain-injury–related insanity
acquittals appears to be even rarer. Steadman and
colleagues studied four states regarding insanity
pleas, acquittals, and diagnostic characteristics
before and after the Hinckley-related reforms
(Steadman et al., 1993). They did not specifically
identify brain injury as a diagnostic category, but
they found 69% of those entering insanity pleas
had schizophrenia, another psychosis, or major
affective disorder. Nestor and Haycock studied
murderers committed to a Massachusetts forensic
hospital (Nester & Haycock, 1997). Of the 13
insanity acquittees referred for neuropsycholo-
gical evaluation, 12 were considered psychotic at
the time of the crime. Melton his colleagues
reported the results of six studies that revealed
67% to 97% of insanity acquittees had a signifi-
cant psychosis, suggesting psychosis is usually
required for successful insanity defense (Melton
et al., 2007).
There are no studies identifying the rates of a
neuropsychological basis for insanity. Available
research would suggest the condition would
need to rise to the level of psychosis for success,
particularly in those jurisdictions without the
volitional prong in the insanity standard. Of 456
consecutive referrals for sanity evaluation at the
U.S. Medical Center during the early 1990s, only
17 were diagnosed with an organic mental illness,
and none were considered insane (Denney &
Wynkoop, 2000). Cochrane, Grisso, and Frederick
(2001) combined additional cases (N = 1,170)
from this database to cover a longer period of
time and found little support for insanity opinions
based on organic disorders.
Denney and Wynkoop (2000) provided the
example of an insanity evaluee diagnosed with
dementia caused by Alzheimer’s disease and
considered insane for disorderly conduct and
trespassing on U.S. postal property. The defendant
had delusions that the U.S. Postal Service was
stealing his mail. In this instance, psychosis caused
his insanity, and Alzheimer’s dementia caused his
psychosis.
480 forensic neuropsychology
In many instances, it is apparent that cases are
not referred for evaluation because they are not
prosecuted when an organic mental illness was
severe enough at the time to clearly result in crim-
inal actions (called pretrial diversion). Of those
that are prosecuted, many are dealt with at the
level of competency to stand trial. Given the often
static or degenerative nature of neurological con-
ditions, these people are found not competent to
stand trial and remain so. Consequently, they
never reach a point at which sanity is at issue.
It is apparent that evaluators more often face
insanity evaluations when some form of less-
obvious organic mental disorder is present and
may have had an impact on the defendant’s past
behavior. It is unlikely that mild brain injury cases
without co-morbid psychosis would support an
insanity defense with the current right/wrong
standard (Denney & Wynkoop, 2000; Yates &
Denney, 2008). Under the ALI standard, such
defenses would appear to have a greater chance of
success given the volitional component.
Brain Injury and Insanity: Importance
of the Multiple Data Source Model
and Not Ignoring Data
The following case example demonstrates the
importance of obtaining corroborative informa-
tion as part of a neuropsychological evaluation on
the issue of criminal responsibility. Although it is
important to use the MDSM (Figure 16.1, p. 440,
this volume) for acquiring information, it is imper-
ative the information is integrated in a manner
consistent with the known natural course of TBI.
This is the only way to arrive at a reasonable foren-
sic conclusion regarding such complicated issues.
A 28-year-old man was charged with armed
bank robbery and referred for evaluation of his
sanity. Nine years previously, he was in a serious
motor vehicle accident and experienced a possible
TBI with potential brief loss of consciousness
(medical records were not available). There were
no known complications. Two years later, he
became a police officer and joined the depart-
ment’s Special Weapons and Tactics team. He won
awards on the police force for his excellent work.
He started experiencing significant stress second-
ary to a deathly sick child and overwhelming debt.
He was diagnosed with post-traumatic stress dis-
order (PTSD) and major depression while in the
community. Nine years after the putative TBI, he
robbed a bank.
The defendant was referred for an evaluation
regarding his criminal responsibility in light of his
history of PTSD and major depression. In seeking
other data regarding his mental state at the time
of the offense, investigative records revealed
that when he went into the bank he carried a
handgun. He ushered all the bank employees into
an office. He acquired access to the walk-in safe.
Last, he asked the employees where the videotape
recording device was that videotaped bank robber-
ies. He then went to the room and confiscated the
videotape that had recorded his entrance to the
bank. He locked the employees in the office and
departed. Throughout the robbery, he demanded
employees not look at his face and to turn away
from him. Given the entirety of information
available using the MDSM, the evaluator provided
this opinion:
Although he had been diagnosed prior to the
robbery with PTSD and depression, behavior
described in the offense suggested he well
understood what he was doing and the wrong-
fulness of his actions. He used a gun to gain
control of the bank employees. He carried with
him a bag for money. He ordered them not to
give him bait money or dye packs. He cau-
tioned them against pulling any alarm. He
demanded the video tape from the security
camera. He pulled the telephone out of the
room in which he left them. He repeatedly told
them to not look at him. After leaving the bank,
he changed his outward appearance and
attempted to flee the area.
The defendant was subsequently evaluated by a
neuropsychologist hired by the defense. The neu-
ropsychologist provided this opinion:
He suffers cognitive deterioration from his
head injury, with his IQ 40–50% below his
memory functions and achievement skills. The
weak score on ability to attend and concentrate
is consistent with this deterioration.
Additionally, in the critical area of thinking
abstractly and solve problems in a hypotheti-
cal-deductive fashion, as measured by the
Category Test, he was in the impaired range.
Given these limitations from his 1985 head
injury, when stressed, he had little or no reserve
to call upon for coping skills. I do not agree that
his reality contact was not substantially impaired
at the time of the offense [emphasis added]. In
my opinion, he saw no options and had no
choices. He did not act rationally and did not
appreciate the consequences of his actions.
 Criminal Responsibility and Other Criminal Forensic Issues
This opinion was provided by an expert who
had read the previous report and knew of the
defendant’s actions in the bank. He nonetheless
ignored this vital corroborative information
about the man’s behavior and concluded that not
only was his abstract thinking and hypothetical-
deductive problem-solving skills impaired, but
also his reality contact was impaired. Aside from
ignoring important corroborative information
from the time of the offense, the evaluator also
disregarded the atypical pattern of recovery for
brain injury. The defendant had become a deco-
rated police officer and SWAT team member after
the claimed head injury. Barring some interven-
ing event to the brain, there is no explanation for
that course of recovery from brain injury. A com-
parison of information dealing with past history,
current presentation, and time of the alleged
offense would have revealed these striking incon-
sistencies.
Criminal Responsibility
Assessment Tools
Rogers (1984) developed the Rogers Criminal
Responsibility Assessment Scales (R-CRAS) as a
tool to assist in the evaluation of criminal respon-
sibility. It is designed for use after the evaluator has
completed all clinical interviews and obtained cor-
roborative information (e.g., ancillary interviews,
medical and investigative records, etc.). It contains
30 items grouped in these topic areas: Patient’s
Reliability, Organicity, Psychopathology, Cognitive
Control, and Behavioral Control. Each item is
assigned a score based upon a 5- or 6-point Likert-
type scale. Items focus on areas relevant to the ALI
standard, with additional variables related to the
GBMI standard and right/wrong standard
(M’Naghten and IDRA). The instrument helps cli-
nicians rate the defendant in several areas: reliabil-
ity regarding potential malingering; signs indicative
of organic mental illness, mental retardation, and
mental illness; and whether there were indications
of cognitive impairment or loss of behavioral con-
trol at the time of the alleged offense. The ratings
culminate in a decision tree that guides the exam-
iner to a forensic conclusion: sane, insane, or no
opinion. The R-CRAS manual includes summary
statistics regarding the scales based on three sam-
ples (n = 73, n = 111, n = 76) of individuals consid-
ered sane or insane by forensic examiners based on
the ALI model. Inter-rater reliability and concor-
dance between opinions based on R-CRAS rating
and court verdicts are both respectable (Grisso,
2003; Melton et al., 2007).
481
The R-CRAS promises increased scientific
rigor in the process of sanity evaluations and pro-
vides increased standardization for insanity
assessments as well as an estimate of known error
rates for predictive classification (Grisso, 2003).
However, it has been criticized regarding its
method of “quantifying” vague clinician judg-
ments (Melton et al., 2007). See the work of
Golding and Roesch (1987), Rogers and Ewing
(1992), and Golding, Skeem, Roesch, and Zapf
(1999) for discussion of these criticisms. The
R-CRAS may prove invaluable as a training tool
for evaluators learning to perform criminal
responsibility evaluations, but available research
suggests the R-CRAS is rarely used in forensic
practice (Borum & Grisso, 1995).
Diminished Capacity and
Responsibility
Diminished capacity is considered a mens rea
defense. In other words, it refers to a decreased
level of culpability because of lesser intent (Clark,
1999). In this regard, first-degree murder, second-
degree murder, and manslaughter differ in their
level of intent. Without invoking the insanity
defense, defendants occasionally bring mental
state into play by claiming a decreased level of
intent because of such factors as alcohol or drug
intoxication, medication use, neurological condi-
tions, or extreme emotional disturbance (Melton
et al., 2007; Yates & Denney, 2008). An extreme
example is the automatism defense, by which
defendants claim no conscious awareness of their
acts. Examples have included crimes committed
while sleepwalking, during a seizure, while
unaware secondary to head injury or other
encephalopathic conditions, and even during
dissociative episodes (Barnard, 1998). Although
courts have generally allowed testimony to this
issue, they have limited its use when the defen-
dant experienced the disability previously and
should have taken precautions to prevent a poten-
tial criminal event. An example would be a man
with a known history of aggression secondary to
complex-partial seizure disorder who refuses pro-
phylactic treatment to help avoid seizures (and
thereby aggression and assault).
When considering diminished capacity, it
must be realized that there are both general and
specific intent crimes. Felon in possession of a
weapon is an example of a general intent crime.
By definition, possessing the weapon carries with
it the prerequisite intent as long as the defendant
understood, or should have understood, that it
482 forensic neuropsychology
was illegal for him or her to possess a weapon.
Bank robbery requires specific intent, that is,
resolve for a particular act to occur. Intent must be
differentiated from motive. Motive prompts an
act, whereas intent “refers only to the state of
mind with which the act is done” (West Publishing,
1990, p. 810).
The most common basis for diminished
capacity is intoxication (Marlowe, Lambert, &
Thompson, 1999). An example would include
whether a defendant could form the prerequisite
intent to first-degree murder. It may very well be
that alcohol intoxication made this level of intent
rather unlikely. Under this circumstance, a jury
could use a lesser included offense such as second-
degree murder or even manslaughter, depending
on the facts of the case.
A similar argument can be made for the effects
of neurological compromise. An example would
include a dentist charged with inappropriate dis-
pensing of narcotics and whose judgment was
compromised by early frontal dementia. The com-
promise may not be so severe as to eliminate
intent fully (which should result in an acquittal),
but it can allow the jury to apply the law in a fair
manner.
A related, and often confused, term is dimin-
ished responsibility. This term actually refers to
mitigating circumstances of the crime that war-
rant a lesser punishment (Clark, 1999). Such
issues are brought before the court at the time of
sentencing. Diminished responsibility is particu-
larly relevant in jurisdictions that no longer have
the volitional prong in their insanity standard.
Individuals with frontal lobe damage often have
impulse control problems that potentially impact
their ability to refrain from performing certain
criminal acts. Deficits in cognitive, emotional,
and behavioral controls secondary to neurological
compromise are relevant to a defense against
many criminal charges, either at trial or at
sentencing.
Assessing Risk of Dangerousness
It is not uncommon for neuropsychologists
involved in criminal proceedings to be asked by
the court to assess a criminal defendant’s propen-
sity for violence if released from custody. The
issue of dangerousness is certainly relevant in
cases of neurological compromise (Volavka,
Martell, & Convit, 1992; Barr, 2008). Such ques-
tions can arise during detention hearings at any
phase of the criminal proceedings. Risk assess-
ment findings are also used in the sentencing
phase of death penalty cases in some jurisdictions.
Potential for dangerousness is generally always
an issue for defendants who are considered not
competent to stand trial and unrestorable. In the
federal jurisdiction, the presiding court must
address the defendant’s potential dangerousness
to others and significant property of others on
release because the charges can be dismissed when
a mentally defective defendant is considered
unlikely to become competent in the foreseeable
future (18, U.S.C., § 4241 and 4241).
Unrestorable incompetent defendants in the
federal jurisdiction can be held in a secure
hospital indefinitely if they are considered dan-
gerous because of mental defect (18, U.S.C.,
§ 4246). Nearly the same issue arises after a defen-
dant is found insane and hospitalized in a secure
facility (18, U.S.C., § 4243). The issue can come up
again when a sentenced inmate who is potentially
dangerous because of mental disease or defect
reaches the end of a sentence because federal
statute allows potential extended commitment
(18, U.S.C., § 4246). In each of these scenarios, the
Federal Bureau of Prisons under authority of
the U.S. attorney general has the mandate and
challenge to find suitable state placement—a
placement that will further ensure public safety.
Most states have similar statutory procedures.
Consequently, it is common for mental health
professionals to provide expert opinions on risk of
dangerousness for the deciding court on each of
these occasions.
Assessment of risk in the prediction of future
dangerousness poses certain ethical dilemmas as
it balances the liberty interests of the individual
against the safety needs of the community (Grisso
& Applebaum, 1992). Given the liberty interests
involved, it is imperative neuropsychologists per-
forming this function conform their work to the
standard of practice as outlined in current litera-
ture. In Barefoot v. Estelle (1983), James P. Grigson
testified regarding defendant Barefoot’s danger-
ousness without ever meeting the man. Justice
Blackmun wrote, “Doctor Grigson testified that
whether Barefoot was in society at large or in a
prison society there was a ‘one hundred percent
and absolute’ chance that Barefoot would commit
future acts of violence that would constitute a
continuing threat to society” (emphasis original;
Justice Blackmun, dissent, p. 3408). Although an
egregiously overstated conclusion, recent research
suggests that mental health professionals can pre-
dict violence at a rate significantly better than
chance when they include relevant factors in the
 Criminal Responsibility and Other Criminal Forensic Issues
decision analysis (Bauer et al., 2003; Monahan,
1992; Monahan & Steadman, 1994; Mossman,
1994; Steadman, 2000).
Factors Known to Increase
Risk of Dangerousness
In this section, I focus on factors relevant for the
assessment of future risk of violence. There is
quite a large body of research on risk assessment
in general and specifically on that pertaining to
sex offenders. I consider general issues of risk
assessment and that which logically pertains to
neuropsychology. For a recent review pertaining
to risk assessment of sexual predators, see the
work of Conroy (2003).
Much of the research regarding violence pre-
diction, and certainly that dealing with sex offend-
ers, has dealt with static and dynamic prediction
variables (Bonta, Law, & Hanson, 1998). Static
variables refer to fixed and unchanging facts
regarding an individual’s life (e.g., number and
nature of past violent offenses, demographic char-
acteristics), and dynamic variables can change.
These variables are subdivided into stable and
acute dynamic variables. Stable variables have the
potential for change (e.g., substance abuse his-
tory), and acute variables are clearly situation spe-
cific (e.g., intoxication). The bulk of actuarial
research on violence prediction focuses on static
variables (Conroy, 2003).
The research of Swanson and colleagues sug-
gested that being male, young, of lower socioeco-
nomic status, and an abuser of drugs or alcohol,
having a major mental disorder, and particularly
having a major mental disorder in combination
with substance abuse/dependence are demo-
graphic factors that increase risk of violence in the
community (Swanson, Holzer, Ganju, & Jono,
1990). Meta-analysis suggests that the strongest
predictor of future violence is past violence
(Mossman, 1994). Monahan and colleagues
(2001) reported results of the MacArthur Violence
Risk Assessment Study, the largest study of com-
munity violence prediction of its kind (Monahan,
2003). The study included male and female civilly
committed patients from several facilities, with
follow-up in the community at 20 weeks and 1
year after discharge. They focused on variables
believed to relate to potential violence (see Melton
et al., 2007 [particularly Table 9.4], and Monahan,
2003, for a more thorough review).
Rather than just static and dynamic variables,
the MacArthur study considered variables in four
factors: dispositional, historical, contextual, and
483
clinical. Dispositional factors included demo-
graphic (e.g., age, gender, race), personality
(e.g., impulsivity and psychopathy), and cognitive
concerns (IQ and neurological impairment).
Historical factors included social history (family,
work, and education), mental hospitalization
history (prior hospitalizations and compliance),
and history of crime and violence. Contextual
factors included perceived stress, social support
systems, and physical aspects of the environment
(e.g., presence of weapons). Clinical factors
included Axis I diagnosis, symptoms, Axis II
diagnosis, level of functioning, and substance
abuse.
The MacArthur study (Monahan, 2003;
Monahan et al., 2001) revealed some surprises
and confirmations regarding violence. Prior vio-
lence and criminality were strongly associated
with community violence in this group of psychi-
atric patients. The prevalence rates for men and
women were actually about the same, but the
nature of the violence was different. Women are
more likely to be violent toward family members,
but violence from men is more likely to result in
serious injury. History of childhood physical
abuse, but not sexual abuse, appears associated
with postdischarge violence. As in the Swanson
et al. (1990) study, presence of substance abuse or
dependence in conjunction with mental illness
significantly raised potential for violence; how-
ever, a diagnosis of a major mental illness was
associated with a lower rate of violence compared
to personality or adjustment disorders. Also, pres-
ence of schizophrenia appeared less associated
with violence than depression or bipolar disorder.
Delusions and hallucinations were associated with
violence less than nondelusional suspiciousness
and presence of violent thoughts. Those scoring
high in anger during hospitalization were twice as
likely to commit violent acts after discharge as
those with low anger scores. The nature of the
environment also played a role in violence deter-
mination, with high-crime neighborhoods more
associated with postdischarge violence. There is
little indication in the MacArthur study that neu-
rological compromise contributed to an increased
likelihood of postdischarge violence. The facts
that only a few of these subjects had neurologi-
cally related concerns and that brain injury did
not appear to be assessed thoroughly clouds the
potential contribution that neurological disorder
may have on postdischarge violence.
Neurocognitive contributions to risk have
been studied less thoroughly. Research with
484 forensic neuropsychology
childhood neuropathology implied that early
cerebral deficits can predispose future dangerous-
ness, particularly when combined with the envi-
ronmental factor of an abusive family (Golden,
Jackson, Peterson-Rohne, & Gontkovsky, 2002;
Lewis, Lovely, Yeager, & Della Femina, 1989;
Lewis et al., 1985). It is logical that neuropsycho-
logical factors can play a role in the production of
violence.
Neuropathology and the Potential
for Violence
It is well known that large portions of the brain
are involved in inhibition of behavior. Damage
to the prefrontal cortex and temporal poles or
frontal-subcortical system or diffuse axonal
shearing can cause a behavioral disinhibition
syndrome, often termed “pseudopsychopathic,”
that can surface as a combination of jocularity,
impulsivity, behavioral dyscontrol, and sexual
disinhibition (Benson & Miller, 1997; Mesulam,
2000; Mills, Cassidy, & Katz, 1997). See the work
of Damasio and Anderson (2003) for a review of
clinical cases that manifested these personality
characteristics.
A classic example of this syndrome is found in
the case of Phineas Gage, a 19th century railroad
foreman who survived an explosion in which an
iron tamping bar (about 1 m long, 3 cm wide) was
blasted up under his cheekbone and out through
the top of his head. His physician described the
change in his personality by writing that the “equi-
librium . . . between his intellectual faculties and
animal propensities seems to have been destroyed”
(Harlow, 1868, reprinted in Macmillan, 2000,
p. 414). One—possibly augmented—account of
Gage described him as “so loudmouthed, boister-
ous, and profane that eventually ‘the police drove
him from Boston Common’” (Blackington, 1956,
cited in Macmillan, 2000, p. 97).
Many researchers are implicating the prefron-
tal and frontal lobes in violence and criminal
behavior (Best, Williams, & Coccaro, 2002;
Brower & Price, 2001; New et al., 2002; Raine,
2002; Raine et al., 1998; Volkow et al., 1995).
Correspondingly, decreased executive function-
ing appears to be associated with an increase in
some forms of aggression (Barratt, Stanford, Kent,
& Felthous, 1997; Giancola, Moss, Martin, Kirisci,
& Tarter, 1996; Paschall & Fishbein, 2002;
Villemarette-Pittman, Stanford, & Greve, 2003).
Electroencephalogram and evoked potential
alterations have been implicated in violence as
well (Bars, Heyrend, Simpson, & Munger, 2001;
Conklin & Stanford, 2002; Drake, Hietter, &
Pakalnis, 1992; Drake, Pakalnis, Brown, & Hietter,
1988; Evans, 1997; Gerstle, Mathias, & Stanford,
1998; Houston & Stanford, 2001; Kiehl, Hare,
Liddle, & McDonald, 1999; Mathias & Stanford,
1999; Raine & Venables, 1988; Raine, Venables, &
Williams, 1990). There are also lines of research
implicating neurochemical alterations and vio-
lence (Gregg & Siegel, 2001; Linnoila & Charney,
1999; Miczek, 1987; Siegal & Shaikah, 1992), with
a particular emphasis on decreased 5-HT
(serotonin) and its treatment with selective
serotonin reuptake inhibitors (Coccaro, 1992;
Coccaro & Kavoussi, 1997; Dolan, Deakin,
Roberts, & Anderson, 2002; Kavoussi, Liu, &
Coccaro, 1994; Kent et al., 1988; Krakowski, 2003;
Shaikah, De Lanerolle, & Siegel, 1997; Volavka,
2002). The research appears to support the pro-
posed two-part classification of violent behavior
as either premeditated or impulsive (Barratt,
Stanford, Dowdy, Liebman, & Kent, 1999; Frick,
1995; A. B. Heilbrun, Heilbrun, & Heilbrun, 1978;
Hubbard et al., 2002; Malone et al., 1998;
Pulkkinen, 1996; Scarpa & Raine, 2000;
Smithmyer, Hubbard, & Simons, 2000; Vitaro,
Gendreau, Tremblay, & Oligny, 1998; Weinshenker
& Siegel, 2002).
Among the impulsively aggressive, there
appears to be substantial evidence of neurocog-
nitive compromise consistent with previous
research regarding executive dysfunction among
the violent (Blair, 2001; Giancola et al., 1996;
Morgan & Lilienfeld, 2000; Mungus, 1988;
Stanford, Greve, & Gerstle, 1997). In addition, the
impulsively aggressive appear responsive to
treatment with certain antiseizure medications
(Barratt, Stanford, Felthous, & Kent, 1997;
Houston & Stanford, 2006; Sieberer & Emrich,
2009; Stanford et al., 2001).
Houston, Stanford, Villemarette-Pittman,
Conklin, and Helfritz (2003) suggested “growing
evidence of neurobiological deficits specific to
impulsive aggressive behavior (i.e., reduced
central serotonergic functioning, executive dys-
function, [and] prefrontal deficits) may serve as
markers of an ineffective behavioral control
system in these individuals” (p. 82). The nature of
the deficits in those with impulsive, reactive
aggression, in concert with apparent treatment
benefits of antiseizure medication, may even sug-
gest the possibility of neuroregulatory abnormal-
ity. Overall, there appears to be enough research
implicating a relationship between neurocogni-
tive functioning and aggression, particularly the
 Criminal Responsibility and Other Criminal Forensic Issues
impulsive type, to indicate neuropsychology
has a place in the evaluation of violent criminal
defendants (Brower & Price, 2001; Barr, 2008).
Risk Assessment Tools
Given the generally improved prediction accuracy
of actuarial information over clinical judgment,
several successful efforts to develop risk assess-
ment tools have occurred (Monahan, 2003).
The Hare Psychopathy Checklist–Revised
(PCL-R; Hare, 1991) and the screening version
(PCL-SV; Hart, Cox, & Hare, 1995) have the larg-
est research base. There is also a more recently
adapted youth version (Forth, Kosson, & Hare,
2003). The PCL-R is considered a “robust predic-
tor of future violent behavior” (Conroy, 2003),
particularly when predicting violence in the com-
munity (Walsh & Walsh, 2006). The PCL-R is a
structured interview and file review that produces
20 scales loaded on two broad factors within
the conceptual domain of psychopathy (Hare,
Harpur, & Hakstian, 1990). The measure requires
specialized training and is rather lengthy, but it is
considered to have good inter-rater reliability (see
Melton et al., 2007).
Webster, Douglas, Eaves, and Hart (1995)
developed the HCR-20, which consists of 20 rat-
ings of historical, clinical, and risk management
factors. Douglas and Webster (1999) identified
retrospectively that scores above the median
increased the likelihood of past violence and anti-
social behavior on average by a factor of 4.
Douglas, Ogloff, Nicholls, and Grant (1999) found
that scores above median increased the risk of
violence by factors of 6 to 13 in a group of civilly
committed patients during the 2 years after their
hospital discharge. The HCR-20 has also been
shown effective at predicting risk of violence
among those with intellectual deficiencies
(Lindsay et al., 2008).
The Violence Risk Appraisal Guide (VRAG;
Harris, Rice, & Quinsey, 1993) was developed in
Canada on a large number of men with serious
criminal offenses housed in a maximum security
hospital. Of 50 predictor variables, a series of
regression equations identified 12 variables that
became the VRAG. The 12 final variables are rated
and totaled to obtain a global score which can be
compared to a table of probabilities for violence
recidivism over seven- and ten-year periods.
Considerable amount of research now exists sug-
gesting the VRAG has moderate to high correla-
tions to violent recidivism, with Receiver Operator
Characteristic AUCs of 0.70 to 0.85 (Quinsey,
485
Harris, Rice, & Cormier, 2005). The VRAG is a
somewhat time-consuming file review because it
includes the PCL-R as one of its variables. This
weakness not withstanding, it has demonstrated
itself as a useful predictive tool (Quinsey et al,
2005.; Rice & Harris, 1995).
The last risk assessment method reviewed here
was developed from the MacArthur Violence
Risk Assessment Study data and called the
Classification of Violence Risk (COVR; Monahan,
Steadman, Applebaum et al., 2005). The
MacArthur researchers developed an iterative
classification tree “approach to violence risk
assessment . . . predicated on an interactive and
contingent model of violence, one that allows
many different combinations of risk factors to
classify a person as high or low risk” (Monahan,
2003, pp. 533–534). The goal was to incorporate
the type of information reasonably available in
clinical records in a manner that does not make
the assessment of risk arduously long. The tree
incorporates a sequence of questions that classify
subjects as either high or low risk.
Monahan and colleagues (2001) evaluated the
iterative classification tree in a multiple model
approach that combined risk assessment meth-
ods. They classified all the civilly committed
patients in to one of five categories of risk and fol-
lowed their progress for 20 weeks after discharge.
Results of this method were favorable. In
Monahan’s words (2003), “This combination of
models produced results not only superior to
those of any of its constituent models, but supe-
rior to any other actuarial violence risk assess-
ment procedure reported in the literature to date”
(p. 534). Subsequently, the authors validated the
computerized program (Monahan, Steadman,
Robbins et al., 2005), and it is now available from
Psychological Assessment Resources, Inc. One
caveat regarding the COVR is that it has only been
validated on psychiatric inpatients preparing for
release (McCusker, 2007; Monahan et al., 2006).
Evaluating risk of violence has become increas-
ingly sophisticated with the development of spe-
cific assessment methods. Each of these methods
was developed with prisoners or psychiatric
patients at risk for violence, and none has been
validated with neurological patients. Logic would
dictate a similar profile of risk-increasing vari-
ables between the two populations (particularly
with the apparent prevalence rate for neurocog-
nitive compromise in violent offenders; Martell,
1992), but ultimately this remains an empirical
question. Until that research materializes,
486 forensic neuropsychology
neuropsychologists who practice risk assessment
in the criminal setting must rely on clinical judg-
ment predicated on other, established nonneuro-
logical risk factors.
D E AT H P E N A LT Y I S S U E S
Nowhere does the need for competent and ethical
practice demonstrate itself greater than in the
practice of capital cases. As with any criminal
case, neuropsychologists can be called on to pro-
vide expertise at any phase of the process; none-
theless, there are unique issues in capital cases
that go beyond the obvious life-or-death outcome.
These issues include a priori ethical consider-
ations, competency to be executed and to waive
appeals, age requirements for imposing a death
sentence, mental retardation, and death penalty
mitigation.
A Priori Ethical Considerations
Before accepting the responsibility of practicing
in capital cases, the neuropsychologist must con-
sider his or her personal position on the death
penalty in general. Ethical standards dictate that
psychologists recognize when personal views have
the potential to interfere with our professional
work. As I reviewed in chapter 16, the roles of
forensic evaluators are different from that of clini-
cal providers. There are times when our decisions
may have untoward implications for criminal
defendants. Each neuropsychologist must objec-
tively evaluate his or her feelings toward the death
penalty and decide if he or she is capable of accept-
ing the possibility of providing an opinion that, in
some aspect, might pave the way for an execution
of a human being (Denney, 2005).
For example, forensic evaluators are occasion-
ally requested to provide an opinion on whether a
criminal defendant is competent to be executed.
A neuropsychologist should not accept this role if
unwilling to provide an affirmative opinion if the
data support such a conclusion. As in any other
forensic endeavor, forensic practitioners need to
remain objective in their roles and remember the
client in this instance is the court, not the defen-
dant. In my opinion, clinicians who are strongly
opposed to the death penalty have too great a pos-
sibility of inadvertent bias to participate in capital
cases as nonpartisan evaluators.
Competence to Be Executed
In 1986, the U.S. Supreme Court ruled in a com-
plicated and lengthy criminal due process and
competency case called Ford v. Wainwright.
Defendant Ford was convicted of a capital offense
and sentenced to death. While on death row, the
issue of his mental health and competency arose.
The Florida state procedure at that time did not
allow an adversarial or judicial determination of
competency because it was determined by the
governor with the assistance of a panel of mental
health professionals. In ruling Florida’s procedure
unconstitutional, the U.S. Supreme Court also
held that executing a person not competent
because of mental illness is a violation of the 8th
Amendment right to be free from cruel and
unusual punishment. The Court concluded that
doing so (a) has questionable retributive value,
(b) has no deterrence value, and (c) simply affronts
humanity. Fascinating quotations that give insight
to the reasoning behind this decision include the
need to protect the “condemned from fear and
pain without the comfort of understanding” and
the need to protect the “dignity of society from
barbarity.”
In deciding Ford, the U.S. Supreme Court did
not address the specific aspects of competency to
be executed much beyond the basic Dusky require-
ments (Dusky v. United States, 1960; see chapter
16). The Court referenced Florida’s standard that
the person must have the mental capacity to
understand the nature of the death penalty and
why it was imposed. Justice Powell, in the concur-
ring opinion, pointed out that a person needs to
understand the connection between the crime
and the punishment. Most other jurisdictions that
allow execution have more detailed standards. An
example description is presented in Reisner and
Slobogin (1990); the test of competency is whether
the prisoner lacks, as a result of:
defects of his faculties, sufficient intelligence to
understand the nature of the proceedings
against him, what he was tried for, the purpose
of his punishment, the impending fate which
awaits him, a sufficient understanding to know
any fact which might exist which would make
his punishment unjust or unlawful, and the
intelligence requisite to convey such informa-
tion to his attorneys or the court (p. 946).
This more detailed inquiry suggests the prisoner
must have capacity to assist in any potential
appeals in addition to an understanding of his
current legal situation (as indicated in Dusky) and
an appreciation of impending death. Heilbrun
and colleagues (Heilbrun, 1987; Heilbrun &
McClaren, 1988; Heilbrun, Radelet, & Dvoskin,
 Criminal Responsibility and Other Criminal Forensic Issues
1992) suggested the ability to prepare for death
spiritually and psychologically as a needed com-
ponent of competency as well.
Related to the issue of evaluating competency
for execution is the controversial concern over the
ethical appropriateness of providing treatment for
condemned prisoners for the purpose of restoring
their competency to be executed. The issue has
been debated at length (Ferris, 1997; Leong,
Weinstock, Silva, & Eth, 1993). The American
Medical Association (1995) put forth a statement
that providing treatment for the restoration of
competence for such reasons is ethically unac-
ceptable unless it is to relieve extreme suffering.
Bonnie (1990) outlined an analysis that revealed
the issue as a complex one with no easy answers.
Much of the concern pertains to the greater
harm in facilitating a person’s death versus reliev-
ing suffering. There are instances when individu-
als would rather receive treatment and die a sane
person than languish away on death row in a state
of mental deterioration (see Singleton v. Norris,
1997, Heaney concurring; Singleton v. Norris,
2003). The issue could be resolved by adopting the
recommendation of commuting a death row
inmate’s sentence to life without parole if the
inmate is found incompetent for execution
(Wexler & Winick, 1991). Of course, this decision
could raise the potential for malingering to new
heights.
Whether one should provide competency
restoration treatment to death row inmates is an
issue that will likely continue in debate for many
years. Until some definitive guidance is provided
in this thorny ethical area, it is doubly incumbent
for neuropsychologists to be aware of their views
and the potential impact these views can have on
professional opinions in capital cases.
Competency to Waive Death
Penalty Appeals
As of December 31, 2009, death row inmates spent
an average of 169 months on death row (U.S.
Department of Justice, 2009). It is not uncommon
under prolonged housing on the unique setting of
death row for individuals to grow weary of the
ongoing appeals process. In death penalty cases,
prisoners receive legal representation even when
they do not wish it; consequently, they can find
themselves in a position to refuse appeals filed on
their behalf. Refusing further appeal amounts to
the prisoner “volunteering” for execution. Just
over 12% of those executed between 1977 and
2001 chose to drop their appeals (Amnesty
487
International, 2001). This situation becomes
complicated because it is not uncommon for
prisoners to develop mental health concerns
while on death row (Cunningham & Goldstein,
2003). While rare, suicide is not unheard of for
inmates living on death row. Three of 3,254 pris-
oners held on death row in 36 states and the fed-
eral prison system died by suicide in 2005 (U.S.
Department of Justice, 2005). It is not surprising
that appeals courts request mental health evalua-
tion for prisoners wishing to waive their appeals.
There is no unique standard for waiving death
penalty appeals beyond that generally spelled out
in case law. It can be deduced from Dusky v.
United States (1960), Godinez v. Moran (1993),
and North Carolina v. Alford (1970) that individu-
als must have a factual and rational understand-
ing of their situation and are waiving their appeal
in a knowing, intelligent, and voluntary manner
(see chapter 16 for a discussion of this aspect of
competency). In addition to other possible mental
health concerns, it is important for the mental
health evaluator to rule out depression as the pre-
cipitating cause for such a waiver.
Death Penalty and
Mental Retardation
In 2002, the U.S. Supreme Court decided the case
of Atkins v. Virginia, a case spelling out that it is
excessive to execute a mentally retarded individ-
ual. It is rare for the High Court to overturn its
own previous decision, but it did just that in
Atkins. The court previously addressed this issue
in Penry v. Lynaugh (1989). In Penry, the court
decided it was not necessarily “cruel and unusual
punishment” to execute a mentally retarded indi-
vidual based on an analysis of societal views at
that time as evidenced by state laws. Societal views
dictate the “evolving standards of decency” as it
relates to cruel and unusual. Because very few
states had prohibitions against executing the men-
tally retarded, the court concluded the prevailing
societal thought suggested it was not so extreme
as to be considered cruel and unusual. The court
did spell out, however, that the cruel and unusual
clause of the 8th Amendment requires a case-by-
case analysis. In the case of mental retardation,
the jury must be able to consider the impact of
mental retardation evidence in its decision about
sentencing. The Penry case was a controversial
5-to-4 decision, so it was not surprising to see the
issue addressed again in Atkins.
During August 1996, Daryl Atkins and an
accomplice abducted Eric Nesbitt, robbed him,
488 forensic neuropsychology
forced him to withdraw an additional $200 from
an ATM, and then drove him to an isolated loca-
tion, where he was shot eight times and killed.
Atkins was convicted of abduction, armed rob-
bery, and capital murder. During the penalty
phase of his trial, a psychologist for the defense
testified that he had a full-scale IQ of 59 and con-
cluded he was mildly mentally retarded. A rebut-
tal psychiatrist testified he was a psychopath and
not mentally retarded. The jury, nonetheless, sen-
tenced Atkins to death. The Supreme Court of
Virginia affirmed the judgment of the trial court,
and the case was appealed to the U.S. Supreme
Court.
In July 2002, the U.S. Supreme Court reversed
the judgment of the Virginia Supreme Court and
remanded the case back to the sentencing court to
consider sentencing other than the death penalty.
In coming to this conclusion, the U.S. Supreme
Court reevaluated society’s perspective on the
issue in a similar fashion as was done in Penry.
The court outlined that a punishment is excessive
and therefore prohibited by the 8th Amendment
as cruel and unusual if it is not “graduated and
proportioned to the offense.” A claim that a judg-
ment is excessive must be judged by the standards
that currently prevail. Society’s evolving standards
of decency must allow for a proportionality review
that is informed by “objective factors to the maxi-
mum possible extent.”
As in Penry, the Court viewed legislation
enacted by the country’s legislatures to be the
clearest and most reliable objective evidence of
contemporary values. At the time of Penry, there
were only two states with statutes against execut-
ing the mentally retarded. Although an additional
16 states enacted statutes prohibiting the execu-
tion of mentally retarded offenders since Penry, “It
is not so much the number of these states that is
significant, but the consistency of the direction of
the change.” The Court further concluded that
mental retardation does not necessarily eliminate
a person’s ability to appreciate right from wrong,
but the condition causes diminished capacities to
understand and process information, communi-
cate, abstract from mistakes and learn from expe-
rience, engage in logical reasoning, control
impulses, and understand the reaction of others.
The Court noted “their deficiencies do not warrant
an exemption from criminal sanctions, but they
do diminish their personal culpability” (p. 348).
The U.S. Supreme Court considered two
additional reasons to agree with the legislative
consensus. First, the Court maintained there is
uncertainty as to whether either justification
underpinning the death penalty—retribution and
deterrence of capital crimes—applies to mentally
retarded offenders. With respect to retribution,
the severity of the appropriate punishment neces-
sarily depends on the offender’s culpability. If the
culpability of the average murderer is insufficient
to justify imposition of the death penalty, the
reduced culpability of the mentally retarded
criminal surely does not merit that form of retri-
bution. Regarding deterrence, the same cognitive
and behavioral deficits that lessen the culpability
of mentally retarded defendants also make it less
likely that they can control their conduct based on
the possibility of execution. Second, mentally
retarded offenders face an increased risk for
wrongful execution because they may unwittingly
provide false confessions, be less able to provide
meaningful assistance to their counsel, are typi-
cally poorer witnesses, and may inadvertently
foster the perception they lack remorse for their
crimes based on their demeanor in court.
The Atkins (2002) decision makes the diag-
nostic aspect of forensic assessment in capital
cases even more important. Although each state
must follow the Atkins decision, the U.S. Supreme
Court did not spell out the specifics of how mental
retardation is defined or, for that matter, how
much mental retardation is needed to obviate the
death penalty. The Court left these details up to
the states to decide. In addition to sub-average
intelligence, the diagnosis requires impairments
in adaptive functioning and evidence of the con-
dition prior to age 18 years. It is not difficult to
fathom a situation in which an individual is raised
in an extremely rural setting with no access to
special education assessments or classes. In this
situation, there may be little evidence of sub-
average intelligence prior to the age of 18 years.
For individuals who have been incarcerated since
they were young juveniles, adaptive functioning
may be rather difficult to assess. Common mea-
sures of adaptive functioning have not been vali-
dated in the correctional environment and do not
appear to translate well.
Last, what is the evaluator to do with illegal
aliens and those from other countries and
cultures? These concerns place an additional
burden on the evaluator and the profession’s
measurement tools. It is absolutely imperative
that evaluations done in capital cases proceed
with utmost care and consideration, particularly
before empirically derived methods to address
these concerns are developed.
 Criminal Responsibility and Other Criminal Forensic Issues
Death Penalty Mitigation
In 1972, the U.S. Supreme Court considered the
death penalty in the United States at that time to
be cruel and unusual punishment because the
manner in which capital sentences were decided
in Georgia was capricious (Furman v. Georgia,
1972). This decision discontinued death penalty
litigation in the United States at the time because
none of the states had a system that was substan-
tially different. The death penalty statutes were
rewritten by 35 states to correct the problem
(Latzer, 1998). In 2002, the U.S. Supreme Court
determined that juries, rather judges, must make
the decision whether or not to impose a death
sentence (Ring v. Arizona, 2002).
The U.S. Supreme Court accepted as constitu-
tional Georgia’s rewrite of their state statute (Gregg
v. Georgia, 1976). Georgia’s capital sentencing
process included the presentation of aggravating
and mitigating factors. With the exception of trea-
son and aircraft hijacking, it required at least one
of ten specified aggravating circumstances to be
established beyond reasonable doubt to impose
the death penalty. The process also allowed the
defense to introduce mitigating circumstances,
but the jury was not bound to cite any particular
mitigating fact to make the binding recommenda-
tion against the death penalty. The Court noted,
“No longer can a jury wantonly and freakishly
impose the death sentence; it is always circum-
scribed by the legislative guidelines” (Gregg v.
Georgia, p. 893).
Regarding mitigating circumstances, the U.S.
Supreme Court referenced the American Law
Institute’s Model Penal Code (Tent. Draft No. 9,
1959, comment 3, p. 71) list of potential facts:
(a) The defendant has no significant history
of prior criminal activity.
(b) The murder was committed while the
defendant was under the influence of
extreme mental or emotional disturbance.
(c) The victim was a participant in the
defendant’s homicidal conduct or
consented to the homicidal act.
(d) The murder was committed under
circumstances which the defendant
believed to provide a moral justification
or extenuation for his conduct.
(e) The defendant was an accomplice in a
murder committed by another person
and his participation in the homicidal act
was relatively minor.
489
(f) The defendant acted under duress or
under the domination of another person.
(g) At the time of the murder, the capacity of
the defendant to appreciate the criminality
[wrongfulness] of his conduct or to
conform his conduct to the requirements
of law was impaired as a result of mental
disease or defect or intoxication.
The defense is certainly not limited to this partic-
ular list of mitigating facts. In Lockett v. Ohio
(1978), the U.S. Supreme Court held the trier of
fact could “not be precluded from considering as
a mitigating factor, any aspect of the defendant’s
character or record and any circumstances of the
offense that the defendant proffers as a basis for a
sentence of less than death” (p. 604). Regarding
this decision, Cunningham and Goldstein (2003)
noted these possibilities for mitigation:
Any information regarding the defendant’s
background, as a child or as an adult, could be
considered relevant. Thus, factors such as a his-
tory of childhood trauma (e.g., physical or
sexual abuse), verbal abuse, exposure to drugs
and alcohol, neglect and abandonment, undi-
agnosed or misdiagnosed conditions (e.g.,
mental retardation, emotional disturbance,
learning disability, attention deficit/hyperac-
tivity disorder), gang or cult membership, wit-
nessing a death of a family member or friend
could be considered nonstatutory mitigation.
In addition, any circumstances related to the
crime could be considered mitigating. Such
nonstatutory factors as the minor role played
by the defendant in the crime, his or her sug-
gestibility quiescence to authority, perceived
coercion, a sense desperation based on real or
imaginary beliefs, or a need for self-perceived
moral retribution could be introduced as non-
statutory mitigators. Lockett requires defense
attorneys, forensic psychological and psychiat-
ric experts to explore all avenues of mitigation
because the factors that can be introduced are
not limited to those specifically delineated by
statute (p. 412, emphasis in the original).
The neuropsychologist contemplating death pen-
alty mitigation work is referred to the work of
Cunningham and Goldstein (2003); Reynolds,
Price, and Niland (2003); and Heilbronner
and Waller (2008) for a thorough review of impor-
tant aspects of this work. The time involvement
in death penalty mitigation is certainly not
490 forensic neuropsychology
consistent with common neuropsychological, or
even forensic, work (see the survey of Sweet,
Peck, Abramowitz, & Etzweiler, 2002, in which
clinical interview and history time in minutes
was M = 57, SD = 27). Cunningham and Goldstein
note, “Obtaining a history in this comprehensive
detail routinely requires 8 to 20 hours of interview
with the defendant, exclusive of any psychological
testing” (p. 422). Although in many instances
this amount of interviewing can be done by
a mitigation specialist or other forensic specialist
and incorporated in to the neuropsychological
evaluation (Heilbronner & Waller, 2008).
Cunningham and Goldstein also note neuro-
psychological and neurological assessments are
“indicated” in most cases because, first, such
findings could have a significant mitigating effect,
and second, there is a growing body of research
implicating neurocognitive compromise in vio-
lent offenders.
Neuropsychological assessment in death
penalty litigation could also focus on aggravating
factors, but in this regard it is likely limited to
addressing increased risk of dangerousness.
Other aggravating factors are uniquely not related
to mental health (e.g., particularly heinous crime,
killing in association with another crime, etc.).
Neuropsychologists can evaluate capital defen-
dants to demonstrate the absence of mitigating
factors (i.e., rebut a defense expert). It is important
for evaluators to remain objective regardless of
who requests their services. Death penalty mitiga-
tion is truly a unique area of practice and one that
requires the utmost competence, integrity, and
ethical conduct. As Cunningham and Goldstein
(2003) pointed out, “In no situation is professional
competence more important than in death
penalty cases . . . it is imperative to present find-
ings in a thorough, objective fashion” (p. 416).
ETHICAL AND
PROFES SIONAL IS SUES IN
CRIMINAL FORENSICS
The unique aspect of practicing neuropsychology
in the criminal forensic setting carries with it a
unique set of ethical concerns. As this volume
contains a chapter specifically covering ethical
considerations in forensic neuropsychological
practice, I focus on only those issues specific to
the criminal forensic setting. In addition to famil-
iarity with the “Ethical Principles of Psychologists
and Code of Conduct” (American Psychological
Association, 2002), neuropsychologists need to be
fluently aware of the “Specialty Guidelines for
Forensic Psychology,” issues of confidentiality, and
5th Amendment protections.
Specialty Guidelines for
Forensic Psychology
The Specialty Guidelines for Forensic Psychology
(“Guidelines” hereafter) are currently in draft
form. The original document had a slightly differ-
ent name “Specialty Guidelines for Forensic
Psychologists” (Committee on Ethical Guidelines,
1991). While these 1991 “Guidelines” are still in
effect, they have been going through the revision
process since 2002. The current draft, dated March
18, 2011, as well as any more current drafts, is
available at http://www.ap-ls.org/links/profes-
sionalsgfp.html (Committee on the Revision of
the Specialty Guidelines for Forensic Psychology,
2008). The “Guidelines” are jointly developed and
adopted by Division 41 of the American
Psychological Association (American Psychology–
Law Society) and the American Academy of
Forensic Psychology (members of the forensic
board affiliated with the American Board of
Forensic Psychology). The 2011 “Guidelines” are
meant to be consistent with the Ethical Principles
of Psychologists and Code of Conduct as well as
“improve the quality of forensic psychological
services; enhance the practice and facilitate the
systematic development of forensic psychology;
encourage a high level of quality in professional
practice; and encourage forensic practitioners to
acknowledge and respect the rights of those they
serve” (p. 2).
The “Guidelines” are aspirational in nature
and serve to guide the psychologist when dealing
with forensic issues. The importance of this cannot
be overstated. The “Guidelines” are not meant
as guidance only for those professionals who
consider themselves “forensic psychologists.” The
introduction provides this summary:
For the purposes of these Guidelines, forensic
psychology refers to professional practice by
any psychologist working within any sub-
discipline of psychology (e.g., clinical, develop-
mental, social, cognitive) when applying the
scientific, technical, or specialized knowledge
of psychology to the law to assist in addressing
legal, contractual, and administrative matters.
Application of the Guidelines does not depend
on the practitioner’s typical areas of practice or
expertise, but rather on the service provided in
the case at hand. . . . Such professional conduct
is considered forensic from the time the
 Criminal Responsibility and Other Criminal Forensic Issues
practitioner reasonably expects to, agrees to, or
is legally mandated to, provide expertise on an
explicitly psycholegal issue. (p. 2)
The “Guidelines” were not written to apply to
psychologists asked to provide professional
psychological services when the psychologist was
not aware at the time of the service that it would
become forensic in nature. For these individuals,
however, they may be helpful in preparing to
communicate professional opinions in the foren-
sic arena. See the work of Denney (2005) for an
application of the “Guidelines” to two neuropsy-
chology cases completed in the criminal forensic
setting. Bush, Connell, and Denney (2006) also
provide a model of ethical decision-making when
participating in the forensic arena. It is important
for neuropsychologists practicing in the criminal
forensic arena to be familiar with the “Guidelines.”
The “Guidelines” cover many more aspects of
forensic practice, but I cover just two critical
areas in the criminal setting, confidentiality and
protecting criminal defendant rights.
Confidentiality in Criminal Forensics
A correct understanding of confidentiality is
imperative in the criminal setting. Some jurisdic-
tions provide confidentiality between the evalua-
tor and defendant under the “work product rule”
as set out by case law (United States v. Alvarez,
1975). Other jurisdictions do not provide for
mental health evaluation confidentiality; in other
words, the fact of the evaluation and the evalua-
tor’s opinion are discoverable even if there was no
report written and the requesting attorney does
not wish testimony (Edney v. Smith, 1976). When
providing evaluations as a result of a direct court
order, confidentiality does not exist. It is impera-
tive for the evaluator to understand the rule in use
within that case jurisdiction. The evaluator must
describe his or her understanding of the use of the
information to the defendant. This difficulty arises
when a clinician evaluates competency to stand
trial, but the clinician’s testimony is requested for
issues of rebutting an insanity defense or, worse,
to provide an opinion regarding potential aggra-
vating issues prior to sentencing. Such an occur-
rence is not unusual in death penalty cases and
has been the issue of U.S. Supreme Court rulings
(e.g., Estelle v. Smith, 1981).
Estelle v. Smith (1981) is another case in which
James Grigson, MD, provided testimony. The dif-
ficulty in this case was that Dr. Grigson may have
informed Smith that he was evaluating him on his
491
competency to stand trial, but he said nothing
about any future testimony on other potential
issues. Subsequent to the evaluation, Smith was
found competent to proceed and convicted of
capital murder. Texas maintains a bifurcated
capital trial process by which the defendant
undergoes trial regarding guilt initially, and then
he or she undergoes another trial by the same jury
regarding whether to impose the death penalty.
For the jury to impose a death penalty, the prose-
cution must demonstrate potential for future vio-
lence. During the sentencing phase of Smith’s
case, Dr. Grigson testified that the man was
a psychopath and likely to kill again. The jury
sentenced Smith to death. The ethical concern
here is that Dr. Grigson did not provide Smith
with a full disclosure of potential uses for the
information gained in the competency evaluation.
The 1991 “Guidelines” addressed this issue at
IV.E.3:
After a psychologist has advised the subject of
a clinical forensic evaluation of the intended
uses of the evaluation and its work product, the
psychologist may not use the evaluation work
product for other purposes without explicit
waiver to do so by the client or the client’s legal
representative.
The issue is less clearly stated in the 2011
“Guidelines,” but they are present under section 6
“Informed Consent, Notification and Assent”:
Because substantial rights, liberties, and prop-
erties are often at risk in forensic matters and
because the methods and procedures of forensic
practitioners are complex and may not be accu-
rately anticipated by the recipients of forensic
services, forensic practitioners strive to inform
service recipients about the nature and param-
eters of the services to be provided. (p. 9)
Additional clarification comes at section 6.03 with
the words, “including potential consequences of
participation” (p. 10). Neuropsychologists must
be cognizant of criminal defendant’s rights regard-
ing limits of confidentiality and informed assent.
Related to this specific event is the duty to watch
out for the constitutional rights of criminal
defendants.
Fifth Amendment Protections
In the example in the preceding section, the U.S.
Supreme Court held that Smith’s 5th Amendment
492 forensic neuropsychology
right to be protected from self-incrimination was
violated by allowing Dr. Grigson to testify on the
issue of future dangerousness at the penalty phase
of the proceedings. The High Court noted:
When Dr. Grigson went beyond simply report-
ing to the court on the issue of competence and
testified for the prosecution at the penalty
phase on the crucial issue of respondent’s
future dangerousness, his role changed and
became essentially like that of an agent of the
state recounting unwarned statements made in
a post-arrest custodial setting.
Even though he warned the defendant about the
limits of confidentiality, Dr. Grigson provided
him with no indication the information used in
the competency evaluation could be used against
him at a future penalty proceeding. Actions that
cause an infringement on a defendant’s constitu-
tional rights, such as was done here, not only
violate the “Ethical Principles” (Principle E as well
as Informed Consent), but also are counter to the
goals aspired to in the “Guidelines.”
The “Ethical Principles” also point out psy-
chologists’ responsibility to avoid harm. It is clear
that, in the case of Estelle v. Smith (1981), Dr.
Grigson did not avoid harm. One could argue that
providing potentially damaging testimony in any
capital case is tantamount to causing harm. By
that reasoning, any unbiased ethical forensic work
could be considered unethical. Clearly, this is not
the case. There is a difference between providing
an unfavorable opinion and violating a defen-
dant’s constitutional rights. It is important to keep
this distinction clear (Denney, 2005; Denney &
Wynkoop, 2000; Heilbrun, 2001).
It is generally important for forensic examin-
ers to limit the scope of their opinions to the refer-
ral questions and the related and supporting
conclusions. In the example, Dr. Grigson did not
limit his opinion to competency. When asked to
testify at the sentencing phase, the safest course of
action would have been to refuse to do so based
on the fact he did not provide Smith with a warn-
ing that information derived from the evaluation
could be used against him in a sentencing pro-
ceeding (Denney, 2005). In addition, an evalua-
tion regarding dangerousness is an entirely
different endeavor with a potentially substantial
difference in data sources and evaluative mea-
sures. Dr. Grigson should have recommended
that the attorney requesting such testimony
seek another evaluation from an independent
examiner. Relatedly, it is important for examiners
to limit their opinions in written reports to strictly
the referral question and supporting conclusion
as well. Additional non-requested opinions in
forensic reports can play havoc on the legal pro-
ceedings. Forensic examiners are asked to provide
expert opinions about very specific issues; well-
trained and competent forensic psychologists
realize this fact.
Training and Certification in
Criminal Forensics
It is hoped this chapter and chapter 16 have
made it clear that performing neuropsychological
evaluations in the criminal forensic arena is a
unique endeavor that requires a unique knowl-
edge domain. The “Ethical Principles” make it
clear that psychologists do not perform activities
for which they are not adequately trained. The
amount of specialized forensic training required
for ethical and competent practice is not clear.
The issue was preliminarily addressed by Otto and
Heilbrun (2002). Some states have developed
minimal requirements for criminal forensic prac-
tice (Farkas, DeLeon, & Newman, 1997). Often,
these requirements include a few hours attending
state-sponsored educational events with varying
amounts of mandated supervision.
Sullivan and Denney (2003) present basic and
aspirational requirements for competent criminal
forensic neuropsychological practice. In discuss-
ing “authentic professional competence,” Sullivan
and Denney (2008) expand their ideas by incor-
porating “Entry, Proficiency, and Specialty” levels
of competence in forensic matters based upon the
Villanova Conference (Bersoff et al., 1997). They
note that not all neuropsychologists will desire to
seek “specialty” level of practice within the sub-
specialty of forensic neuropsychology, but aware-
ness of these different levels will protect the
clinical from practicing beyond their authentic
level of professional competence.
No one really knows the exact point at which
clinical neuropsychological practice ends and
criminal forensic practice begins. The “Guidelines”
suggest criminal forensic work begins when one
knowingly accepts such a case. In addition to
Sullivan and Denney (2003, 2008), Heilbronner
and Frumkin (2003) raised the issue of this “divid-
ing line” and make a recommendation for one
potential model of practice. It is good that these
issues are beginning to be discussed in the profes-
sional literature. Time will reveal how well such
suggestions are accepted.
 Criminal Responsibility and Other Criminal Forensic Issues
Neuropsychologists interested in developing
criminal forensic practices can begin acquiring
knowledge content from texts and seminars. I
strongly recommend Psychological Evaluations for
the Courts (Melton et al., 2007). It is an astounding
text that covers nearly the entirety of forensic prac-
tice, both civil and criminal. This endorsement is
not intended to mean there are no other good
texts; there are. Denney and Sullivan (2008) is the
first text devoted to the application of clinical neu-
ropsychology to the criminal forensic arena.
Seminar training can be obtained from
national workshops by the AAFP. These work-
shops are uniformly strong in content and
presented at various times during the year and in
various locations around the country. Supervision
is also a necessary component of training in
criminal forensics. I recommend receiving
supervision from an individual who has proven
competency to provide psychological services
in the criminal forensic setting. Attainment of
board certification in forensic psychology by the
American Board of Forensic Psychology is
the clearest example of this achievement and
would represent the “specialty” level of practice
(Bersoff et al., 1997; Sullivan & Denney, 2008).
I admonish eager neuropsychologists to be wary
of board-certifying bodies that bestow “diplo-
mate” status with the ease of signing a credit
card (so-called vanity boards and checkbook
credentials). These bodies have attempted to
improve their appearance by including multiple
choice examinations, but still do not require face-
to-face, oral examinations of knowledge base
and practice skill at the hands of documented
experts in the field. Otto and Heilbrun (2002) and
Fisher (2008) present clear and even poignant
discussion on this issue. Last, the National
Benchbook on Psychiatric and Psychological
Evidence and Testimony (Parry, 1998), a judge’s
handbook, addresses the issue of board certifica-
tion and vanity boards specifically:
The court should be aware that while specialty
board certification is prestigious within the
various professions, witnesses who have not
obtained this level of credentialing are not
automatically presumed to be deficient by
comparison, nor are they unsuited per se to
provide expert testimony. Judges must also be
wary of witnesses claiming certification by
various “mail-order” boards, that do not
require an oral examination or other indicia of
a rigorous qualifying process. (p. 55)
493
Neuropsychologists entering the arena of forensic
practice need to prepare adequately for the
heightened scrutiny that comes with the court of
law (Sullivan & Denney, 2003, 2008). Attempting
to bypass this preparation by presenting oneself as
competent based on a vanity board is misrepre-
sentation to the public. Although the public, and
many in the judicial system, will not recognize
this ruse, misrepresentation nonetheless remains
ethically inappropriate (American Psychological
Association, 2002; Committee on Ethical
Guidelines, 1991; Committee on the Revision of
the Specialty Guidelines for Forensic Psychology,
2011).
S U M M A RY
This chapter builds on chapter 16 by reviewing
major areas of importance to neuropsychological
practice in the criminal forensic arena. Covered
were the nature of the forensic mental health eval-
uation in general, criminal responsibility, sentenc-
ing issues, risk assessment, competency to be
executed, death penalty mitigation, and impor-
tant professional and ethical concerns. The chap-
ter dealt strictly with adult criminal proceedings.
There is a host of other issues inherent in juvenile
work. Although there is a considerable body of
literature dealing with psychological evaluation of
individuals in the juvenile justice system (see
Grisso’s work), the first step in application of clin-
ical neuropsychology and neurodevelopmental
issues to that population has only recently begun
(Grisso et al., 2003; Wynkoop, 2003; Wynkoop,
2008).
The application of clinical neuropsychology to
assist parties in the criminal justice system is a
unique practice opportunity. It requires a dis-
tinctly different knowledge base in addition to
solid, empirically based, clinical neuropsycho-
logical knowledge and skill. Neuropsychologists
interested in working in the criminal forensic
setting are encouraged to acquire that knowledge
base and skill in a manner sufficient for compe-
tent and ethical practice of an applied empirical
science.
N OT E S
Opinions expressed in this chapter are those of the
author and do not necessarily represent the position of
the Federal Bureau of Prisons or the U.S. Department
of Justice.
1. There are several variants in spelling for
M’Naghten. Moran (1981), in his 18-month period of
research, found documents that appeared to indicate
494 forensic neuropsychology
the man actually spelled his name “McNaughtan,” but
M’Naghten is used here because it was used in the orig-
inal legal case.
2. Formally adopted by the ALI on May 24, 1962.
3. Very loosely drawn from Texas v. Andrea Yates
(2003).
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 18
Trends in Forensic Practice and Research
J E R RY J. S W E E T A N D D AW N G I U F F R E M E Y E R

Adversary system. A procedural system, such

as the Anglo-American legal system, involving
active and unhindered parties contesting with
each other to put forth a case before an independent
decision-maker. Black’s Law Dictionary. Seventh Ed.
—garner, 1999 , p. 54

The American civil and criminal legal systems
rely on experts in a variety of capacities, most
fundamentally to provide relevant information
that can assist in important decision making. The
same is true for other adjudicatory proceedings
that are less formal and take place outside of
courtrooms. Though not all forensic contexts in
which clinical neuropsychologists consult regard-
ing civil litigants and claimants and criminal
defendants are literally adversarial (i.e., involving
antagonistic elements), all have the potential to be
so and many actually will be. This omnipresent
possibility represents a salient distinction from
clinical contexts, with the latter characterized by a
shared goal between neuropsychologist and
patient regarding seeking to understand and
improve the patient’s identified problems. The
various implications of this context for all involved
parties have been well identified by various
neuropsychology writers and researchers, who
have over the years created a very large relevant
literature. The question we will address within the
closing chapter of this text fundamentally con-
cerns the future of forensic neuropsychology.
More specifically, in interrogatory form and
adopting a common phrase used by attorneys,
do we have an opinion within a reasonable degree
of certainty as neuropsychologists regarding where
the practice and scientific study of forensic neuro-
psychology is going from here? The bases of the
opinions to follow will be numerous, including
historical data from a search of federal and state
case opinions, trends evident in practice surveys
and relevant empirical research, the impact of
pertinent legal rulings, and the growing literature
providing guidance on a range of forensic
matters specifically written for clinical neuro-
psychologists.
PA R T I C I PAT I O N I N T H E
LEGAL SYSTEM
Psychologists have been participating in the
American legal system for decades. In fact,
Division 41 (American Psychology-Law Society)
within the largest psychology professional organi-
zation in the world, the American Psychological
Association (APA), was formed first in 1981 as a
forensic division and then in 1984 as the American
Psychology-Law Society because of the meaning-
ful involvement of psychologists specializing in
forensic matters. More broadly, APA itself has
participated in the legal system for decades, by
filing numerous amicus briefs that are intended to
inform the judiciary regarding psychological
topics of relevance to rulings (American Psycho-
logical Association, 2010). Some of these topics
concern matters of import to clinical neuro-
psychology (e.g., confidentiality, misuse of psy-
chological test materials, test security).
We have previously defined forensic neuro-
psychology and some key concepts as
. . . all neuropsychological practice in which a
clinician provides evaluation or consultative
services to an individual involved in a proceed-
ing that is potentially adversarial in nature.
502 forensic neuropsychology
Adversarial proceedings are those that involve
two or more interested parties who must reach
a resolution of a common concern or disagree-
ment from potentially antagonistic positions.
Adversarial proceedings may be either formal,
often taking place in a courtroom and involv-
ing criminal, civil (including personal injury
and medical malpractice), or family (including
divorce and child custody) law or informal,
often involving administrative matters, such as
disability determination, fitness for duty, and
due process educational hearings. In all these
proceedings, the offering of specialty knowl-
edge by the clinical neuropsychologist is to
inform a “trier-of-fact” or an administrative
process regarding an individual who is desig-
nated a litigant, if involved in formal court
proceedings, or as a claimant, if involved in less
formal proceedings (e.g., seeking disability
status or seeking special considerations
in an educational system).” (Sweet, Ecklund-
Johnson, & Malina, 2008, p. 869)
Related to formal proceedings associated with
forensic neuropsychology, electronic databases
containing historical documentation of civil and
criminal proceedings in the United States federal
and state court systems are available for public
scrutiny, and afford us the opportunity to gather
information pertaining to clinical neuropsycho-
logists. Perhaps the most well known of these
databases is LexisNexis® Academic, with searches
of this database often referred to simply as Lexis
searches. Previously, Taylor (1999) used such a
search as the basis for his observation that prior to
April 1997, the number of cases in a database of
state and federal court decisions in which the term
“neuropsychologist” occurred was 401. Taylor
also reported that 98% of these decisions occurred
after 1980. A major implication of these observa-
tions is that formal forensic involvement by
neuropsychologists is a relatively recent phenom-
enon. For clinicians who have practiced over the
last several decades, there is anecdotal informa-
tion that such involvement has increased over the
years.
To capture a more exact depiction of the growth
of forensic neuropsychology, Lexis searches were
carried out in June 2010. The first search consisted
of identifying cases in the state and federal courts in
which the terms “neuropsychologist” or “neuropsy-
chology” or “neuropsychological” were found. The
resulting graph is shown in Figure 18.1. Categorized
into decades, it is apparent that the involvement of
4000 3786
3500
3000
2500
2000
1500
1130
1000
500
222
1 3 23
0
1950–59 1960–69 1970–79 1980–89 1990–99 2000–10
FIGURE 18.1: Cases identified in legal search
engine LexisNexis® Academic by decade that men-
tion “neuropsychologist” or “neuropsychology” or
“neuropsychological.”
neuropsychologists and/or reference to the subject
matter of neuropsychology by name has increased
dramatically over time. In reality, the numbers
shown do not include instances in which neuro-
psychologists consulted with attorneys about cases,
but were not disclosed and did not participate at
testifying experts. And, as a reminder, the Lexis
database would not include informal forensic cases,
such as disability determination, fitness for duty,
and due process educational hearings. Thus, the
numbers depicted in Figure 18.1 represent only a
subset of actual cases involving neuropsychologists
or our subject matter.
LexisNexis® Academic also contains an archive
of legal materials that are primarily for, and pri-
marily written by, attorneys. A second search, the
resulting graphic of which is shown in Figure 18.2,
was conducted to identify the number and type
of legal materials containing the terms “neuro-
psychologist” or “neuropsychology” or “neuro-
psychological.” Again, it is apparent from the
dramatic increases over time that attorneys are
producing and consuming an increasing number
of legal materials that contain information rele-
vant to the specialty of clinical neuropsychology.
It does not require a leap of logic to conclude that
this is because the cases they handle in litigation
increasingly require input of neuropsychologists
as expert witnesses.
TRENDS
Additional evidence of the growth of forensic
neuropsychology can be found within our own

600
559
550
500
450
400
350
300
250
193
200
150
100
50 18
0 0 2
0 conflicts that occur frequently during forensic
1950–59 1960–69 1970–79 1980–89 1990–99 2000–10
FIGURE 18.2: Law reviews, legal journal articles,
and other publications for attorneys identified by
legal search engine (LexisNexis® Academic) by
decade that mention “neuropsychologist” or “neuro-
psychology” or “neuropsychological.”
Note. The above information was obtained on June 11, 2010. The
“Easy” search function was used, searching “Legal” document
sources and then excluding individual case documents.
literature. Survey data suggests that over time,
neuropsychologists have increased their involve-
ment in forensic cases (Sweet, Moberg, & Suchy,
2000). More recent data (Sweet, Nelson, &
Moberg, 2006) indicates that for adult neuro-
psychologists, forensic activities account for an
average of 12% of their practice, with a mean
of 4.0 hours per week (SD = 7.7). For pediatric
neuropsychologists the average is somewhat less,
accounting for approximately 6% of their activi-
ties, or 1.7 hours per week (SD = 3.9). For those
who identify as both pediatric and adult neurop-
sychologists, forensic activities account for an
average of nearly 21% of their practice (6.9 hours
per week; SD = 10.0). Compared to clinical evalu-
ations, forensic evaluations typically require more
time to complete; they also apparently contribute
disproportionately to neuropsychologists’ incomes
and there is a positive correlation between time
spent in forensic activities and income level
(Sweet et al., 2006).
As neuropsychologists increased their involve-
ment in forensic activities, they have encountered
new challenges to their ability to provide objec-
tive, ethical, scientifically informed evaluations,
and opinions. Ethical challenges may arise from
the differences in psychologists’ roles in clinical
and forensic settings, while others occur due to
the differences in psychologists’ and lawyers’ roles
(for elaboration of these issues, see Grote, earlier
Trends in Forensic Practice and Research 503
in this volume; Greiffenstein & Kaufmann, earlier
in this volume; and Sweet, Ecklund-Johnson, &
Malina, 2008). Additionally, there are issues
inherent to the forensic context that occur less
commonly in general clinical practice, which
must be addressed to ensure a complete, sound
evaluation (e.g., secondary gain issues). While the
American Psychological Association’s (APA)
Ethical Principles of Psychologists and Code of
Conduct (1992; 2002) provides general guidance
on psychologists’ ethical conduct and practice,
additional assistance, specifically addressing
activities, became necessary.
Leading forensic practitioners and researchers
provided a preponderance of articles, book chap-
ters, and texts, which clarified practice issues
common to forensic neuropsychologists, and
offered direction on ethical conduct in situations
confronted by practitioners within the field (e.g.,
Bush, 2005; Bush & Drexler, 2002). While benefi-
cial, practitioners were left with a myriad of infor-
mation and opinions to sift through and synthesize
independently. Thus, the National Academy of
Neuropsychology (NAN) and the American
Academy of Clinical Neuropsychology (AACN)
have created a number of position papers, intended
to provide the official stance of these organizations
on acceptable practices. Topics addressed have
included test security (AACN, 2007; NAN, 2000b),
third party observers (AACN, 2001; NAN, 2000a),
ethical complaints filed against neuropsycholo-
gists engaged in forensic activities (AACN, 2003),
and the use of symptom validity tests (Bush et al.,
2005; Heilbronner, Sweet, Morgan, Larrabee,
Millis, & Conference Participants, 2009).
Forensic research involving all types of forensic
evaluations, including disability/independent
medical examinations, civil litigation cases, and
criminal proceedings, has flourished as the field
has grown. In 2002, Sweet and colleagues invento-
ried the contents from 1990 to 2000 of the most
popular clinical neuropsychology journals, for
topics related to forensic practice. They found that
publications focusing upon forensic neuropsychol-
ogy had increased substantially within the prior
decade, from approximately 4% to 14% (Sweet,
King, Malina, Bergman, & Simmons, 2002).
During the same period of time, presentations on
relevant forensic topics at the annual meetings of
NAN and Division 40 (which occurs at the annual
meeting of APA) correspondingly increased.
While the scientific literature has advanced,
rulings within the legal world have evolved to
504 forensic neuropsychology
reinforce the need for a scientifically grounded
approach to forensic neuropsychology. In 1993,
with the Daubert v. Merrell Dow Pharmaceuticals,
Inc. ruling, the United States Supreme Court spec-
ified four criteria by which the admissibility of
evidence should be determined, clarifying that
evidence presented by expert witnesses should be
derived by methods that are generally accepted
within the scientific community (the sole crite-
rion elaborated by the previous relevant ruling,
known as the Frye standard from Frye v. United
States, 1923); they are able to have been subjected
to empirical testing; they have a known error
rate (which is acceptable); and/or they have been
subjected to peer review. While judges retain the
capacity to decide which of the criteria to apply
and how to apply them, and a number of states
retain the Frye standard rather than Daubert,
this Supreme Court ruling clearly demonstrates
that the forensic psychology community will
be expected to employ scientifically accepted
methods in their work, or risk having expert
testimony excluded.
Following the Daubert ruling, many within
the field expressed the concern that courts may
apply the Daubert standards in a manner that
could constrain neuropsychological practice, for
example, by limiting admissible evidence to
include data collected via fixed assessment batter-
ies only. There is no evidence suggesting that neu-
ropsychologists working with a flexible test battery
approach have had their testimony excluded with
greater frequency than those who employ a fixed
test battery approach (Greiffenstein, 2009). It is
the case that since the Daubert ruling, challenges
to evidence presented by neuropsychologists have
increased, related to a number of different issues
that do not represent a pattern. There is no indica-
tion to suggest that evidence from neuropsychol-
ogists is challenged or deemed inadmissible more
frequently than evidence given by other profes-
sionals (Sweet, Ecklund-Johnson, & Malina,
2008). When individual neuropsychologists have
been excluded by a judge, it was because the prac-
titioner did not adhere to scientifically sound
practice, the outcome of which is reasonable.
However, this does not mean that neuropsy-
chologists should simply ignore the goings-on of
the legal world and trust that the courts will figure
out the best way to apply the Daubert standard to
psychologists’ testimony (or the Frye standard, as
the case may be). It appears that Daubert has
raised awareness of the need to consider the
scientific validity of evidence offered by expert
witnesses (Cheng & Yoon, 2005; Groscup, Penrod,
Studebaker, Huss, & O’Neil, 2002); however,
judges receive limited training in scientific meth-
ods, which may impede their ability to appropri-
ately apply Daubert criteria to evidence offered by
expert witnesses (Dahir et al., 2005; Faigman &
Monahan, 2005). When judges fail to exclude
testimony of questionable scientific validity, it is
left to jurors to evaluate the merit of expert
witnesses’ opinions, to consider possibly (likely)
conflicting information from expert witnesses
retained by the opposing sides, and to determine
how to integrate information presented by wit-
nesses with other evidence to develop a verdict.
Research has indicated that jurors lack knowledge
of complex scientific methodology, and that while
having opposing experts may sensitize jurors to
empirically relevant issues, it may also increase
their uncertainty regarding all expert testimony in
a case and fail to assist them with forming deci-
sions that are grounded in science (e.g., Levett &
Kovera, 2008). Psychologists and neuropsycholo-
gists may serve as educators to the court, for exam-
ple, as technical advisors to assist federal judges or
as court-appointed experts to federal juries, and,
in light of the increased emphasis that courts have
placed upon scientifically valid testimony since
Daubert, medical and legal experts alike have
urged courts to increase their use of court-
appointed experts (Faigman & Monahan, 2005).
When Daubert or other evidentiary standards
are applied to neuropsychologists’ testimony, or
in some cases misapplied, judicial rulings can set
precedent that is adopted in other jurisdictions
and can have the effect of widely affecting forensic
activities. As an example of a ruling that might
have broadly affected neuropsychologists, but
ultimately did not only because a higher court
ruling turned back the precedent, we can consider
a case from New Hampshire involving opposing
neuropsychology experts. In 2005, a case came
before the New Hampshire Supreme Court, in
which a lower court had excluded the testimony
of a pediatric neuropsychologist, via a Daubert
challenge initiated by the defendant. In this case,
Baxter v. Temple, the plaintiff ’s neuropsychologist
was characterized as having administered a bat-
tery of tests that represented a flexible battery
approach. In response to a Daubert challenge by
the defendant, in which the defense-retained neu-
ropsychologist claimed that only a fixed battery,
such as the Halstead-Reitan battery is valid, the
trial court considered excluding the plaintiff ’s
neuropsychologist. In fact, after considering

relevant evidence the trial court decided that the
battery of tests administered by the plaintiff ’s
neuropsychologist had not been validated in a
forensic context, and because the battery itself
(i.e., the set of tests together) had not been sub-
jected to peer review and did not have a known
error rate, the neuropsychologist’s testimony was
inadmissible. The New Hampshire Supreme Court
noted “distilled to its essence, the defendants’
position is that Dr. X [the plaintiff ’s pediatric
neuropsychologist] should have used a fixed bat-
tery, such as the Halstead-Reitan battery, rather
than devising her own. . . .” Ultimately, assisted by
an amicus brief submitted by AACN (2007), the
New Hampshire Supreme Court disagreed with
that position, reversed the trial court’s decision,
and found that the neuropsychologist’s testimony
based on a flexible battery was admissible.
A U. S. Supreme Court ruling provides another
example of the importance of forensic psycholo-
gists’ utilization of scientifically grounded assess-
ment techniques. In Atkins v. Virginia (2002) the
Supreme Court ruled that the death penalty
should not be applied to individuals who are
mentally retarded/intellectually impaired. The
need for forensic psychologists and neuropsy-
chologists to use thorough, well-validated assess-
ment techniques is never more apparent than in
legal circumstances that may result in an indivi-
dual receiving the death sentence. This ruling also
illustrates the role that psychologists who abide by
a scientist-practitioner model could play in the
evolution of the legal application of significant
judicial actions. Duvall and Morris (2006) provide
a discussion of the means by which states have
enacted the Atkins ruling, each having determined
a definition of mental retardation/intellectual
impairment, which in numerous cases apparently
has not been well informed by principles of psy-
chometric theory. As with the Baxter v. Temple
New Hampshire case, Atkins illustrates the oppor-
tunities that may be created by the judicial system
for psychologists to educate and assist triers-of-
fact within the legal system. In the case of Baxter,
occurring within the smaller venue of one state’s
court system, the necessary assistance was very
focused (an amicus brief provided by AACN).
With regard to Atkins-like decisions, the process
of influencing the creation or modification of
extant statutes and related regulations can require
broad efforts (e.g., regarding Atkins in particular,
defining operationally at what psychometric
point mental retardation/intellectual impairment
begins and the consideration of standard error of
Trends in Forensic Practice and Research 505
measurement). Neuropsychologists have scien-
tific clinical training that makes them particularly
well suited to inform the triers-of-fact in such
matters, as well as others that will arise in the
future. Moreover, the specialty of clinical neuro-
psychology would be well advised to look for
relevant and appropriate opportunities to educate
the legal system regarding our area of practice, in
much the same way as has occurred with the topic
of ensuring test security (cf. Kaufmann’s 2009
treatise regarding strategies and legal arguments
for protection of raw data that are the subject of
forensic proceedings).
L O O K I N G F O RWA R D
The Future Involvement of Practitioners
As is evident from the Lexis data in Figure 18.1,
involvement of clinical neuropsychologists in the
legal system as expert witnesses is a relatively
recent phenomenon. Arguably, this involvement
did not occur in meaningful numbers until the
1990s. The curvilinear steep increase of this
growth likely cannot continue, and may in the
next ten to twenty years reach asymptote, with
subsequent growth yoked proportionately to the
number of relevant new civil litigants and claim-
ants and criminal defendants. Importantly, there
is no reason to believe that the initial factors that
created interest by the legal community in the
expertise of clinical neuropsychologists will cause
a waning of future interest. That is, the specialty
will continue to be heavily wedded to empiricism,
which is foundational to the scientist-practitioner
that has in the past been, and will continue in the
future to be, the prevailing conceptual framework
of neuropsychology’s training model and approach
to clinical practice. It is this orientation to scien-
tific inquiry and objective hypothesis testing that
leads to knowledge growth and refinement of
practice procedures, and assures that opinions of
neuropsychologist expert witnesses have solid
foundations.
Increasingly, health care has invested intellec-
tually and economically in “empirically proven”
assessments and interventions. Though represent-
ing a foreign and new approach in some areas of
health care, such as in some forms of psychother-
apy, this is a familiar, and one can even character-
ize it as a “tried-and-true,” approach in clinical
neuropsychology. There has been no evidence
across decades of lessened interest in research
among clinical neuropsychologists, though as
the majority of practitioners transferred from
506 forensic neuropsychology
institutional employment to private practice, a
smaller proportion are producing practice-related
research, which is mirrored by “psychologists in
all areas of psychology and for scientists in all
disciplines” (Norcross, Karpiak, & Santoro, 2005,
pp. 1481–1482). In fact, the productivity evident
within the most popular journals of the field
suggests sustained scientific interest and appre-
ciable growth of practice-related scientific
research. Additionally, the clinical patient groups
with which clinical neuropsychologists work will
continue to include a nontrivial percentage who,
because of acquired or perceived injury, go on to
file lawsuits or seek disability status. Thus,
neuropsychological practices will continue to be
relevant to the legal system and administrative
processes in which claims of impairment must be
adjudicated.
The increasing numbers of neuropsycholo-
gists specializing in pediatric cases reflects an
interesting phenomenon, which mirrors the his-
torical development and identity distinction of
pediatric neurologists. This development has
forensic implications. To be sure, there are many
more adult than pediatric forensic cases in crimi-
nal and civil courts. There are also disability cases,
which are nearly exclusively adult. It seems
unlikely that as a group pediatric neuropsycholo-
gists will proportionately ever be as involved in
forensic practice as their adult colleagues have
become. However, to the extent that the subspe-
cialty of pediatric neuropsychology expands its
scientific literature regarding differential diagno-
sis, including the influences of emotional states,
motivation, and effort on neuropsychological
measures, there will be increasing demands for
involvement with relevant pediatric civil litigants
and claimants and criminal defendants. In recent
years, relevant pediatric literature has in fact been
growing (e.g., Donders, 2005; Flaro & Boone,
2009; McCaffrey & Lynch, 2009; Wills & Sweet,
2006). Forensic applications unique to pediatric
practice include issues of due process in the
educational settings, and medical malpractice
claims including birth trauma (see Taylor chapter,
this volume). Wynkoop (2008) presents an infor-
mative review of forensic neuropsychology in the
juvenile justice system.
Future Directions of Forensic Research
Response Bias and Related Topics
The adage that “past behavior is the best predictor
of future behavior” is likely to apply to those
who conduct research relevant to forensic
neuropsychology. Related, the inventory of the
forensic neuropsychology literature in the three
most popular clinical practice journals (Archives
of Clinical Neuropsychology, Journal of Clinical
and Experimental Neuropsychology, and The
Clinical Neuropsychologist) from 1990 to 2000
carried out by Sweet, King, Malina, Bergman, and
Simmons (2002) provides evidence that is very
suggestive regarding the future of research in this
area. This inventory revealed that the journals
contained a greater proportion of forensic articles
from 1990 to 2000. Moreover, there were 139 arti-
cles published during this era that were “substan-
tially” addressing forensic practice, as opposed to
“partially” or “not” addressing forensic practice.
The top ten topics of these forensic articles are
shown in Table 18.1.
Will the future resemble the past in terms of
forensic research topics? There are at least four
reasons to believe that response bias and malin-
gering research will continue to be the most
frequent topic studied by forensic investigators.
First, psychology is the discipline that historically
has addressed whether samples of behavior are
valid. Specifically, since the early 1990s neuropsy-
chologists have accomplished a great deal related
to devising procedures that can effectively dis-
criminate between valid and invalid responses, a
subset of which can be determined to be the result
of deliberate deception. This research area has
TABLE 18.1 TOP TEN FORENSIC TOPICS
PUBLISHED IN THE THREE MOST
POPULAR CLINICAL NEUROPSYCHOLOGY
JOURNALS 1 FROM 1990 TO 2000
1. Malingering
2. Measures of cognitive abilities
3. Decision making
4. Psychometrics (including test validity and
reliability)
5. Litigation effects
6. Base rates
7. Ethics
8. Appropriate tests
9. Expert testimony
10. Use of norms
1
Archives of Clinical Neuropsychology, Journal of Clinical and
Experimental Neuropsychology, and The Clinical Neuropsychologist.
Source: Sweet, J. J., King, J., Malina, A., Bergman, M., & Simmons, A.
(2002). Documenting the prominence of forensic neuropsychology
at national meetings and in relevant professional journals from
1990–2000. The Clinical Neuropsychologist, 16, 481–494.

established clinical neuropsychologists as the
most likely experts in a decision-making arena to
have an objective methodology on which to base
an opinion that responses are invalid and the
extent to which the invalid responses represent
malingering. Second, base-rate studies of response
invalidity and malingering have demonstrated
that the context within which an evaluation takes
place is highly associated with the risk of insuffi-
cient effort and symptom over-reporting, which
can invalidate test results (Ardolf, Denney, &
Houston; 2007; Mittenberg, Patton, Canyock, &
Condit, 2002). Such research has established
clearly that involvement in a forensic context
raises the risk of invalid responding, which of
course needs to be identified in order that deci-
sions by judges, juries, disability insurance carri-
ers, and so forth are based on valid information.
Societal resources are finite; resources given to
nondeserving individuals diminish unnecessarily
the remaining resources available for those who
are deserving. Third, the domains of interest in
assigning awards or in allowing alternate conse-
quences (e.g., psychiatric hospitalization rather
than prison incarceration) to individuals who are
injured or ill are frequently the very practice
domains of clinical neuropsychologists (e.g.,
cognitive function, differential diagnosis of
acquired brain dysfunction versus serious psychi-
atric illness). Fourth, there is a constant tension
between the profession of clinical neuropsychol-
ogy and the legal system with regard to sharing
detailed information regarding practice tech-
niques and decision rules. Though practitioners
strive to maintain test security and not share the
intricate details of our response-bias detection
methods, the legal system and the more general
interest of behavioral scientists to publish openly
in peer-review journals in order to allow inde-
pendent validation ensures that eventually new
methods must be devised, which requires more
scientific research. For these reasons, it seems
almost certain that topics related to response bias,
such as in the reporting of cognitive, somatic, and
affective symptoms and response validity in the
performance of tests of ability that depend on the
effort of the examinee, will continue to be the
most widely researched of forensic topics. As these
topics inform the general topic, malingering will
continue to receive the highest degree of interest
from forensic neuropsychologists.
Reinforcing this view, consider that in 2007
two edited textbooks were published that focused
exclusively on feigned cognitive impairment
Trends in Forensic Practice and Research 507
(Boone, 2007) and malingered neuropsychologi-
cal deficits (Larrabee, 2007). In no preceding year
were two such books published. Even more
recently, the first neuropsychology of malingering
casebook was published (Morgan & Sweet, 2009).
If anything, the amount of interest and the
related activity of forensic researchers are increas-
ing on this topic. The fact that the American
Academy of Clinical Neuropsychology held its
first ever consensus conference on the topic of
“Neuropsychological Assessment of Effort,
Response Bias, and Malingering” (Heilbronner,
Sweet, Morgan, Larrabee, Millis, & Conference
Participants, 2009) should serve to underscore
that this area of investigation will continue to be
prominent to practitioners and researchers.
Continued Investigation of
Assessment Context
There is no question that the influence of context
on assessment results will continue to be a major
part of forensic neuropsychology research. There
are likely to be more refined and sophisticated
approaches used by researchers, especially as
archival databases grow in size, allowing for more
specific analyses of subgroups. As a straightfor-
ward case example, consider that within a forensic
context of civil litigation there are circumstances
that can create opposite motivations for litigants.
Figure 18.3 demonstrates a comparison of pre-
sumptive negative and positive motivation within
a comparable secondary gain context of individu-
als suing for damages after motor vehicle acci-
dents. Litigant A is pursuing a litigation claim of
persistent brain injury years subsequent to motor
vehicle accident involving a documented mild
traumatic brain injury. Litigant B is pursuing a
litigation claim of chronic pain and physical
changes years subsequent to a motor vehicle acci-
dent involving an uncomplicated mild traumatic
brain injury, as well as multiple well-documented,
non-central nervous system injuries. The head
injury of Litigant B was thought to be benign and
not to have caused persisting brain injury, which
explains why Litigant B has not claimed altered
cognitive status as a result of the accident. In fact,
Litigant B’s claim of physical injury being caused
by the defendant requires that his memory of the
accident scenario is considered intact because
Litigant B’s recollection of the events of the acci-
dent does not match that of other witnesses, and
has therefore been called into question. The other
witnesses described circumstances, which, if
true, would prove that the defendant was not at
508 forensic neuropsychology

Test of Memory Malingering multiple sclerosis that had been judged in a rou-
100 tine clinical context to have caused memory
80 impairment. Again, as databases of forensic
experts increase in size, more fine-tuned group
60
Litigant A studies involving such contrasting subcontexts
40 will be possible.
Litigant B
20
0 Integrative Assessment Research
Trial 1 Trial 2 Retention Apart from the research topic of malingering and
its numerous subtopics, the primary bases of clin-
Victoria Symptom Validity Test ical practice and forensic practice for neuro-
100 psychologists are our test procedures, which are a
80 constant focus of research investigation. These
60 tests and the manner in which neuropsychologists
Litigant A integrate a wide variety of assessment information
40
Litigant B from multiple sources and ultimately reach
20 diagnostic and treatment decisions are topics that
0 are data based and on which we strive to make
Easy Difficult Total improvements via scientific research. There is an
ongoing need for research to provide guidance to
Green’s Word Memory Test
clinicians who must integrate many different indi-
100
vidual data, representing what in isolation may
80 vary from low reliability to high reliability, into a
60 robust opinion (Larrabee, 2008; Victor, Boone,
40 Litigant A Serpa, Buehler, & Ziegler, 2008). Related, among
Litigant B the extensions of current research approaches
20 that are likely to become more common is the
0 use of statistical analyses and decision rules
Immed. Delayed Consist. that consider multiple points of information to
Recall Recall
strengthen conclusions (e.g., Larrabee, 2008).
FIGURE 18.3: Positive and negative effects on
motivation within civil litigation (percent correct on Development of Diversity-related
three common effort measures). Specific Norms
The federal government and large professional
organizations, such as the American Psychological
fault. Therefore, if Litigant B’s memory is not Association, have in recent years emphasized the
accurate, the liability portion of the case is likely importance of identifying and respecting ethnic
to be dismissed. Moreover, a preexisting condi- and cultural diversity in our society. In a field, like
tion of multiple sclerosis of more than 20 years clinical neuropsychology, in which the fundamen-
and medical documentation by a neurologist tal assessment approach is normative, it is espe-
prior to the accident raised doubt regarding cially important to develop norms that can be
Litigant B’s ability to recall the accident accurately. applied appropriately to examinees. To be clear,
To summarize, whereas Litigant A may receive a this is not a new issue or a new development within
litigation award if memory is impaired by the the specialty. Rather, it is an issue that is receiving
accident at issue, Litigant B’s case may be dis- new emphasis, related to which a greater amount
missed if capable memory is not demonstrated. of energy is being invested. Related neuropsycho-
Within Figure 18.3, it is apparent that even the logical literature is growing, and will need to con-
same forensic context of civil litigation can have tinue to grow in order to keep professionals abreast
opposite effects on motivation on three com- of the rapidly changing language, racial, and ethnic
monly used effort measures that appear on the population demographics that comprise “culture”
surface to be tests of memory ability. Litigant A in the United States (Manly, 2008). Increasingly,
demonstrated obvious insufficient effort on the modal person being evaluated in the office of a
all three effort measures, whereas Litigant B U.S. clinical neuropsychologist will appear less
performed nearly flawlessly, despite longstanding well represented by past normative data, requiring

development and application of new normative
datasets that are more refined with regard to cul-
tural diversity, including influences of low socio-
economic status and low levels of literacy. More
pertinent to this textbook, increasingly, the indi-
viduals involved in civil and criminal proceedings,
workers’ compensation claims, and disability
claims will have culturally diverse backgrounds,
presenting new challenges in understanding their
presentations on psychometric instruments.
A recent summit conference focused on
“Challenges in the Neuropsychological Assess-
ment of Ethnic Minorities: A Problem Solving
Summit” (Romero, Lageman, Kamath, Irani, Sim,
Suarez, et al., & the Summit Participants, 2009).
Experts on this topic and leaders of key neuropsy-
chology organizations met for the purpose of dis-
cussing scientific advances, challenges, education
and training, organizational change, and involve-
ment related to ensuring the accuracy of neuropsy-
chological assessment results that could be
affected by cultural background and ethnic minor-
ity status. Using statistics from the Pew Hispanic
Center as an example, the participants noted the
increasing diversity of examinees in the United
States in terms of language, culture, education,
and ethnic minority status, which is not matched
by the diversity of neuropsychological examiners
in these same variables. As the specialty of clinical
neuropsychology develops procedures and guide-
lines for meeting these challenges, there will
be implications for forensic neuropsychological
evaluations. Related, forensic examiners will need
to keep abreast of best practices and the means of
applying relevant norms.
Neuroimaging
At this point, a perennial question pertaining to
neuroimaging might be raised by some readers.
That is, will progress in neuroimaging have a neg-
ative impact on clinical and forensic practice in
years to come? The answer, borne out by historical
facts, is simply and emphatically “No.” In fact, the
opposite has been true. Consider, for example,
that in the nascent days of American clinical neu-
ropsychology, there were no computerized tomog-
raphy (CT) and magnetic resonance image (MRI)
scans of the brain. Those technologies had not yet
been applied clinically. It was during the era of
applications of CT and MRI to clinical conditions
of the brain that the specialty of clinical neuropsy-
chology has seen its greatest growth in terms of
training programs, job positions, and growth of
the private practice sector, all healthy signs
Trends in Forensic Practice and Research 509
(cf. practice surveys, such as Sweet, Nelson, &
Moberg, 2006). The same is true with regard to
other technologies, such as positron emission
tomography (PET), single photon emission com-
puterized tomography (SPECT), functional MRI
(fMRI), functional near-infrared spectroscopy
(fNIRS), and newer magnetic resonance-based
technologies, such as diffusion tensor imaging
(DTI). In fact, neuropsychologists have frequently
collaborated with physicians in terms of clinical
research involving sophisticated neuroimaging
technologies, as is evident in the relevant litera-
ture (see structural imaging review by Kurth &
Bigler, 2008; and functional imaging review by
Ricker & Arenth, 2008). With regard to functional
brain imaging, neuropsychologists are so involved
that the Division of Clinical Neuropsychology
(Division 40) of the American Psychological
Association published an official position paper
on the topic (APA Division 40, 2004). It seems
that with each new sophisticated development of
an imaging technology that can be applied to the
brain, the opportunities for neuropsychological
research and growth of knowledge related to the
brain and behavior expands further (see special
issue of The Clinical Neuropsychologist, 2007,
Issue 1 on “Neuropsychological Technologies” for
additional information).
What then of the application of neuroimaging
technologies and other new experimental brain
investigation techniques to forensic practice?
Some, like the so-called “brain fingerprinting” are
unique commercial ventures that have received
sharp-edged critique by fellow psychophysiology
experts (cf. Rosenfeld, 2005). Other technologies,
such as PET, SPECT, and fMRI are more widely
accepted in the scientific interdisciplinary neuro-
science research community, with a growing
number of clinical applications in at least some
medical centers. However, related to these latter,
more widely known technologies, numerous legal
authorities over time have provided cautionary
tones regarding premature adoption of new imag-
ing technologies by the legal system (e.g., Khoshbin
& Khoshbin, 2007, Moriarty, 2008) and courts
have been understandably conservative in allow-
ing such information into evidence. Petit (2007), a
law school professor who reviewed the status of
federal court rulings related to admitting or exclud-
ing results of functional imaging and “brain fin-
gerprinting” into evidence, provided an apt quote:
We have been and should continue to be
cautious about bringing science into the
510 forensic neuropsychology
courtroom. We should keep the use of science
in judicial inquiries some distance behind the
vanguards of scientific inquiry. But we have
been and should continue to be open to what is
helpful in the pursuit of the goals of our legal
system, even if the result is a profound transfor-
mation of how that system operates. (p. 340)
Given that neuropsychologists are very involved
in pushing the envelope of research technologies
that can expand our understanding of brain-
behavior relationships, we can look forward to an
augmentation, rather than a diminution, of our
current activities, as historical developments in
technology have already shown. Perhaps as sug-
gested by Ricker and Arenth (2008), functional
neuroimaging will become “a common adjunct
to traditional assessment and intervention.”
However, in terms of near term application to
forensic practice, there are two developments that
are prerequisite for reliance on these technologies.
First, extensive experience in clinical settings that
establishes clear practice guidelines for the disor-
der in question would need to be developed. The
American College of Radiology (ACR) develops
“appropriateness” guidelines, and in fact has done
so with regard to specific clinical conditions, such
as head trauma. At the time of last revision in
2008 (ACR, 2008), the appropriateness of such
functional technologies as PET and SPECT for
evaluating head trauma of any severity was at the
lowest possible rating. If the technologies under
consideration are deemed inappropriate in a rou-
tine clinical context, it is difficult to imagine a
forensic context within which these technologies
would be considered probative by a judge. Second,
if sufficient scientific and clinical knowledge is
eventually accrued for these technologies, such
that they are considered clinically appropriate, the
behavioral and real life implications of abnormal
findings will still need to be defined. To state it
simply, an anatomical image in isolation is not of
use in a clinical or forensic context, unless the
image has a known relationship to function and
quality of life, or impacts on issues of competence
or criminal responsibility. An imaging abnormal-
ity is not synonymous with a deficiency in the
ability to function in daily life. This is well known
in mainstream neuroradiology. As a concrete
example, frequently, neuroradiologists find evi-
dence of brain tissue density changes that form a
patchy appearance described as “periventricular
white matter changes” on CT or MRI structural
scans of the brain. These findings can be found in
individuals who are functioning normally and are
often interpreted using terms that indicate possi-
ble age-related change in small blood vessels,
which is of unknown clinical significance.
Ultimately, it is behavior, not images of brain
tissue, which is relevant to clinical and forensic
consultations by neuropsychologists. Within neu-
ropsychology, this position has been clearly stated
by imaging expert Bigler (2001), in an article
the title of which addresses the topic directly,
“Neuropsychological testing defines the neuro-
behavioral significance of neuro-imaging defined
abnormalities.” Outside of neuropsychology,
Khobshin and Khobshin (2007) have expounded
on this point and noted:
The risks of the misuse of brain imaging in the
courtroom are undeniable. We have strongly
recommended that even structural brain images
be used only for the purpose of linking a struc-
tural abnormality or injury to a specific deficit,
and then to be used only as a tool for interpreta-
tion by the expert witness to assess its clinical
significance. Furthermore, we have recom-
mended that functional brain images not be
used for the purpose of linking a particular
functional change in a modular fashion in the
brain to assess motivation, propensity, or respon-
sibility for a complex behavior or an inability to
inhibit it (very similar to the inadequacies of
polygraphs currently used for lie-detection).
Given the current state of medical and scientific
knowledge about brain science, once functional
brain images are admitted as evidence for these
purposes, the adversarial system is an inade-
quate forum for determining the evidentiary
validity of such evidence. Guidance is needed
for judges who must make evidentiary determi-
nations from the medical profession, in con-
junction with relevant scientific societies,
concerning the proper use of the images and of
the accompanying testimony in the courtroom.
. . . We would like to emphasize that the image
alone used as evidence of behavior is at this time
and for many years to come at best wishful
thinking and material for science fiction, and at
worst, pseudoscience. (pp. 191-192)
To state an obvious truism about a fundamen-
tal aspect of the relationship of brain function to
behavior . . . the brain is involved in all behavior,
whether that behavior is a simple correct response
to a well-researched “effort test,” known to be
objectively easy in terms of producing few errors,

or more complex behavior that involves pretend-
ing to be impaired when one is not actually
impaired. In fact, the nature of some behaviors,
such as deliberately concealing information that is
known by simply disavowing the knowledge actu-
ally involves a greater degree of brain activity and
different networks of activity within the brain.
This well-known fact has been extensively docu-
mented in years of research related to psychophys-
iological means of detecting deception (e.g., see
review by Rosenfeld, 1999). Nevertheless, if one
ignores what is already known and applies func-
tional imaging technology in a naïve manner to
the question of whether responding is effortful
(e.g., Allen, Bigler, Larsen, Goodrich-Hunseker, &
Hopkins, 2007), erroneous logic can produce
unfounded interpretations. Much more reason-
ably and consistent with prior relevant research,
Browndyke et al. (2008) used a common effort
test in concert with event-related fMRI to show
that neural circuits involved in feigned memory
vary with response demand and error type.
Indeed, the truism remains that the brain is
involved in all behavior, including withholding of
effort during evaluations.
Though future developments in technology,
especially imaging technology, will at times pro-
duce exciting advances, for any context in which
causation is important, such as is true in forensic
applications, new technologies will need to be
scrutinized in a number of ways. The well-known
criteria of causation proposed by Sir Austin
Bradford Hill (Hill, 1965) are relevant. Van
Reekum, Streiner, and Conn (2001) discussed
Hill’s causation criteria in the context of their
possible application in the field of neuropsychia-
try, which is quite relevant to consideration of
neuroimaging technologies. According to Reekum
et al., Hill’s causation criteria involve (1) demon-
strated strong association between possible
causative agent and outcome, (2) consistency of
findings across sites and methodologies of
research, (3) demonstrated specificity of outcomes
produced by possible causative agent, (4) tempo-
ral sequence of possible causative agent occurring
before the outcome of interest, (5) a dose-response
or “biological gradient” between possible caus-
ative agent and outcome, (6) a “biologic rationale”
that plausibly explains the relationship between
the possible causative agent and the outcome,
(7) “coherence,” such that what is already
known is in agreement with the causation argu-
ment, (8) evidence from experimental studies,
and (9) evidence from analogous conditions.
Trends in Forensic Practice and Research 511
Even when new technologies reveal new
means of creating images of the brain, this new
information is not automatically relevant to foren-
sic proceedings. With Hill’s criteria of causation in
mind, what is first needed in order to be relevant
is the determination of whether such new images
support causation. As Ricker (this volume) has
discussed, imaging technologies such as SPECT,
PET, and fMRI remain investigational, in part due
to the poor specificity of abnormal findings, a
problem that significantly limits determination of
causation. What is also needed, as noted earlier in
this section of our chapter, is the determination
of whether the new images offer information
pertaining to real-life functioning.
Overview of Future Research
With no factor identified on the horizon that is
likely to alter greatly the fundamental activities of
clinical neuropsychologists, or the need for empir-
ical research as a means of making additional
progress, these topics are very likely to continue
to receive a great deal of attention from forensic
researchers. Their current status in terms of rank-
ing second and third, respectively, in Table 18.1 is
unlikely to change in the next ten years.
Beyond Scientific Practice—The Final
Frontier: Ethics and Objectivity
One might conclude from the above that perhaps
continued scientific investigation will be the only
driving force that creates progress in forensic neu-
ropsychology. While true that substantial progress
will require continued scientific research, there
are important topics that are relatively difficult,
and in some instances impossible, to scrutinize by
means of the scientific method. We turn our atten-
tion now to topics of ethics and objectivity.
Ethics
A clear signal that the subspecialty practice of
forensic neuropsychology has begun to mature is
evidence of greater guidance in the literature
regarding relevant professional behavior (within
general practice guidelines: AACN, 2007; within
official position papers related to forensic prac-
tice: Bush, Barth, et al., 2005; Bush, Ruff, et al.,
2005), and in particular greater guidance regard-
ing ethics. As readers know by reaching the end of
this text, a complete chapter (chapter 4) by Grote
on ethics is contained in this current volume.
Increasingly, ethics pertaining to forensic neurop-
sychology is a topic that is being addressed, in the
form of journal articles (e.g., Grote, Lewin, Sweet,
512 forensic neuropsychology
& Van Gorp, 2000; Johnson-Greene & Bechtold,
2002; Malina, Nelson, & Sweet, 2005) and book
chapters (e.g., Fisher, Johnson-Greene, & Barth,
2002; Grote, 2005; Seward & Connor, 2009; Sweet,
2005; Sweet, Grote, & Van Gorp, 2002). Readers
can also refer to the general textbook on ethics
written specifically for neuropsychologists by
Bush (2007), within which there is a detailed
listing of citations pertaining to forensic activities,
as well as a separate forensic ethics textbook, the
co-authors of which include two neuropsycho-
logists (Bush, Connell, & Denney, 2006).
The trend of increasing attention being paid to
ethics related to forensic activities of neuro-
psychologists is likely to continue. Why? There
are several fundamental aspects of performance
of professional work in forensic contexts that pro-
vide a basis for understanding the ongoing need
to pay attention to ethics. First, as noted earlier, a
forensic context is inherently adversarial. In the
process of providing opinions that are frequently
met with contrary opinions and at times extensive
questioning by attorneys who may favor a set of
supporting opinions, interactions between neu-
ropsychology colleagues can become less than
“collegial.” Second, ethics address areas of
professional conduct that are at times complicated
to understand in a routine clinical situation, which
are compounded by the interface of different
professions (i.e., psychology, law) that may not
share the same viewpoints on key issues. Third,
the change of roles and related practice behaviors
when one is providing clinical services to a patient
versus providing forensic consultation to an
attorney regarding a plaintiff can be substantial,
and at times contradictory. Fourth, as noted previ-
ously, it appears that clinical neuropsychology as a
specialty is continuing to develop a greater
involvement in forensic activities.
Objectivity versus Bias: The Roles
and Behavior of Experts
Related to ethics, the specific topic of the impor-
tance of maintaining objectivity while engaged as
a neuropsychologist in forensic tasks has been
discussed increasingly. Early on in this discussion,
Sweet and Moulthrop (1999a, 1999b) published a
series of self-examination questions aimed at
encouraging individual practitioners to proac-
tively consider whether their opinions were objec-
tive. Johnson-Greene and Bechtold (2002) offered
guidance from an ethics perspective regarding
appropriate conduct when reviewing the work of
a forensic expert retained on the opposite side of a
litigated case. It is well known that expert
witnesses often “collide” when offering opinions to
legal decision-makers. Within the legal commu-
nity, there has been debate regarding how to resolve
the often-observed “battle of experts” in litigation
(cf. Rein, Todd, & Howell, 2006). In fact, the fric-
tion between experts has at times boiled over inap-
propriately into accusations of ethical violations, to
the point that AACN created a position paper to
offer guidance regarding resolution of concerns
about an expert’s behavior that arise during adver-
sarial proceedings, such as civil litigation (AACN,
2003). As noted by Sweet (2005), it is axiomatic
that (1) “. . .no one can claim a more ethical posi-
tion simply by virtue of the fact that he or she is
retained more by the plaintiff or more by the
defense in adversarial proceedings.” (p. 59), and (2)
“. . .the rate of actual ethical violations is not pro-
portionate to the increased number of ethical con-
cerns raised during forensic proceedings.” (p. 60)
Because of the increasing prominence of
forensic neuropsychology within the broader
specialty of clinical neuropsychology, it seems
likely that issues related to objectivity versus bias
will continue to be addressed at professional
conferences and workshops, and in relevant
peer-reviewed journals. That this occurs is not an
indication that neuropsychologists have any
greater degree of frequency or severity of these
problems. Rather, it is an indication that as a
group of specialists whose training and clinical
practice is firmly rooted in a scientist-practitioner
perspective, neuropsychologists strive to remain
objectively focused, even when applying our
knowledge base in an adversarial context creates
pressures to do otherwise.
S U M M A RY A N D
FINAL ARGUMENTS
As noted within this chapter and indeed evident
throughout this textbook, forensic neuropsycho-
logy has become well recognized and well estab-
lished within the American civil and criminal
legal system, as well as in other forensic settings.
Though the majority of our analysis has focused
on relevant data and scientific investigations, the
evidence that forensic neuropsychology has
“arrived” is also easy to find on an anecdotal level.
Any experienced forensic neuropsychologist can
provide examples of the now common place
agreement of other experts in medical specialties
to defer to the opinions of clinical neuropsycho-
logists regarding the selection, administration,
scoring, and interpretation of neuropsychological

assessment procedures. This was not always the
case, as perhaps even 15–20 years ago, physicians
were commonly expected to be deferred to by
psychologists on all matters pertaining to injury
and health status, and the reverse scenario of a
physician deferring to a psychologist was not at all
common.
Whereas popular media have occasionally
depicted assessment procedures, such as testing
with inkblots, well-known television shows such
as Law and Order now explicitly refer to specific
expertise of a “neuropsychologist.” The Alaska Bar
Association newsletter known as “The Alaska Bar
Rag” reported on the disciplinary action of an
attorney whose requirement to be reinstated was
to submit the expert opinion “from a board-
certified psychologist or neuropsychologist that
he is fit to engage in the practice of law” (Alaska
Bar Association, April-June 2008). And, perhaps
the most interesting example of all is the state
court appeal of an individual convicted of murder
and sentenced to death. The appeal (Clark v.
Mitchell, 1992/2005) alleged that the conviction
occurred in large part because the defense lawyer
had not retained a neuropsychologist to present
evidence!
There seems little doubt that continued scien-
tific investigation related to neuropsychological
assessment procedures will continue to bolster
the credibility of scientifically oriented forensic
neuropsychologists who provide evidence that
informs the triers of fact in adversarial proceed-
ings, whether in the courtroom or in other
contexts. As involvement in forensic settings
continues to increase, there is a strong likelihood
that relevant graduate coursework and post-
graduate residency opportunities will increase.
A strong likelihood exists that forensic neuro-
psychologists will be board certified, which,
with the exception of the specialty of clinical
neuropsychology, is still not well established in
other psychology practice specialties. In fact,
AACN, the membership organization of American
board-certified clinical neuropsychologists, has,
since its inception of an annual meeting, recog-
nized the importance of forensic practice by
assigning a substantial portion of its meeting
program to workshops by experts in forensic
neuropsychology. Related, as more individuals
within the specialty of clinical neuropsychology
take on the identity of a “forensic neuropsycholo-
gist,” there is a strong likelihood that a board
certification subspecialty in forensic neuropsy-
chology will be created. In many ways, this future
Trends in Forensic Practice and Research 513
action could be envisioned to parallel what is
currently taking place at present in the form of
steps being taken within the American Board
of Professional Psychology (ABPP) to create a
subspecialization in pediatric neuropsychology,
within ABPP’s specialty board of the American
Board of Clinical Neuropsychology.
The career length of a clinical neuropsycholo-
gist can easily be thirty years. In the span of a
single career of that length, the specialty practice
area of forensic neuropsychology has literally
come into existence and become a visible and
substantial part of clinical neuropsychology. We
have no way of knowing what another thirty-year
span will bring, but no factor yet identified sug-
gests that the current trajectory and presence of
forensic neuropsychology will diminish.
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 INDEX

Page numbers followed by an “f, ” “t,” or “n” denote figures, tables, or notes, respectively.

AACN. See American Academy of Clinical dangerousness and, 484–85

Neuropsychology SPECT and, 166, 170
AAN. See American Academy of Neurology TBI and, 265
ABA. See American Bar Association alcohol, 283
ABA Model Rules of Professional Conduct, 26–27, 27t amnesia from, 464
ABCN. See American Board of Clinical diminished capacity from, 482
Neuropsychology MTBI and, 236, 243, 251
abduction, 60n1 neurotoxic injury from, 291
Ability Focused Battery (AFB), 14–15 neurotoxic symptoms from, 288t
ability to assist, 446 pediatric TBI and, 211
abnormal performance on tests, 17 SPECT for, 166
absolute discovery, 31–32 ALI. See American Law Institute
AC. See Attention Concentration Index aluminum, 284t
N-acetylaspartate: creatine ratio, 290 Alzheimer’s disease (AD), 8, 401
ACRM. See American Congress of Rehabilitation capacity with, 407–9, 409t
Medicine FC with, 417–20
ACS. See Advanced Clinical Solutions informed consent with, 407–9
activated imaging, 161 MTBI and, 240
activities of daily living (ADL), 415 PCS and, 246
actus reus, 475 TBI and, 270–71
AD. See Alzheimer’s disease American Academy of Clinical Neuropsychology
ADC. See apparent diffusion coefficient (AACN), 77, 503
ADHD. See attention deficit hyperactivity disorder on ethics, 102, 104
ad hoc hypotheses, 3 on raw data, 104, 105f, 108–9
ADL. See activities of daily living American Academy of Forensic Psychology, 40
administrative law, 38t American Academy of Neurology (AAN), 13
admissibility MTBI and, 233
Daubert and, 88, 90–91 QEEG and, 169SPECT and, 166
expert testimony and, 70–94 American Bar Association (ABA), 402
in trial phase, 50–52 American Board of Clinical Neuropsychology
wrongful disclosure and, 91–93 (ABCN), 25
zealous advocacy and, 79 MTBI and, 236
Advanced Clinical Solutions (ACS), 16, 125–26 American College of Occupational and Environmental
adversarial setting, 26 Health Medicine, 283
advocacy. See also zealous advocacy American College of Radiology, 161
expert testimony and, 60n12 SPECT and, 166
AFB. See Ability Focused Battery American Congress of Rehabilitation Medicine
affective lability, 265 (ACRM), 232
affirmative defense, 474, 477t American Law Institute (ALI), 476–77
Afghanistan, 244 American Psychological Association (APA), 102,
age. See also dementia 402, 503
pediatric TBI and, 216 ethics and, 103, 104, 111
aggression. See also dangerousness risk on informed consent, 111
518 index
amicus brief, 24 Atypical Response (ATR), 377–78
in Baxter, 77 AUC. See area under curve
amnesia. See also post-traumatic amnesia Auditory Number Search Test, 266
anterograde, 264 Auditory Verbal Learning Test. See Rey Auditory Verbal
CST and, 464–67, 465t Learning Test
GOAT, 262 authority figures, 43
amphetamine, 288t Average Impairment Rating, 342
amyotrophic lateral sclerosis, 241 AVLT. See Rey Auditory Verbal Learning Test
analogy, 9
ANAM, 239–40 badgering, 55
Andreasen, Nancy, 368–69 Balance Error Scoring System (BESS), 238f
Andrews. See United States v. Andrews Barefoot v. Estelle, 482
anonymity, 39 basal ganglia/thalamus pattern, 187
anterograde amnesia, 264 base rate, 11–12, 507
anxiety, 350 COI, 12
chronic pain and, 307 for malingering, 141, 145
generalized anxiety disorders, 166 for MTBI, 4–5, 246t
medically unexplained symptoms and, 341 for neurotoxic injury, 294–98, 295t–296t
MTBI and, 240 Bates stamped, 60n14
neurotoxic injury and, 296 Baxter v. Temple, 24, 75–77, 504, 505
PTSD and, 388 amicus brief in, 77
TBI and, 265 fixed battery and, 70
APA. See American Psychological Association flexible battery and, 70
Apgar, 184 in limine in, 75
IQ and, 187 Bayes Information Criterion (BIC), 15
apnea, 183 Bayley Scales of Infant Development (BSID), 181
apolipoprotein E, 212 Behavior Rating Inventory of Executive Function
apoptosis, 184 (BRIEF), 221
apparent diffusion coefficient (ADC), 252 behavior therapy, 318, 389
area under curve (AUC), 11 Bendectin, 73
ACS and, 125–26 Benton, Arthur, 12
AFB and, 15 Benton Visual Form Discrimination (VFD), 125,
malingering and, 124 125t, 136
TBI and, 134 benzodiazepines, 248, 249f
Arithmetic, WAIS-IV, 7 BESS. See Balance Error Scoring System
arsenic, 169, 284t beyond a reasonable doubt, 28, 475
arterial end zones, 180 bias
arthritis, 329 CARB, 122
arthrography, 333 confirmation, 5, 57
assessment phase, 40–49 Consensus Conference Statement on the
general contours and, 40–45 Neuropsychological Assessment of Effort, Response
report writing in, 45–49 Bias, and Malingering, 77
association, 8 debiasing procedures, 45
asthma, 181 ethics and, 107
Atkins v. Virginia, 487–88, 505 hindsight bias, 5–6
ATP. See Atypical Presentation Scale in neuropsychological evaluation, 4–6
ATR. See Atypical Response vs. objectivity, 512
Attention Concentration Index (AC), 6 RBS, 138–40, 147
MTBI and, 236 response bias, 77, 120–25
attention deficit hyperactivity disorder (ADHD), in testimony, 57
181–82, 183 BIC. See Bayes Information Criterion
MTBI and, 248, 249f, 250 binomial theorem, 17, 122
neurotoxic injury and, 291 bio-associative mechanisms, 340
pediatric TBI and, 213–14, 217 biological gradient, 8
attorney interactions, 24–26 biological plausibility, 289
phases of, 35–57 biological severity indexing, 7
principles of, 59t biomarkers, 212
attributions, 338 bipolar disorder, 241, 248, 249f
Atypical Presentation Scale (ATP), 461 birth defects, 74
 index 519

Block Design carpal tunnel syndrome, 329

raw data from, 104 Carpenter v. Yamaha Motor Corp., 92
WAIS-IV, 7 CAST*MR. See Competence Assessment for Standing
blood oxygen level dependent (BOLD), 163–64 Trial for Defendants with Mental Retardation
Boston Diagnostic Aphasia Exam, 266, 293 catastrophizing, 306
Boston Process Approach (BPA), 75–77 Category Test, 16
Boulder Conference, 71 malingering and, 124, 131
BPA. See Boston Process Approach MTBI and, 234
BPD. See bronchopulmonary dysplasia WAIS-IV, 7
Brady, James, 82 causation, 8, 511
brain. See also perinatal brain injury; traumatic brain competency and, 447–48
injury; specific features of brain expert testimony and, 80–81
intrapartum brain damage, 56 perinatal brain injury and, 193–94
pediatric TBI and, 216 CBT. See cognitive behavior therapy
plasticity of, 216 CCTI. See Capacity to Consent to Treatment Instrument
BRIEF. See Behavior Rating Inventory of Executive CDC. See Centers for Disease Control
Function CDR. See Clinical Dementia Rating
Brief Symptom Inventory (BSI), 239 Centers for Disease Control (CDC), 232, 260
bronchopulmonary dysplasia (BPD), 180 central nervous system (CNS). See also brain; spine
Broyles v. Reilly, 92 injury to, 5
Bruno-Golden, Barbara, 75–7 neurotoxic injury in, 290, 298
BSI. See Brief Symptom Inventory toxins and, 283
BSID. See Bayley Scales of Infant Development central sinovenous thrombosis, 191
b Test, 121–22 cerebellum
burden of proof, 454–55 pediatric TBI and, 212
SPECT and, 162
CAI. See Competency Assessment Instrument cerebral palsy (CP), 180–81
calcium, 184 cerebral sinovenous thrombosis and, 191
California Verbal Learning Test-Children’s Version HIE and, 186, 188
(CVLT-C), 214, 218, 218t, 221–22 IPS and, 188–90
California Verbal Learning Test-Second Edition cerebral reserve, 242–43
(CVLT-II), 6, 13, 15 cerebrovascular accident. See stroke
malingering and, 124–25, 129 cerebrovascular disease, 166
neurotoxic injury and, 293 certiorari, 74
raw data from, 104 cesarean section, 189
Cameron. See United States v. Cameron CFS. See chronic fatigue syndrome
cannabis. See marijuana Chandler Exterminators v. Morris, 51
CAP. See Confusion Assessment Protocol Chappelle v. Ganger, 60n17
capacity. See also diminished capacity; financial capacity; CHI. See closed head injury
testamentary capacity child abuse
with AD, 407–9, 409t chronic pain and, 304–5
vs. competency, 403 pediatric TBI and, 211, 218–19
FC, 415–21 Chiperas v. Rubin, 31
FCEs, 333–34 chorioamnionitis, 189
FCI, 417–421, 418t, 419t, 420t, 422t, 423t chronic fatigue syndrome (CFS), 141, 339–40, 344–45
for informed consent, 405–15 chronic pain, 302–19
with MCI, 409–10 anxiety and, 307
with PD, 410–14 behavior therapy for, 317–19
with PDDS, 413t catastrophizing with, 306
TC, 421–31 child abuse and, 304–5
Capacity to Consent to Treatment Instrument (CCTI), diagnosis and assessment of, 311–15, 332–34
406–9, 407t, 408t, 409t Digit Span and, 128
for PDDS, 411–15, 411t, 412t, 413t, factitious disorder and, 312–13
CAPS. See Clinician Administered PTSD Scale FBS and, 136
CARB. See Computerized Assessment of Response Bias fear-avoidance with, 307–8, 308f
carbon disulfide, 286t interventions for, 316–19
carbon monoxide (CO), 283, 288t, 289, 290–91 malingering and, 147, 306–7, 313–15
carbon tetrachloride, 286t mood disorders and, 307
carboxyhemoglobin, 169, 290 MPQ and, 147
520 index
chronic pain (continued) Community Integration Questionnaire (CIQ), 268
MTBI and, 250 compelling inconsistency, 118
personality disorders and, 306–7 compensation for services
psychological screening for, 316–17 ethics and, 107
psychosocial factors in, 304–8 pre-assessment phase and, 39–40
risk factors for, 309–11, 317t Competence Assessment for Standing Trial for
somatization disorder and, 305–6 Defendants with Mental Retardation (CAST*MR),
somatoform disorders and, 312 459–60
specific conditions, 329–32 competency, 82
treatment for, 334–35 assessment tools for, 456–64
chronic widespread pain, 329–30 vs. capacity, 403
cingulate gyrus, 290 causation and, 447–48
CIQ. See Community Integration Questionnaire as Constitutional right, 445–46
civil law, 38t as contextual issue, 447
TPO and, 35 in criminal law, 444t
Clark v. Arizona, 478 for death penalty, 486–87
Classification of Violence Risk (COVR), 485 as decisional capacity, 451–52
classification statistics, 9–12 definition of, 402–3
clear and convincing evidence, 28 with dementia, 401–32
Cline v. Firestone Tire, 33 evaluation of, 450t
clinical assessment general, 403–4
competency requirements of neuropsychologists for, intermittent, 404
102–3 limited, 403
instruments for, 43 malingering and, 148
Clinical Dementia Rating (CDR), 429 to plead guilty, 452–54
clinical psychology, five noble traditions of, 4 prescriptive remediation for, 448–49
clinical reports, 45–49, 45t to refuse insanity defense, 455–56
Clinician Administered PTSD Scale (CAPS), 372, 374, restoration of, 404
379, 384–87 specific, 403–4
closed head injury (CHI) SVT for, 466
b Test and, 122 test scores for, 463t
malingering and, 124, 149 treatment for, 467–68
SPECT and, 166 to waive counsel, 452–54
CNS. See central nervous system to waive death penalty appeals, 487
CO. See carbon monoxide Competency Assessment Instrument (CAI), 457, 458t
coagulation disorders, 190 competency requirements of neuropsychologists
cocaine, 283 for clinical assessment, 102–3
neurotoxic symptoms from, 288t ethics and, 106–7
SPECT and, 166 competency to stand trial (CST), 40
Coccidioides immitis, 347 amnesia and, 464–67, 465t
coercion, 451–52 in criminal law, 438–69
cognitive abnormalities, 354 diminished capacity and, 442–44
cognitive behavior therapy (CBT), 318, 389 expert testimony and, 82–83
cognitive deficits. See also competency neuroimaging and, 171
alternative explanations for, 338–39 plea entering with, 83
death penalty and, 84, 487–88 punishment and, 84
HIE and, 185–86 trial and, 83–84
with MTBI, 242 videotaping and, 442–44
from neurotoxic injury, 289f Complex Figure Test. See Rey Complex Figure Test
with PTSD, 379–81 complex regional pain syndrome (CRPS), 330
VLBW/VPTB and, 181–82, 195 compressed spectral array (CSA), 164–65
cognitive symptoms, 336–37 computed tomography (CT), 333, 509
Cohen’s d, 240 for MTBI, 233, 241–42
coherence, 9 for neurotoxic injury, 298
COI. See condition of interest for pediatric TBI, 212
collegiality versus opposition, 29 for TBI, 265
collusion, 107 for toxic exposure, 169–70
Colorado v. Connelly, 451–52 Computerized Assessment of Response Bias (CARB), 122
Coma Recovery Scale, 266 computerized dynamic posturography (CPD), 147
 index 521

conceptual bracket creep, 370 CST. See competency to stand trial

concussion, 233 CT. See computed tomography
condition of interest (COI), 10 current ability, 446
base rate, 12 insanity defense and, 479–80
confidentiality, in criminal law, 491 cutoff scores, 9–10
confirmation bias, 5, 57 CVLT-C. See California Verbal Learning Test-Children’s
integrity check and, 57 Version
confusion CVLT-II. See California Verbal Learning Test-Second
from expert testimony, 89–90 Edition
PTCS, 262, 264 cytokines, 184
with TBI, 263–64
Confusion Assessment Protocol (CAP), 264, 266 dangerousness risk
Consensus Conference Statement on the assessment of, 482–83
Neuropsychological Assessment of Effort, Response assessment tools for, 485–86
Bias, and Malingering, 77 neuropathology of, 484–85
consistency analysis, 6–8 risk factors for, 483–84
consistency of association, 8 DAPS. See Detailed Assessment of Posttraumatic Stress
Consonant Trigrams, neurotoxic injury and, 293 Daubert v. Merrell Dow, 3, 50–52, 56, 74, 504
consulting admissibility and, 71, 73, 88, 90–91
fixed battery for, 75–77 criminal law and, 88, 90
flexible battery for, 75–77 expert testimony and, 90–91
litigation, 36–38 Frye and, 90
Continuous Recognition Memory Test (CRM), 130 lie detection and, 86
Continuous Visual Memory Test (CVMT), 130 trilogy of, 74–75
Controlled Oral Word Association, 35 wrongful disclosure and, 92
MTBI and, 237 death penalty
Cooley, Wes, 351 cognitive deficits and, 84
Cooper v. Oklahoma, 455 competency for, 486–87
coping, 240 criminal responsibility and, 486–90
corpus callosum, 212 mental retardation and, 487–88
corrective mechanisms, 39 mitigating circumstances with, 489–90
corticosteroids, 334–35 de bene esse deposition, 52
courtroom familiar, 26 debiasing procedures, 45
COVR. See Classification of Violence Risk deception
CP. See cerebral palsy fMRI for, 171–72
CPD. See computerized dynamic posturography neuroimaging for, 171–72
criminal law, 38t test for, 72–73
competency in, 444t Decosta. See Limbaugh-Kirker v. Decosta
confidentiality in, 491 definition by exclusion, 87
CST in, 438–69 delayed onset syndrome, 185, 187
Daubert and, 88 HIE and, 194
ethics in, 490–93 delayed PTSD, 375–76
expert testimony in, 87–90 dementia. See also Alzheimer’s disease
FRE and, 88 competency with, 401–32
IDRA and, 88 SPECT and, 166
neuroimaging in, 170–72 TBI and, 270–71
self-report in, 474 dementia pugilistica, 243
TPO and, 35 denial of evaluation, 108
criminal responsibility, 475–86 Department of Veteran Affairs (VA), 366
death penalty and, 486–90 deposition, 52–56
diminished capacity and, 481–82 depression. See also major depressive disorder;
criterion-groups, 119, 314 manic-depressive disorder
cross examination, 52–53 MTBI and, 240, 248, 249f, 250
crowding hypothesis, 190 neurotoxic injury and, 296
Crown, Barry, 81 PCS and, 246
CRPS. See complex regional pain syndrome PTSD and, 388
cruel and unusual punishment, 84 SPECT and, 166
Cryptococcus spp., 347 symptoms of, 337
CSA. See compressed spectral array TBI and, 265
522 index
detail, 48 Durham v. United States, 476
Detailed Assessment of Posttraumatic Stress (DAPS), 377 Dusky v. United States, 83, 446–47, 449–51, 487
Detroit Edison Co. v. National Labor Relations Board, 31 Dyer v.Trachtman, 37
wrongful disclosure and, 92
DFA. See discriminant function analysis Ecstasy. See MDMA
diabetes ECST-R. See Evaluation of Competency to Stand
maternal, 183 Trial-Revised
neurotoxic injury and, 296 edema, 212
diagnosis threat, 43 educating the jury, 53
PCS and, 247–48 Edwards v. Indiana, 464
diagnostic error management, 44 EEG. See electroencephalography
Diagnostic & Statistical Manual (DSM), 367–69, 368t Eighth Amendment, 84
dicta, 60n16, 93n2 electroencephalography (EEG), 85, 164–65
dictionary for laymen, 47, 47t IPS and, 190
differential prevalence design, 119 for neurotoxic injury, 298
diffuse edema, 212 for pseudoneurological illness, 342–43
diffusion tensor imaging (DTI), 252, 509 electromyography (EMG), 333
Digit Memory Test (DMT), 119, 122–24 elements of expert witness control, 53
Digit Span, 266. See also Reliable Digit Span EMDR. See eye movement desensitization and
malingering and, 124, 128–29, 144 reprocessing
MTBI and, 239 EMG. See electromyography
WAIS-IV, 7 encephalopathy. See also hypoxic ischemic
Digit Symbol encephalopathy
TBI and, 273 solvents and, 281, 282t
WAIS-IV, 7 epilepsy, 189
diminished capacity, 84–85, 88 episodic memory, 168
criminal responsibility and, 481–82 ergo propter hoc, 48
CST and, 442–43 ergotism, 347
diminished responsibility, 84–85, 482 Estelle v. Smith, 491, 492
direct examination, in deposition, 52–53 Ethical Principles of Psychologists and Code of Conduct
Disability Rating Scale (DRS), 267–68 (APA), 30–32, 503
disc bulge and herniation, 330 ethics, 26, 30, 101–13, 511–12
discectomy, 334 accurate and full reporting and, 112
discipline, for testimony, 56 APA and, 103, 104, 111
discography, 333 bias and, 107
disconfirmatory information, 6 collusion and, 107
discovery, 30 compensation for services and, 107
in trial phase, 49 competency requirements of neuropsychologists and,
discovery deposition, 52 106–7
discriminant function analysis (DFA), 412 in criminal law, 490–93
disinhibition, 265 death penalty and, 486
Dissimulation Scale-Revised, 134 informed consent and, 109–12
DMT. See Digit Memory Test interpretation and, 112–13
doctor-patient relationship, 37 interviews and, 109
dose-response relationship, 25 obstacles to, 106–13
inverse, 44–45 patient examination and, 107–8
with malingering, 144–45 protecting the public and, 113
with MTBI, 235 pull of affiliation and, 38
with neurotic injury, 289 raw data and, 103–6, 105f, 108–9
Dot-Counting Test, 121 records and, 107–8
double hazard, 216 in trial phase, 56
Drope v. Missouri, 445 ethylene glycol, 286t
DRS. See Disability Rating Scale Evaluation of Competency to Stand Trial-Revised
DRS Memory, 412–14 (ECST-R), 461–62
DSM. See Diagnostic & Statistical Manual event-related potentials, 170
DTI. See diffusion tensor imaging exaggeration. See symptom exaggeration
Dubray. See United States v. Dubray exceptionalism, 60n6
due process, 82 EXIT 25, 412–14
duration of unconsciousness, 261 expectations, 338
 index 523

experiment, 9 malingering and, 124, 125, 127t

expert testimony, 36–38 neurotoxic injury and, 294
admissibility and, 70–94 Finger Tip Number Writing, 124
advocacy and, 60n12 FIQ. See Full Scale IQ
causation and, 80–81 Fitness Interview Test (FIT), 457–59
confusion from, 89–90 five noble traditions, of clinical psychology, 4
in criminal law, 87–90 fixed battery, 24
CST and, 82–83 admissibility of, 51
Daubert and, 90–91 Baxter v. Temple and, 70
discrediting of, 80 for consulting, 75–77
elements of expert witness control, 53 ethics of, 39
MMPI-2 FBS and, 79–80 Fla. DOT v. Piccolo, 31
qualification of, 72–75 FLD. See frontal lobe defense
relevance of, 89 flexible battery, 24
reliability of, 79, 88–89 admissibility of, 51
scope of, 74 Baxter v. Temple and, 70
unqualification for, 81–82 for consulting, 75–77
wrongful disclosure and, 91–93 18-F-fluorodeoxyglucose (FDG), 163
extrapyramidal syndrome, 185, 194 fluoroscopy, 333
eye movement desensitization and reprocessing FM. See fibromyalgia
(EMDR), 389 fMRI. See functional magnetic resonance imaging
FMS. See Wisconsin Failure-to-Maintain Set
FA. See fractional anisotropy fNIRS. See functional near-infrared spectroscopy
facet joint syndrome, 330 football. See sports
factitious disorder, 116, 312–13 forced-choice testing, 122–23
fact witness, 36–38 Ford v. Wainwright, 486–87
Fake Bad Scale (FBS). See Symptom Validity Scale forensically relevant instruments, 43
false alternatives, 54–55 forensically specific instruments, 43
false conceit gambit, 56 Forensic Psychia!, 73f
false negatives, 10, 44 Forensic Psycholo!, 73f
false positive, 44 forensic reports, 45–49, 45t
for malingering, 141, 143 Fourteenth Amendment, 82, 439
family-wise error, 28 fractional anisotropy (FA), 252
Faretta v. California, 452–54 FRE. See Federal Rules of Evidence
fashionable illnesses, 339 free radicals, 184
fatigue. See chronic fatigue syndrome Frendak v. United States, 455–56
Faust, David, 75–76 frontal lobe defense (FLD), 85, 484
FBS. See Symptom Validity Scale neuroimaging and, 170
FC. See financial capacity PET and, 170
FCI. See Financial Capacity Instrument Frye v. United States, 3, 50–52, 60n16, 504
FDG. See 18-F-fluorodeoxyglucose admissibility and, 72–73
fear-avoidance, 307–8, 308f Daubert and, 90
Federal Rules of Evidence (FRE), 27, fMRI and, 86
on admissibility, 50 general acceptance and, 74
criminal law and, 88 SVT and, 70
on expert testimony, 72 FT. See Finger Tapping
on general acceptance, 74 Full Scale IQ (FIQ), 16
fibromyalgia (FM), 141, 329–30, 343–44 neurotoxic injury and, 293
malingering and, 147 functional capacity exams (FCEs), 333–34
15-Item Test. See Rey 15-Item Test functional magnetic resonance imaging (fMRI), 85–86,
Fifth Amendment, 83, 439, 491–92 163–64, 509
financial capacity (FC), 415–21, 418t for deception, 171–72
with AD, 417–20 for TBI, 167–69
with MCI, 420–21 functional near-infrared spectroscopy (fNIRS), 509
Financial Capacity Instrument (FCI), 417–21, 419t, 420t, fungi. See toxic mold
422t, 423t
Finger Agnosia, 124 GA. See gestational age
Finger Tapping (FT), 6, 7, 15, 125t, 135 Gage, Phineas, 484
CHI and, 126 Galveston Orientation and Amnesia Test (GOAT), 262, 264
524 index
gambits, 54–56 MTBI and, 234
Gansler, David, 88, 89 neurotoxic injury and, 293
GBMI. See guilty but mentally ill and pseudoneurological illness, 341–42
GCCT. See Georgia Court Competency Test Hand Dynamometer, 124
GCS. See Glasgow Coma Scale HCR-20, 485
GDS. See Global Deterioration Scale headache, 332
general acceptance, 51 migraine, 331
Frye and, 74 head injury. See also closed head injury; traumatic brain
general competency, 403–4 injury
general contours, 40–45 PTSD and, 373–75
General Electric v. Joiner, 25, 56, 74 Health Insurance Portability and Accountability Act
expert testimony and, 88–91 (HIPAA), 104, 105–6
general intent, 88 hearsay rule, 79
generalized anxiety disorders, 166 heavy metals, 282
General Memory Index (GM), 6 symptoms from, 284t–285t
Georgia Court Competency Test (GCCT), 459 Henry-Heilbronner Index (HHI), 138, 139–40
germinal matrix, 182 N-hexane, 286t, 291
gestational age (GA), 179 HIE. See hypoxic ischemic encephalopathy
Glasgow Coma Scale (GCS), 7 Hinckley, John, 82, 477
for MTBI, 231, 233, 241–42, 249 hindsight bias, 5
for PCS, 247 HIPAA. See Health Insurance Portability and
for pediatric TBI, 212 Accountability Act
and pseudoneurological illness, 342 hippocampus
and PTSD, 366 pediatric TBI and, 212
QEEG and, 169 PTSD and, 371
for TBI, 261, 262 Histoplasma spp., 347
Glasgow Outcome Scale (GOS), 268–69 HIV, 236, 243
Global Deterioration Scale (GDS), 429 holdings, 93n2
glutamate, 180 Hopkins Verbal Learning Test, 237
HIE and, 184 Houston Conference, 103
GM. See General Memory Index; gray matter HPA. See hypothalamic-pituitary-adrenal axis
GOAT. See Galveston Orientation and Amnesia Test HRB. See Halstead-Reitan Battery
Godinez v. Moran, 452–54, 487 Huntington’s disease, 13
good recovery, 269 H-words, 14–15
GOS. See Glasgow Outcome Scale hydrops fetalis, 183
G-PIPE. See Group Protecting the Integrity of hyperbilirubinemia, 180
Psychological Examinations hypertension
gray matter (GM), 179 maternal, 191
HIE and, 184 neurotoxic injury and, 296
neurotoxic injury and, 290 hypotension, 183
VLBW/VPTB and, 180 hypothalamic-pituitary-adrenal axis (HPA), 305
Grenitz v. Tomlian, 56, 70 hypothermia, 212
on expert testimony, 81 hypotheses, 3–4
Griggs et al. v. Duke Power, 28 hypothyroxinemia, 183
Grip Strength, 15 hypoxic ischemic encephalopathy (HIE), 179
PCS and, 126 delayed onset syndrome and, 194
Grisso, Thomas, 444–45 MRI for, 185, 185f, 187–88
Grooved Pegboard, 6, 7, 15 pediatric TBI and, 212
neurotoxic injury and, 294 stroke and, 188
Group for the Advancement of Psychiatry, 450, 450t in term infants, 183–88
Group Protecting the Integrity of Psychological
Examinations (G-PIPE), 92 IADL. See instrumental activity of daily living
guilty but mentally ill (GBMI), 479 IAMP. See 123-I-para iodoamphetamine
Gulf War, 340–41 IASP. See International Association for the Study of Pain
iatrogenic PTSD, 388–89
hallucinogenics, SPECT and, 166 idiopathic environmental intolerance (IEI), 297
Halstead, Ward, 12–13 IDRA. See Insanity Defense Reform Act of 1984
Halstead-Reitan Battery (HRB), 8, 13–14 IEDs. See improvised explosive devices
malingering and, 119, 124 IEI. See idiopathic environmental intolerance
 index 525

IEPC. See Individualized Educational Planning interpreters, informed consent for, 110–12
Committee interviews, 6–7
illusory correlations, 5 ethics and, 109
illusory mental health, 350 for perinatal brain injury, 192
IMEs. See independent medical examinations for PTSD, 383–88
Immigration and Nationality Act, 87 intracranial hemorrhage, 190–91
Impairment Index, 234 intrapartum brain damage, 56
improbability, 118, 146, 314 intraventricular hemorrhage (IVH), 180
improvised explosive devices (IEDs), 244 cerebral sinovenous thrombosis and, 191
impulsivity intracranial hemorrhage and, 191
dangerousness and, 484–85 in utero, 56
TBI and, 265 inverse dose-response effect, 44–45
inadmissible character evidence, 78–79 in vitro studies, 73–74
incompetency. See competency IOM. See Institute of Medicine
independent medical examinations (IMEs), 32–35 123-I-para iodoamphetamine (IAMP), 162
doctor-patient relationship and, 37 IPS. See ischemic perinatal stroke
informed consent for, 110 IQ, 16
for PTSD, 366, 390–91, 390t Apgar and, 187
Index Scores, of WAIS-IV, 16–17 FIQ, 16, 293
Indiana v. Edwards, 453–54 HIE and, 185–86
Individualized Educational Planning Committee IPS and, 189–90
(IEPC), 215 Performance IQ, 7, 57
Individuals with Disabilities Education Act, 215–16 Verbal IQ, 7, 57
Individuals with Disabilities Education Improvement VLBW/VPTB and, 182
Act of 2004, 215 Iraq, 244
informed consent ischemic perinatal stroke (IPS), 188–90
with AD, 407–9 ISTSS. See International Society for Traumatic Stress
capacity for, 405–15 Studies
ethics and, 109–12 IVH. See intraventricular hemorrhage
for interpreters, 110–12
for videotaping, 111–12 Jackson v. Indiana, 467
initial meeting, 35–36 Jenkins v. United States, 50
injections, for chronic pain, 332–33, 334–35 expert witness testimony and, 71
injury and (CVMT). See Continuous Visual Memory Test Joiner. See General Electric v. Joiner
in limine, 52
in Baxter v. Temple, 75 known-groups design, 119
in Santos-Buenos and, 87 for malingering, 314
SVT and, 78 Kumbo Tire Co. v. Carmichael, 56, 74
INS. See International Neuropsychological Society
insanity defense, 446 Larry P. v. Riles, 28
competency to refuse, 455–56 law. See also attorney interactions; civil law;
criminal responsibility and, 475–86 criminal law
expert testimony and, 82–83 administrative, 38t
TBI and, 479–81 conflicts in, 26–29
Insanity Defense Reform Act of 1984 (IDRA), 70, 82, FN and, 23–61
84–87, 477 probate, 38t
criminal law and, 88 lead poisoning, 76, 283, 284t, 292
Institute of Medicine (IOM), 283 learned treatise, 55
instrumental activity of daily living (IADL), 415 learning disabilities, 181
insula, 290 MTBI and, 250
integrity check, 57 pediatric TBI and, 217
intermediate evidentiary standard, 94n11 legal bases, 25
intermittent competency, 404 legal primacy, 60n6
International Association for the Study of Pain (IASP), 302 legal settings, 38t
International Neuropsychological Society (INS), 101 Letter Memory Test, 123–24
International Society for Traumatic Stress Studies LexisNexis Academic, 502, 502f
(ISTSS), 378–79 lie detection, 86, 86f
interpretation, 30 likelihood ratio (LR), 10
ethics and, 112–13 for malingering, 143–44, 145
526 index
Limbaugh-Kirker v. Decosta, 79, 80 MMPI-2 for, 146
limited competency, 404 MND and, 146
List Learning and Memory, 239 MPRD and, 146
litigation consulting, 36–38 MTBI and, 251
LNNB. See Luria Nebraska Neuropsychological Battery patterns of, 117
Logical Memory, 125 PCS and, 247–48
logistic regression, 10–11 perinatal brain injury and, 193
loss of consciousness problem-solving ability measures and, 130–31
with MTBI, 232, 233, 240 PTSD and, 376–77
with PCS, 244 RDS and, 128–29, 144
with PTSD, 374–75 recognition memory measurements and, 129–30
LR. See likelihood ratio research designs for, 118–20
Lumsden v. United States, 31 ROC for, 11f
Luria Nebraska Neuropsychological Battery (LNNB), simulation studies for, 144
13–14 subtypes of, 147–48
lying, 350–52 SVT for, 142–44, 149
lie detection, 86, 86f symptom exaggeration with, 131–41
testimony about, 146–47
MacArthur Competency Assessment Tool-Criminal Malingering Index, 132
Adjudication (MacCAT-CA), 460–61 manganese, 282, 285t
MacArthur Violence Risk Assessment Study, 485 manic-depressive disorder
magnetic resonance imaging (MRI), 333, 509 MTBI and, 241, 249f
for chronic pain, 303 SPECT and, 166
for HIE, 185, 185f, 187–88 marijuana, 248, 249f, 283, 296
for MTBI, 241–42 neurotoxic symptoms from, 288t
for neurotoxic injury, 298 marketing, 60n2
for pediatric TBI, 212 maternal diabetes, 183
for PVL, 180 maternal hypertension, 191
for toxic exposure, 169 maternal hypotension, 183
for VLBW/VPTB, 182 MBK. See methyl-N-butyl ketone
WM and, 180 McGill Pain Questionnaire (MPQ), 131–32
magnetoencephalography (MEG), 165 chronic pain and, 147
major depressive disorder (MDD), 13 MCI. See mild cognitive impairment
MTBI and, 249f, 250 MCS. See multiple chemical sensitivity
PCS and, 246 MCs. See medical controls
malingered neurocognitive dysfunction (MND), 117–18, MDD. See major depressive disorder
313–14 MDMA, 283, 296
malingering and, 146 neurotoxic symptoms from, 288t
MTBI and, 248, 249f MDSM. See multiple data source model
response bias and, 120–24 medical controls (MCs), 5
TBI and, 141 medical history
malingered pain-related disability (MPRD), 118, 146, accuracy of, 349
307, 314 distortion of, 352
malingering, 6, 507 medically unexplained symptoms, 336–55
assessment of, 116–50 assessment of, 352–53
base rate of, 141, 145 with CFS, 344–45
CHI and, 149 characteristics of, 339–41
chronic pain and, 147, 306–7, 313–15 with FM, 343–44
criteria for, 117 lying and, 350–52
definition of, 116–18 with MCS, 345–46
diagnosis of, 141–46 medical history accuracy and, 349
Digit Span for, 128–29, 144 medical history distortion and, 352
dose-response relationship with, 144–45 pseudoneurological illness, 341–43
false positive for, 141, 143 psychological stress and, 348–49
FBS and, 137t self-appraisal and, 349–50
FM and, 147 symptom exaggeration and, 350–52
FT for, 127t with toxic mold, 346–48
incompetency and, 148 Medical Symptom Validity Test (MSVT), 139
LR for, 143–44, 145 Medina v. California, 454–55

MEG. See magnetoencephalography
memory. See also specific memory types and tests
LNNB for, 14
MTBI and, 232, 235, 250
neurotoxins and, 283
pediatric TBI and, 213
TBI and, 264
Memory and Location, 124
meniscal tears, 330–31
mens rea, 84, 87, 94n14, 475
MENT. See Morel Emotional Numbing Test
mental retardation. See cognitive deficits
mental state at offense (MSO), 474–75
mental status examination (MSE), 41
mercury, 169, 283, 285t
mere conclusory comment, 48
methamphetamine, 283
method conflicts, 28
methyl alcohol, 286t
methyl-N-butyl ketone (MBK), 282, 286t
Meyers Neuropsychological Battery, 14
migraine, 331
mild cognitive impairment (MCI), 402
capacity with, 409–10
FC with, 420–21
mild traumatic brain injury (MTBI), 231–53
complaint base rates for, 4–5, 246t
diagnostic criteria for, 231–34
differential diagnosis for, 248–51
neuropsychological effect sizes for, 249f
outcomes with, 236–41
PCS and, 244–48
persistent problems following, 241–44
recovery curves for, 238f
research designs for, 234–36
severity of, 235t
SVT and, 145
Miller-Forensic Assessment of Symptoms, 378
Mini Token Test, 266
Minner v. American Mortg., 24
Minnesota Multiphasic Personality Inventory-2
(MMPI-2), 11, 11f, 13, 49
for chronic pain, 305–6, 315
expert testimony and, 80
FBS and, 133–38
for malingering, 117, 124, 125, 146
for MTBI, 250
for PCS, 126, 247
for pseudoneurological illness, 342–43
for PTSD, 136–37, 381–83
symptom exaggeration and, 132–33
TPO and, 34
Miranda v. Arizona, 83, 451–52, 474
miserable minority, 233
MMPI-2. See Minnesota Multiphasic Personality
Inventory-2
M’Naghten, Daniel, 475–77
MND. See malingered neurocognitive dysfunction
Model Penal Code, 476
index 527
moderate TBI, 260–73
incidence of, 262–63
neuropsychological assessment of, 265–68
outcomes after, 268–71
prediction of outcome for, 271–73
Modified Somatic Perception Questionnaire
(MSPQ), 147
modus tollens, 4
mold, 283
monoparesis, 188
Monte Carlo method, 17
mood disorders
chronic pain and, 307
MTBI and, 250
neurotoxic injury and, 296
Morel Emotional Numbing Test (MENT), 377
motivation impairments, 126–27
motor function tests, 126–27
motor vehicle accidents (MVA), 372–73
MPQ. See McGill Pain Questionnaire
MPRD. See malingered pain-related disability
MRI. See magnetic resonance imaging
MSE. See mental status examination
MSO. See mental state at offense
MSPQ. See Modified Somatic Perception Questionnaire
MSVT. See Medical Symptom Validity Test
MTBI. See mild traumatic brain injury
muddying the record, 49
multi-method convergent means of data gathering, 40
multiple chemical sensitivity (MCS), 298, 345–46
multiple data source model (MDSM), 473–75, 480–81
multiple measures, 15
multiple sclerosis, 13
chronic pain with, 302
MTBI and, 241
Munchausen by proxy, 85
muscle ligament injuries, 331
MVA. See motor vehicle accidents
mycotoxins, 283
myelography, 333
myofascial pain syndrome, 331
NAART, 282
NAB. See Neuropsychological Assessment Battery
National Academy of Neuropsychology (NAN), 101,
102, 503
on raw data, 109
National Center for Injury Prevention and Control, 232
National Computer systems (NCS), 136
National Institute of Neurological and Communicative
Disorders and Stroke-Alzheimer’s Disease and
Released Disorders Association (NINCDS-
ADRDA), 404
National Standardized Test, 292
nature, 477–78
N-Back, 167–68
NBW. See normal birth weight
NCS. See National Computer systems; nerve conduction
study
528 index
necrotizing enterocolitis, 180, 183 nonsteroidal anti-inflammatories (NSAIDs), 334
negative predictive power (NPP), 10 nonverbal behaviors, 54
formula for, 11 normal birth weight (NBW), 181
PPP, 11–12 normative basis for tests, 43
sensitivity and, 142 North Carolina v. Alford, 452, 487
specificity and, 142 novel problem solving, 213
Nelson v. Nelson, 71 NPP. See negative predictive power
nerve conduction study (NCS), 333 NSAIDs. See nonsteroidal anti-inflammatories
nerve decompression, 334 null hypothesis, 4
NES. See Neurobehavioral Evaluation System
Neurobehavioral Evaluation System (NES), 292 OA. See osteoarthritis
Neurobehavioral Functioning Inventory, 266 objectivity, 48–49, 57
Neurobehavioral Rating Scale, 266 vs. bias, 512
neuroimaging, 85–86, 160–72, 509–11. See also specific in deposition, 53–54
neuroimaging modalities vs. zealous advocacy, 26–27
activated, 161 obsessive-compulsive disorder, 166
in criminal law, 170–72 ODA. See Optimal Data Analysis
CST and, 171 odds ratio (OR), 10
for deception, 171–72 Oklahoma Premorbid Intelligence Estimate (OPIE), 16
electrophysiological techniques for, 164–65 oligohydramnios, 189
evidence classes and, 161 opiates
FLD and, 170 neurotoxic symptoms from, 288t
for neurotoxic injury, 290 SPECT and, 166
radioligand-based, 161–64 OPIE. See Oklahoma Premorbid Intelligence Estimate
resting, 161 Optimal Data Analysis (ODA), 139
for toxic exposure, 169–70 OR. See odds ratio
neurolytic blockade, 334 organization, 48
Neuropsychia!, 73f organophosphates, 283, 288t
Neuropsycholo!, 73f, 438 Orientation Log, 266
Neuropsychological Assessment Battery (NAB), 17 orthopedic injuries, MTBI and, 234, 252–53
neuropsychological diagnosis. See also specific conditions osteoarthritis (OA), 329
classification statistics in, 9–12 OTBM. See overall test battery mean
neuropsychological evaluation. See also specific conditions overall test battery mean (OTBM), 7, 14
bias in, 4–5 oxyhemoglobin, 163
errors in, 4–5
with science, 4–9 Paced Auditory Serial Addition Test (PASAT), 7, 250
SVT in, 77–80 PAI. See Personality Assessment Inventory
videotaping of, 33t pain. See also chronic pain
neuropsychological testing, 12–18 CRPS, 330
neurotoxic injury, 281–98 IASP, 302
base rate for, 294–98, 295t–296t MPQ, 131–32, 147
cognitive deficits from, 289f MPRD, 118, 146, 307, 314
exposure assessment for, 290–98, 297f myofascial pain syndrome, 331
interpretation of findings for, 294–98 painter’s syndrome, 281–82
medical history and, 291 paint thinners, 292
occupational and environmental history and, 291–92 parens patriae, 439
social, academic, and psychiatric history and, 292 Parkinson’s disease (PD), 13, 401
sufficient exposure for, 291 consent capacity with, 410–15
toxin categories, 283, 288 chronic pain with, 302
nexus, 48 PD-CIND, 414
NINCDS-ADRDA. See National Institute of Neurological Parkinson’s disease dementia syndrome (PDDS), 411–15
and Communicative Disorders and Stroke-Alzheimer’s consent capacity with, 411t, 412t, 413t
Disease and Released Disorders Association paroxetine (Paxil), 389
nitric oxide, 184 PASAT. See Paced Auditory Serial Addition Test
non-CNS litigants, 5 passive answering, 54
nondisclosure privilege, 31–32 patent ductus arteriosis, 180, 183
nonepileptic seizures, 342–43 Pate v. Robinson, 445
nonevaluation, 108 Paxil. See paroxetine
non obstante veredicto, 28 PCBs. See polychlorinated biphenyls
 index 529

PCD. See persistent post-concussional disorder polychlorinated biphenyls (PCBs), 74

PCL-R. See Psychopathy Checklist-Revised portal to portal billing, 39
PCS. See post-concussion syndrome Portland Digit Recognition Test (PDRT), 44
PCSC. See Post-Concussion Symptom Checklist for malingering, 117, 124, 129
PD. See Parkinson’s disease for MTBI, 236
PD and cognitive impairment without dementia for pseudoneurological illness, 342
(PD-CIND), 414 positive predictive power (PPP), 10
PDDS. See Parkinson’s disease dementia syndrome of FBS, 137
PDRT. See Portland Digit Recognition Test formula for, 11
PDS. See Posttraumatic Stress Diagnostic Scale NPP, 11–12
pediatric TBI, 211–22 sensitivity and, 142
child abuse and, 218–19 specificity and, 142
complicating premorbid histories with, 217–18 positron emission tomography (PET), 163, 509
epidemiology of, 211 FLD and, 170
family functioning and, 217 for TBI, 166–67
moderating and mediating variables with, 215–17 for toxic exposure, 169–70
neurobehavioral sequelae from, 213–14 Post-Concussion Symptom Checklist (PCSC), 239, 245
neuropsychological evaluation of, 219–21 post-concussion syndrome (PCS), 126
pathophysiology of, 212 MTBI and, 237, 240, 244–48
severity of, 211–12 QEEG for, 169
special education for, 214–15 SPECT for, 166
SVT for, 221–22 symptoms of, 244, 246t, 337
Penry v. Lynaugh, 487–88 post hoc, 48
People v. Sebastianelli, 24 post-traumatic amnesia (PTA), 232, 233
per diem, 39 MTBI and, 239, 241, 249
Performance IQ, 7 PTSD and, 375
perinatal brain injury, 179–200 TBI and, 261–64
central sinovenous thrombosis, 191 post-traumatic confusional state (PTCS), 262, 264
forensic assessments for, 192–99 post-traumatic hydrocephalus, 265
HIE, 183–88 Posttraumatic Stress Diagnostic Scale (PDS), 387–88
intracranial hemorrhage, 190–91 post-traumatic stress disorder (PTSD), 51, 365–93
IPS, 188–90 cognitive deficits with, 379–81
recommendations for, 196t–197t definition of, 367
socioeconomic status and, 194 delayed, 375–76
testimony for, 195–97 DSM and, 367–69, 368t
VLBW, 179–83 epidemiological studies on, 369–70
VPTB, 179–83 forensic evaluation for, 378–88
periventricular hemorrhagic infarction (PHI), 180 head injury and, 373–75
VLBW/VPTB and, 182 iatrogenic, 388–89
periventricular leukomalacia (PVL), 180 interviews for, 383–87
persistent post-concussional disorder (PCD), 246 malingering and, 376–77
personal attacks, 60n3 MMPI-2 for, 136–37
Personality Assessment Inventory (PAI), 132, 379 MTBI and, 240, 244, 250
personality disorders, 306–7 MVA and, 372–73
persuasion, 49 neurobiology of, 370–72
pesticides, 283, 292 neurotoxic injury and, 296–97
PET. See positron emission tomography psychological stress and, 348–49
PHI. See periventricular hemorrhagic infarction self-report of, 387–88
physical examinations, 333–34 symptom exaggeration and, 133
Picture Completion, 16 symptoms of, 338
placenta post-trial phase, 56–57
cerebral sinovenous thrombosis and, 191 post-Vietnam syndrome, 369
HIE and, 183–84 PPP. See positive predictive power
intracranial hemorrhage and, 190–91 practice pattern surveys, 24
VLBW/VPTB and, 183 practicing competent neuropsychology, 25
plausibility, 8–9 pre-assessment phase
pneumothorax, 180 compensation for services and, 39–40
PNS. See Pseudoneurologic Scale initial meeting in, 35–36
police power, 439 role selection in, 36–38
530 index
predictive value statistics, 10 RDS. See Reliable Digit Span
preeclampsia, 189 Reagan, Ronald, 82
cerebral sinovenous thrombosis and, 191 reasonable level of understanding, 446
preexisting conditions, 7 receiver operating characteristic (ROC), 11, 78
pediatric TBI and, 220 for malingering, 11f, 124
premorbid psychopathy, 42t for TBI, 134
preponderance of evidence standard, 28, 48 recognition memory measurements, 129–30
pretrial diversion, 480 recognition trials, 121
prevailing school of thought, 73 Recognition Word List, 132
prevalence/base rate. See base rate records
priorities, 49 ethics and, 107–8
probability mapping, 165 for MTBI, 232
probable assistance, 29 SGFFP and, 37
probable MPRD, 118 testimony from, 37
probate law, 38t regional cerebral blood flow (rCBF), 161
problem-solving ability measures, 130–31 fMRI and, 163
pro bono, 107 PET and, 167
pro se, 452 regional cerebral metabolic rate for glucose
protecting the public, 113 (rCMRglc), 163
proximate cause, 46 PET and,163, 167
pseudoneurological illness, 341–43 regional cerebral metabolic rate for oxygen
pseudoneurological symptoms, 337–38 (rCMRO2), 163
Pseudoneurologic Scale (PNS), 139–40 Rehnquist, William, 74
pseudoscience, 3 Reitan, Ralph, 13
psychological stress, 348–49 relevance
Psychopathy Checklist-Revised (PCL-R), 485 of evidence, 78
psychotic disorders, 265 of expert testimony, 89
PTA. See post-traumatic amnesia reliability, of expert testimony, 79, 88–89
PTCS. See post-traumatic confusional state Reliable Digit Span (RDS), 124, 125t, 126, 135
PTSD. See post-traumatic stress disorder malingering and, 125, 128–29, 144
PTSD Checklist, 387 symptom exaggeration and, 132
pull of affiliation, 35, 38 remittitur, 60n4
Purdue Pegboard, 294 reports
PVL. See periventricular leukomalacia in assessment phase, 45–49
clinical, 45–49, 45t
QEEG. See quantitative electroencephalography forensic, 45–49, 45t
Q-PTSD. See Quick Test for Posttraumatic Stress self-report, 387–88, 473–74
Disorder response bias, 77
quadriparesis, 188 forced-choice testing and, 122–24
quality, 477–78 MND and, 120, 122–24
quantitative electroencephalography (QEEG), 164–65, Response Bias Scale (RBS), 138–40, 147
169, 237 responsibility. See also criminal responsibility
Quick Test for Posttraumatic Stress Disorder diminished, 84–85, 482
(Q-PTSD), 377 responsivity to social and political forces, 28
resting imaging, 161
RA. See rheumatoid arthritis Restructured Clinical Scales, 138
radiculopathy, 331 retinopathy, 180, 183
radiofrequency (RF), 163 pediatric TBI and, 219
radioligand-based imaging, 161–64 retrospective competency determinations, 83
Ragge v. MCA/Universal Studios, 34 Rey 15-Item Test, 120–21, 135
raw data, 29–32 symptom exaggeration and, 132
ethics and, 103–6, 105f, 108–9 Rey Auditory Verbal Learning Test (AVLT), 14, 124
wrongful disclosure and, 92 malingering and, 129
RBS. See Response Bias Scale neurotoxic injury and, 293
rCBF. See regional cerebral blood flow PCS and, 247
rCMRglc. See regional cerebral metabolic rate for glucose Rey Complex Figure Test, 130
rCMRO2. See regional cerebral metabolic rate for oxygen MTBI and, 235, 250
R-CRAS. See Rogers Criminal Responsibility Assessment neurotoxic injury and, 294
Scales PCS and, 247
 index 531

Rey’s Dot-Counting Test, 121 sepsis, 180, 183

Rey Word List, 135 Serial Digit Learning test, 294
RF. See radiofrequency serotonin, 484
rheumatoid arthritis (RA), 329 sertraline (Zoloft), 389
Riggins v. Nevada, 467 serum biomarkers, 212
right/wrong test, 476 severe TBI, 260–73
Rinchack. See United States v. Rinchack incidence of, 262–63
Rivermead Post-concussion Symptoms Questionnaire, 245 neuropsychological assessment of, 265–68
ROC. See receiver operating characteristic outcomes after, 268–71
Rogers Criminal Responsibility Assessment Scales prediction of outcome for, 271–73
(R-CRAS), 481 SGA. See small for GA
roles, 440–41, 440t, 442f SGFFP. See Specialty Guidelines for Forensic Psychology
conflicts with, 28–29 Shaheen, Sandra, 75
in pre-assessment phase, 36–38 shaken-baby syndrome, 218
rotator cuff tears, 331 Sharrer & Sharrer v. Sunscape Landscape Nursery, Inc.
Rush v. Megee, 71 et al., 79
shunt-dependent hydrocephalus, 182
Santos-Bueno. See United States v. Jose Santos-Bueno sick building syndrome, 346–48
Saylor, F. Dennis, 88 Sieling v. Eyman, 452–53
schizophrenia, 13 Sierra v. Reyes, 80
b Test and, 122 Simmons v. Mullen, 71–72, 75
MTBI and, 250 Simple Visual Reaction Time, 293
SPECT and, 166 simulation studies, for malingering, 119, 144
Schudel v. General Electric, 50 single photon emission computed tomography (SPECT),
sciatica, 331 161–62, 509
science, 3–4 aggression and, 170
neuropsychological evaluation with, 4–9 cerebellum and, 162
neuropsychological testing and, 12–18 for CFS, 344
scope for TBI, 165–66
of expert testimony, 74 for toxic exposure, 169–70
of testimony, 50–51 SIRS. See Structured Interview of Reported Symptoms
Seashore Rhythm Test, 124 Sixth Amendment, 439
Sebastianelli. See People v. Sebastianelli skull fracture, 197, 219, 233
SEE. See standard errors of estimate TBI and, 261
Segna. See United States v. Segna small for GA (SGA), 179
seizures smoking, 290
cerebral sinovenous thrombosis and, 191 social judgment, 213
HIE and, 185 socioeconomic status
IPS and, 190 pediatric TBI and, 216
nonepileptic, 342–43 perinatal brain injury and, 194
pediatric TBI and, 219 TBI and, 273
pseudoneurological illness and, 342 VLBW/VPTB and, 183
self-appraisal, 57 soft psychology, 4
medically unexplained symptoms and, 349–50 solvents
MTBI and, 243 encephalopathy and, 281, 282t
perinatal brain injury and, 193 symptoms with, 286t–287t
self-awareness, 265 somatization disorder
self-incrimination, 439 chronic pain and, 305–6
self-regulation, 216 PCS and, 247
self-report SPECT and, 166
in criminal law, 473–74 somatoform disorders, 141
of PTSD, 387–88 chronic pain and, 312
Sell v. United States, 467–68 PCS and, 247
sensitivity, 5, 11–12 Spatial Span, 104
MCS, 298 special education, 214–15
NPP and, 142 Specialty Guidelines for Forensic Psychology (SGFFP), 32,
PPP and, 142 490–91
of Rey 15-Item Test, 120 on compensation for services, 40
SVT and, 12 records and, 37
532 index
specific competency, 403–4 Symptom Improbability Rating Scale, 135
specific intent, 88, 94n13 symptom validity, 77–80
specificity, 5, 8, 11–12 Symptom Validity Scale (FBS), 11, 11f, 49, 70, 125t
NPP and, 142 for chronic pain, 136
PPP and, 142 expert testimony and, 80
of Rey 15-Item Test, 120 for malingering, 137t
SPECT. See single photon emission computed MMPI-2 and, 138
tomography PPP of, 137
Speech Sounds Perception Errors, 124 symptom exaggeration and, 133–38
spine for TBI, 133–35, 138
chronic pain with, 303 WMT and, 138–39
disc bulge and herniation in, 330 symptom validity test (SVT), 10–11, 44
spinal fusion, 334 for chronic pain, 315
spinal stenosis, 331 for competency, 466
spondylolisthesis, 331–32 Daubert and, 51
spondylolysis, 331–32 forced-choice testing for, 122
spondylosis, 332 Frye and, 70
sports hearsay rule and, 79
MTBI and, 233–34, 236–37, 243, 251 in limine and, 78
pediatric TBI and, 214 for malingering, 142–44, 149
Spot-the-Word-Test, 381 for MTBI, 145
SQUIDs. See superconducting quantum-interference in neuropsychological evaluations, 77–80
devices for pediatric TBI, 221–22
SRS. See Supervision Rating Scale for PTSD, 366
standard errors of estimate (SEE), 16 sensitivity and, 12
standard of proof, 28, 454–55 specificity and, 12
star witness mentality, 57 for TBI, 145
steroids, 183 systolic blood pressure deception test, 72–73
for chronic pain, 334–35
strength of association, 8 Tactual Performance Test Total Time, 124
stress, 348–49. See also post-traumatic stress disorder Tarver v. State, 25
stroke Task Force for Test User Qualifications (TTFUQ), 102
b Test and, 122 taxon based malingering, 148
HIE and, 188 TBI. See traumatic brain injury
IPS, 188–90 TBI Model Systems protocol, 267
Stroop Test, 293 TC. See testamentary capacity
Structured Interview of Reported Symptoms (SIRS), TCE. See trichloroethylene
132, 378 TCI. See Testamentary Capacity Instrument
sua sponte, 444 Technetium, 162
subarachnoid hemorrhage, 190–91 temporality, 8
subdural hemorrhage, 190–91 temporomandibular disorder (TMD), 332
pediatric TBI and, 219 TENS. See transcutaneous electrical nerve stimulation
subpoenas, 60n9 tension-type headache, 332
substance abuse. See specific substances tests, 12–18. See also specific tests
sufficient present ability standard, 83 in common use, 43–44
Sullivan. See United States v. Sullivan cutting score, 12
superconducting quantum-interference devices data, 104
(SQUIDs), 165 materials for, 104
Supervision Rating Scale (SRS), 268 security, 31
supporting board certification, 25 validity of, 44
SVT. See symptom validity test wrongful disclosure of, 91–93
Symbol Digit Modalities Test, 243 testamentary capacity (TC), 421–31
MTBI and, 250 undue influence and, 430–31
for PTSD, 381 Testamentary Capacity Instrument (TCI), 426–27
Symbol Digit Paired Associate Learning Task, 293 testimony. See also expert testimony
symptom exaggeration bias in, 57
with malingering, 131–41 discipline for, 56
medically unexplained symptoms and, 350–52 about malingering, 146–47
MTBI and, 248 for perinatal brain injury, 195–97
 index 533

scope of, 50–51 MND and, 141

in trial phase, 52–56 neuropsychological assessment of, 267t, 268t
Test of Memory Malingering (TOMM), 117, 123 PET for, 166–67
FBS and, 138 prediction of outcome from, 272t
PCS and, 245 QEEG for, 169
pediatric TBI and, 218, 221–22 ROC and, 134
perinatal brain injury and, 193 SPECT for, 165–66
Test of Premorbid Functioning (TOPF), 16 SVT and, 145
TFCBT. See trauma-focused cognitive behavioral therapy symptom exaggeration and, 133–34
therapeutic alliances, 441 symptoms and, 337
Therapeutics and Technology Assessment Subcommittee, 13 treater versus expert, 29, 440t, 442f
QEEG and, 169 trial phase, 49–56
third-party observations (TPO), 32–35 admissibility in, 50–52
G-PIPE and, 92 deposition in, 52–56
threshold effect, 243 discovery in, 49
threshold limit values (TLV), 290 ethics in, 56
thrombocytopenia, 189 testimony in, 52–56
intracranial hemorrhage and, 191 trichloroethylene (TCE), 287t
thyroid disease, 296 trilogy of Daubert, 74–75
TLV. See threshold limit values TRIN. See True Response Inconsistency scale
TMD. See temporomandibular disorder tripod, 40–41
toluene, 283, 287t true negatives, 10
Tomlin v. Holecek, 33–34 True Response Inconsistency scale (TRIN), 132
TOMM. See Test of Memory Malingering T-scores, 43
TOPF. See Test of Premorbid Functioning TSI. See Trauma Symptom Inventory
topographical mapping, 165 TTFUQ. See Task Force for Test User Qualifications
Toronto Test of Acute Recovery After TBI, 266 21-Item Test, 122
toxic exposure, neuroimaging for, 169–70 type I error, 28
toxic mold, 283, 346–48
TPO. See third-party observations UGPPA. See Uniform Guardianship and Protective
Trail Making A, 7 Proceedings Act
for competency, 463t ultimate issue, 448
for neurotoxic injury, 293 undue influence, 430–31
Trail Making B, 6, 7, 14 Uniform Guardianship and Protective Proceedings Act
for competency, 463t (UGPPA), 415
for malingering, 124 United States v. Andrews, 466
for MTBI, 239, 243 United States v. Cameron, 84–85
for neurotoxic injury, 293 United States v. Dubray, 478
for PDDS, 414 United States v. Jose Santos-Bueno, 87–90
for TBI, 273 United States v. Rinchack, 465
Trail Making Test, 13, 266 United States v. Segna, 478
transcutaneous electrical nerve stimulation United States v. Sullivan, 478
(TENS), 334 upsetting the witness, 55
trauma-focused cognitive behavioral therapy
(TFCBT), 389 VA. See Department of Veteran Affairs
Trauma Symptom Inventory (TSI), 377–78 Validity Indicator Profile (VIP), 123
traumatic brain injury (TBI). See also mild traumatic brain Validity Quotient (VQ), 47
injury; moderate TBI; pediatric TBI; severe TBI validity threats, 41
AUC and, 134 Variable Response Inconsistency scale (VRIN), 132
chronic pain with, 302 vegetative state, 269
classification of, 261–62 Verbal IQ, 7
course of recovery from, 263–65 Verbal Paired Associates, 125
Digit Span for, 128–29 Verbal Selective Reminding Test, 6, 14
FBS and, 133–35, 137t, 138 MTBI and, 239, 250
fMRI for, 167–69 verbal working memory, 167–68
hindsight bias with, 5–6 very low birth weight (VLBW), 179–83
insanity defense and, 479–81 very preterm birth (VPTB), 179–83
malingering and, 119, 124, 125 VFD. See Benton Visual Form Discrimination
MDSM for, 480 Victoria Symptom Validity Test, 122
534 index
videotaping Wechsler Memory Scale-Third Edition (WMS-III), 13
informed consent for, 111–12 raw data from, 104
of neuropsychological evaluation, 33t weight, 51–52
Vietnam, 369 Westbrook v. Arizona, 452–53
Violence Risk Appraisal Guide (VRAG), 485 Western Aphasia Battery, 293
VIP. See Validity Indicator Profile Whalem v. United States, 455
Visual Number Search Test, 266 whiplash-associated disorder (WAD), 332
Visual Reproduction, 125 Whitaker v. Parker, 71
VLBW. See very low birth weight white matter (WM), 179
Vocabulary Subtest, 16 HIE and, 184, 188
for malingering, 124 IPS and, 188
for neurotoxic injury, 293 neurotoxic injury and, 290
voir dire, 52–53 pediatric TBI and, 212
VPTB. See very preterm birth VLBW/VPTB and, 180
VQ. See Validity Quotient WHO. See World Health Organization
VRAG. See Violence Risk Appraisal Guide Wide-Range Achievement Test-Revised (WRAT-R), 463t
VRIN. See Variable Response Inconsistency scale Wieter v. Settle, 450, 464
VSVT, 149 Williams v. CSX Transportation Inc., 78
Wilson v. United States, 464–65
WAD. See whiplash-associated disorder Winnans v. N.Y. & Erie Railroad Co., 71
Wade v. United States, 478 Wisconsin Card Sorting Test (WCST), 6, 52, 124, 136
WAIS-III. See Wechsler Adult Intelligence Scale, for malingering, 125, 130–31
Third Edition for MTBI, 250
WAIS-IV. See Wechsler Adult Intelligence Scale, for neurotoxic injury, 293
Fourth Edition Wisconsin Failure-to-Maintain Set (FMS), 125, 125t
WAIS-R. See Wechsler Adult Intelligence Scale-Revised WM. See white matter
war, 244, 369 WMS-III. See Wechsler Memory Scale-Third Edition
MTBI and, 244 WMS-R. See Wechsler Memory Scale-Revised
Washington v. Harper, 467 WMT. See Word Memory Test
watershed pattern, 187 Word Choice Test, 125
WCST. See Wisconsin Card Sorting Test Word Memory Test (WMT), 122
Wechsler Adult Intelligence Scale, Third Edition for deception, 171–72
(WAIS-III) FBS and, 138
for chronic pain, 315 for malingering, 117, 129
for malingering, 124 for PCS, 248
for neurotoxic injury, 293 Working Memory Index, 7
Wechsler Adult Intelligence Scale, Fourth Edition work product rule, 491
(WAIS-IV), 7, 16 World Health Organization (WHO), 232–33, 241
for chronic pain, 315 neurotoxic injury and, 292
for malingering, 125 on solvents, 281
for neurotoxic injury, 293 WRAT-R. See Wide-Range Achievement Test-Revised
for TBI, 273 wrongful disclosure, 91–93
Wechsler Adult Intelligence Scale-Revised (WAIS-R), 8, wrongfulness, 477–79
14, 16–17
for competency, 463t X-ray, 333
malingering and, 119
MTBI and, 236 Youtsey v. United States, 446
for PDDS, 414
Wechsler Intelligence Scale for Children—Fourth zealous advocacy
Edition, 220–21 admissibility and, 79
Wechsler Memory Scale-Revised (WMS-R), 6, 13, 17 vs. objectivity, 26–27
for competency, 463t zero-order validity study, 28
malingering and, 119 Zoloft. See sertraline
MTBI and, 236 z-scores, 43