Acta Psychiatr Scand 2013: 127 (Suppl. 441): 147 2012 John Wiley & Sons A/S.

& Sons A/S. Published by Blackwell Publishing Ltd

All rights reserved ACTA PSYCHIATRICA SCANDINAVICA
DOI: 10.1111/acps.12038

Rediscovering catatonia: the biography of a

treatable syndrome
Fink Max. Rediscovering catatonia: the biography of a treatable Max Fink
syndrome. Department of Psychiatry and Neurology Emeritus, Stony
Brook University, Long Island, NY, USA
Objective: Catatonia, a disorder of movement and mood, was described
and named in 1874. Other observers quickly made the same recognition.
By the turn of the century, however, catatonia was incorporated as a
type within a conjured syndrome of schizophrenia. There, catatonia has
lain in the psychiatric classication for more than a century.
Method: We review the history of catatonia and its present status. In
the 1970s, the tie was questioned when catatonia was recognized among
those with mood disorders. The recognition of catatonia within the
neuroleptic malignant syndrome oered eective treatments of high
doses of benzodiazepines and electroconvulsive therapy (ECT), again
questioning the tie. A verifying test for catatonia (the lorazepam
sedation test) was developed. Soon the syndromes of delirious mania,
toxic serotonin syndrome, and the repetitive behaviors in adolescents
with autism were recognized as treatable variations of catatonia.
Results: Ongoing studies now recognize catatonia among patients
labeled as suering from the Gilles de la Tourettes syndrome, anti- Key words: schizophrenia; treatment; diagnosis;
classification; catatonia; tonic immobility
NMDAR encephalitis, obsessivecompulsive disease, and various
mutisms. Max Fink, 23 Spring Hollow Road, PO Box 457, St.
Conclusion: Applying the treatments for catatonia to patients with these James, NY 11780, USA.
E-mail: mfink@attglobal.net or max.fink@stonybrook.edu
syndromes oers opportunities for clinical relief. Catatonia is a
recognizable and eectively treatable neuropsychiatric syndrome. It has
many faces. It warrants recognition outside schizophrenia in the
psychiatric disease classication. Accepted for publication October 4, 2012

Introduction: liberating catatonia from

schizophrenia
The ultimate court of appeal is observation and experi-
ment, and not authority. Thomas H. Huxley (1)
For an illness to be eectively treated, it has rst
to be recognized; only then can physicians apply
their knowledge and skills. Catatonia is an identi-
able syndrome of abnormal movement and emo-
tion rst described by the German psychiatrist
Karl Kahlbaum in 1874 among the patients in his
psychiatric asylum. His description was soon
armed by other physicians and broadly accepted
as an identiable syndrome among psychiatric dis-
orders. Within two decades, another German psy-
chiatrist, Emil Kraepelin also recognized
catatonia. But Kraepelin included catatonia and
two other syndromes, hebephrenia and paranoia,
as markers within a grand scheme that he labeled
dementia praecox (later, schizophrenia).
Kraepelin was a prolic writer of textbooks
widely regarded as gospel truth. As a result, for
more than a century, catatonia was buried within
schizophrenia as one of many types. To this day,
when clinicians recognize catatonia, they immedi-
ately see schizophrenia and reexively prescribe
neuroleptic drugs even when the signs of psychosis
are absent. The Kraepelin equation of catato-

1
Max Fink
nia = schizophrenia dominates clinical thought
and writing. Such prescription is not helpful;
indeed, it is often harmful as neuroleptic drugs
often precipitate a toxic syndrome in patients with
catatonia that is recognized as the neuroleptic
malignant syndrome. More egregious, however, is
the failure to prescribe the specic and eective
treatments for catatonia as they are not recognized
as treatments for schizophrenia. This mistaken
conception has plagued patients for more than a
century and has distorted the classication of psy-
chiatric diseases.
These chapters of Rediscovering Catatonia trace
the biography of catatonia, relate how it is identi-
ed, describe its many forms, look forward to
identifying other forms of catatonia that are now
not recognized and inadequately treated, discuss
the fear hypothesis that explains catatonias origin,
and discuss catatonias history within psychiatric
classications with the present promise of relief in
the DSM-5 iteration.
Catatonia is a syndrome of body movement and
speech related to disorders of emotion. Mutism
(not speaking), negativism (refusing commands),
posturing and rigidity (holding unusual bodily pos-
tures), and repetitive speech and acts (repeating
meaningless words, phrases, or motor movements,
often self-injurious) are its main signs. The charac-
teristic delusions, hallucinations, and disturbances
in thought that are central to the image of schizo-
phrenia are not features of catatonia. Catatonia is a
distinct syndrome that in the past half century has
been increasingly reported outside schizophrenia.
Eective treatments for catatonia were devel-
oped in the 1930s rst the barbiturates and then
electroconvulsive therapy (ECT). In the 1980s, the
barbiturates were replaced by the benzodiazepines
for clinical use. Neither the sedative drugs nor
ECT are considered eective in schizophrenia and
are therefore not applied in cases of catatonia
when it is presumed to be a manifestation of
schizophrenia. Inadequate treatment and pro-
longed illness result when this error of diagnosis is
made. The neuroleptic drugs that are promoted as
treatments for schizophrenia are ineective for cat-
atonia; indeed, they increase toxicity and occasion-
ally lead to death.
I was trained as a neurologist and psychiatrist
and began my academic career as a researcher in
1954. Like many of my peers, only occasionally
did I recognize catatonia in practice. I was not
awakened to the extent of catatonia until the 1980s
when as an Attending Physician at the University
Hospital of Stony Brook University on Long
Island I supervised the care of hospitalized patients
and its ECT treatment unit.
2
Neuroleptic drugs such as chlorpromazine and
haloperidol, the drugs used to relieve psychosis,
aect the bodys motor functions. They induce
tremors, peculiar rhythmic movements of mouth
and tongue (dyskinesia), and stien and slow body
movement (rigidity). They induce acute toxic states
of fever and delirium that are accompanied by the
catatonia signs of mutism, repetitive acts, and
rigidities. These toxic signs were increasingly rec-
ognized during the 1970s as the reports of fatalities
grew; by 1980, the toxic consequences were named
the neuroleptic malignant syndrome (NMS).
By 1984 at Stony Brook, we had identied three
patients with NMS, and each exhibited signs of
catatonia. We applied the promoted treatments of
the time; one slowly recovered but two did not.
The lifesaving benets of ECT in these conditions
had been described in 1952 and repeatedly con-
rmed (2). When the two patients who had not
responded to medications were treated with ECT,
they recovered quickly (3).
Although we lacked understanding of the causes
of malignant catatonia, we did know that ECT
relieved it. Relatively few hospitals had ECT treat-
ment units, but all could prescribe agents like bro-
mocriptine that increased the brain levels of the
dopamine neurotransmitter that is directly inhib-
ited by neuroleptic drugs. A national debate
ensued, carried on for more than two decades,
whether the neuroleptic-induced malignant syn-
drome was an abnormality of dopamine metabo-
lism and best treated with dopamine agonists or an
example of malignant catatonia that was best trea-
ted with ECT. The debate focused my interest in
catatonia (46).
Two former students, Michael A. Taylor and
Richard Abrams, had been instrumental in report-
ing catatonia in patients with manicdepressive ill-
nesses and in 1976 had questioned the teaching
that catatonia was necessarily an aspect of schizo-
phrenia (7, 8). In 1990, I began to collaborate with
Taylor, and in our rst essay, we argued that cata-
tonia was best seen as a distinct syndrome indepen-
dent of schizophrenia, arguing for their separation
(9). At the time, the Diagnostic and Statistical
Manual of psychiatric disorders of the American
Psychiatric Association was undergoing its fourth
revision, and we urged that catatonia be separated
from schizophrenia. To accommodate our view,
although still beholden to the dominant perspec-
tive of catatonia as a form of schizophrenia, the
DSM-IV committees added a class of Catatonia
secondary to a medical condition with a distinct
code of 293.89 (10).
Our interest in catatonia its main features,
how it is found, in what forms, and how best trea-

Fig. 1. Average annual number of citations marked as cata-
tonia in each 5-year period.
ted led us to publish the textbook Catatonia:
A Clinicians Guide to Diagnosis and Treatment in
2003 (11) and to urge again that catatonia war-
ranted a home of its own in the classication (12).
This publication was the rst text on catatonia
since the original publication by Karl Kahlbaum
130 years earlier (13).
Much has changed since then catatonia is
more often recognized, eective treatments are
commonly applied, favorable outcomes are
increasingly reported, and death rates for medica-
tion-induced neurotoxic syndromes have fallen.
Increasing numbers of citations to catatonia in
the medical literature are reected in the NIH Pub-
Med indices (Fig. 1).
Two new forms of catatonia have been recog-
nized since our publication. In 2007 the syndrome
of anti-NMDAR encephalitis was described as a
neuropsychiatric disorder of diverse manifestations
connected to an autoimmune etiology. More than
70% of the diagnosed patients exhibit catatonia
that is neither recognized nor properly treated.
Instead, patients are subjected to intensive searches
for hidden tumors, oered surgery if a silent tumor
is recognized, and prescribed potent steroids,
immunotherapy, and plasma exchange with
minimal benet.
A more dramatic impetus to tracing this history
has been the recognition that the self-injurious
behaviors of children and adolescents suering
from autism spectrum disorders may be signs of
catatonia that are responsive to catatonia treat-
ments. The recognition of catatonia in these disor-
ders and demonstrations of the ecacy of catatonia
treatments are largely the eorts of Drs. Lee Wach-
tel at Johns Hopkins Medical Center and Dirk
Dhossche at the University of Mississippi (14).
Rediscovering catatonia
As the connection to schizophrenia has been
loosened, catatonia is increasingly recognized
among the childhood disorders of Gilles de la Tou-
rettes syndrome, obsessivecompulsive disorder,
and diverse mutisms the selective or elective
and the pervasive refusal syndrome recognized in
the classication of diseases. Catatonia is also seen
in patients with post-traumatic stress disorders,
passive acceptance of rape assault, and fear-
induced freezing in urban violence and military
disasters. These connections support a hypothesis
of catatonia as a residual response to fear of immi-
nent doom from the time when humans feared
predators (15).
Most psychiatric disorders are identied by
the presence of symptoms from symptom check-
lists. No laboratory tests, common in clinical
medicine, are used. But catatonia is among the
few psychiatric diagnoses that are operationally
dened. In the chapters that follow, catatonia is
dened as published by Michael Taylor and
myself in 2003: Patients who exhibit two or more
motor signs of catatonia (recognized in Catatonia
Rating Scales) for more than 24 h and that
quickly improve with test doses of lorazepam are
presumptively diagnosed as suering from catato-
nia. Recovery of the illness with relief of the
motor and vegetative signs after treatment with
benzodiazepines and ECT validates the diagnosis.
An operational diagnostic procedure assures
recognition of the syndrome and oers patients
typically eective and prompt relief. For those
who are misidentied as catatonic when they are
not, the principal hazard is the delay in instituting
a more appropriate treatment, if there is one. The
benzodiazepines are not hazardous, and the test
doses are well within clinical experience for safety.
Although ECT is widely stigmatized as brain dam-
aging and capable of erasing memories, these haz-
ards pale before the risks to life inherent in the
more malignant forms of catatonia and the pro-
longed illness that follows inappropriate diagnosis
and ineective treatment.
The American Psychiatric Association DSM-5
Psychosis Work Group presented its recommenda-
tions on catatonia online in May 2012, listing
many proposed changes. When these are published
in DSM-5, the much needed separation of catato-
nia from schizophrenia will be accomplished.
Much will then need to be done in professional
and public education to assure recognition and
treatment of catatonia as an independent psychiat-
ric syndrome.
3
Max Fink

Chapter 1: catatonia is discovered

In some ways disease does not exist until we have agreed mania and melancholia, the stupidities (mental
that it does by perceiving, naming, and responding retardation), epilepsies, and the dementias of
to it. CE Rosenberg 1986 (16) aging, as a result of head trauma or alcoholism.
Among the patients were some who postured
Catatonia is a syndrome of dysfunctions in
and stared, frequently mute but occasionally repet-
movement and emotion. It was rst culled in the
itive in speech and movement, occasionally
1870s from the welter of behaviors that are com-
appearing in stupor as if dead, or in delirious furor
mon in every asylum. Unlike diseases of a single
and unresponsive to painful stimuli. In 1874, Karl
body organ and narrowly dened functions,
Kahlbaum, the 46-year-old director of a private
abnormal behaviors encompass the whole organ-
psychiatric sanitarium in the German town of
ism. What did practitioners see when they entered
Gorlitz, described his experience with such patients
an asylum in the mid-1800s and tried to make
in a small book of 104 pages that he labeled Die
sense of what they encountered?
Katatonie. It was his third attempt to classify the
The entrance door is locked, and one of a ring of
behaviors of his patients (17).
large keys is used to enter. The moment the door
From an extensive clinical practice, Kahlbaum
opens, the entrance is lled with a cacophony of
described 26 case histories that included disabling
cries and the pungent odors of urine, sweat, and
disorders of movement and speech among their
the medicine paraldehyde (a liquid sedative with
symptoms. The patients were immobile and postur-
the odor of vinegar). Loud voices, some sing-song
ing, remaining in one position for hours; or moving
and some cackling, and occasional screams ll the
continually, pacing, or hitting a wall or themselves;
entranceway. Some patients are tied down on a
or standing and staring, unblinking, repeating
pallet, while others sit motionless seemingly una-
words or phrases over and over again, sometimes
ware of the activities around them, unresponsive to
in whispers or in repetitive shouts. They had other
questions and even to painful stimuli; and yet, oth-
signs of mental illness melancholia (depression,
ers are rocking, posturing Christ-like, staring, and
withdrawal to stupor, and suicide risk), mania
pacing. When they do respond, many are sad and
(continuous movement, grandiosity, delirium), psy-
despondent, or frightened, or grandiose, or angry.
chosis (peculiar thoughts that brought forth unu-
Speech may be normal, but more often it is repeti-
sual speech), and dementia (poor memory,
tive and meaningless. Occasionally a patient has an
disorientation, poor self-care). Many were also suf-
epileptic seizure.
fering the systemic diseases of syphilis, tuberculo-
Trying to distinguish causes and predict the
sis, or epilepsy. Onsets and courses of illness
course of an illness in an individual patient was chal-
uctuated with sudden changes in retardation and
lenging. Over time, the behaviors of individual
withdrawal, or mania and excitement, or delusional
patients may remain the same day after day but more
and suicidal thoughts, so much so that one school
often the symptoms evolve, sadness and despon-
of professional thought described the behaviors as
dency alternating with excitement and mania, for
expressions of a single disease of many causes.
example, deteriorating to ever poorer self-care, until
Before specic syndromes were described, the vari-
dementia and a vegetative state ensues.
ations in symptoms seemed to appear and disap-
How was one to extract a recognizable disease
pear but no single pattern was discerned. The term
from this welter of dysfunctions? No help was
Einheitspsychose unitary psychosis was in
likely to be gleaned from studies of the brain after
common use until Kahlbaum and his colleague
death, either in the search for abnormal tissues in
Heckers description of hebephrenia and catatonia
the sliced brain or cellular changes in stained brain
and Kraepelins images of dementia praecox and
tissues, even when examined with the nest micro-
manicdepressive insanity were accepted.
scopes. At the time, dementia paralytica had been
Kahlbaum describes a young man admitted to
described as the neurological consequence of syph-
the sanitarium who becomes intensely fearful when
ilis. It was recognized during life by progressive
he is told that he has syphilis. (This case record is
paralyses accompanied by grandiose thoughts,
paraphrased from Case #2 of the English transla-
impaired memory, and silly comments. After
tion of the Kahlbaum text by George Mora on the
death, thickened brain coverings were found as
publications 100th anniversary. Mora was a pedi-
evidence of the fatal disease. But such direct patho-
atric psychiatrist lecturing at Yale and New York
logical evidence was the exception. Also demar-
Universities.)
cated and generally accepted at the time were

4

A 33-year-old peasant terminates a love aair, becomes
depressed and is reluctant to talk or participate in social
activity. His depressed moods become constant after he
develops a syphilitic infection. Muscular twitching in the
face and extremities and severe tonic contractions of the
back muscles follow. He retires to his bed without inter-
est in his surroundings; his eyes remain shut, refuses to
reply when addressed or even to speak. He eats little. On
admission to the sanitarium he is inactive, lies prone in
bed, giving no answer to questions put to him. He main-
tains any posture he is made to assume for long periods.
It is possible to place his extremities in the most extrava-
gant postures that he changes gradually to an original
passive position. When induced to walk, he moves for-
ward slowly, leaning to the right and extending his right
leg stiy. Sensory responses are greatly reduced over the
entire body with little reaction to needle pricking.
Three months later he suddenly begins to speak inces-
santly, expressing a few monotonous phrases over and
over as Love is God, Love, Love, Love is God, Love is
God with permutations, adding short phrases as Is it
so? or I say, spoken softly or at times shouting loudly.
While voicing these phrases he sometimes lies at on his
back; at times the upper part of his body is raised and
head bent stiy back. He becomes hoarse, speaking
softly with intermittent shouting. This condition per-
sisted with brief interruptions. He died a year later after
contracting tuberculosis (13).
A detailed analysis of Kahlbaums cases was
undertaken by Daniel Rogers who nds 25 case
vignettes (18). Rogers analyzes 21 vignettes for
motor signs characterized as signs of catatonia.
Kahlbaum recognized 17 motor signs. Since then,
additional signs, altogether about 40, have been
listed in Catatonia Rating Scales. The most recent
addition to the recognized catatonia signs is the
repetitive self-injuries seen in children and adoles-
cents suering from autism spectrum disorders
(19).
Consider the eort entailed by Kahlbaums
attempt at classication. No catalog of psychiatric
diseases existed nor had criteria been described
with which to label an illness or to predict a per-
sons fate. No eective treatments were known,
and persons recovered, remained ill, or died inde-
pendent of physicians eorts. Some patients sud-
denly recovered after a severe systemic infection or
after an epileptic seizure and could leave the asy-
lum. At best, physical restraints and sedation with
opiates were prescribed for the unruly, and feeding
was forced to maintain life in the stuporous
and negativistic. By providing a clean, protected
home, the physicians hoped that recovery would
be spontaneous.
Rediscovering catatonia
Attempts at classication were being made in
other branches of medicine, especially in bacteriol-
ogy. Unique infectious diseases were identied by
the patterns of clinical symptoms and the course of
the illness. Pathogens were identied in body u-
ids, and illnesses were labeled by the name of the
invading pathogen, oering opportunities to test
treatments in homogeneous samples of one illness
type. These eorts in clinical medicine were models
for Kahlbaum. He saw his eorts as similar to
those that described the motor disorders of tabes
dorsalis, the loss of motor control of the limbs
when syphilis aected the spinal cord and the para-
noia and dementia of dementia paralytica. Kahl-
baums descriptions and demarcations of catatonia
were so well dened that others soon recognized
similar cases.
Kahlbaums first classification of psychiatric disorders
Born in eastern Germany on December 28, 1828,
Kahlbaum had been schooled at the universities of
Konigsberg, Wurzburg, and Leipzig. He was
awarded an MD in Berlin with a thesis on the
anatomy and histology of the intestinal tract of
birds in 1854. After joining the faculty at Konigs-
berg, he established training courses in psychiatry
for medical students and published a monograph
on sensory delusions. By 1863, he had developed a
complex glossary of mental disorders that he pub-
lished as Die Gruppierung der psychischen Krankhe-
iten und die Einteilung der Seelenstorungen (20).
He listed many peculiar behaviors and clustered
the symptoms into disorders according to their
principal features (depression, mania, psychosis)
and course of illness (continuous, recurrent, and
episodic). In an obsessively detailed organization,
he gave each form a unique name. Vesania typica
anticipated the manicdepressive illness of Kraepe-
lin and vesania progressiva described a deteriora-
tion in mood to delirium and dementia. Vecordia
were disorders beginning in puberty, including
paraphrenia hebetica, a disorder that later was
labeled hebephrenia. A disorder in mood labeled
dysthymia exhibited a retarded form dysthymia
atra and an agitated form, dysthymia elata. In
that burst of creativity, he had not yet described
the concept of catatonia.
Kahlbaums rst classication was lled with
obsessive details and not based on any logical prin-
ciple that could be explained to others, so it is no
surprise that this creation was deemed too complex
to be understood and was not accepted by his col-
leagues. In similar fashion, the iterations of the
DSM classication describe illnesses without a
5
Max Fink
basis in biological or medical principles. The class
names and descriptions are committee-driven, and
depending on the skills and enthusiasm of vocal
leaders, a diagnosis is either included or eliminated
from the accepted list. The criteria are descriptive
based on the presence of symptoms, with some
attention to course. The few biological criteria that
have been developed are excluded.
Kahlbaum left the university faculty in 1866 to
become a sta physician at the Reimer Sanitarium,
a private sanitarium in Gorlitz, a village in eastern
Germany that bordered Poland. A year later, he
bought the hospital, became its director, and main-
tained it until his death in 1899.
In his personal life, Kahlbaum was liberal in
politics, ascetic in not using tobacco or alcohol,
regular in church attendance, and active in the
church choir. He traveled frequently to meetings
and to art museums. In 1866, he married the cou-
sin of his colleague Ewald Hecker. The union pro-
duced three sons and one daughter. Kahlbaums
wife died in 1884 and he remarried in 1888, pro-
ducing two more sons. After his death, his son
Siegfried, who had trained in psychiatry with Carl
Wernicke, directed the sanitarium until 1943 when
it was taken over by the government for military
uses.
Hebephrenia
In 1866, the same year that he became hospital
director, Kahlbaum was joined by Ewald Hecker
as a sta physician. Together, they continued an
interest in classication. In Die Gruppierung
Kahlbaum had described a syndrome of para-
phrenia hebetica, and together, they described
the syndrome that became a model for the
description of catatonia. It began as a disorder
in thought and speech with an onset in adoles-
cence. By early adulthood, it had progressed to
dementia. Child-like, often imbecilic behaviors
limited the ability of the patients to take part in
normal schooling and even in adequate self-care.
In 1871, Ewald Hecker described these condi-
tions in seven cases in the 35-page essay Die
Hebephrenie (21).
The illness begins its progressive course with
melancholia and mania between the ages of 18 and
22 years. Over time, thinking becomes confused
and speech becomes silly and repetitive, a course
that ends in dementia. Hecker said:
In most cases the disease apparently begins as a sequel
to a profound alteration in emotions with decidedly mel-
ancholic symptoms.
6
The melancholia expresses itself rst as a sadness and
depression of mood that gradually consolidates into
delusions ending in a brooding persecutory mania or
a delusion of injury. A shallowness of aect appears
Side by side with his morbid lamentations of his terrible
misery [the patient] frequently cannot suppress an
impulse to laughter and silly jokes.
Of special importance are disturbances of form [of
speech] First there is a peculiar deviation from logical
sentence formation [with] a noticeable tendency to
remain stuck on a topic once he has taken it up
The mode of speech and expression sinks well below
his level of education [and] we see a propensity to gush,
a preference for sentimental descriptions, a seemingly
poetic diction, and consequently an overow of empty
misshapen phrases.
On etiology, Hecker wrote:
the rst striking fact is that we are mostly (although not
always) dealing with individuals who have been slightly
retarded in their physical and in their mental develop-
ment from early on a certain weakness of intellect,
laziness, and inability to do mental work is already
noticed in childhood, but this is not as extreme or as
noticeable as in idiotism.
The condition was commonly recognized among
patients in the asylums. A few decades later, hebe-
phrenia, like catatonia, was co-opted by the Ger-
man psychiatrist Emil Kraepelin within his
conjured disorder of dementia praecox. Hebe-
phrenia was the principal form of the syndrome
later labeled schizophrenia. In successive psychiat-
ric disease classications, hebephrenia has often
been relabeled. The present term disorganized
schizophrenia is one of the ve recognized types
of schizophrenia (22, 23).
At one time, hebephrenia was frequently seen in
chronic care institutions. The illness was consid-
ered progressive, poorly responsive to treatments,
often ending in silly behaviors and dementia.
Patients became lifelong wards of society as they
were unable to care for themselves. The processes
of deinstitutionalization that closed the sanitaria in
the last quarter of the twentieth century shifted
patients with hebephrenia to adult homes and
chronic disease institutions.
Catatonia
As Hecker and Kahlbaum were collaborating at
Gorlitz, we can picture their discussions of each
patient and their search for other examples of
hebephrenia. And just as Hecker was riveted by

hebephrenia, Kahlbaum focused his attention
upon what is now recognized as catatonia. His
rst public discussion of catatonia was before an
audience at the University of Konigsberg in
1866 (24). At Innsbruck 3 years later, he
described two cases of melancholia with stupor
that exhibited the signs of catatonia. The discus-
sion after his presentation was sparse, but a
published comment noted that enlarging the
classication with a new diagnosis focused on a
muscular tension psychosis would not be help-
ful. (25)
In 1874, 3 years after Heckers 1871 article on
hebephrenia, Kahlbaum formally introduced
catatonia to psychiatry. His description is valid
today.
Catatonia is a brain disease with a cyclic, alternating
course, in which the mental symptoms are, consecu-
tively, melancholy, mania, stupor, confusion, and even-
tually dementia. One or more of these symptoms may be
absent from the complete series of psychic symptom
complexes. In addition to the mental symptoms, loco-
motor neural processes with the general character of
convulsions occur as typical symptoms.
Lacking eective treatment, Kahlbaum observed
the full course that marked the disease:
The typical signs of the condition termed atonic melan-
cholia [a depressive illness with the characteristic motor
signs of catatonia] may be described as a state in which
the patient remains entirely motionless, without speak-
ing, and with a rigid, masklike facies; the eyes focused
at a distance; he seems devoid of any will to move or
react to any stimuli; there may be fully developed
waxen exibility, as in cataleptic states, or only
indications, distinct, nevertheless, of this striking
phenomenon.
The motor-inhibited form of the illness is distin-
guishable from its excited forms, often resolving
dramatically and suddenly, a resolution that
clearly distinguished catatonia from an association
with schizophrenia.
The general impression conveyed by such patients is one
of profound mental anguish, or an immobility induced
by severe mental shock; it has been classied either
among the states of depression (which explains the term
atonic melancholia) or among the conditions of feeble-
mindedness (stupor or dementia stupida); others have
regarded it as a combination of the two.
Here Kahlbaum oers a clue to his thinking of
the cause of catatonia. His patients appeared to be
astonished or thunderstruck. The syndrome
appeared:
Rediscovering catatonia
after very severe physical or mental stress such as a
terrifying experience. The patient remains motionless,
without speaking, and with a rigid masklike facies, the
eyes focused at a distance . The general impression
conveyed is one of profound mental anguish, or an
immobility induced by severe mental shock (13).
Citing fear as central to the syndrome, Kahl-
baum titled his book Die Katatonie, oder das Span-
nungs-Irresein, translated as Catatonia, the
tension insanity.
Other observers wrote that a subject suering
Kahlbaums disease might lay like a log of wood,
stretched out, able to behold with his eyes but
unable to speak a word for several days. The
malady occurs suddenly and he stops as if he were
frozen, his eyes open, xed and motionless (26).
On recovery, patients say that they desired to
speak but were unable to do so, sensing impending
doom. Persons in catatonic stupor are frozen,
petried, and experience extreme fear (27).
Recent authors also describe patients as giving the
appearance of intense anxiety (2830).
Kahlbaum compared his image of catatonia to
what at that time had recently been demarcated as
dementia paralytica, the general paralysis of the
insane associated with syphilis:
In this newly dened group of disorders, similar to gen-
eral paralysis of the insane (GPI) with or without
delusions of grandeur clinical changes in the locomotor
apparatus form the main and typical features of the dis-
ease; in addition, each disease (GPI and this disease)
exhibits manifold patterns of symptoms. In GPI the par-
alytic components are of many varying grades of severity
and type; one or other may be absent in any particular
case. In the same way as in GPI, the spastic signs in
the newly described clinical form of the disease are also
manifold and varied These muscular symptoms dis-
play alterations in muscular tone and I would like to
name this disease entity the tonic mental disorder (Span-
nungs-Irresein) or vesania katatonica (catatonia) (13).
In this progressive understanding, we see Kahl-
baum identifying the principal signs of the disor-
der, the emotional basis, and the progressive
course. His model was the developing understand-
ing of neurosyphilis. Although no connection to an
infection had been made, a search for brain lesions
in anatomy and histology for each psychiatric dis-
order was ongoing. New techniques for staining
brain tissues identied dierent cellular forms
(e.g., neurons and glia), and many authors
searched for brain lesions and cell forms to associ-
ate with behaviors. Kahlbaum was not enthusiastic
about this search:
7
Max Fink
This anatomicopathological work produced much valu-
able material but contributed nothing to the basic views
on the origin of mental illness or on the anatomical locus
of their diverse and signicant manifestations; the view
is now spreading that only comprehensive clinical obser-
vation of cases can bring order and clarity into the mate-
rial by using the method of clinical pathology. It is
futile to search for an anatomy of melancholy or mania,
etc. because each of these forms occurs under the most
varied relationships and combinations with other states,
and they are just as little the expressions of an inner
pathological process as the complex of symptoms called
fever. How wrong it inevitably was to expect patho-
logical anatomy alone to reform the obsolete psychiatric
framework.
In the nal chapter, Kahlbaum, nding no bene-
cial treatments, argued for supportive and non-
punitive hospital care at a time when the debilitat-
ing treatments of bleeding, purging, and dunking
sped many persons to untimely deaths. An interest
in electricity as a source of treatments for psy-
chiatric diseases both the symptoms of the
patients and the characteristics of electricity were
ephemeral led to many imaginative experimental
applications. Kahlbaum ends his discussion of
treatments, possibly anticipating the role of
electricity:
On the other hand it seems we have methods of very
great therapeutic importance in faradic and galvanic
electricity, although for the time being the indications
have not yet been worked out, and in many cases the
action might be explained more on the basis of mental
than of physiopathological eects.
The catatonia that we envision today is not the
result of structural tissue changes (as in strokes,
tumors, traumatic injury) nor infections or singu-
lar systemic disorders, but as extensions of physio-
logical functions. The signs of catatonia are not
novel behaviors but exaggerations of every
humans repertoire of tics, mannerisms, compul-
sions, rituals, speech interjections, and postures.
So long as these habits do not interfere with nor-
mal living, the subjects and the observers adjust,
considering the peculiarities as part of the individ-
uals personality. When the changes in behavior
are acute and by their severity impede normal
living, an illness is perceived and relief is sought.
Many patients, including some severely ill, recover
normal functions and do so rapidly, without per-
manent eects, an indication that the catatonia
motor signs result from variations in physiology
and not from changes in structures or tissues. We
do not view catatonia as similar to neurosyphilis
as Kahlbaum conjectured. But when the repetitive
8
behavior is self-injurious, when the withdrawal is
to stupor or to delirious mania, and when the
changes in autonomic activity are severe, catato-
nia becomes life-threatening. In most instances,
the signs are well tolerated, and with the eective
treatments known today, the subject returns to
the state of functioning before the onset of the
illness.
Kahlbaum after catatonia
As a hospital director, Kahlbaum shared the belief
in moral treatment for the psychiatric ill the
benevolent, supportive, non-punitive, socially
encouraging environment that emphasized rehabil-
itation measures. By 1887, his hospital consisted of
18 buildings with 130 patient rooms; large dining
and recreation halls; theater, library, and reading
rooms; tennis and croquet courts, and an indoor-
heated gymnasium, all in a park-like setting with
gardens and a farm. He developed a special child
treatment unit, the Padagogicum, with school-
rooms, employed trained teachers, and specialists
in handicrafts and educational programs. His
asylum became a model for the care of children
and adolescents.
Kahlbaums interest in the psychiatric care of
children was enduring. In 1883, he published an
essay on child psychiatry, rening the concept of
hebephrenia and arguing for special treatment for
juveniles, much as he had developed in his Pada-
gogicum. His rened description of the condition
[hebephrenia or pubertal neurosis], wrote Ernest
Harms in 1962,
must be designated the rst realistically established con-
cept of child psychiatry. (31)
What is Kahlbaums place in the history of
psychiatry? In celebrating the centenary of the
publication of Die Katatonie, Rafael Katzenstein
cited Kahlbaum as
the rst German psychiatrist to systematically elaborate
forms of mental diseases from the pure clinical view-
point. He identied the defects in earlier formulations
[ie, the Einheitspsychose] and sought to organize psychi-
atric states according to observations of onset, course,
and outcome (25).
Late in life, Emil Kraepelin assessed Kahl-
baums role in clinical medicine in this way:
He [Kahlbaum] was the rst to stress the necessity of
juxtaposing the condition of the patient, his transitory
symptoms and the basic pattern underlying his disease.
The condition of a patient may change often and in
diverse ways, with the result that in the absence of other

clues any attempt to rescue him from his plight is
doomed to failure. Moreover, identical or remarkably
similar symptoms may accompany dierent diseases.
Their inner nature may only be revealed through their
progress and termination and, in some instances, at post
mortem.
On the basis of such considerations Kahlbaum sought to
delineate a second pattern of illness similar to that of
[general] paralysis and, like it, including both mental dis-
orders and physical concomitants: catatonia, in which
muscular tension provided a basis for comparison with
[general] paralysis. Although his interpretation is open
to criticism, Kahlbaum deserves credit for having
suggested the right approach. Careful attention to the
progress and termination of mental disorders, informa-
tion gleaned in some instances from autopsies, and
insight into underlying causes have made possible the
juxtaposition of a vast array of evidence and often diag-
nosis on the basis of symptom pattern. We can today
formulate in specic terms what earlier doctors could
surmise but not prove (32).
Kahlbaums work was praised by Karl Jaspers,
a German psychopathologist and author of the
denitive text of psychiatry after Kraepelin:
Kahlbaum formulated two fundamental requirements:
rstly, the entire course of the mental illness must be
taken as basically the most important thing for any for-
mulation of disease entities and, secondly, one must base
Rediscovering catatonia
oneself on the total picture of the psychosis as obtained
by comprehensive clinical observation. In emphasizing
the course of the illness, he added a new viewpoint (33).
By the end of the twentieth century, Kahlbaums
contribution in extracting catatonia from the
welter of altered behaviors was increasingly appre-
ciated and biographies appeared (3436).
In my view, as a clinician, Kahlbaum made the
best of the knowledge of his time and extracted
two clinical entities that are still appreciated by cli-
nicians today. He had the misfortune, however, to
have his work co-opted by a fellow German psy-
chiatrist whose skill as a textbook writer (that went
through eight editions) hid Kahlbaums work
within the shadow of a poorly dened abnormal
behavior syndrome that even today, after more
than a century, lacks any measurable and veriable
characteristics and also lacks eective treatment.
In the past few decades, a few intrepid clinicians
have resurrected Kahlbaums image of catatonia
and rened its characteristics in a way that are
both objectively veriable and eminently treatable.
Present-day clinical skills indicate that many
syndromes that are actually forms of catatonia are
hidden in plain sight. As these are reframed as
treatable aspects of catatonia, the place of Karl
Kahlbaum as a father of modern clinical psychia-
try will be assured.
9
Max Fink

Chapter 2: catatonia disappears

It is true that man is still, as he has always been, subject baums catatonia, and a paranoid psychosis (a
to error; his judgments are often incorrect, his beliefs delusional fear of impending harm) as one disease,
false, his opinions changeable from age to age. But expe- a position that under the later name of schizophre-
rience of error is his best guide to truth, often dearly nia has persisted in psychiatric classications until
bought, and therefore, the more to be relied upon. the present.
Alfred Russel Wallace, 1905 (37) Manicdepressive insanity began later in life,
Kraepelin said, with uctuations into relative
Kahlbaums 1874 account of catatonia was
health and recurrent illness without progressing to
delineated so well that others quickly recognized
dementia. Although he found instances of catatonia
the disorder that he described. Within 3 years, cat-
in both the dementia praecox and manicdepressive
atonia as Kahlbaum delineated was reported in
populations, he marked catatonia as a principal
four patients with depression and mania (38).
sign of dementia praecox. He established a cate-
From New York Citys Wards Island in 1883, cat-
gorical rewall in his system between these two
atonia was recognized in patients with melancholia
disorders, a rewall that persists to this day in the
(39). Four years later, a German report cited cata-
worlds principal psychiatric classications.
tonia in manic patients (40). By 1898, six subtypes
For neither illness did Kraepelin oer dening
of catatonia had been described (41), and catatonia
characteristics. Nor were his descriptions improved
had been distinguished from dementia paralytica
upon in the succeeding century to develop a well-
(neurosyphilis) in a study of 227 psychiatric
dened disease description, or to dene specic
patients (42).
tests, or to identify eective treatments. In psychi-
An active academic industry commenting on
atric manuals, schizophrenia remains a heteroge-
catatonia quickly followed among German,
neous conglomeration of disturbances of speech,
French, and American authors (11). Each eort, in
thought, and aect. Manicdepressive illness has
samples of 112 patients, conrmed Kahlbaums
undergone greater development into two major
descriptions and took a position on whether the
syndromes, one characterized by depressive mood
syndrome was best explained by systemic medical
disorder and one by mania. Each has been divided
or by psychologic mechanisms. As each recogni-
into non-specic overlapping types without den-
tion sharpened the image of the syndrome, catato-
ing characteristics, without eective treatments,
nia became more strongly established as an
and ignoring the extensive evidence that the two
identiable psychiatric entity, making the eventual
syndromes appear in the same subjects as their
development of treatments increasingly likely.
illnesses progress (44).
Then catatonia was recognized by the German
Kraepelin regarded catatonia only as a type
psychiatrist Emil Kraepelin (18561926), the head
within his concept of dementia praecox. The demo-
of psychiatry at Heidelberg and then at Munich.
tion of catatonia from an individual syndrome to
As an asylum physician, Kraepelin cared for
that of a subtype, a marker, and in the present
chronically ill psychiatric patients whose prognosis
classications as a specier of dementia praecox
was poor. In the absence of eective treatments,
has hidden catatonia from recognition as a unique
the illness of many patients ended in dementia. In
syndrome for more than a century. This is in no
the nineteenth-century tradition of the study of
small part a tribute to the enormous inuence
diseases, Kraepelin sought to classify his patients
Kraepelin has had in the history of psychiatry.
illnesses. He adopted Kahlbaums course of
A prolic writer of psychiatric textbooks, Kraepe-
illness as a dening characteristic for his own diag-
lin was the most prominent German psychiatrist
nostic formulations (43). He periodically organized
up to World War I. He published his rst textbook
and re-organized his case records into clusters of
in 1883 (45) with revisions through an 8th edition,
similar symptoms and outcome. After much shuf-
which appeared in four volumes between 1909 and
ing of the le cards describing the observations in
1915. It is little wonder that Kraepelins image of
his patients, by 1899, he described two main
catatonia overwhelmed that of Kahlbaum. Kahl-
groups with dierent courses of illness, dementia
baum published his small book of 104 pages in
praecox and manicdepressive insanity.
1874, but the voices of the many authors who
Dementia praecox, as he described it, was a dis-
endorsed his work were faint compared with the
order in thought, speech, and aect that began in
booming of Kraepelin, Eugen Bleuler, and Adolf
adolescence and progressed to dementia. Kraepelin
Meyer, among many others. It was not until 1973
lumped together Heckers hebephrenia, Kahl-

10

that the English translation of Kahlbaums book
became available and sparked the studies that
found catatonia outside schizophrenia.
Kraepelin received his MD in 1878 and begun
his academic travels rst as Professor at Dorpat
(Estonia) in 1886, then at Heidelberg in 1890. He
moved to Munich in 1903 where he founded a
German Institute for Psychiatric Research with
extensive funds from American philanthropists,
the banker James Loeb, and the Rockefeller
Foundation. The Institute established Kraepelin
and Munich as a world center for biological psy-
chiatric research.
Kraepelin was nurtured in a world that saw
the brain as the seat of psychiatric illness. At the
opposite end of the psychopathology spectrum
stood Sigmund Freud with an emphasis on individ-
ual psychology. Psychiatric symptoms typically
arose from the mental experience of the patient
rather than as a result of a brain disorder, a seduc-
tive paradigm that captivated clinicians interest
especially in the United States. An image of
dementia praecox as a brain disease was replaced
by an image of disorganization induced by child-
hood experiences and memories, best relieved by
individual psychoanalysis, a philosophy enthusias-
tically adopted by Paul Eugen Bleuler (1857
1939).
Bleuler obtained his MD in Zurich in 1881 and,
after various positions in psychiatric hospitals,
became a professor in Zurich and head of the Bur-
gholzli Sanitarium in 1898. He studied hypnotism
with Sigmund Freud, published a textbook on
schizophrenia in 1911 and a general psychiatry text
in 1918.
Bleuler restructured Kraepelins image of
dementia praecox using psychological theory and
terms. It was he who created the name schizophre-
nia, the favored name that reies the syndrome to
this day. He described mutism, negativism, and
rigidity as generalised and persistent blocking
an exaggeration of the phenomenon seen in
healthy individuals when they are overwhelmed
by emotional disturbance. (46). The patient with
catatonia was suppressing unpleasant memories
by silence (mutism), by tenseness and rigidity
(holds back acts that are compelled by memories),
by refusal to obey commands, and by displacing
rising emotions and tension into motor acts that
shut out reality (posturing, grimacing, staring,
stereotypes).
By the end of World War I, the writings of
Kraepelin and Bleuler dominated psychiatric
thinking until the philosophy of Sigmund Freud
achieved dominance in America during and after
World War II. Kahlbaums perception of catato-
Rediscovering catatonia
nia as an independent syndrome was buried. Until
the end of the twentieth century, Kahlbaums
catatonia was viewed within Kraepelins conjured
formulation of dementia praecox and subsequently
within Bleulers concept of schizophrenia.
Conflict of paradigms in psychiatry
As catatonia was incorporated as a feature within
more severe chronic psychoses, a new inuence in
its recognition was the worldwide inuenza pan-
demic of 19171919. Many who survived the infec-
tions developed chronic illnesses. Stupors were
common with active periods of slow movements,
shuing gait, rigid posturing, xed facies,
decreased eye blinking, and extended staring. (In
retrospect, these signs are better seen as examples
of infection-induced catatonia.)
Labeled encephalitis lethargica, the syndrome
was classied and treated as a form of Parkinsons
disease that is commonly found in the elderly
(47). But these signs were also identical to those
of catatonia, which by this time was accepted as
an aspect of schizophrenia, leading the Viennese
psychiatrist Cosimo von Economo to describe the
patients as suering the same schizophrenia illness
that Kraepelin had described (48). For many
patients, the illness was progressive, leading to
long-term hospitalization either in neurologic cen-
ters or in psychiatric sanitaria. Whether the label
of encephalitis lethargica or of catatonic schizo-
phrenia was applied in an individual patient
depended not on any distinguishing ndings but
on the attitude and experience of the observer and
the setting.
The lesson that catatonia is a treatable syn-
drome in postencephalitic states is still ignored. In
the successful book and lm Awakenings, the neu-
rologist Oliver Sacks describes the patients exhibit-
ing prolonged and severe motor inhibition,
posturing, rigidity, and mutism that began during
the encephalitis epidemic (49). The patients resided
in a home for the elderly chronic ill. Their syn-
drome was labeled parkinsonism, and the newly
heralded treatment of high-dose l-dopa was
applied. Limited relief occurred but was hailed in
the book and lm as a revolutionary discovery. At
a meeting of the Society of Biological Psychiatry in
1996, I asked Dr. Sacks whether he had considered
the patients to have catatonia. He averred that
they did not, nor had he considered using the treat-
ments for catatonia for these patients (50).
The conict of paradigms between clinical neu-
rology and psychiatry is ongoing, to the detriment
of the clinical sciences and the welfare of the
patients. (51) Examples are discussed in the assess-
11
Max Fink
ment and treatment of the neuroleptic malignant
syndrome (Chapter 3) and anti-NMDAR encepha-
litis (Chapter 5).
Daniel Rogers, in an excellent recent review of
motor disorders in psychiatry, presents portraits of
patients with dementia praecox by Kraepelin and
comparable portraits of postencephalitic motor
signs. The pictures are indistinguishable (18). The
label of schizophrenia or of a neurological disease
again depends not on objective ndings but on the
accident whether the referral was to the neurologic
or the psychiatric clinic. And the outcomes are
determined by the treatments associated with each
diagnosis parkinsonism with l-dopa and similar
medications and schizophrenia with neuroleptic
drugs.
A retrospective note on the increasing domi-
nance of psychology during the rst half of the
twentieth century stated The fact that an
undoubted neurological disease, encephalitis
lethargica, could produce a wide spectrum of
psychiatric illness challenged the central idea of the
so-called functional psychoses [i.e., not derived
from brain pathology] in an era that had come to
be dominated by the teachings of psychoanalysis
(52).
The identication of catatonia within and out-
side schizophrenia varied in the twentieth cen-
tury. In 1912, catatonia was described in 30
patients with infectious diseases, toxic states,
depression, mania, and delirium, encouraging the
belief that catatonia occurred outside schizophre-
nia (53). The prognoses varied, being good when
episodes were few and worsening as the episodes
increased in number. In a 1922 study of 200
patients who met Kraepelins constructs, catato-
nia was found more often among the manic
depressive patients than among those with
dementia praecox (54).
August Hochs 1921 monograph Benign Stupors
described 25 psychiatric patients treated at the
Wards Island Hospital in New York City. Their
behaviors, motor signs, course, and outcomes are
similar to the patients described by Kahlbaum.
Classifying the patients using the Kraepelin/Bleul-
er distinctions, Hoch reported the prognoses were
favorable with remission of symptoms and return
to the community in 13 manicdepressive patients.
The outcomes were poor in the 12 patients with
general medical illnesses or schizophrenia (55).
(Hoch lacked the eective treatments for catatonia
developed a decade later.)
Reviewing the twentieth-century psychiatric
literature nds many articles both in Europe and
the United States that describe catatonia as an
independent entity, but many more accept the
12
Kraepelin/Bleuler incorporation within schizo-
phrenia. Interest in catatonia as an identiable
independent syndrome waned so much that when
the American Psychiatric Association presented its
classications of psychiatric illnesses in 1952, cata-
tonia was only recognized as a type of schizophre-
nia and remained so in the succeeding revisions in
1968, 1980, and 1994.
Psychiatry leaves the asylum
Catatonia was further pushed into the background
by changes in psychiatry. First, the enthusiasm for
the psychodynamic philosophy that blossomed
during World War II decreased interest in systemic
medical illnesses and moved the focus of psychiat-
ric practice from the asylum to the private oce
and clinic. A principal inuence was the rapid
expansion of the numbers of physicians trained in
psychiatry.
Involuntary military conscription of millions
of men brought many who were not t for such
service, leading to an expansion of the need for
physicians trained in psychiatry to evaluate and
treat those who became ill. Many physicians
entering military service without prior psychiatric
experience, myself included, were trained in
schools of military neuropsychiatry. That
training was dominated by the psychodynamic
philosophy.
William Menninger, a conrmed Freudian ana-
lyst, was the head of the US Armys Department
of Psychiatry. Schools for military neuropsychia-
try were established in San Antonio, Texas, and
in Topeka, Kansas. I was a eld medical ocer
in the US Army in 1946 when I was assigned to
the school in Texas. For 4 months, I attended
daily classes in psychoanalysis, clinical psychia-
try, and clinical neurology. Diagnosis and treat-
ments were almost wholly psychodynamic. Lip
service was played to the teaching of the biologi-
cal treatments of ECT, insulin coma, and lobot-
omy. In that prepsychopharmacology era,
pharmacology was focused on the used of sedat-
ing drugs. When I left military service, I was
helped by the Servicemans Readjustment Act,
known as the GI Bill, to pay tuition to attend
the William Alanson White Institute of Psycho-
analysis in New York City during my postgradu-
ate residency training in neurology and
psychiatry at Monteore, Bellevue, and Hillside
Hospitals. When the war ended, many physicians
used government education benets to extend
their training in psychoanalysis and then to open
private oces separate from hospitals for their
clinical practices.

Few connected with the large sanitaria where
the more severely ill were housed, and psychiatry
increasingly became an out-patient oce practice
focused on psychotherapy. A few clinicians applied
their skills among those who were in hospital care,
but it was soon clear that the severely ill were no
longer of interest to most practitioners as their
attention was focused on the young, alert, intelli-
gent, attractive, emotionally ill who did not require
institutional care. The acute illnesses of catatonia
did not lend themselves to oce care, and as inter-
est shifted from the psychoses to the less ill, interest
in catatonia dissipated.
A second factor in the virtual disappearance of
catatonia from the psychiatric radar screen was the
development in the 1930s of treatments that could
eectively and quickly relieve it. In 1930, William
Bleckwenn demonstrated the immediate relief of
catatonia by injections of sodium amobarbital, a
medication that decreases anxiety and induces
sleep (56, 57). The eects ended mutism, relieved
posturing and staring, and encouraged speech,
feeding, drinking, and self-care. For some, relief
was immediate and complete. For others, the bene-
ts were transient and treatments had to be contin-
ued. The ease with which a retarded and excited
patient with catatonia could be relieved by a single
chemical injection made the sodium amytal glass
vials in wooden cylinders ubiquitous features of
clinical care in psychiatric hospitals and emergency
rooms.
During my medical school training in psychia-
try at Bellevue Psychiatric Hospital in 1945, and
again during neurology and psychiatry residency
training between 1948 and 1951, I was equipped
with vials of sodium amytal and sterile water
and was frequently called upon to treat mutism
and negativism for feeding and to relieve excited
catatonic states by these injections. In retrospect,
the relief of catatonia by amobarbital was the
rst sign of the approaching era of psychophar-
macology.
Treatments for the most seriously ill psychiatric
patients appeared next insulin coma therapy in
1933, chemically induced seizures in 1934, frontal
leucotomy in 1936, and electrically induced
seizures in 1938.
Insulin coma patients were injected with large
doses of the hormone insulin that reduced blood
sugar to minimal survival levels, inducing coma
until blood sugar levels were normalized by intra-
venous injections or tube-feeding into the stomach
of high concentrations of glucose sugars. In treat-
ment programs, comas were induced daily for
4050 comas over 3 months. Seizures occurred in
up to 20% of the treatments, and for those who
Rediscovering catatonia
were not responding rapidly, electric-induced sei-
zures were added during the coma.
Seizures were rst induced chemically using
intramuscular injections of camphor, later with
intravenous pentylenetetrazol (metrazol). Other
chemical methods of inducing seizures were
examined. In the 1950s, the inhalant urothyl
(Indoklon) was tested in random assignment
studies vis a vis ECT. Flurothyl, an ether with
the ether aroma and volatility, was presented to
the patient by way of a mask that covered
mouth and nose. Within three to four breaths,
the patient was asleep and a seizure quickly fol-
lowed. These treatments were as eective as
ECT, but the complexity of the administration
and chemical cost limited the interest, and the
method was discarded. These chemical induc-
tions were replaced by electricity in what is now
electroconvulsive treatment (ECT). In each treat-
ment, the benet accrues to the number and
frequency of seizures induced.
Frontal leucotomy was the surgical procedure
that severed the connections between the frontal
lobes and the rest of the brain, inducing changes in
thought, reducing obsessions, and often inducing
seizures. Leucotomy was introduced as a full
neurosurgical procedure under sterile operating
room conditions. But one of the proponents, Wal-
ter Freeman, introduced a quick method using an
ECT-induced seizure as anesthetic and cutting the
brain via an ice-pick-like device introduced
through the thin plate over the eyeball. (58) Public
and professional distaste for this procedure is illus-
trated in the book and lm One Flew Over the
Cuckoos Nest by Ken Kesey (59). Interest in
lobotomy ended when chlorpromazine and other
neuroleptic drugs were introduced and shown to
be safer and more eective.
These treatments typically relieved the more
severe and malignant catatonias. The physicians
prescribing the treatments most often labeled the
patients as suering from schizophrenia and only
occasionally focused interest on catatonia. While
continuing treatments were needed to sustain the
benets, the prognosis for full relief became excel-
lent, making catatonia among the most success-
fully treatable conditions in psychiatry. Interest
remained weak as the patients were quickly
returned to their homes and no longer were clinical
challenges.
In the discovery that induced seizures relieved
schizophrenia, it was most fortuitous that Ladislas
Meduna selected patients with catatonia for his
rst experiments. Nine of the rst 11 patients were
catatonic requiring nursing care and naso-gastric
feedings. Had he selected subjects from among
13
Max Fink
those with hebephrenia, his experiences would not
have been encouraging (60).
Were these treatments, lobotomy, insulin coma,
and ECT eective in relieving schizophrenia? The
answer depends on the populations selected and
the settings from which they came. For the more
acutely ill patients, mainly from out-patient set-
tings that included those with catatonia and those
with the mixed syndromes of depression and
psychosis (labeled schizoaective illness), the treat-
ments oered dramatic relief. For the more chroni-
cally ill, especially those with long-standing illness
diagnosed as the paranoid, hebephrenic, and non-
catatonic forms of schizophrenia, neither ECT nor
the other biological treatments were benecial. The
site of the assessment, whether in a long-stay
hospital population or in a general hospital
acute treatment center, inuenced the evaluation
(61, 62).
In 1981, the neurologist B. Mahendra posed the
question, Where have all the catatonics gone?
(63). Noting that the psychiatric texts had com-
mented on the decline in the recognition of cata-
tonic schizophrenia and that the decline had
preceded the inuence of neuroleptic drugs,
Mahendra doubted that the disorder of catatonic
schizophrenia ever existed. The frequency of asso-
ciation of catatonia and schizophrenia depended
on the incidence of the many ways in which catato-
nia was elicited. He cited examples of catatonia
secondary to infections (as in encephalitis) and in
the excitement and retardation of the mood disor-
ders. As an analogy, he noted that tuberculosis
had been frequently found among severely ill psy-
chiatric patients but had not been reied as a
tuberculous schizophrenia. Catatonia had not
disappeared, but the connection to psychosis had
been prematurely reied.
14
An example is the 1969 study published by B.
Pauleikho based on 35 years of experience with
552 hospitalized psychiatric patients (24). Pauleik-
ho identied stupor in 100 patients and excite-
ment in 51 patients with catatonia. In 26 patients,
catatonia was malignant, that is, life-threatening
and severe. Presenting his data in 5-year incre-
ments, he reported a drop in the frequency of the
diagnoses after 1953, ascribing the reduced
numbers to changes in clinic administration and
diagnostic styles and not to changes in the inci-
dence of catatonia. In 12 patient histories, he
illustrated catatonia variants that are readily rec-
ognizable today as a syndrome distinct from
schizophrenia.
In the 1970s, James Morrison at the University
of Iowa examined hospital chart records and
reported an increased incidence of catatonia in
patients with mood disorders, chiey those with
mania (64, 65). An examination of patients admit-
ted to a New York City hospital psychiatric unit
in the same period found a higher prevalence of
catatonia among the patients with mania and
depression than in those with schizophrenia (7,
66). The same higher concentration of catatonia
among manic patients than in those with schizo-
phrenia was reported from Germany (67). These
reappraisals had little immediate eect but set the
stage for liberating catatonia from schizophrenia.
As we will see, they made it possible for the
appearance of an acute, often lethal syndrome
associated with high-potency neuroleptic drugs to
rekindle interest in catatonia as independent of
schizophrenia.
 Rediscovering catatonia

Chapter 3: the neuroleptic malignant

syndrome
With all these disadvantages of re-examination, I can for these eects were prescribed, but with little
only expect to dig my new species [of clinical case] from relief. Despite the increasingly severe impacts on
the mass of rubbish of confused, irregular conglomera- movement and speech, the balance between the
tions of amorphous appearance, to separate it from the reduction in expressed delusions and hallucina-
encumbrance of incidental matters, and so present it, tions, aggressive acts, screaming behaviors, and
that others may be able to satisfy themselves of its frightening thoughts was considered favorably by
individuality, and then enter upon the critical and exact administrators, so that continued prescription was
analysis of its true and essential essence; or else to decide widely endorsed.
that it is only an old variety with some accidental and The benets were also considered sucient to
illusive peculiarities. Luther V. Bell, 1849 (68) replace insulin coma (ICT), a more dangerous and
unpleasant treatment then in use. In 1933, the Aus-
Catatonia faded from psychiatrys awareness
trian psychiatrist Manfred Sakel proposed treating
until the hazards of the neuroleptic malignant syn-
schizophrenia by daily injection of increasing high
drome brought it to professional attention. Fre-
doses of the hormone insulin to lower blood glu-
quently fatal, the stupor, rigid posturing, mutism,
cose levels to states of coma (69). After an hour of
and repetitive speech of critically ill delirious
observed coma, an intravenous injection or naso-
patients renewed interest in catatonia, especially
gastric gavage of concentrated glucose quickly
when the treatments for catatonia were found to
returned the patient to consciousness. Within an
relieve the neurotoxic syndrome.
hour, patients were alert having showered, toileted,
Chlorpromazine (CPZ), the rst of the neurolep-
and been fed, able to return to their treatment
tic drugs, was introduced in 1954 as a sedating
ward. Psychotic thoughts and aggressive behaviors
agent for excited psychotic patients. The aggres-
were inhibited so that about one-third of the
sion, screaming, re setting, breaking furniture,
patients left the hospital and returned to their
and physical injuries that were common in the
families after courses of up to 50 comas.
sanitaria were quickly reduced, benets that were
In the 1940s and 1950s, about 40 patients were
recognized in every psychiatric center where it was
treated with ICT each year at Hillside Hospital. In
used. As the director of psychiatric research at
the 5 years, I treated about 200 patients. Pro-
Hillside Hospital in Long Island, New York, a
longed coma, the failure of the patient to recover
200-bed sanitarium, I also studied its eects.
consciousness as glucose was administered,
Within a few weeks, the nurses who rst saw the
occurred in 3% of the treatments. The patients
benets eagerly referred their most disturbed
required intensive nursing care and careful man-
patients for the experimental treatment. By 1957,
agement of uids and blood electrolytes. We tried
the antidepressant imipramine was introduced
many medications, including the newly introduced
followed by a ood of new chemicals for the relief
steroids, with none proving useful. Three patients
of anxiety, depression, and psychosis. The enthusi-
died. Spontaneous seizures occurred in up to 20%
asms of psychopharmacology soon dominated
of the treatments, and when no benets were
both the profession and the public media and have
apparent after a month of comas, we added ECT
done so to the present.
to the comas. ICT was a laborious and riskful
But patients paid heavily for these benets.
treatment of marginal benet.
Motor movements slowed and gait became
We soon recognized that the patients who
ungainly. Sti and rigid posturing was accompa-
improved with ICT were also relieved by CPZ.
nied by tremors. Drooling slathered their cloth-
Beginning in 1957, the patients referred for ICT
ing. Their faces were emotionally at, without
were randomly assigned to either a 50-coma treat-
smiles or laughter. Some became jaundiced,
ment course of ICT or to daily oral dosing with
itched, and scratched leaving long red trails on
CPZ. In the prior 3 years of experience, we had
their arms and legs. Patients refused their medi-
learned that about 1200 mg/day of CPZ was the
cines, and in that era of paternalism and invol-
eective dosing schedule. In the study, patients
untary treatment, the new drugs were often
received doses beginning at 300 mg/day rising
administered forcibly.
weekly to 1200 mg/day. The median dosage was
We had no knowledge of how to prevent these
800 mg/day for the 10-week course.
eects. Many chemicals thought to be prophylactic

15
Max Fink
Within 15 months, we had treated 50 patients,
half with CPZ and half with ICT. A seminal 1958
paper in the Journal of the American Medical
Association reported similar reductions in psycho-
sis and aggression with both treatments (70). But
the risks for prolonged coma and death, weight
gain, and nursing care costs of ICT were greater
than the risks and costs of CPZ. By the end of
1958, the hospital discontinued its use, and soon
ICT had been widely abandoned throughout the
nation.
An interesting footnote to the ICT history is
described by the author Sylvia Nasar in the biogra-
phy and lm A Beautiful Mind, the story of the
1994 Nobel Economics Prize winner John Nash.
He had become psychotic soon after completing
his degree at Princeton and had begun a teaching
career. By 1961, he required hospital care for a
paranoid psychosis and was admitted to the Tren-
ton State Hospital where ICT was still available.
His treatment with ICT relieved the principal
symptoms, but he remained chronically ill. (71)
Suppression of interest in movement disorders
More potent neuroleptic drugs, such as uphen-
azine, triuoperazine, and haloperidol, were next
introduced to the psychiatric community and
widely prescribed. Hospital wards became quieter,
and increasing numbers of patients moved from in-
patient to out-patient care. The rapid discharge of
patients and the closing of the asylums, the process
soon labeled deinstitutionalization, began as a
trickle and soon became a ood, closing the major-
ity of the sanitaria in the United States and
throughout the world by the end of the century.
Neuroleptic drugs suppress psychosis but do not
cure. Their eects are more like that of steroids
that suppress symptoms than like those of an anti-
biotic in relieving an infection by destroying the
invading agent. Neuroleptic drugs require contin-
ued prescription to maintain health. As the dos-
ages of neuroleptic drugs are reduced or
withdrawn, symptoms are. We did not know
then, nor do we know now, for how long treat-
ments should be sustained nor did we understand
the risks. Medication treatments, month after
month and year after year are accepted clinical
practice.
As more patients exhibited peculiar motor
movements, the association with neuroleptic drugs
was increasingly recognized. Tremors interfered
with writing and speaking, gait became slow and
shuing, and as eyelids did not blink, patients
appeared to be constantly staring. After long expo-
16
sures, especially in older patients, voices became
husky. Feeding and talking were made dicult by
worm-like writhing mouth movements. Labeled
tardive dyskinesia and tardive dystonia, the move-
ments were uncontrollable, becoming progressively
more severe and unsightly. No eective treatment
or prevention was known as patients risked the
Scylla of psychosis or the Charybdis of dyskinesia.
The sanitaria were soon lled by slow, shuing,
trembling, shadows of human beings, occasionally
laughing or giggling uncontrollably (72). The
motor eects of the neuroleptic drugs were so com-
monly recognized that measuring the severity of
tremors in handwriting was suggested as a criterion
to identify an active clinical agent (73).
The enthusiasm for prescribing these agents
would be severely lessened if the eects on move-
ment were widely discussed. The pharmaceutical
industry, frightened that their sales would be
impeded, encouraged leading psychiatrists
(known opinion leaders) to publicly opine that
the motor changes were inconsequential and toler-
able. The movement eects were widely denied
and pushed out of professional and public aware-
ness. In hospital settings where physicians exam-
ined patients at their bedsides, the measuring and
recording of the motor signs were feasible. But in
oce settings, physicians sat behind their desks,
and physical examinations were not carried out,
further minimizing the recognition of motor signs
of illness.
When newly introduced the second-generation
or atypical neuroleptic drugs clozapine, risperi-
done, olanzapine, and quetiapine were marketed
in the 1990s, the banner argument for their use was
their lesser motor eects. It took more than two
decades after the rst appreciation of the motor
toxicity of neuroleptic drugs for these eects to be
publicly acknowledged and then mainly as an
advertising strategy to encourage prescription of
the second-generation neuroleptics. It took
another two decades to recognize that the lesser
movement eects were tied to the lesser antipsy-
chotic potency of the new agents: their benets
were only slightly better than those of placebos
(74).
The active suppression of the recognition of
abnormal movements with neuroleptic drugs also
suppressed the recognition of catatonia. The belief
that catatonia had disappeared was further
encouraged by the segregation of the severe psychi-
atrically ill outside the experience of community
physicians and the many psychiatrists now active
only in their oce settings. The full range of motor
signs of parkinsonism, tardive dyskinesias, and

catatonia was only identied in long-stay facilities
(75).
The neuroleptic malignant syndrome enables
recognition of catatonia
The recognition of catatonia was energized by the
awareness that the more potent neuroleptic drugs
risked inducing acute febrile catatonic syndromes.
Described within the decade after CPZ was
introduced and labeled, the syndrom malin des
neuroleptiques an acute neuroleptic toxic syn-
drome patients suddenly became feverish, stu-
porous, and delirious (76, 77). Heart rate, blood
pressure, breathing rate, and sweating increased
without evidence of infection. Catatonic signs
became prominent. This life-threatening syndrome
appeared without warning, often following a tran-
sient inuenza-like syndrome of malaise, fever, and
weakness (7880).
As agents with greater neuroleptic potency than
CPZ were marketed, severity of the toxicity
increased. Evidence of the syndrome in eight
patients treated with high-potency neuroleptic
drugs described by Alan Gelenberg of Bostons
Massachusetts General Hospital compelled atten-
tion, and clinicians became frantic to understand
these phenomena (81, 82).
The cause was puzzling. Were these acute symp-
toms evidence of the blockade of dopamine neuro-
transmission that was reported in laboratory
studies and considered the basis for the relief of
thought disorders? Dopamine was one of the
brains principal intercellular communication sys-
tems impaired by the new drugs. Perhaps prescrip-
tion of dopamine agonists, drugs that increased
brain dopamine levels, would reverse toxicity?
A 1980 review of more than 60 published cases
brought particular attention to the syndrome that
was labeled the neuroleptic malignant syndrome
(NMS), a name that was widely accepted (83). The
syndrome was labeled malignant in recognition
that many patients died in an acute autonomic
storm of high fever, elevated blood pressure,
increased heart rate, irregular heart rhythms, and
sweating. Each case report recognized rigidity,
dyskinesia (abnormal motor movements), postur-
ing, mutism, and negativism, the classic signs of
catatonia. This publication cited dopamine block-
ade as the cause of NMS and endorsed treatment
with the dopamine agonists bromocriptine and
amantadine.
When it was realized that the same neuroleptic
drugs that inadvertently led to the appearance of
these catatonic signs were used to relieve
Rediscovering catatonia
schizophrenia, including the cases labeled as the
catatonic form of schizophrenia, treatment options
became confused. When patients exhibited signs of
psychosis, physicians prescribed neuroleptic drugs.
But these also increased neurotoxicity. It took
some time to realize that discontinuation of
neuroleptics was essential to relieve the toxic
syndrome.
Matters were not helped by an assertion that
increased motor rigidity and fever were signs of
malignant hyperthermia (MH), a syndrome of
muscle weakness and fever that follows the use of
inhalation anesthetics (83). This syndrome is
restricted to a few patients with an identiable
genetic fault. For symptomatic relief of MH, the
muscle relaxant dantrolene is prescribed. As a
result of this confused association, dantrolene was
added to the recommended prescriptions for NMS.
In 1997, the newly established NMS Internet Hot-
line made prescription of both bromocriptine and
dantrolene and withdrawal of the oending
neuroleptic the cornerstones of the recommended
management.
Neuroleptic malignant syndrome was soon
sensed as clinically identical to malignant (that is,
lethal) catatonia (MC) that had been described
before the neuroleptic drugs were introduced. Many
forms of MC had been recognized, and the ecacy
of ECT in its relief was reported by 1952 (2).
By 1984, we had recognized NMS in three
patients at the University Hospital at Stony Brook,
each with prominent signs of catatonia (3). We rst
summarized the prior reports of 17 similar cases;
11 had been precipitated by haloperidol, a nding
that since has been repeatedly conrmed. Two
patients had died with the others slowly recovering
after extended nursing care. Dierent psychoactive
agents had been prescribed benztropine, dantro-
lene, amantadine, bromocriptine, and diphenhy-
dramine but none were eective.
Among our patients, a 30-year-old woman had
been treated with the neuroleptic uphenazine and
then admitted to the hospital in an acute state of
rigidity, posturing, mask-like facies, profuse sweat-
ing, and fever. She was treated with the antihista-
mine diphenhydramine, the dopamine agonist
bromocriptine, the antimanic lithium, and the anti-
psychotic mesoridazine, each selected to relieve
one of her symptoms. She received little benet,
and only after all medications were discontinued
and weeks of nursing care did the toxic syndrome
slowly resolve and she was able to return home.
In a 45-year-old disorganized and psychotic
woman with depressed mood, the neuroleptic
haloperidol and then uphenazine had been pre-
17
Max Fink
scribed. NMS was precipitated. A 5 mg diazepam
dose administered intravenously as a sedative
resolved the motor syndrome quickly but tran-
siently. Continued treatment with bromocriptine
and lorazepam oered little benet. In another
patient, a 26-year-old man with bizarre thinking,
slow speech and movement, and the catatonic signs
of posturing and rigidity had been transferred
from a state hospital for treatment with ECT. An
intramuscular injection of the long-acting neuro-
leptic uphenazine decanoate was given and within
72 h NMS was recognized.
Electroconvulsive therapy was prescribed for
both patients, and within 1 day, the toxic syn-
drome had resolved dramatically for each. Their
ECT treatment courses were continued until the
toxic states had fully resolved without residual
motor or toxic signs. We concluded that NMS was
a physician-induced form of malignant catatonia
treatable by ECT.
Over the next few years, other patients with
NMS were successfully treated. We described our
awareness that the neuroleptic drugs, particularly
the high-potency drugs, were also toxic in eliciting
syndromes of catatonia and fever and that the tox-
icity resolved with neuroleptic drug withdrawal;
and if withdrawal alone was not sucient, ECT
was a denitive treatment.
This awareness was documented hesitantly as
ECT was the most stigmatized treatment in psychi-
atry. Yet, by 1990, the recognition of catatonia
warranted immediate treatment with ECT even
before medication trials (4). By 1991, Denise White
reported that catatonia was a risk factor for neuro-
toxic development (84) and then catatonia was
seen as integral to the diagnosis (85). These reports
crystallized the integral role of catatonia in NMS.
That same year, collaborating with Michael Tay-
lor, we suggested to the American Psychiatric
Association DSM-IV commission, then revising
the classication criteria, that catatonia warranted
a place distinct from its role as a type of schizo-
phrenia (9). Increasingly, the argument was made
that NMS was best regarded and treated as a form
of malignant catatonia and that eective relief was
assured when treatments for catatonia were applied
rather than those considered useful for an aberra-
tion of neurotransmitter activity (5, 86). By 1996, a
rating scale was developed for catatonia and a sys-
tematic study established the lorazepam sedative
test as a diagnostic verication of catatonia. Treat-
ment with high doses of lorazepam was shown to
be eective for 80% of the patients with catatonia
and ECT eective for the remainder (87, 88).
In the next decade, numerous reports found
NMS rapidly responsive to ECT, and in 2003,
18
Michael Taylor and I summarized the extensive evi-
dence in the textbook Catatonia: A clinicians guide
to diagnosis and treatment (11). But ECT is much
stigmatized, and many institutions lacked the phys-
ical facility or the trained personnel for its use lead-
ing to ethically troubling reports of prolonged
hospital care and unnecessary deaths in patients
with NMS. Fortunately, the benzodiazepines, a less
controversial and less invasive treatment than
ECT, were also available to relieve NMS.
Catatonia and benzodiazepines
Catatonia had rst been successfully treated with
intravenous injections of the barbiturate amobar-
bital in 1930 by William Bleckwenn in Wisconsin
(56). Within 4 years, relief by inducing grand mal
seizures was described by the Hungarian neuropsy-
chiatrist Ladislas Meduna (89). Both treatments
were widely adopted when catatonia was recog-
nized as such. Once NMS was pictured as a form
of catatonia, the question was raised whether bar-
biturates would relieve NMS. Ever since its rst
description, amobarbital had been the accepted
immediate treatment of catatonia in emergency
room settings. By the 1980s, concerns about the
toxicity and safety of the barbiturates led to their
replacement by benzodiazepines that were used as
sedatives, soporics, and anticonvulsants.
In 1983, Gregory Fricchione and his colleagues
at Massachusetts General Hospital described the
rapid relief of NMS by intravenous lorazepam, a
commonly used benzodiazepine (90). Each of four
patients they treated exhibited catatonia, fever,
agitation, and delirium, with elevated blood pres-
sures, rapid heart rates, and increased sweating.
Haloperidol had been the toxic agent in three
instances and triuoperazine in one. After various
prescribed medications and nursing care had failed
to relieve the syndrome, intravenous lorazepam in
2-mg doses was administered. In each patient,
NMS resolved within a day, with some symptoms
resolving within hours. This dramatic experience
established lorazepam as an eective treatment for
catatonia.
In discussing this experience, Greg Fricchione
relates: I had treated a patient in postcardiotomy
delirium with intramuscular and then intravenous
haloperidol and he developed neuroleptic induced
malignant catatonia. I brought my mentor Ned
Cassem the Director of the MGH Consultation
Psychiatry Service and both a physician and
Jesuit priest with me around 8 pm to see the
patient who had not responded to diphenhydra-
mine or benztropine. Ned chose lorazepam and I
injected 2 mg intravenously in the presence of

several of the nurses. Catatonia lysed [disap-
peared] dramatically in about 1 min; the nurses
who all knew Ned asked in wonderment: What
did you give him Dr Cassem? And as he turned
to leave, Ned said nonchalantly, why holy water
of course era of psychopharmacology, psychiatric disorders
By 1990, Patricia Rosebush and her colleagues
at McMaster University in Hamilton, Canada,
also described complete and dramatic relief of
NMS by lorazepam in a prospectively open trial in
1 mg or 2 mg doses in 12 episodes (29). Other
reports of the ecacy of lorazepam (91, 92) were
followed by descriptions of the ecacy of other
benzodiazepines, clonazepam (93), diazepam (94),
and zolpidem (95).
At Stony Brook University Hospital in 1994, 28
patients with catatonia were systematically treated
with injected and/or oral lorazepam for up to
5 days and with ECT when lorazepam failed. Out-
comes were monitored quantitatively during the
treatment phase with a Catatonia Rating Scale
(87). In 16 of the 21 patients (76%) who received a
treatment trial of lorazepam, catatonia resolved
within 1 day. Three cases were examples of NMS.
In 11 patients to whom we had administered an
intravenous dose of lorazepam, immediate relief of
catatonia was the result, the harbinger of the full
relief that followed treatment with high oral doses
of lorazepam. Four patients who did not have an
immediate response to intravenous lorazepam were
successfully treated with ECT (88).
By 1990, two competing treatment protocols
were prescribed for NMS the bromocriptine
dantrolene model based on the dopamine/malig-
nant hyperthermia association and the benzodiaze-
pineECT model based on the recognition that
NMS is the form of malignant catatonia. Although
no direct comparisons between the two treatments
were made, the ecacy of the benzodiazepine
ECT model assured its widespread use and accep-
tance. By 1991, doubts as to the merit of dopamine
augmentation as the eective treatment for NMS
were expressed (96). By 1995, the hypothesized
connection of NMS to malignant hyperthermia
was also found wanting, and treatment with dan-
trolene was no longer recommended (97). Thereaf-
ter, whether NMS was relieved or a fatality ensued
depended not on the administration of dopamine
agonists or dantrolene but whether the neuroleptic
administration had been promptly discontinued
and uid and metabolic integrity re-established.
Well-documented texts describing the neuroleptic
malignant syndrome as a variant of malignant
catatonia appeared in 2003 (11) and 2004 (98).
What delayed the recognition of NMS as drug-
induced catatonia? The tie of catatonia to schizo-
Rediscovering catatonia
phrenia was so intimate that the prior recognition
of schizophrenia was obligatory before catatonia
could be considered. The recognition of catatonia
outside schizophrenia reported in the 1970s had
yet to become part of psychiatrys teaching. In the
are perceived as errors in neurotransmitter physiol-
ogy, favoring the belief that NMS was the result of
a decrease in brain dopamine activity and making
the prescription of dopamine agonists a logical
treatment. The same beliefs would not support
treatment with benzodiazepines (or ECT) as no
theory of neurotransmitter action had been pro-
moted for catatonia or malignant catatonia. Beliefs
in dopamine aberration in NMS were very strongly
held, and intense public debates were frequent for
more than a decade.
Recognizing catatonia today
With the renewed interest in catatonia and the
appreciation that catatonia often occurs indepen-
dent of schizophrenia, it became important to
develop criteria to dene its many variations. In
clinical medicine, a diagnosis is made, and treat-
ment is oered after the patient relates his symp-
toms and recent history; the physician examines
for signs of dysfunctions; laboratory tests are
requested and assessed; and based on these nd-
ings, the clinician considers a diagnosis from his
glossary of disorders. After identifying the most
likely t, treatment is prescribed. When a specic
treatment leads to recovery, the diagnosis is con-
sidered validated. Patients with catatonia rarely
complain of symptoms; the behaviors are observed
or reported, and examination identies the
presence of identiable catatonia signs. When
motor signs are prominent, a checklist of catatonia
signs sorted in a Catatonia Rating Scale becomes a
useful guide to the examination (11).
Catatonia is an all-or-none phenomenon, so the
presence of two or more catatonia signs for 24 h or
longer is sucient to consider it to be present. Sur-
veys of populations in psychiatric hospital wards
and emergency rooms nd that 715% exhibit
catatonia (11, 12).
Once the diagnosis is entertained, the clinician
can conrm the diagnosis by employing a sedative
relaxation test (lorazepam test). William Bleck-
wenns description of immediate relief of catatonia
by the intravenous injection of amobarbital
sodium in his article The production of sleep and
rest in psychotic cases presented both an eective
treatment and a diagnostic test (56). For patients
who are mute, posturing, rigid, or with other cata-
tonia signs, the return of speech and relaxation of
19
Max Fink
posture and tension are prompt, usually within
10 min after an injection of sodium amobarbital
or, more commonly today, after 1 mg or 2 mg
lorazepam. The change may be transient or may
persist, but the immediate relaxation conrms the
presence of catatonia.
For many decades, amobarbital and other bar-
biturates were essential features of hospital emer-
gency room care. As a medical student and
resident in the 1940s, I was usually in the hospi-
tal carrying a small wooden cigar case with a
glass vial of 500 mg amobarbital powder, syr-
inge, needle, sterile water, and tourniquet
always prepared and often used. In his clinical
review of the diagnosis and management of
catatonia in 1975, James Morrison studied 250
patients with catatonia of whom 97 were exam-
ined by a barbiturate interview, the intravenous
injection of up to 5 g of amobarbital (99). He
reported that 71 (73%) responded favorably,
meaning a quick relief of mutism, tension, pos-
turing, and stereotypy. He gives the example of a
23-year-old single man with a 2-year history of
persecutory and grandiose delusions who exhib-
ited waxy exibility and posturing of the psycho-
logical pillow (head held elevated as if on a
pillow) and not responding to antipsychotic treat-
ments. After the intravenous administration of
four grams of sodium amobarbital, the rigidity,
tension, and posturing lessened and the patient
began to speak of the terror he had felt when he
realized that the television was bugged and the
FBI was gathering information about him.
In the early 1980s, as discussed earlier, ben-
zodiazepines were recommended as safer sedatives
than the barbiturates, and lorazepam and diaze-
20
pam were successfully tested in catatonia treat-
ment. Numerous anecdotes cite the patient with
mute catatonia being sent to a hospital laboratory
for a procedure after an injection of lorazepam to
assure cooperation, only for the ward nurse to be
called with a complaint that the patient is overly
talkative and uncooperative in the procedure
room. Intravenous dosing in a mute, posturing, or
stuporous patient typically relieves the syndrome
within a few minutes.
How assured is the response to an intravenous
injection of 1 mg lorazepam or 2.5 mg diazepam
as verication of catatonia? Almost all patients
with positive scores on the Catatonia Rating Scale
are relieved. Occasionally, a second dose is
required and applied within 10 min. It is not
stretching the comparison too far to say that a
sedative drug acts with the same dose-related speed
as a concentrated acid or base reverses the pH bal-
ance of a chemical solution.
Once the presence of catatonia is veried, treat-
ment today is remarkably eective. More than
80% of the patients are relieved by barbiturates or
benzodiazepines, and when these fail, the others
are relieved by ECT (11).
The availability of both a reliable and quick
diagnosis method and eective treatment has
enabled the discovery of additional forms of cata-
tonia (14, 100). Once catatonia was divorced from
schizophrenia and the main motor signs were
appreciated, other forms of catatonia, such as
delirious mania, toxic serotonin syndrome, and
pediatric catatonia, were recognized and their
diagnostic criteria and treatment algorithms
established.
 Rediscovering catatonia

Chapter 4: new forms are recognized

According to an old story, there are three types of base- lupus erythematosus (a highly varied systemic,
ball umpires. One says: I call them [balls and strikes] as often fatal autoimmune disease) was referred for
they are. The second says I call them as I see them. ECT by Dr. Gregory Fricchione, the head of the
And the third says What I call them is what they hospitals Consultation & Liaison Service (103).
become. Frederick Grinnell, 1992 (101) Her agitated manic behavior, facial grimacing,
mutism, and rigidity were poorly controlled. She
Recognizing the neuroleptic malignant syn-
required high doses of sedative drugs and four-
drome (NMS) as a form of malignant catatonia
limb restraints to sustain her life in intensive
showed that catatonia was found outside schizo-
nursing care. With the consent of her husband, her
phrenia. It also oered eective treatment for the
mother, and her physicians, the rst ECT was
patients and justied the challenge to the hypothe-
given on the 27th day of hospital care.
sis that NMS was the result of dopamine blockade.
Mania and delirium rapidly disappeared, speech
Breaking the association with schizophrenia freed
and self-care improved, posturing, mutism, and
clinicians to see catatonia in broader samples of
screaming were allayed, so much so that after
patients. It encouraged the development of Catato-
seven treatments the family and her physicians
nia Rating Scales and exploration of an injection
withdrew consent for further treatment. But treat-
of lorazepam as a verifying diagnostic test. It stim-
ment was incomplete and symptoms soon
ulated the search for catatonia in other guises.
returned. The ECT course continued, and she
Among patients admitted to the hospital in a
received 10 more treatments. Her psychiatric and
hyperactive agitated delirium, the uctuating signs
medical conditions were relieved, and she left the
of catatonia were commonly recognized. The risk
hospital in psychiatric and systemic remission.
of death led to many descriptions of excited deliri-
On admission, she had exhibited the systemic
ous states with prominent signs of catatonia, vari-
signs of lupus erythematosus supported by positive
ously labeled malignant, pernicious, lethal, fatal, or
antinuclear antibody tests. Treatments with intra-
mortal catatonia; or delirium becomes the focus as
venous methyl prednisolone and three plasmaphe-
in delirious mania or manic delirium; or the eponym
resis exchanges did little to improve her condition.
of Bells mania or Stauders lethal catatonia was
Treatment with cyclophosphamide was begun but
used.
her delirium and excitement led to the referral for
Acute signs of NMS were also identied in sub-
ECT. With ECT, her behavior normalized and
jects who had not been treated with neuroleptics
she returned to her home. Cyclophosphamide
but with psychoactive drugs that aected the
continued monthly, and she was well on 1-year
serotonin neurotransmitter system. These patients
re-examination.
suered what became known as the toxic serotonin
Similar cases of delirium are commonly found in
syndrome, a parallel disorder to NMS.
medical, surgical, and emergency room settings.
Increasingly, the signs of catatonia were found
For more than two centuries, clinicians have
among adolescents admitted to our facility, at
described patients with the acute onset of an
rst among those with peculiar behaviors associ-
excited delirious state, dangerous to themselves
ated with mental retardation and then those with
and to others, frequently so severe as to result in
delirious mania (102). Many patients showed
death. In 1849, Luther Bell, in a 13-year review of
repetitive self-injurious behaviors (SIB), but we
1700 admissions to Bostons McLean Hospital,
did not realize that this behavior was a form of
described 40 patients with delirium, fever, and
catatonia until we read reports from other medi-
uncontrollable excitement that alternated with stu-
cal centers among their patients with neurobe-
por. Three-quarters had died. The syndrome
havioral disorders. That the patients improved
became known as Bells mania (68).
with ECT validated the association (19). Such
In 1934, Karl Heinz Stauder described the
repetitive behaviors are now recognized within
sudden onset of intense excitement, delirium, high
the catatonia spectrum.
fever, and catalepsy in three young adults with a
family history of psychiatric illness but who previ-
Delirious mania as malignant catatonia ously had been in good medical health. In a
matter of minutes, each went from well to
Our experience associating catatonia with delirium extreme excitement and psychosis. During the
increased when an intermittently mute and scream- illness, each injured himself by slamming repeat-
ing 25-year-old woman, ill with a 3-year history of

21
Max Fink
edly into the ground or walls. All three died. Stau-
der termed the syndrome todliche katatonie (fatal
catatonia) (104).
Similar descriptions by many authors conrm
the characteristics of delirious mania as a form of
malignant catatonia (2, 105114). The principal
feature is the acute onset of a nightmarish, dream-
like, overactive state that develops within a few
hours or a few days. Voices, noises, and sights are
misperceived, encouraging frightening thoughts.
Patients hit out and thrash about, harming them-
selves and others. Grimacing, posturing, echolalia
(repeating words), and echopraxia (repeating
movements) are prominent. Negativism (refusing
to obey commands) and automatic obedience
(obeying commands that they are told not to obey)
are almost always present. Patients sleep poorly
and are unable to recall their recent experiences or
the names of objects or numbers given to them.
They are disoriented and they confabulate.
Patients hide in small spaces, close the doors and
blinds on windows, and remove their clothes run-
ning nude in and from their homes. Garrulousness,
ights of ideas, and rambling speech alternate with
mutism. Fever, rapid heart rate, elevated blood
pressure, and rapid breathing are common. An
example is abstracted from my review of delirious
mania (109).
A 29-year-old man with a positive history for HIV had
been found wandering on a beach, naked, confused, and
unable to rationally answer questions. He was admitted
to the psychiatric emergency room of Stony Brook Uni-
versity Hospital. Despondent about his illness, he
stopped taking the prescribed medicines, and said that
he wished to die. The day before admission, he had been
slashing pictures of his friends and walking about the
house with a bloody knife, muttering incoherently.
On admission, he was excited, screaming, confused,
dehydrated, unkempt, and dirty. He required four-limb
restraints and 0.5 mg of the antipsychotic chemical
restraint haloperidol was administered intramuscularly.
Within an hour he was rigid and mute, febrile, dehy-
drated, and urine showed evidence of cannabinoids.
An intravenous injection of 1 mg lorazepam quickly
reduced the catatonia signs. Mutism, rigidity, staring,
and periodic excitement persisted despite daily loraze-
pam dosages to 10 mg per day. Neuroleptic medication
was precluded by his reaction to haloperidol.
Surrogate consent was obtained for ECT. On day 11, the
rst seizure was induced and within 24 h he no longer
required protection. Mutism, rigidity, and staring disap-
peared. Within 2 h his temperature rose to 102F and
resolved to normal over the next 12 h.
22
After the second ECT 2 days later, he became better ori-
ented and cooperative. The next day he came voluntarily
for the third treatment. Delirium, catatonia signs, and
excitement were fully relieved by the sixth treatment,
and he was discharged to the care of his family. Loraze-
pam was discontinued, and lithium therapy was pre-
scribed for persisting mania. Follow-up 2 months later
showed him to be continuing his medical treatment with-
out any persisting signs of psychiatric illness.
In this patient and in additional similar cases
described in texts on ECT, the risks of precipitat-
ing a neuroleptic malignant syndrome precluded
the prescription of haloperidol and other potent
neuroleptic drugs to control behavior (70). Ben-
zodiazepines were preferred. While doses of loraze-
pam to 10 mg/day reduced manic and aggressive
behavior, these did not relieve delirium. ECT,
however, eectively resolved the delirious syn-
drome in each case. We had been encouraged to
apply ECT in delirious patients by reports pub-
lished in 1952 by the Austrian clinicians Otto
Arnold and H. Stepan (115). They were faced with
patients with the life-threatening condition of
malignant catatonia, and lacking any eective
treatment risked the use of ECT. To induce grand
mal seizures in acutely ill moribund patients was
counterintuitive. Yet, 16 of 19 delirious patients
survived when they were treated with ECT within
5 days of the onset of the illness; of the 14 whose
treatment had been delayed, none survived. Daily
ECT and up to three seizures a day were necessary
to relieve the more severe conditions.
Although such published experiences were few,
ECT became the accepted treatment. Not all the
cases were associated with neuroleptic drugs,
although these were the more common forms of
physician-induced deliria (116118).
In the French literature, a dreamy, stuporous
syndrome is described as onirisme (translated as
oneiroid state, oneiroid syndrome, or oneirophre-
nia) (119). In a short delightful 1950 text, Ladislas
Meduna, the developer of convulsive therapy,
described such patients in sucient detail to
identify their syndrome as a form of malignant
catatonia (120). He distinguished the syndrome
from schizophrenia and reported 64% full remis-
sion with ECT.
The cause of delirious mania is unknown, but
the syndrome is often preceded by an acute infec-
tion, a traumatic incident or poisoning (121123).
As delirium dominates the story, the connection to
a prior illness is usually overlooked. A connection
to bipolar disorder or manicdepressive illness is
often assumed, but is rarely conrmed by the
patients history. Considering delirious mania as a

form of catatonia rather than as a form of bipolar
disorder oers a bridge to quick, eective relief
with catatonia treatment.
The sudden appearance of delirious mania in a
public place has been hazardous. One example, as
described by Edward Shorter, is that of a non-
English-speaking immigrant from Poland upon his
arrival at a Canadian airport. Confused by the
requirements of customs control, he could not nd
his mother whom he expected to meet. He became
increasingly agitated, sweating, dehydrated, and
aggressive. Police were called and sought to
control his behavior by electric taser applied
up to four times; he fell to the ground scream-
ing and convulsing, and minutes later was dead
(124). Similar experiences dot the literature (125).
Toxic serotonin syndrome
Occasionally, an acute febrile and toxic reaction
mimicking NMS follows the administration of
drugs that aect the brains serotonin system. In
1994, a woman was admitted to University Hospital
at Stony Brook with the motor and vegetative signs
of NMS. She had not been exposed to neuroleptics
but had been treated with serotonergic drugs.
A 59-year-old married woman with a 21-year history of
psychiatric disorder and three prior hospitalizations for
agitation, mood swings, and psychosis was admitted to
hospital following the addition of a single 25 mg dose of
nortriptyline to a regimen of l-dopa and trazodone. The
l-dopa was prescribed for signs of parkinsonism after
many years of neuroleptic treatment. Trazodone was
prescribed as an antidepressant of the serotonin antago-
nist and reuptake inhibitor class.
Within 5 h she became fearful, tremulous, sweating, and
incontinent of urine. The systemic signs persisted with
waxing and waning of motor restlessness, rigidity, and
tremors. Four days later, she became confused and
reported episodes of explosive diarrhea.
At the psychiatric emergency room, she was mute, rigid,
sweating, and tremulous with rapid heart rate and ele-
vated blood pressure. A single 1 mg intravenous dose of
lorazepam was administered, without benet. On admis-
sion to the psychiatric unit, she was afebrile, her posture
was rigid and she did not obey simple commands. In the
absence of exposure to neuroleptics a toxic serotonin
syndrome (TSS) was diagnosed. Treatment with loraze-
pam did not oer relief. ECT was begun and a day after
the rst treatment, motor rigidity, mutism, and negativ-
ism became more prominent, and additional lorazepam
was prescribed. The afternoon of her second treatment,
motor rigidity and mutism were gone, she was more
interactive and responsive, denied hallucinations, and
Rediscovering catatonia
attended unit activities. Three additional treatments
resolved the psychosis, depressed mood, agitation, and
motor and vegetative signs (126).
Her condition met the diagnostic criteria for the
toxic serotonin syndrome (TSS) (127). Serotonergic
drugs are used widely to relieve depressed mood
and may precipitate an acute febrile syndrome of
twitching muscles, tremors, diarrhea, and mental
changes. Such states follow a rapid increase in dos-
ing or when a selective serotonin reuptake inhibi-
tor (SSRI) is combined with a monoamine oxidase
inhibitor (MAOI).
Patients become restless and sleep poorly, their
sensorium is altered, the skin is ushed, and they
complain of sweating, tremors, shivering, lethargy,
salivation, nausea, diarrhea, and abdominal pain.
Laboratory tests of body functions show signs of
acute toxicity. Temperature and blood pressure are
elevated, tendon reexes are hyperactive, move-
ments ataxic, and myoclonus appears. The big
picture is of a malignant catatonia/neuroleptic
malignant syndrome with gastrointestinal
symptoms (128133).
Although most patients respond rapidly to with-
drawal of the oending medicines and supportive
care, ECT has been used successfully (134, 135).
The overlap in diagnosis of TSS and NMS is
shown in a report of the calls to the NMS Informa-
tion Service, an expert Internet referral service
(136). Of 29 calls requesting information about
NMS, the symptoms of 22 (79%) met criteria for
TSS and 25 (89%) met criteria for NMS (137). The
authors concluded that NMS and TSS are syn-
drome variants of malignant catatonia, a conclu-
sion supported by their rapid relief by
benzodiazepines and by ECT.
The pediatric catatonias
For many years, catatonia was not considered to
exist in children and adolescents. Now we know
dierently. It was hidden under the global diagno-
sis of schizophrenia and the labels of stupor and
catalepsy (muscular rigidity and xity of posture
regardless of external stimuli and decreased sensi-
tivity to pain). The authoritative incorporation of
catatonia as schizophrenia by Emil Kraepelin and
Eugen Bleuler, as we have seen, blocked consider-
ation of catatonia in other conditions. A detailed
history by Edward Shorter of the vagaries of
catatonia in children relates the various ways that
catatonia has been regarded by psychiatrists.
Often, catatonia has been hidden under diagnoses
of encephalitis lethargica, hysteria, hebephrenia,
schizophrenia, and, lately, autism (138).
23
Max Fink
Few childhood disorders were recognized in
early psychiatric classications and are usually
dened as schizophrenia, mental retardation, and
tics and mutisms. In recent classications, conduct
and attention decit disorders have been added. In
DSM-IV, what had been known as mutism
became elective mutism and then pervasive refu-
sal syndrome; echophenomena and stereotypy
were relabeled Tourettes syndrome or obsessive
compulsive disorder (OCD); posturing and nega-
tivism were associated with autism or autism
spectrum disorders; and tantrums and excited
states labeled emotional behavior disorders or
conduct disorders. No one of these behaviors is
well dened, and for none has either an eective
treatment or an understanding of the underlying
pathophysiology been developed. When catatonia
has been recognized, however, it has been possible
to relieve the symptoms with treatments for catato-
nia (139). Here we discuss the experience with chil-
dren suering autism spectrum disorders and
mental retardation in whom the connection to
catatonia is well dened; in the next chapter, we
discuss other pediatric syndromes that meet crite-
ria for catatonia and warrant further study.
Autism spectrum disorders
Autism, a disorder of socialization and speech with
an onset in early childhood, was brought to profes-
sional attention by Leo Kanner in 1943 (140) and
by Hans Asperger in 1944 (141). They described
children with delayed maturation, poor socializa-
tion, and a plethora of repetitive behaviors. Much
debate ensued as to the distinction between child-
hood autism, mental retardation, and childhood
schizophrenia. Mainstreaming the education of
these children, increased information on the Inter-
net, and the rise of active parent organizations
have established autism as a diagnosis for which
special support is provided by many American
school services. Children are oered aides in
classrooms and psychological assistance and
speech therapy at home. In communities with ben-
ets for the children and their families, the number
of children labeled autistic has risen rapidly with
recent estimates running as high as one of every
eight children (142). Severity of illness ranges from
children who can be maintained at home and in
community schools to those who require highly
specialized institutional care.
Autism is marked by mutism, echolalia, echopr-
axia, odd hand postures, freezing of ongoing
movements, rigidities, forced vocalizations, stereo-
typy, self-injurious behaviors, and insensitivity to
24
pain. All are signs of catatonia. Two formal sur-
veys nd catatonia in 1217% of adolescents
otherwise labeled with autism (143, 144). Although
we lack systematic studies identifying and treating
catatonia in autism, case reports now dot the liter-
ature indicating instances of relief for even the
most severely ill (139, 145). Children who are
bound to their home, unable to participate in
regular schooling, are relieved of their repetitive
behaviors, especially those who are injurious to self
and aggressive to their families. The behaviors are
self re-enforcing and result in bodily harm with
bone fractures or the loss of eyes, teeth, and n-
gers. Here is one of many case reports from the
Stony Brook University Hospital:
A 14-year-old intellectually disadvantaged boy was
admitted for persistent head-banging, which required
him to wear a protective helmet and be restrained most
of the day. Donalds mental age was measured as
4.3 years. He communicated by guttural sounds. The
unusual behaviors began at age 10 and persisted despite
various medications and both positive and negative rein-
forcement treatments. He wore large gloves in addition
to the helmet, and was sedated to control his high-
pitched wailing and prolonged screaming. After 4 years
of failed treatment, Donald was evaluated for ECT. On
admission to the hospital, examination found no bodily
disorders to preclude further treatment. Consent was
obtained from his legal guardian.
After the sixth of twice-weekly ECT, screaming, scratch-
ing, and head-banging were reduced. By the 10th treat-
ment, Donald no longer needed the helmet, gloves, or
restraints. Treatments were reduced to once weekly, and
after 16 treatments he was returned to his residence. For
another 2 months, treatments were given once every
2 weeks and then stopped, because the psychiatrists were
satised with his progress. Anticonvulsants were pre-
scribed and he participated in group activities without
restraints or life-threatening behaviors (146).
Other reports cite the successful relief of catato-
nia in a child with Down syndrome (147), in
autistic twins (148), and in malignant catatonia in
an adolescent with a cerebellar malformation from
birth (149). Another report cites two adolescent
patients with tics successfully treated with ECT
(150). The successful relief of self-inicted injuries
in youth with autism spectrum disorders is increas-
ingly recognized (151154). While some relief
occurs with high doses of lorazepam, ECT is
more eective (155, 156). The immediate
changes are dramatic, and the benets become
persistent when treatments are continued over
many weeks.

Another example of successful treatment is
related by Dr. Lee Wachtel, the medical director of
the Neurobehavioral Unit at the Kennedy Krieger
Institute in Baltimore, Maryland.
Robert was the product of a full-term pregnancy and
spontaneous vaginal delivery. Developmental mile-
stones were within normal limits for the rst
15 months of life, when he stopped interacting with
others and lost acquired speech. A pervasive develop-
mental disorder was diagnosed and he began intensive
early intervention services at a private clinic, lived at
home, and attended a specialized school for the next
15 years. He was estimated to have attained upper ele-
mentary school skills; at his best, he was learning the
names of European capitals and completing multi-digit
multiplication.
At age 14, Robert evinced grunting and other abrupt
vocalizations, progressing to repetitive rocking, lunging,
head shaking and nger apping, multiple stereotypies
and hair-combing echopraxia. The symptoms waxed and
waned for the next 3 years. He continued to attend
school.
Three years and 5 months after symptom onset, Robert
suddenly stopped eating and required manual feeding by
others. Food spooned onto his tongue would remain for
several minutes until extensive prompting evoked swal-
lowing. He lost about 50 lbs in weight in the next few
months. Rigid posturing occurred intermittently
throughout the day, particularly evident at mealtimes
when utensils would remain suspended in his hand in the
air, or he would clamp down so forcefully that sta
members feared breaking his jaw to pry out the utensils.
Periods of stupor, slow gait and shuing steps became
frequent. Aggression and self-injury ensued. Unpro-
voked physical attacks of his family and sta members
necessitated physical holds frequently using canvas belts
for limb immobilization. Self-injury included frenetic
twisting movements of ngers deep into the nares, self-
biting of hands, arms and tongue with wound formation.
He was no longer able to attend school or to leave his
home.
For lack of local inpatient services, Robert was only
hospitalized 7 months after these symptoms began.
Prior to hospitalization his days were spent sleeping
from 4 AM to 10 AM, then lying or crouching unre-
sponsive in his bed requiring full care in toileting,
bathing and feeding, until early evening when agita-
tion, self-injury, aggressive episodes, leaping, lunging,
jumping, screeching and nonsensical vocalizations
would commence.
Local psychiatric and neurological assessments oered
no diagnosis or treatment. Extensive laboratory and
imaging studies were within normal limits. Olanzapine
Rediscovering catatonia
30 mg daily (a neuroleptic) was prescribed leading to
further deterioration. Lorazepam 3 mg/day yielded mild
improvement. Self-injury escalated to the frank loss of
oral tissue and tongue bleeding.
Robert was admitted to hospital in January, 2012 with a
diagnosis of delirious mania/agitated catatonia, and
commenced ECT 2 days after admission. ECT thrice
weekly was pursued with standard methohexital
sedation, succinylcholine muscle relaxation, and bilat-
eral electrode placement. Within 2 weeks self-injury,
aggression and agitation ceased, (with the exception of a
few episodes of slapping when redirected from mastur-
bation) but other motor, vocal and behavioral symptoms
of catatonia persisted. Tissue wounds healed.
ECT frequency was increased to 45 times weekly for
the next 2 weeks, which led to overall symptom resolu-
tion. Lithium monotherapy was begun with ECT thrice
weekly and Robert showed consistent improvement
despite waxing and waning of symptoms.
On evaluation after ECT #26, Robert independently
walked into the room at a normal pace, waved to the
doctor, greeted her by name, and then began to read out
loud from a book. He answered multiple questions with
minimal hesitation in the same sing-song cadence he had
demonstrated from an early age. He interacted appropri-
ately with his mother and caregiver and independently
selected multiple songs and videos on his IPad, deftly
using the touch screen. The only abnormal physical
movements observed were brief episodes of nger ap-
ping. His father said that ECT had released Robert
from the shackles of Hell.
At the time of writing Robert had received 44 treatments
and was in the maintenance ECT phase with gradual
tapering of the frequency. Medications included lithium
600 mg BID with a serum level of 0.8 meq/l, lorazepam
2 mg TID, and memantine 5 mg BID. Robert was still
unable to transition to home for lack of appropriate
ECT services in his home area.
An interesting feature of this boys history and
that of numerous other similar reports is the
gradual onset of catatonia in childhood and then
a rapid escalation during adolescence. Because
ECT carries a heavy burden of stigma, however,
families are extremely reluctant to consider ECT,
despite the persistence of abnormal behaviors,
poor maturation, and poor socialization. Parents
who agree to treatment insist that only a
minimum number of treatments be applied, with-
drawing consent at the earliest favorable change.
We now know that successful relief requires ECT
continuation treatments. With eective care,
adolescents are able to remain at home as a
participating family member, manage their daily
25
Max Fink
self-care, and participate in schooling and social
activities.
Mental retardation
Before the recent enthusiasm for the autism diag-
nosis, patients with the same symptoms and signs
of delayed speech and learning, poor socialization,
and peculiar movements were labeled as suering
from mental retardation. Labels are sensitive to
social acceptance and undergo change when they
are deemed oensive. Intellectual disability,
intellectually challenged, mental handicap, and
learning disability are alternative terms. For a
time, the scores under 70 on intelligence quotient
tests were a measure of severity. The labels of aut-
ism or autism spectrum disorders include many of
these subjects as well as a cluster of patients with
high intellectual capacities that are seen as having
Asperger syndrome.
But like normal persons, they develop mood dis-
orders, acute excitements, deliria, and catatonia.
They were often prescribed neuroleptic drugs to
control aggressive behaviors, and from time to
time, the neuroleptic malignant syndrome was
induced. But even when these signs would have
recommended treatment with ECT, the recommen-
dation was precluded by the belief that these chil-
dren were already suering brain damage and that
ECT would worsen the condition. From time to
time, clinicians would treat such patients with
ECT, often successfully and without a worsening
of the subjects communication or language skills.
In 1999, we reviewed chart records for the diagno-
sis of mental retardation of the patients admitted
to Stony Brook University Hospital. We had trea-
ted ve patients from ages 1864: two with depres-
sive mood, two with NMS, and one with a toxic
response to hallucinogens. All responded well
to ECT without worsening of their intellectual
abilities (157).
The treatment for catatonia in a woman with a
life history of mental retardation was also safe and
successful.
On admission Claudia appeared her stated age of 23, not
speaking for long periods. She would assume postures
imitating others or after the examiner moved her limbs.
26
The catatonic signs were accompanied by screaming and
aggressive outbursts; she often required physical
restraint. She appeared depressed, refused to eat, and
was incontinent. Her speech was not intelligible to us
but was interpretable by her mother.
High doses of lorazepam diminished the catatonia signs,
but depressed mood, excitement, and incontinence con-
tinued as before. When ECT was recommended, both
parents signed the consent form. After two treatments,
Claudias mood and sleep improved, her appetite
returned, she was tractable, and she responded to ques-
tions and directions. After the third ECT, catatonia was
gone and her behavior was easily manageable. She was
discharged to her parents home for continuation treat-
ment with lorazepam and weekly ECT. She took part in
a day treatment programme for patients with mental
handicaps and required no additional medications. After
5 months, ECT treatments were discontinued and Clau-
dia remained in the community with lorazepam as her
principal medication. (146)
A recent literature review in patients with intel-
lectual disability treated with ECT found 72
reports with positive outcomes in 79% of the cases
(158). The patients include disabilities from mild to
profound. Transient complications were cited in
13% of the reports; these included memory impair-
ment, drowsiness, delirium, and spontaneous sei-
zures. Relapse occurred in 32% despite continuing
treatment with medications. The reviewers discuss
the under-use of ECT because of diagnostic over-
shadowing the presence of the label of intellec-
tual disability prejudiced caretakers against
consideration of ECT as riskful and brain damag-
ing. A second hurdle was that of informed consent
as the disability calls into play legal issues of guard-
ianship, surrogate consent, and judicial consent.
At this writing, delirious mania (malignant
catatonia) in all its variations, toxic serotonin syn-
drome, and many forms of pediatric catatonia are
widely considered among the diagnosable and
treatable catatonia disorders. These recent recogni-
tions are positive outcomes of our appreciation
that catatonia is readily found outside schizophre-
nia and that we now are able to verify the diagno-
sis and have eective treatments to validate the
diagnosis. The next challenge is to consider other
disorders as possible forms of catatonia.
 Rediscovering catatonia

Chapter 5: are these forms of catatonia?

That a new disease should be manifested at this (repeating words), and coprolalia (repeating
advanced day, in the calendar of medical history, is not scatological words), a cluster of behaviors that is
without many precedents. That such should occur in the now known as the Gilles de la Tourettes syndrome
great family of maladies involving the nervous system, (GTS). (159). It was distinguished around the same
would be the least improbable, when we reect how less time that Karl Kahlbaum described catatonia and
than all others these have been studied, comprehended was one of many attempts to identify psycho-
and treated, until within a comparatively recent period. pathological conditions with predictable outcomes.
Luther V. Bell, 1849 (68) GTS has a childhood age-of-onset and persists
to adulthood. Repetitive vocalizations, antisocial
The recognition that catatonia is the treatable
and inappropriate sexual acts, self-injury, and
core of the neuroleptic malignant syndrome
sleep disturbances are the principal features. In a
released catatonia from its steel-bound tie to
systematic examination of 55 adults with GTS,
schizophrenia and encouraged questions whether
87% exhibited echophenomena, perseveration,
other psychiatric syndromes were better considered
staring, grimacing, posturing, mannerisms, and
catatonia in disguise and be brought under the
stereotypy (160). The signs of autism and GTS
same treatment umbrella. The life-threatening syn-
overlap, and in many cases, the choice of diagnosis
dromes of delirious mania and the toxic serotonin
is in the eyes of the beholder and not in any
syndrome were the rst to be appreciated as forms
distinguishing criteria (161).
of catatonia. Next, the self-injurious behaviors that
No fully eective treatment is known. For mild
are commonly described in children and adoles-
tics, the behavior is tolerated and treatment is con-
cents with autism spectrum disorders were found
sidered unnecessary. For more severe forms, both
to be part of a catatonia syndrome that responded
negative and positive behavior re-enforcement ritu-
to ECT. But that was just the beginning.
als are prescribed, but success is limited (162, 163).
Within the DSM-IV classication of psychiatric
Reductions in the number of verbalizations are
disorders are many entities that readily meet cata-
reported with treatment with the neuroleptics
tonia criteria selective (or elective) mutism; Gilles
haloperidol and pimozide (164). Recent industry-
de la Tourettes syndrome, vocal, and transient tic
sponsored studies of olanzapine nd decreases in
disorders; the neuroleptic-induced Parkinson syn-
symptoms with greater reduction of tics compared
drome; stereotypic movement disorders; and
with placebo treatment (165). For the more
obsessivecompulsive disorder. For none are
severely debilitating forms of the illness, experi-
dened biological markers nor eective treatments
mental deep brain stimulation has been tried with
known. These mutisms and stereotypical behaviors
teasingly favorable reports. The studies lack
bear sucient characteristics of catatonia to war-
proper controls, however, so are considered
rant re-examination as catatonia variants.
exploratory (166).
In the past decade, a new diagnostic entity of
From time to time, tics have been so severe as to
anti-NMDAR encephalitis has been enthusiasti-
warrant trials with ECT. A PubMed review found
cally promoted as a unique neuropsychiatric disor-
10 reports of modest relief. In an 18-year-old man
der. Although catatonia is recognized in 70% of
with depressed mood, facial tics, grimacing, repeti-
the subjects so diagnosed, the connection to cata-
tive hand-washing, and self-injurious behavior,
tonia is not credited in the disorders evaluation
ECT resolved both the mood and the tic disorders,
nor in its treatment.
a benet that was sustained over the next year.
And, among neurologic syndromes, akinetic
When treatments stopped, he relapsed, but when
mutism, the prolonged state of stupor and paraly-
ECT was re-instated, the tics did not return and he
sis with apparent vigilance, has many characteris-
continued symptom-free while attending college.
tics of catatonia, such that exploring its relation to
In the same review, the tics and self-injurious
catatonia would be useful.
behavior of a 19-year-old autistic man were
reduced but not fully relieved with ECT (150).
Gilles de la Tourettes syndrome (GTS) Another example comes from my own experi-
ence. A 64-year-old widowed woman with recur-
In 1885, the French neuropsychiatrist Georges rent episodes of depressive illness relapsed with
Gilles de la Tourette described nine patients with repetitive scatological expressions in response to
multiple tics (sudden, repetitive, non-rhythmic any query. The tics disappeared quickly with ECT
motor movements or vocalizations), echolalia

27
Max Fink
(167). Individual case reports of the relief of GTS
with ECT are frequent (168172).
For all the similarity of GTS and catatonia
many descriptions of GTS meet the criteria for
catatonia reports of treatment with benzodiaze-
pines are surprisingly sparse. When the benzodiaz-
epine clonazepam was introduced to clinical trials,
reductions in symptoms were reported (173175).
The lack of interest in such experimentation is par-
ticularly surprising considering the persistence of
GTS and the failure of recommended treatments.
Given the safety and ecacy of benzodiazepines,
further study of GTS as a form of catatonia
certainly is warranted.
Elective mutism and pervasive refusal syndrome
In 1991, four young British girls between 9 and 14
years of age were described as suering a poten-
tially life-threatening condition manifested by pro-
found and pervasive refusal to eat, drink, walk,
talk, or care of themselves in any way over a period
of several months. The children required nasogas-
tric tube-feeding and spent such prolonged periods
in bed that they were occasionally requiring
manipulations of the joints under general anesthetic
to prevent contractures (176). They eventually
recovered after extended periods of hospital care.
The cases were labeled pervasive refusal syn-
drome (177). Since then <30 additional cases are
cited in the literature, with a 3 : 1 ratio of girls to
boys (178180). None of the reported cases had a
fatal outcome, although each required prolonged
hospital care. In the few patients who have been
the subject of long-term follow-up, the recovery
has been complete.
In discussing the four cases, Brian Lask and his
colleagues specically consider the diagnoses of
anorexia nervosa, elective mutism, post-traumatic
stress disorder, and stupor, but they do not list cat-
atonia (176). Yet, the children exhibit mutism, neg-
ativism, posturing, and rigidity and require
parenteral feeding for survival. These are cardinal
signs of catatonia, but no catatonia treatments had
apparently been tried.
Separately, in one patient in Ireland, a diagnosis
of catatonia was formally considered in an
11-year-old girl. Video images of her behavior
clearly met the criteria for catatonia, but her
parents refused a benzodiazepine treatment trial.
She recovered after 18 months of nursing care in
hospital (181).
Dirk Dhossche, a child psychiatrist in Jackson,
Mississippi, has looked further into similar cases,
applying the present criteria for catatonia. He
28
describes children and adolescents diagnosed with
childhood disintegrative disorder, Kleine-Levin
syndrome (a disorder of excessive eating and sleep-
ing), PraderWilli syndrome (a disorder of low
muscular tone, small stature, and incomplete sex-
ual development), tic disorder, and autoimmune
encephalitis as examples of catatonia (182). In each
case, the illness resolved safely once it was recog-
nized and treated with benzodiazepines and ECT.
The frequency of catatonia in such a wide range of
child and adolescent disorders indicates that pedi-
atric catatonias are not rare, particularly in epony-
mous disorders that are a principal part of
pediatric medicine. Dhossche also cites depriva-
tion, abuse, and trauma in the etiology of pediatric
catatonia (183) and presents examples of catatonia
among asylum-seeking children in Sweden (184,
185).
As with other pediatric syndromes that are
poorly dened and dicult to treat, it behooves
clinicians responsible for patients with persistent
and severe forms of mutism to consider the
connection to catatonia. But too few do so.
Anti-N-methyl-D-aspartate receptor encephalitis
Limbic encephalitis, an acute neurological
disorder, was rst described in the 1960s as a
paraneoplastic condition one resulting from
tissue changes induced by tumors that stimulate a
form of self-poisoning. It is considered an autoim-
mune disorder, a condition in which the immune
system mistakenly attacks and destroys healthy
body tissue. More than 80 dierent autoimmune
disorders are described in the medical literature.
The pathophysiology is poorly understood, and
the treatments are empiric and of limited ecacy.
The presumed connection to tumors sends
patients to whole-body searches, but the syn-
drome is also accepted as a diagnosis without
nding a tumor. In normal life, various tissue
receptors, one of which is the n-methyl-D-
aspartate receptor, are part of the bodys natural
physiology. In the words of enthusiasts, an anti-
NMDAR encephalitis reaction is present in
patients who develop:
an acute multistage illness that progresses from
psychosis, memory decits, seizures and language disin-
tegration into a state of unresponsiveness with catatonic
features often associated with abnormal movements and
autonomic and breathing instability.
About 70% of patients have prodromal [early onset]
symptoms consisting of headache, fever, nausea, vomit-
ing, diarrhea or upper respiratory symptoms. [The

psychiatric syndrome] follows within a few days or a
few weeks with a rapid disintegration of language, from
reduction of verbal output and echolalia [and echopraxia]
to frank mutism.
The initial phase of the illness is usually followed by
decreased responsiveness that can alternate between
periods of agitation and catatonia [with] autonomic
movements and autonomic instability (186).
The descriptions readily meet the criteria for cat-
atonia disturbances of behavior marked by
unresponsiveness with catatonic features, a febrile
course, followed by reduction in verbal output
and echolalia to frank mutism, followed by peri-
ods of agitation and catatonia, in which patients
resist eye opening but show no response to pain-
ful stimuli. Although experience with the
syndrome is limited, the descriptions clearly t
within the present conception of catatonia as a
systemic syndrome unrelated to psychosis and
schizophrenia.
A 2008 case report in the New England Journal
of Medicine describes a 26-year-old woman admit-
ted for headache, behavioral changes, abnormal
movements, and mutism of 7 weeks duration.
After extensive laboratory test examinations, an
anti-NMDAR encephalitis was diagnosed.
Throughout her illness, signs of catatonia were
recorded but neither recognized as such nor trea-
ted. An ovarian teratoma was found, surgically
removed under anesthesia, and the syndrome
resolved within a day. Was the removal of the
tumor or the anesthesia the therapeutic agent?
The rapidity of the resolution and her course
favor the relief of catatonia from the sedation
(187).
Another report, this one in the American Journal
of Psychiatry, described a 16-year-old boy with
protracted stupor, psychomotor retardation, mut-
ism, posturing, stereotypical movement, refusal to
eat and drink, and episodic agitation (188). A posi-
tive blood test supported an anti-NMDAR diag-
nosis. No clear medical or toxic cause was found,
nor were any of the prescribed psychotropic medi-
cations or immune therapies benecial. The pres-
ence of catatonia was not recognized; as a
consequence, no consideration was given to its
treatments. Instead, after treatment with haloperi-
dol and other antipsychotic agents, the symptoms
worsened. The syndrome eventually abated with
nursing care with the patient slowly returning to
baseline function 7 months after the onset of
symptoms. The failure to recognize catatonia or to
consider its treatment was criticized as a disservice
to the patient as well as unnecessary trumpeting of
a poor clinical lesson (189).
Rediscovering catatonia
The diagnosis of anti-NMDAR encephalitis
depends on a specic positive serum or cerebrospi-
nal uid antibody test (186). When the diagnosis is
considered, much interest is paid to the coexistence
of encapsulated teratoma tumors. The recom-
mended treatments are tumor resection and non-
specic immunotherapy (corticosteroids, intrave-
nous immunoglobulin, or plasma exchange) or
immunotherapy medications (rituximab or cyclo-
phosphamide).
A report of 100 cases of this syndrome exqui-
sitely describes the signs of catatonia in the
patients, but neither catatonia nor its treatments
are discussed (190). Case reports now dot the
literature with most patients being female and with
resolution after resection of ovarian teratomas
when found. But the syndrome is also reported in
males and among many patients without evidence
of tumors (191).
The heightened enthusiasm for this diagnosis is
reected in an Editorial in the British Journal of
Psychiatry in April 2012 calling for laboratory
tests for anti-NMDAR encephalitis in all individ-
uals with a rst presentation of psychosis, or peo-
ple with psychosis and features of autonomic
disturbance, movement disorder, disorientation,
seizures, hyponatremia, or rapid deterioration
with the possibility of antibody-mediated encepha-
litis in mind. The recommendation continues:
This assessment should include, as a minimum, a
neurological and cognitive examination and early
serum testing for antibodies against the NMDA
receptor and voltage-gated potassium channel. All
patients testing positive for these serum antibodies
should be referred to neurological centers with
expertise in managing these cases (192).
Support for the suggestion followed quickly with
the unproven assertion that NMDA receptor anti-
body encephalitis is a condition that responds to
immunotherapy (193). Such a recommendation is
inconsistent with good medical practice, however,
as the diagnosis directs attention to a treatment
that has not been proven eective.
The popular enthusiasm for this diagnosis is
illustrated by the rapidly increasing case report lit-
erature. The initial references to anti-NMDAR
encephalitis cited in PubMed are dated 2007. By
September 2011, 68 reports are listed with 2 coau-
thored by Josef Dalmau; by February 2012, the
number has increased to 126 with 32 by Dalmau;
and by October 24, 2012 the number of reports had
increased to 166 with 40 co-authored by Dalmau.
Considering these cases as examples of catatonia
is veried by the reported ecacy of ECT, cited in
reports in ve patients (194197). One example is
described (198):
29
Max Fink
An 11-year-old girl became uncooperative, confused,
and agitated with slurred speech and hallucinations
after an upper respiratory tract infection. She was
admitted to the hospital with a diagnosis of acute psy-
chosis and was prescribed a low dose of the atypical
neuroleptic risperidone with little eect. After adminis-
tration of chlorpromazine for agitation, she became
febrile, with rapid pulse rates and body rigidity. Malig-
nant catatonia was diagnosed, and a course of ECT
was begun. After eight treatments she resumed normal
functioning. Ongoing abdominal complaints prompted
ultrasound and abdominal CT that revealed an ovarian
tumor. Surgical removal of the ovarian teratoma may
have contributed to the full recovery of the patient.
Absent controlled studies, however, proof for this con-
clusion is lacking as the patient had already achieved
near remission after an intensive 2-week course of
ECT.
Clinical accounts of patients suering from
autoimmune limbic encephalitis commonly
describe catatonia, but the syndrome is seldom so
labeled nor are the eective treatments attempted.
As catatonia is present in a majority of patients
and we lack evidence of a specic treatable patho-
physiology, it is prudent to consider catatonia in
the dierential diagnosis and oer its tests and
treatments.
Obsessivecompulsive disorders
Obsessivecompulsive disorder is characterized by
repetitive thoughts and persistent motor acts that
interfere with normal life. The behaviors are simi-
lar to those of GTS except that the expressions are
not scatological and onset occurs later in life. It is
a persistent disorder for which no eective treat-
ment is known. Suggested treatments, which vary
with the severity of the symptoms, ll the full range
of psychotherapy, negative and positive behavioral
conditioning, medications, deep brain stimulation,
and surgical ablation of brain regions. Historically,
OCD has been interpreted as an anxiety disorder,
and the syndrome is classied in the DSM under
this umbrella. But the treatments for anxiety disor-
ders are not eective in OCD, which throws the
association into question.
Patients diagnosed with OCD exhibit signs of
catatonia (199, 200), and when these patients have
been treated with clonazepam (201203) and with
ECT (204208,) benet has been reported. My per-
sonal experience is similar.
Faced with a severely incapacitated 24-year-old man
with inability to leave his room, feed or toilet himself
because of checking actions, a trial of ECT was under-
30
taken, using a standard ECT protocol. After 2 weeks,
the checking was reduced and he was able to leave his
room, feed and care for himself. After 3 weeks, he left
the ward and went to a meal at a restaurant accompa-
nied by his mother. After 5 weeks he was discharged
with a prescription for the selective serotonin reuptake
inhibitor clomipramine. He was able to care for himself
for 2 months and then the checking returned. A second
ECT trial was less eective.
An additional seven patients I treated showed
short-term benets. Because we had not developed
a protocol for out-patient ECT, we did not
examine the merit of continuation ECT in these
cases.
Considering the inecacy of present treatments
and the lack of understanding of the pathophysiol-
ogy of obsessivecompulsive disorder, greater
attention to the role of catatonia and its treatments
is surely warranted.
Akinetic mutism
Neurologic texts describe patients who lie inert
and mute, appear alert, and regarding the clinician
by only moving their eyes. They may follow the
movement of objects or be diverted by sound. Nei-
ther voluntary movements nor restlessness or nega-
tivism is seen. A painful stimulus may produce
reex withdrawal or no movement. Patients have
to be fed and are incontinent of urine and feces
(209). They appear lifeless and may be mistaken
for dead (124). Initially labeled akinetic mutism,
this condition has since been described under such
names as coma vigil, apallic syndrome, sti-
man syndrome, locked-in syndrome, encephale
isole, and stupor of unknown etiology. The terms
vegetative state and minimally conscious state
are now used frequently. The symptoms dier little
from those of the more severe forms of inhibited
catatonia. Whether the subject is seen as a form of
akinetic mutism on a neurologic medical service or
as a form of catatonia on a psychiatric service is in
the eyes of the beholder and not in any specic
characteristic behavior (210).
Akinetic mutism was described in 1941 in a
14-year-old girl whose illness had lasted for
8 years. She experienced headaches localized over
the left eye, disturbances in vision, and vomiting.
A cyst had distended the third ventricle of the
brain, and relief followed the removal of its uid;
permanent relief followed its excision (211). Simi-
lar descriptions dot the medical literature in
patients with tumors and blood vessel abnormali-
ties in and around the brains third ventricle and

the basilar artery (212218). The stuporous state is
thought to result from the direct structural involve-
ment of the base of the brain (209). States of
stupor with the same neurologic signs are also
found in the acute toxic states associated with
hallucinogenic and other toxic drugs and in
chronic infections (219221).
Patients in chronic stupors or catatonia-like
states form a portion of every chronic neurological
medical service. When rst seen, each patient is
thoroughly examined for brain stem lesions, and
when found, may be relieved medically or surgi-
cally. But in many cases, lesions are not found, and
it is in such instances that the question arises
whether the signs meet the criteria for catatonia.
One description of akinetic mutism describes the
state as similar to that of catatonic schizophrenia.
In those catatonic schizophrenic states that simu-
late akinetic mutism, there is awareness, as these
patients do have memory of the events happening
during the catatonic state (213). Another writer,
discussing the range of etiologies, some with identi-
ed brain lesions and some without, noted: Varia-
tions occur: the patient may be almost totally
immobile and mute, or may have only a suggestion
of hampering of speech and movement (208). In
each description, the signs of catatonia are among
the physical signs noted in the examination, but
because the accompanying behaviors, thoughts, or
course are not those of schizophrenia, catatonia is
not identied. The author of a detailed 1962
review of akinetic mutism and its symptoms from
New York State Psychiatric Institute writes that
these simulate, in many respects, catatonic
schizophrenia (214).
The following personal experience reects the
overlap between catatonia and one of the descrip-
tive terms for akinetic mutism, that of a stupor of
unknown etiology.
A 22-year-old woman, lying mute in stupor, not moving
to sound or pinprick is seen in a bed lled with furry ani-
mal gures on the Neurology Service of an academic
medical center. Her illness began a month earlier with
acute malaise and somnolence followed by headaches
and abnormal movements, and then a seizure. Medical
and extensive neurologic examinations identied no
cause, treatments for epilepsy were prescribed, with the
Rediscovering catatonia
diagnosis of record of stupor of unknown etiology.
Plans for transfer to a long stay at a neurologic center
were underway.
A psychiatric consultant suggested an intravenous lo-
razepam test to rule out catatonia. Within a few minutes
of injection she opened her eyes, verbalized hoarsely,
and then moved her hands to pick up an animal gure
and to smile. Over the next few days increasing dosages
of lorazepam resulted in some speech, and aided sitting,
standing, and walking. With family consent, ECT was
begun and after four treatments the patient was fully
responsive, able to feed and care for herself, talking
responsively. Within 2 weeks she was discharged to her
home as recovered.
Early in the literature of this syndrome, relief
was described by inducing phenobarbital coma
(222). Zolpidem brought back to life the motor
movements and speech of a 48-year-old woman
who developed akinetic mutism after a suicide
attempt by hanging (223). Failure to properly iden-
tify the locked-in syndrome as a form of catatonia
in one instance resulted in a subject remaining in a
paralyzed state for 16 years (224). The tragedy of
motor paralysis in a conscious state is not readily
describable (225).
Descriptions of catatonia in the historical litera-
ture nd many subjects at rst believed to be dead
and their sudden revival fortuitously preventing
their burial (124). When a brain stem lesion is iden-
tied and is successfully treated surgically or medi-
cally, the outcome is determined by the site and
pathology of the lesion and the ecacy of the
treatments. But patients without an identiable
lesion who are residing on neurologic and medical
hospital services in chronic care under any of the
cluster of labels designating akinetic mutism war-
rant examination for catatonia.
We have explored the merits of separating cata-
tonia from schizophrenia, seen its many clinical
forms, and questioned whether other illnesses can
be included under the catatonia umbrella. It is now
useful to ask how the recognition of catatonia
faltered and look at the recent developments that
identify catatonia as an independent syndrome in
the classication of psychiatric diseases. The pro-
cess, while not complete, is well underway.
31
Max Fink

Chapter 6: classifying catatonia

The modern system of elevating every minor group, When Eugen Bleuler relabeled Kraepelins image
however triing the characters by which it is distin- of dementia praecox as schizophrenia, he retained
guished, to the rank of genus, evinces, we think, a want catatonia as its marker.
of appreciation of the true value of classication. And there catatonia has lain, a marker for
Sir Joseph Dalton Hooker, 1855 (226) schizophrenia for a 100 years, in repeated editions
of the ocial diagnostic classications until the lat-
How is catatonia recognized in psychiatric texts
est revision, the DSM-5, oers some relief.
today? For a syndrome to be recognized, it must
The rst Diagnostic and Statistical Manual of
be identied in the classications by a name, a
the American Psychiatric Association, published
description, and a coding number. Only then is it
in 1952, designated catatonia simply as schizo-
established as a disorder of professional interest.
phrenic reactions, catatonic type. These reac-
Two ocial classications, the International Classi-
tions are characterized by conspicuous motor
cation of Diseases (ICD) by the World Health
behavior, exhibiting either generalized inhibition
Organisation (227) and the Diagnostic Statistical
(stupor, mutism, negativism, and waxy exibil-
Manual (DSM) by the American Psychiatric Asso-
ity) or excessive motor activity and excitement.
ciation (228), are mainstays of clinical recognition.
The individual may regress to a state of vegeta-
The rst classications agreed on disease names
tion (228).
and characteristics for statistical purposes of
The revision in 1968 (DSM-II) described two
admissions, discharges, and deaths, but in the past
types of catatonia, both within the category of
half century, the labels have been increasingly
schizophrenia: It is frequently possible and useful
used for selecting treatment, research studies, and
to distinguish two sub-types of catatonic schizo-
physician and hospital payments. Guidelines for
phrenia. One is marked by excessive and sometime
the prescription of treatments are tied to specic
violent motor activity and excitement and the other
diagnoses. In evaluating the ecacy and safety of
by generalized inhibition manifested by stupor,
treatments, each subject is selected with narrow
mutism, negativism, or waxy exibility. In time,
diagnostic criteria to assure homogeneity of the
some cases deteriorate to a vegetative state (229).
samples. As treatments are better dened, the pay-
The third revision of 1980 mentioned catatonia
ments for physician and hospital care are tied to
under the classication catatonic type of
specic procedures. Durations of hospital care can
schizophrenia dominated by catatonic stupor,
be matched against standard care experiences,
negativism, rigidity, excitement, or posturing
allowing insurers and government agencies to eval-
(230). By the time of this formulation, however,
uate the eciency of treatment procedures and
researchers had recognized many instances of
treatment teams. Indeed, the quality and applica-
catatonia outside schizophrenia, especially among
bility of the classication system is central to the
the aectively ill.
concept of governmental control and insurance for
For half a century, it was also known that cata-
health care.
tonic patients responded well to barbiturates and
When Karl Kahlbaum described catatonia, he
to ECT, while patients identied as schizophrenic
saw many variations in the signs of the syndrome
but without evidence of catatonia did not.
and in the associated disorders. He presented 26
Although members of the DSM-III committees
cases that spanned a variety of illnesses, some that
were acquainted with this literature, they chose to
meet the present criteria for psychosis and mood
ignore it (231).
disorder and some ill with the systemic diseases of
Largely through the writings of intrepid catato-
tuberculosis and syphilis. As we have described,
nia scholars, the revision of 1994 (DSM-IV) added
two decades later, Emil Kraepelin recognized cata-
catatonia secondary to a medical disorder, a sin-
tonia just as Kahlbaum had described it. As Krae-
gular recognition outside schizophrenia (10). For
pelin shued his case record cards seeking
the mood disorders, a catatonia specier was
patterns in the main signs, he saw catatonia in
added to encourage awareness of its possible asso-
many instances, particularly in those who became
ciation with mood disorders. The absence of a cod-
models of dementia praecox. He also perceived
ing number, however, discouraged the use of a
catatonia among his other described diseases, in
specier term in diagnosis or in research studies.
patients with manicdepressive insanity and with
Literature searches now nd few citations to a cat-
paranoia, but his belief that catatonia was a mar-
atonia specier.
ker of dementia praecox dominated his writings.

32

These changes did not inuence clinical practice.
Catatonia was regarded as a sign of schizophrenia,
and whenever catatonia was recognized, neurolep-
tic drugs were routinely prescribed even in patients
showing no evidence of disturbed thought or
speech.
Perhaps, the failure to recognize catatonia out-
side schizophrenia could be excused as the argu-
ment was lost in the growing cacophony of pleas
by dierent constituencies. Each DSM revision
expanded the numbers of principal diagnoses:
DSM-I: 106; DSM-II: 182; DSM-III: 265; DSM-
III-R: 292; and DSM-IV: 297 (232).
Recognition that the neuroleptic malignant
syndrome (NMS) was more eectively relieved
by benzodiazepines and by ECT, as we have
seen, established catatonia as a well-dened syn-
drome outside schizophrenia. By 2003, Michael
Taylor and I summarized the accumulated 130-
year experience in Catatonia: A clinicians guide
to diagnosis and treatment (11). We argued that
catatonia met the criteria for a distinct clinical
syndrome; that the singular linkage to schizo-
phrenia was not justied; that assigning catatonia
to a separate DSM class in a home of its own
was consistent with the known experience; and
that such a designation would optimize recogni-
tion and treatment (12).
Catatonia in DSM-5
In 2008, the American Psychiatric Association
designated Work Groups of clinicians to examine
the experience with the existing classications
and to recommend changes for a revision to be
published as DSM-5 in 2013. Catatonia was
assigned to the members of the Psychosis Work
Group, still tying catatonia to the Kraepelin and
Bleuler conceptual tradition, despite the extensive
literature nding catatonia more often outside
schizophrenia. As none of the Work Group
members had been associated with the new learn-
ing on catatonia, any changes would necessarily
be based on the eects of special pleadings from
outside groups.
In 2010, 35 clinicianscholars, each with catato-
nia experience, joined together to urge simplica-
tion of catatonia as a unique, single diagnostic
class and to discard the connection to schizophre-
nia (233). The same-year child psychiatrists who
had clinical experience with catatonia, especially
among those patients with autism spectrum disor-
ders, published their evidence in support of giving
catatonia a classicatory home of its own (234).
Responding to these submissions, William Car-
penter, the Psychosis Work Group chairman and
Rediscovering catatonia
editor of the Schizophrenia Bulletin, invited
Michael Taylor, Edward Shorter, and me to argue
the case for catatonia as an independent class
(235). He solicited comments from others (236,
237), and with these in hand, he published the
responses and an overall critique by three members
of the Psychosis Work Group (238).
In our submission, we reiterated the arguments
for catatonia as an independent syndrome that we
had documented in our writings of 2003 and
throughout these essays (11, 12). Patricia Rose-
bush and Michael Mazurek of the McMaster Uni-
versity in Canada had often written on the ecacy
of benzodiazepines in malignant catatonia. They
reported catatonia in about 10% of acutely ill
psychiatric patients, only a minority having met
criteria for schizophrenia. Among those with
aective disorders, who comprise the largest sub-
group of patients with catatonia, the catatonia
signs typically resolve dramatically and completely
with benzodiazepine therapy. Rosebush and
Mazurek warned that failure to treat catatonia
properly before administering neuroleptic medica-
tions increased the risk of inducing a malignant
reaction. Establishing catatonia as a separate
diagnostic entity, the researchers argued, would
increase recognition of a treatable neuropsychiatric
syndrome (236).
Gabor Ungvari, Stanley Caro, and Jozsef
Gerevich opined that catatonia was historically
established, universally accepted as integral to
schizophrenia, and the form should be retained.
They cited the failure of benzodiazepines to relieve
catatonia among chronic psychotic patients in
Hong Kong. (ECT was not tried.) While these
authors accepted that patients in stuporous catato-
nia did respond well to benzodiazepines and ECT,
and could be distinguished from those with
schizophrenia, the failure of patients with
chronic catatonia to do so justied retention of
catatonic schizophrenia as a unique entity in the
classication (237)
Stephan Heckers, Tajiv Tandon, and Juan
Bustillo, members of the DSM-5 Work Group,
responded that a prominent position for catatonia
would pave the way for better recognition of the
syndrome, facilitate eective treatment, and cata-
lyze studies of the neural and genetic mechanisms
of catatonia. Although they encouraged better
labeling of catatonia in the classication, they did
not support the single designation. They see cata-
tonia as a marker of other syndromes, of many
entities in the psychiatric disease classication.
They also noted that a single designation for cata-
tonia would be beyond the limits of the charge
given the Work Group (238).
33
Max Fink
These authors also oered the jarring note that
If such a consolidation does occur, it should likely
be in the section on Psychotic Disorders because
catatonia is a dimension of psychosis (238)
Rosebush and Mazurek expressed the same con-
viction: The majority of patients with catatonia
have concurrent psychosis (236). These assertions
are beliefs, holdovers that catatonia is integral to
schizophrenia for which the primary treatment is
the prescription of neuroleptic drugs. Such associa-
tion is unfortunate because many forms of
catatonia are not accompanied by the delusions,
hallucinations, and disorders of thought that
characterize schizophrenia. Also, such patients
respond to the specic treatments of catato-
nia without resort to those used in the relief of
psychosis.
The proposed recommendations (Spring 2012)
Following consideration of various revisions, the
latest proposal published on the American Psychi-
atric Associations DSM-5 Development website
in May 2012 recommended (239):
i) Catatonia as a type of schizophrenia is to be
deleted.
ii) The class of Catatonia secondary to a general
medical condition created in 1994 is to be
retained.
iii) A new class of Catatonia Not Elsewhere Clas-
sied is to be created.
iv) A catatonia specier is to be added for 10 pri-
mary diagnoses with the coding of xxx.x5.
v) A list of catatonia signs is adopted from
DSM-IV.
These recommendations were reviewed by the
informal group of catatonia scholars in June 2012
and were endorsed as consistent with the ongoing
experience. The elimination of the designation of
schizophrenia, catatonic type, was hailed as nec-
essary. The inclusion of a single class of Catato-
nia Not Elsewhere Classied is responsive to the
experience and publications repeatedly expressed
by the catatonia scholars. It will serve the
requests for a single catatonia term and do
much to cut the tie between schizophrenia and
catatonia.
The designation of Catatonia Secondary to a
Medical Disorder introduced in 1994 is to be
maintained. The distinction between this label and
that of Catatonia NEC is unclear, but the experi-
ence was considered insucient to justify elimina-
tion. It is expected that the professions experience
34
will determine the relationship between these two
diagnoses.
The designation of catatonia speciers for 10
primary diagnoses sustains the secondary position
of catatonia in the prior classications. Whether
such is necessary is unclear because as we describe
in these essays, the recognition of catatonia identi-
es a syndrome for which eective treatments are
known. Adopting a specier model creates treat-
ment dilemmas. For example, the present recom-
mendations sustain a problematic inconsistency
with a class of Schizophrenia with catatonia speci-
er. Is the prescription of a neuroleptic agent (the
standard prescription for schizophrenia) to precede
that of the benzodiazepine or are both to be pre-
scribed simultaneously? We know that catatonia
sets the stage for a malignant response when a
patient is treated with neuroleptic drugs. Treat-
ment consistent with the specier label will subject
patients to unnecessary risks.
For an excited and delirious patient with signs
of catatonia, categorized as Bipolar disorder with
catatonia specier is the treatment to be the com-
monly prescribed high-potency neuroleptic drug
haloperidol for restraint, thereby risking a toxic
response? Or is the eective prescription to be high
doses of benzodiazepines and ECT, the treatments
for catatonia? Or are both drugs to be prescribed
simultaneously? Similar conicts follow each desig-
nation of a catatonia specier.
Despite these questions, the DSM-5 recommen-
dation for catatonia as an independent syndrome
not tied to schizophrenia corrects a long-standing
error that has plagued patient care and clinical
research for more than a century (235, 240). The
present recommendations are suciently broad to
allow experience to rene the place of catatonia in
clinical care. It may encourage clinicians to appre-
ciate catatonia in the many syndromes cited in
these pages, to do so early, and to oer the
eective treatments that assure catatonia its unique
place in medicine.
The changes recommended in the DSM-5 are
impressive and are sucient to signicantly
improve clinical diagnosis. With the known treat-
ments, patient care will surely be improved. The
main issue for these recommended changes will be
their acceptance in guidelines for treatment and
forthcoming textbooks. The known experience
nds about 80% of the patients with catatonia
respond to the benzodiazepines, but for the
remainder, the consideration of ECT brings out
the broad prejudice against its use, a prejudice that
often blocks eective treatment.
 Rediscovering catatonia

Chapter 7: the fear response

Mans mind stretched to a new idea never goes back to but unable to speak a word for several days. The
its original dimension. malady occurs suddenly and he stops as if he were
Oliver Wendell Holmes, Sr., 1859 (241) frozen, his eyes open, xed and motionless (26).
On recovery, patients say that they desired to
How is catatonia related to other medical and
speak but were unable to do so, sensing impending
psychiatric disorders? Catatonia usually has an
doom. Persons in catatonic stupor are frozen,
acute onset and once expressed, persists for days,
petried, and experience extreme fear (27). They
months, even years if not treated. It is as common
give the appearance of intense anxiety (2830).
in children and adolescents as it is in adults. Many
In discussing catatonia in children, the historian
forms are now recognized, some not ordinarily
Edward Shorter cites an eighteenth-century French
destructive but lethal when accompanied by fever
physician who delayed the funeral services of a girl
and systemic distress. The behaviors are seen either
from the lower classes because her color had not
as inhibited and retarded and regarded as stupor
changed at all. And she recovered a few hours
or as excited and aggressive and seen as delirium
later. The girl would already have been buried sev-
or delirious mania. Catatonia is mainly a disorder
eral times, if we had not been familiar with her
of body posture, movement, and speech, although
attacks of hysterical vapors (138).
some patients report intense anxiety and fear.
In a history of malignant catatonia, Shorter
Catatonia has not been traced to a defect in a
describes the progressively severe stages of catato-
single-body organ nor to a specic physiologic
nia, malignant catatonia, neuroleptic malignant
dysfunction. After catatonia is relieved, we see no
syndrome, and delirious mania, the latter some-
residuals; it is as if the blackboard has been erased
times prompted by the horrors of war: As the ter-
with a few smudges left at the corners. It is a
ried civilian population of northern France ed
behavior of the whole organism, more like waking
the advancing German armies in 1940 there was
and sleeping or like a childs crying.
massive fear. Some of the worse aicted found
The phenomenology is distinct from that of
their way to the psychiatric hospital at Auxerre,
other psychiatric diagnoses. Some authors see
where there were 17 cases of delire aigu [delirious
catatonia as a common end-state response to
mania], almost all with a fever and ending fatally
the feeling of imminent doom inherited from
(124).
ancestral encounters with carnivores, an adapta-
In 1982, a perceptive Australian psychiatrist
tion that has changed over the millennia of
described four patients with systemic physical ill-
human development but remains a common fea-
ness who exhibited catatonia in association with
ture of life (15). In this fear hypothesis, catato-
intense fear (242). Although the patients were pre-
nia is a whole-body phenomenon, and support
scribed eective treatments for catatonia, recovery
for the hypothesis is found in the quick relief
depended, he believed, on attention to and treat-
aorded by the anxiolytic qualities of drugs used
ment of the psychological stressors. He regarded
to relieve its symptoms.
catatonia as regression to a primitive expression
When Kahlbaum envisioned catatonia as a syn-
elicited by overwhelming fear.
drome, he described his patients as astonished or
In a systematic inquiry, Georg Northo and his
thunderstruck. The syndrome appeared after
colleagues in Frankfurt, Germany, assessed the
very severe physical or mental stress such as a
experiences 3 weeks after recovery of 24 patients
terrifying experience. He said that the patient
(15 excited, 9 inhibited) who met the criteria of
remains motionless, without speaking, and with a
four or more catatonia signs (28). The patients
rigid masklike facies, the eyes focused at a distance
greatest fears were their inability to control their
devoid of any will to move or to react to any
intense anxiety. They felt threatened and feared
stimulus. He continues: The general impression
dying. They were less concerned about their lack
conveyed is one of profound mental anguish, or
of control of body movement or of self-care.
an immobility induced by severe mental shock
The association of the fear response with catato-
(13). Citing fear as the central theme of the syn-
nia among children and adolescents with autism
drome, Kahlbaum titled his book Die Katatonie,
and with tics has recently been detailed by Dirk
oder das Spannungs-Irresein, translated as Catato-
Dhossche. He reports deprivation, abuse, and
nia, The Tension Insanity.
trauma to be frequent in the expression of catato-
A writer nds subjects who lay like a log of
nia among them (148).
wood, stretched out, able to behold with his eyes

35
Max Fink
After cardiac surgery, immobilization reactions
with the characteristics of catatonia have been
encountered. One patient was immobilized and
almost like a statue; another was frozen and
expressionless. She spoke barely audibly in a
monotone with long pauses and made no sponta-
neous comments. The postoperative reaction has
been described as experiencing a catastrophe, the
patients resembling the photographed faces of sur-
vivors of civil disasters, and the countenances pres-
ent staring and vacant expressions of seeming
frozen terror. Immobile, apathetic, and completely
indierent to their fate, they respond to inquiries
in monosyllables devoid of aect (243).
A one-person experimental study demonstrated
the relation of catatonia to fear. A 42-year-old
woman with a long history of recurring depressions
was admitted to hospital for a recurrent episode.
Treatment with the antidepressant maprotiline was
discontinued, and the next day she was mute and
stuporous. A single oral dose of 2.5 mg lorazepam
relieved the stupor and the depressed mood, and
she asked to be discharged. With her consent, an
experiment was undertaken to verify the diagnosis
of catatonia. She was given an intravenous bolus
of 0.7 mg umazenil, a benzodiazepine antagonist
that blocks the receptor and reverses the actions of
lorazepam. Almost immediately she became dizzy,
nauseous, and anxious and feared impending acci-
dents to family members. The fears quickly con-
densed to certainty, and within 2 min, she was
again mute and stuporous and remained so for
2 h. She was treated with lorazepam and recov-
ered. After the rst treatment and reversal, the
experiment was repeated with the same results. The
patient was discharged from hospital with prescrip-
tions for lorazepam and carbamazepine and
remained well (244).
Seizures, whether naturally or experimentally
induced, may immediately be followed by immo-
bility and stupor. The sudden loss of conscious-
ness, posture, and spontaneous motor acts with
tongue biting and urinary wetting is a severely
frightening experience. Consequences are often
described as either rigid-catatonic or accid-
cataleptic states that bear the characteristics of
catatonia (245, 246).
Barbiturates and benzodiazepines that relieve
anxious depression also relieve catatonia, an expe-
rience that, as previously noted, is consonant with
the fear hypothesis. The rapid eect of these
agents is demonstrated by reports that administer-
ing parenteral lorazepam to mute and negativistic
patients en route to MRI or EEG laboratories
makes them cooperative and talkative for the
procedure.
36
Tonic Immobility
These diverse human experiences are found in ani-
mals described as tonic immobility and negative
conditioning. Tonic immobility is the elicitation of
a xed posture, usually rigid, that is elicited by qui-
etly holding an animal down, slowly stroking, and
then gradually releasing the hold. The animal
remains immobile with limbs in the unusual pos-
tures that they are placed. The phenomenon is
demonstrated in chickens and other fowl, frogs,
snakes, guinea pigs, and rabbits (247). A tradition
of pretending to be dead is described as the behav-
ior of the Virginia opossum playing possum, as
it is described in childhood play (248).
A loud noise terminates the imposed posture.
The duration of the pose is lengthened when pre-
ceded by a frightening stimulus such as loud noise,
electric shock, adrenalin injections, or simulated
predation as when a chicken is held under the head
of a model of a Coopers Hawk for 15 s before
immobilization. The duration is shortened in a
dose-related fashion by pretreatment with tran-
quilizers that sedate and inhibit fear (247).
Intense fear is pictured as the evolutionary basis
for both tonic immobilization and for catatonia.
Recognition that catatonia is present in 10% of
acutely ill psychiatric inpatients, that it is relieved
by the potent anxiolytic drugs, and that patients
give the appearance of intense anxiety, led the New
Zealand psychologist Andrew Moskowitz to pro-
pose that catatonia is a relic of ancient defensive
strategies, developed during an extended period of
evolution in which humans had to face predators
in much the same way many animals do today and
designed to maximize an individuals chances of
surviving a potentially lethal attack (15).
Among the defenses of prey animals are ight,
ght, and dissimulation. Flight is stimulated when
the predator is seen at a distance; ght is an
option when escape is not possible; and hiding,
dissimulation, and lack of movement are encour-
aged when the predator is at a distance that would
permit not seeing an immobile prey. The core cata-
tonic symptoms of stupor, mutism, and immobility
can be linked to tonic immobilization.
Fear conditioning, a form of emotional learning
that connects a neutral stimulus to one eliciting
fear, also suggests a link to catatonia. Repeated
exposure to a neutral stimulus (e.g., ringing of a
bell) with a painful shock stimulus ties the stimulus
and response together so that ringing the bell elicits
physiologic autonomic changes (e.g., catechol-
amine release from the adrenal medulla and
sympathetic nerves) and endocrine release (e.g.,
glucocorticoids of the adrenal cortex) (249).

The most compelling daily life images of
immobility in the face of intense fear are
reported in accounts of rape assault. The actress
Kelly McGillis presented a detailed description
of being assaulted and raped by two men in an
article on the lm The Accused, noting that,
although she was conscious, crying, and scream-
ing, she was unable to move (250). Studies of
tonic immobility during rape and assault describe
intense fear, inability to move, and perceived
physical restraint (251, 252). Fear-induced freez-
ing is also reported in military disasters and in
urban violence (253).
Cyber bullying, the sending of hostile denigrating
messages through social media, is an increasing
stressor among adolescents, severe enough to lead to
withdrawal from school, hospital care, and suicide.
A 14-year-old girl without prior psychiatric history
was admitted to hospital with anxiety, tearfulness,
and insomnia, which matured to an oneiroid state
with mutism, immobility, waxy exibility, postur-
ing, and negativism. Treatment with daily ECT
relieved the condition in 2 weeks (254).
The experiences with tonic immobility are rele-
vant to our understanding of post-traumatic stress
disorders (PTSD). In an experiment, both normal
and PTSD subjects related their most disturbing
experiences, and the stories were recorded and edi-
ted into 100-word scripts. A script was then read
to the subject standing on a platform that mea-
sures body sway. The record of the sway is broad
in normal subjects but very narrow in PTSD
subjects reecting increased immobility (255).
If tonic immobility is a human phenomenon, we
would expect the signs to occur in patients with
panic disorders. In a questionnaire study of 1118
community-based subjects with a history of panic
attacks, 18% reported being immobilized always,
36% sometimes, and 16% rarely during their tions allow the view of catatonia outside the
attacks (256).
These many diverse experiences and descriptions
encourage attention to the role of fear in our image
of catatonia. Stupor, rigidity, posturing, and mut-
Rediscovering catatonia
ism are behaviors that are analogous to tonic
immobilization. Repetitive words and acts, postur-
ing, and grimacing are dissimulations attempts to
appear other than oneself. A childs fear and dis-
comfort stimulates crying that brings nursing, cud-
dling, and relief. Older children develop a
repertoire of calls, screams, cries, postures, hiding,
throwing, and breaking of objects to bring similar
relief. Being mute and not responding brings
desired attention. The behaviors may be active or
passive, and for each, the caretakers and other
children respond, and soon postures, grimaces,
repetitive acts, repetitive speech, and withholding
of speech become learned behaviors that elicit
reassuring responses.
Catatonia may be regarded as a relic of the per-
iod in human history in which being prey for
aggressive animals led to the same defenses that
are seen in prey animals. Such imagery is consis-
tent with the ecacy of the anxiolytic treatments
of barbiturates and benzodiazepines. The ecacy
of ECT in relieving catatonia is a puzzlement,
however. We do not understand the mechanism
by which induced seizures alter behavior,
although a viable hypothesis considers the brains
release of neuroendocrine hormones in the course
of the seizure as instrumental (257). Such hor-
mone studies have not been of interest to catato-
nia scholars. It would be timely to study the
neuroendocrine action of the eective treatments
now that catatonia is appreciated as a unique
behavior syndrome.
Catatonia is an abnormal behavior that is identi-
ed by observation alone. Changes in movement,
posture, and speech are sucient to identify the
syndrome. No damage to the body remains after
recovery, indicating that the abnormal behavior is
an exaggeration of the normal state. Such observa-
conventional causes of the bodys systemic
disorders and encourage its consideration as an
inherited adaptive syndrome.
37
Max Fink

Chapter 8: Lenvoi
The art of drawing conclusions from experiments and relieved catatonia as eectively as do the treat-
observations consists in evaluating probabilities and ments for neurosyphilis today.
estimating if they are large and numerous enough to We see immediate benets in identifying catato-
constitute proofs. The type of calculation is more com- nia as a unique syndrome outside schizophrenia.
plicated and more dicult than we think; it demands Ever since its creation, schizophrenia has been pic-
great sagacity. Antoine Lavoisier (258) tured as an illness of disorganized thought and
speech associated with delusions, hallucinations,
The birth of catatonia as a concept in 1874 was
and emotional attening. When catatonia was
followed by a stormy childhood. Within two
incorporated within schizophrenia, its recognition
decades, it was abducted into the concept of
led physicians to interpret their patients peculiar
dementia praecox and was hidden, like Cinderella,
movements and speech as psychotic even when
for almost a century. Despite the miraculous tting
thought disorder, emotional attening, and the
slippers of sodium amobarbital and induced sei-
other signs of psychosis were not present. The phy-
zures, the eective treatments devised in the 1930s
sicians reexively prescribed neuroleptic drugs as
that should have been liberating, the sequestration
treatment. Little merit has been found in this asso-
of catatonia within schizophrenia remained all but
ciation; indeed, as we have seen, such prescription
complete until the 1970s when catatonia was again
is fraught with the risk of precipitating a malignant
reported in patients with mood disorders and in
syndrome and even death.
neurotoxic states. The recognition that the neuro-
Patients meeting the criteria of catatonic schizo-
leptic malignant syndrome was a form of catatonia
phrenia respond to ECT with relief of catatonia. In
that could be eectively relieved by its treatments
most instances, the relief is accompanied with a
opened clinicians eyes to catatonia outside Krae-
disappearance of the signs that were interpreted as
pelins schizophrenia.
evidence of psychosis. But patients with other
Recognizing catatonia in NMS revived our inter-
forms of schizophrenia, the paranoid, disorga-
est in the unique syndrome and taught us its signs.
nized, undierentiated, and residual forms,
When we perceived the signs of catatonia among
respond poorly to ECT. The benet in the relief of
our delirious manic patients, we were able to treat
catatonia clearly accrues to the signs of catatonia
them eectively and save lives. Cases of NMS in
and not to those of schizophrenia.
patients who had not been exposed to neuroleptics
In the rst half of the twentieth century, catato-
led to recognition of the toxic serotonin syndrome
nia was interpreted in psychologic terms, often
as a treatable example of catatonia. The associa-
labeled as hysteria. Once the syndrome was
tion of catatonia in patients in excited delirious
relieved by amobarbital and by ECT, however, a
states and the remarkable ecacy of induced sei-
biological image took precedence. The ecacy of
zures and benzodiazepines for rapid relief brought
these treatments is now established, an experience
delirious mania within the catatonia tent.
that would be the envy of the clinicians who rst
The recognition that self-injurious behavior in
recognized catatonia but whose knowledge
patients with autism and neurodevelopmental
provided no relief for their patients.
defects were signs of catatonia argued for treat-
The appreciation of catatonia as an indepen-
ment trials that were successful. Catatonia was
dent syndrome in clinical medicine is an example
next appreciated in the repetitive behaviors of
of the successful application of the medical model
patients with Gilles de la Tourette and other tic
of diagnosis the established method of disease
disorders, obsessivecompulsive disorder, anti-
identication by history, physical examination,
NMDAR encephalitis, elective mutism, pervasive
laboratory tests, and validation by response to
refusal syndrome, and akinetic mutism. The evi-
treatment (259). Unfortunately, this medical diag-
dence for viewing these disorders as forms of cata-
nostic model is rejected for psychiatric classica-
tonia is suciently compelling to revisit their
tion and is replaced by an image match-up based
classication, clarify their diagnostic criteria, and
on the main symptoms alone. After listening to
test alternate treatment possibilities.
the patients history, the physician examines
The immediate relief of catatonia by intravenous
symptom checklists to nd a comparable classied
injections of benzodiazepines oered a useful bio-
symptom pattern. No physical examination is
logical marker that veried the clinical diagnosis.
made. No laboratory tests are applied. No refer-
Treatment with high doses of benzodiazepines
ence to prior responses to treatments is consid-
(followed by ECT when the medications failed)

38

ered. As a result, the DSM classication is a mel-
ange of arbitrary and ill-dened labels, and each
individual diagnosis is almost exclusively in the
eyes of the beholder.
The melancholia error
Like the arbitrary classication of catatonia as a
form of schizophrenia, melancholia is rejected in
the DSM classication. Melancholia is a psycho-
pathological syndrome that was well described
throughout history, beginning in ancient Greek
and Roman medical texts. In the 1850s, a circular
insanity of severe depressions alternating with
manic episodes was delineated by the French
psychopathologists Jules-Gabriel Baillerger and
Jean-Pierre Falret. Other authors conrmed their
description, but it was the formulation by Emil
Kraepelin of manicdepressive insanity that took
hold and was appreciated throughout the twentieth
century. In 1980, the DSM-III discarded the con-
cept of a single illness of alternating phases and
divided the mood disorders into major depression
and bipolar disorder. In splitting the disease
entity by polarity, the classiers sought to accom-
modate reports that the family patterns and the
new treatments with anticonvulsants seemed to
distinguish the entities. The label of manicdepres-
sive reaction described in DSM-II was discarded,
and melancholia was denigrated to a specier of
mood disorders without a code number, thereby
inhibiting its use (260).
Melancholia is a distinct identiable syndrome
with four consistent features (44). The mood is of
severe depression or mania or both. Suicide risk is
high. Motor behavior is always altered with
agitation and restlessness or retardation and stu-
por (261). The vegetative signs of anorexia, weight
loss, and insomnia are always present. And, cogni-
tive inability to concentrate thoughts or recall
memories is a common feature.
Extensive studies of cortisol, the adrenal gland
hormone, nd hypercortisolemia elevated levels
of cortisol in the blood at the height of the illness
and a return to normal levels with eective treat-
ment and clinical relief. With relapse, the abnor-
mality returns. Because systemic hormones exhibit
diurnal rhythms, the abnormality is best measured
by the dexamethasone suppression test, a measure
of serum cortisol over 24 h. An abnormal test is
considered a marker of melancholia and is used to
verify the diagnosis (44).
Physiologic abnormality in melancholia is also
reected in abnormal sleep EEG studies and in
dysfunction of thyroid metabolism. That melan-
cholia is a specic form of mood disorder is
Rediscovering catatonia
reected in its strong response to tricyclic antide-
pressants and to ECT, and the inecacy of SSRI
and SNRI antidepressants, various psychothera-
pies, and placebos (44, 262).
This error in the classication of melancholia
parallels the error that plagued catatonia. Despite
extensive writings justifying melancholia as a dis-
tinct medical syndrome (44, 261264) and even
pleadings (265), the members of the present DSM-
5 Work Group on mood disorders have rejected
any consideration of melancholia as a distinct
entity. The present proposals for the mood disor-
ders continue the classication much as developed
for DSM-IV.
The position in the classication and treatment
of the depressive mood disorders is reminiscent of
the arguments that developed in the 1980s regard-
ing the recommended treatments of the neuroleptic
malignant syndrome. Once the syndrome was rec-
ognized as a toxic eect of neuroleptic drugs, the
connection to the dopamine neurotransmitters was
invoked and treatments with dopamine agonists
recommended. It took two decades to replace the
neurotransmitter model and treatment with that of
catatonia and its specic treatment. Splitting the
mood disorders according to the unipolar or bipo-
lar model has yielded little benet in either the
understanding of mood disorders or eective treat-
ments. The alternative model, that of melancholia
as a dened entity with specic symptoms and
signs, laboratory test evidence of cortisol abnor-
mality as a diagnosis verier, and rapidity of
treatment response to tricyclic antidepressants and
ECT as validating criteria, warrants better consid-
eration in the classication.
The challenges
The relations of melancholia and catatonia is a
challenge. The early reports of catatonia recog-
nized its appearance in patients with disorders in
mood, and the ndings of catatonia among
patients with manic and depressive mood disorders
were the rst awareness that the identity of catato-
nia with schizophrenia was false. As we have
shown, patients with catatonia suer intense emo-
tions, often as severe as those with melancholia for
which suicide is the major risk. Both catatonia and
melancholia are rapidly resolved with ECT, sug-
gesting an inherent commonality that is not under-
stood and warrants exploration. Our lack of
experimental evidence makes us believe that mel-
ancholia does not resolve with benzodiazepines or
barbiturates and that catatonia does not resolve
with tricyclic antidepressant drugs. But these
assumptions are not secured by clinical trials; they
39
Max Fink
may be wrong and testing is warranted. The neuro-
endocrine abnormality in melancholia is well docu-
mented, but that in catatonia is not. These
questions need attention to clarify the relationship
between melancholia and catatonia.
The connection of catatonia with seizures is
another challenge. We know how to induce seizures
and can oer eective treatment. We know that the
benet for the patient resides in the seizure and not
in any aspect of the inducing agent whether the
stimulus is chemical, electrical, or magnetic is irrel-
evant. The eects are immediate, being appreciated
within a day, but repeated seizures are required to
sustain relief. Each seizure aects the neuroendo-
crine system, releasing a massive discharge of hor-
mones into the brain and throughout the body.
Some hormone eects are persistent and seem cor-
related with recovery and sustained benet (257,
264). While we have some information on the hor-
monal eects of induced seizures, we have very lit-
tle on the hormone changes in catatonia. The
relationships between seizures and catatonia war-
rant greater attention.
Another intriguing aspect of catatonia is its simi-
larity to the animal condition of tonic immobility,
a reex that can be experimentally induced in prey
animals under conditions of acute threat. Many
authors, beginning with Kahlbaum, noted the fear
and tension of patients with catatonia. The evi-
dence for a relationship between fear and catatonia
encourages more detailed study.
But while we have made much progress in iden-
tifying the patients who have catatonia and in our
ability to help them, the position of patients with
catatonia in our society is perilous. First, the
recognition of catatonia and its teaching are poor.
Catatonia is typically hidden in textbooks as a type
of schizophrenia, nothing more, and its eective
treatments are disregarded. Published case reports
describe prolonged illness and even fatalities
because catatonia was not appreciated and not
appropriately treated.
The stigmatization of ECT is widely encouraged
by the failure of medical school faculties and psy-
chiatric and neurologic residency training programs
to consider the treatment a necessary part of the
education of their students. The failure of many
psychiatric hospitals and medical schools to equip
and maintain ECT treatment facilities is evidence of
the stigma. Such failures are unethical in the princi-
ple of justice, the necessity for society to make
known eective treatments available to all citizens
regardless of their illness and social status (266).
Further, while the state has a duty to protect the
interests of minors and the psychiatrically ill, spe-
cial regulations have come to inhibit eective treat-
40
ment for patients with catatonia. Patients who are
mute, negativistic, and in stupor, delirium, or furor
may be unable to give verbal or written consent for
their care. In many treatment venues, the use of
intravenous sedatives, and more so, the application
of ECT is severely restricted; in some US states, it
is even proscribed by law.
Two cases illustrate how legislative obstacles to
appropriate treatment of catatonia can adversely
aect individual patients and their families:
A 22-year-old woman, without any prior psychiatric
illness, developed malignant catatonia following a
Caesarean delivery. The legal hurdles to obtaining
consent under the highly restrictive rules of California
severely impeded her treatment for 33 days, risking her
life and causing unnecessary additional expense for her
and for society. Within 36 h of treatment she no longer
required special nursing care and proceeded to full
recovery (266).
A 16-year-old adolescent suering from autism spectrum
disorder developed life-threatening self-injurious behav-
ior. After the failure of extensive psychological and medi-
cal treatment trials a course of ECT in Baltimore
resolved the injurious behavior and allowed him to return
to his home to be maintained by periodic continuation
ECT. But the family lived in Los Angeles where ECT in
children and adolescents under age 18 is legislatively
interdicted. For his treatments the family had to y every
7 to 10 days to Tucson, Arizona in order for the boy and
the family to experience a more healthy home life.
Kahlbaum envisioned catatonia as a disorder of
movement and mood, and in the more than a
century since his description, we have learned to
identify the syndrome as he saw it. We have added
veriable tests and developed eective and safe
treatments. We are now able to detect many forms
that catatonia takes in the clinic. The recognition
of catatonia assures not only advances in wellbeing
of patients but also oers personal gratication for
clinicians as they restore a sick person, often mori-
bund, to full health. In liberating catatonia as an
independent treatable syndrome in the dictionary
of psychiatric illnesses, we honor the vision of Karl
Kahlbaum and bring his image of catatonia out of
the shadows.
Acknowledgements
Michael Taylor brought catatonia out of the shadows of
schizophrenia by his diagnostic studies in the 1970s. When my
interest in catatonia was aroused in the 1980s, Mickey
explained the many variations of the syndrome and together
we challenged the DSM classication. We went on to collabo-
rate in expanded texts on Catatonia (2003) and Melancholia
(2006).

Edward Shorter dramatically extended my education in the
history of psychiatry. His 1997 History of Psychiatry is the
classic modern text. In 2007, with David Healy, he wrote
Shock Therapy: A History of Electroconvulsive Treatment in
Mental Illness. He went on to write Endocrine Psychiatry
(Oxford 2010) and asked me to add a clinical chapter. Since
then, he has written extensively on the history of malignant
catatonia and delirious mania. He stimulated much of my
enthusiasm for the stories of the clinicians who went before
us, on whose eyes we depend for our images and on whose
shoulders we stand.
Dirk Dhossche and Lee Wachtel are intrepid child and ado-
lescent psychiatrists who broadened our concepts of catatonia
to include many childhood disorders now labeled by epony-
mous names. The recognition of these behaviors as forms of
catatonia has improved the lives of many disadvantaged and
disabled youth.
When Taylor and I rst described catatonia as a common
medical syndrome, David Healy challenged our interpretation
that catatonia was a frequently diagnosable illness. He sent out
registrars to hospitals in Wales and India, used our rating
scale, and found patients with the syndrome, as predicted. He
also challenged us to defend catatonia as an independent
identiable and treatable syndrome.
Edward Shorter, David Healy, Jan-Otto Ottosson, Tom
Bolwig, and Kennedy Cosgrove were readers and critics of
early drafts of this biography. I am indebted to my wife
Martha and the editor Jonathan Cobb who read each revision
demanding increasing clarity and simplication. The text was
ably copyedited by Susan Belanger. The index was assured by
Kristin Nyitray and Lynn Toscano, archivists at the Stony
Brook University Library.
I am grateful to the Directors of the Scion Natural Science
Foundation and the predecessor International Association
for Psychiatric Research who supported my studies of
catatonia, melancholia, convulsive therapy, and quantitative
electroencephalography.
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