Frontal Lobes

The frontal lobes are considered our emotional control center and home to our personality.
There is no other part of the brain where lesions can cause such a wide variety of symptoms
(Kolb & Wishaw, 1990). The frontal lobes are involved in motor function, problem solving,
spontaneity, memory, language, initiation, judgement, impulse control, and social and sexual
behavior. The frontal lobes are extremely vulnerable to injury due to their location at the front
of the cranium, proximity to the sphenoid wing and their large size. MRI studies have shown
that the frontal area is the most common region of injury following mild to moderate
traumatic brain injury (Levin et al., 1987).
There are important asymmetrical differences in the frontal lobes. The left frontal lobe is
involved in controlling language related movement, whereas the right frontal lobe plays a role
in non-verbal abilities. Some researchers emphasize that this rule is not absolute and that
with many people, both lobes are involved in nearly all behavior.
Disturbance of motor function is typically characterized by loss of fine movements and
strength of the arms, hands and fingers (Kuypers, 1981). Complex chains of motor movement
also seem to be controlled by the frontal lobes (Leonard et al., 1988). Patients with frontal
lobe damage exhibit little spontaneous facial expression, which points to the role of the frontal
lobes in facial expression (Kolb & Milner, 1981). Broca's Aphasia, or difficulty in speaking, has
been associated with frontal damage by Brown (1972).
An interesting phenomenon of frontal lobe damage is the insignificant effect it can have on
traditional IQ testing. Researchers believe that this may have to do with IQ tests typically
assessing convergent rather than divergent thinking. Frontal lobe damage seems to have an
impact on divergent thinking, or flexibility and problem solving ability. There is also evidence
showing lingering interference with attention and memory even after good recovery from a
TBI (Stuss et al., 1985).
Another area often associated with frontal damage is that of "behavioral sponteneity." Kolb &
Milner (1981) found that individual with frontal damage displayed fewer spontaneous facial
movements, spoke fewer words (left frontal lesions) or excessively (right frontal lesions).
One of the most common characteristics of frontal lobe damage is difficulty in interpreting
feedback from the environment. Perseverating on a response (Milner, 1964), risk taking, and
non-compliance with rules (Miller, 1985), and impaired associated learning (using external
cues to help guide behavior) (Drewe, 1975) are a few examples of this type of deficit.
The frontal lobes are also thought to play a part in our spatial orientation, including our body's
orientation in space (Semmes et al., 1963).
One of the most common effects of frontal damage can be a dramatic change in social
behavior. A person's personality can undergo significant changes after an injury to the frontal
lobes, especially when both lobes are involved. There are some differences in the left versus
right frontal lobes in this area. Left frontal damage usually manifests as pseudodepression
and right frontal damage as pseudopsychopathic (Blumer and Benson, 1975).
Sexual behavior can also be effected by frontal lesions. Orbital frontal damage can introduce
abnormal sexual behavior, while dorolateral lesions may reduce sexual interest (Walker and
Blummer, 1975).
Some common tests for frontal lobe function are: Wisconsin Card Sorting (response
inhibition); Finger Tapping (motor skills); Token Test (language skills).
References:
Blumer, D., & Benson, D. Personality changes with frontal and temporal lobe lesions. In D.
Benson and D. Blumer, eds. Psychiatric Aspects of Neurologic Disease. New York: Grune &
Stratton, 1975.
Brown, J. Aphasia, Apraxia and Agnosia. Springfield, IL: Charles C. Thomas, 1972.
Drewe, E. (1975). Go-no-go learning after frontal lobe lesion in humans. Cortex, 11:8-16.
Kolb, B., & Milner, B. (1981). Performance of complex arm and facial movements after focal
brain lesions. Neuropsychologia, 19:505-514.
Kuypers, H. Anatomy of the descending pathways. In V. Brooks, ed. The Nervous System,
Handbook of Physiology, vol. 2. Baltimore: Williams and Wilkins, 1981.
Leonard, G., Jones, L., & Milner, B. (1988). Residual impairment in handgrip strength after
unilateral frontal-lobe lesions. Neuropsychologia, 26:555-564.
Levin et al. (1987). Magnetic resonance imaging and computerized tomography in relation to
the neurobehavioral sequelae of mild and moderate head injuries. Journal of Neurosurgery,
66, 706-713.
Miller, L. (1985). Cognitive risk taking after frontal or temporal lobectomy. I. The synthesis
of fragmented visual information. Neuropsychologia, 23:359-369.
 Milner, B. Some effects of frontal lobectomy in man. In J. Warren and K. Akert, eds. The
Frontal Granular Cortex and Behavior. New York: McGraw-Hill, 1964.
Semmes, J., Weinstein, S., Ghent, L., & Teuber, H. (1963). Impaired orientation in personal
and extrapersonal space. Brain, 86:747-772.
Stuss, D. et al. (1985). Subtle neuropsychological deficits in patients with good recovery after
closed head injury. Neurosurgery, 17, 41-47.
Walker, E., & Blumer, D. The localization of sex in the brain. In K.J. Zulch, O. Creutzfeldt,
and G. Galbraith, eds. Cerebral Localization, Berlin and New York: Springer-Verlag, 1975.

https://www.neuroskills.com/brain-injury/frontal-lobes.php

Frontal Lobe Syndromes

Updated: Jun 08, 2018

 Author: Stephen L Nelson, Jr, MD, PhD, FAAP; Chief Editor: Jasvinder Chawla, MD,
MBA more...
Background
The frontal lobe is the largest lobe in the brain, yet it is often not specifically
evaluated in routine neurologic examinations. This may in part be due to the
attention to detail and rigorous testing strategies required to probe frontal lobe
functions. As successful completion of any cognitive task considered a frontal
lobe function requires multiple brain regions both within and outside the frontal
lobe, some authors prefer the term frontal systems disease. In any case,
dysfunctions of the frontal lobe can give rise to relatively specific clinical
syndromes. When a patient's history suggests frontal lobe dysfunction,
detailed neurobehavioral evaluation is necessary.
Traditional classification systems divide the frontal lobes into the precentral
cortex (the strip immediately anterior to the central or Sylvian fissure) and
prefrontal cortex (extending from the frontal poles to the precentral cortex and
includes the frontal operculum), which is broken into: orbitofrontal cortex
(including the orbitobasal or ventromedial and the inferior mesial regions),
ventrolateral prefrontal cortex, dorsolateral prefrontal cortex, medial prefrontal
cortex (containing the anterior cingulate gyrus, and prelimbic and infralimbic
cortices), and the caudal prefrontal cortex (which includes the frontal eye
fields). Each of these areas has widespread connectivity.
Given the unique connectivity between the frontal regions and deeper brain
structures, lesions of these areas or their connections generate relatively
distinctive clinical behaviors.
  The dorsolateral frontal cortex is concerned with planning, strategy
formation, and executive function. Patients with dorsolateral frontal
lesions tend to have apathy, personality changes, abulia, and lack of
ability to plan or to sequence actions or tasks. These patients have poor
working memory for verbal information (if the left hemisphere is
predominantly affected) or spatial information (if the right hemisphere
bears the lesion brunt).
 The frontal operculum contains the center for expression of language.
Patients with left frontal operculum lesions may demonstrate Broca
aphasia and defective verb retrieval, whereas patients with exclusively
right opercular lesions tend to develop expressive aprosodia.
 The orbitofrontal cortex is concerned with response inhibition. Patients
with orbitofrontal lesions tend to have difficulty with disinhibition,
emotional lability, and memory disorders. Patients with such acquired
sociopathy, or pseudopsychopathic disorder, are said to have
an orbital personality. Personality changes from orbital damage include
impulsiveness, puerility, a jocular attitude, sexual disinhibition, and
complete lack of concern for others.
 Patients with lesions affecting the cingulate cortex typically develop
akinetic mutism.
 Patients with inferior mesial (basal forebrain) lesions tend to manifest
anterograde and retrograde amnesia and confabulation.
Broca aphasia from a lesion in areas 44 and 45 on the left hemisphere leads
to nonfluent speech, agrammatism, paraphasias, anomia, and poor repetition.
Lesions anterior, superior, and deep to (but sparing) the Broca area produce
abnormal syntax and grammar but repetition and automatic language are
preserved. This disorder is known as transcortical motor aphasia (also called
commissural dysphasia) and uninhibited echolalia is common. Memory
disturbances only develop with lesion extension into the septal nucleus of the
basal forebrain. Appreciation of verbal humor is most impaired in right frontal
polar pathology.
The image below shows an MRI that is suggestive of frontotemporal
dementia.
 Axial brain MRI of a patient with progressive tremorless
parkinsonism and frontal-predominant dementia (Mini Mental State
Examination = 23/30; Frontal Assessment Battery = 10/18; abnormal clock
drawing task and additional constructional impairment) with moderate
ideomotor apraxia. The MRI demonstrates predominantly frontal (A) and
anterior temporal atrophy (B) suggestive of frontotemporal dementia.
Pathophysiology
A detailed discussion of the pathophysiology of frontal lobe dysfunction is
beyond the scope of this review and the reader is referred to 2 excellent
reviews by Mesulam (2002) and Bonelli and Cummings (2007). [1, 2] As
Mesulam has discussed, one way to think about the role of the frontal lobe is
that it is the brain's way of modifying and interposing constraints on basic
reflexive behaviors. For example, taking food when one is hungry is reflexive.
Nonetheless, most adults can inhibit this behavior until the context is
appropriate. Most hungry diners waiting in line at a restaurant do not usually
help themselves to food from the plates of diners who have already been
served, but some patients with frontal lobe dysfunction cannot inhibit this
response.
Unlike most animals, a human's mental state is preoccupied a great deal with
what has happened in the past or what may happen in the future. Parts of the
frontal lobe are essential for this type of "time travel." Indeed, good judgment
requires evaluating the possible consequences of a variety of future activities
and selecting the one with the most good consequences and the fewest bad
consequences.
This frontal lobe-mediated responsibility of decision-making depends on the
valuation of a choice, such as its costs, benefits, and probability of success,
as well as the assessment of the outcome of a given choice, in order to adapt
future behaviors appropriately. The anterior cingulate cortex is primarily
responsible for selecting choices and evaluating the outcome of that selection
to ensure adaptation to the environment. [1] The orbitofrontal cortex is
responsible for changes in behavior in response to unexpected
outcomes. [2] Poor judgment and inappropriately weighting of the value of past
experiences may, as a result, occur with frontal lobe dysfunction.
Working memory involves a complex circuit that involves many brain regions,
including the dorsolateral frontal cortex, thalamus, and parts of the temporal
and parietal cortices. Working memory is defined as memory for a limited
amount of information (such as a telephone number) that needs to be kept in
consciousness for a few seconds (until the number is dialed) and then may be
lost forever. Most patients are able to hold 6 or 7 digits in working memory.
Patients with frontal lobe impairment may have decreased capacity in working
memory (eg, shortened digit span) or difficulty manipulating information in
working memory (eg, impaired reverse digit span test).
Epidemiology
Frequency
United States
Data are not available for the epidemiology of frontal lobe dysfunction as a
clinical syndrome, but data are available concerning the incidence and
prevalence of the major causes of syndromes of frontal lobe dysfunction. For
specifics on these data, please refer to the following linked Medscape
Reference articles. Common causes (see also Causes) include the following:
 Intellectual disability
 Traumatic brain injury (see Classification and Complications of Traumatic
Brain Injury and Traumatic Brain Injury: Definition, Epidemiology,
Pathophysiology
 Brain tumors (see Brain Metastatis and EEG in Brain Tumors)
 Degenerative dementias including Alzheimer disease, dementia with
Lewy bodies, Parkinson-Plus Syndromes, and frontotemporal dementias
 Cerebrovascular disease
 Normal-pressure hydrocephalus and other hydrocephalic disorders
 Psychiatric diseases such as schizophrenia and major depression
  In addition, any neurologic or psychiatric disease that can affect the
frontal lobe (eg, multiple sclerosis, CNS lupus) may be associated with
frontal lobe dysfunction.
 Frontal lobe dysfunction is associated with blood alcohol level and occurs
during acute intoxication with many recreational drugs.
Sex
Traumatic brain injury is much more common in men than women both in the
United States and worldwide. Gender predominance depends on the specific
underlying neurologic disorder.
Age
The relative likelihood of different causes of frontal lobe dysfunction is a
function of patient age. In teenagers and young adults, the most common
causes are intellectual disability, traumatic brain injury, and drug intoxication.
In middle-aged patients, brain tumors, cerebrovascular disease, infections
such as HIV, multiple sclerosis, and early onset degenerative dementias are
common. In late life, cerebrovascular disease and degenerative dementias
are predominant causes of frontal lobe dysfunction. The main degenerative
dementias with frontal lobe predominance, frontotemporal lobar
degenerations, together with Alzheimer disease, are the most common
degenerative dementias in the pre-senile age (younger than 65 years).
History
The examiner must obtain a history from an informant who knows the patient
well. One of the seeming paradoxes of frontal lobe dysfunction is that
informants may complain about the patient's "inability to do anything," yet on
at least cursory mental status testing, the patient appears normal or only
mildly impaired. This dissociation should be a clue that frontal lobe
dysfunction may be present. Symptoms of possible frontal lobe dysfunction
that should be probed include change in performance at work and changes
organizing and executing difficult tasks such as holiday dinners or travel
itineraries. [3] The examiner should inquire about the following changes:
 Appropriateness of behavior: Does the patient say things that he or she
would never have said before, such as "You are so fat" or "That is a really
ugly dress"?
 Patient's table manners: Does the patient now take food and start eating
before everyone else, or take food from other people's plates without
asking?
 Patient's empathy and ability to infer the mental state of others: This kind
of dysfunction often leads to inappropriate behavior.
  Possible apathy: Does the patient care less about hobbies, family
members, and finances than previously?
 An increase or decrease in the patient's sexuality or in his or her
judgment about possible liaisons.
In addition to these data, the examiner should obtain careful developmental,
head trauma, and social histories, including educational and personal
attainments. The examiner should also probe about possible substance
abuse, whether the patient was a victim of past abuse (physical, sexual, or
psychiatric) and about major psychiatric stressor (eg, deaths of friends or
family, divorce or separation, job loss or financial reversals). Indeed, a
detailed past psychiatric history is required.
Physical
Dysfunction of parts of the frontal lobe is sometimes associated with aphasia
or severe impairment of attention and can make formal neuropsychologic
testing or neurobehavioral evaluation problematic.
Many commonly used brief mental state tests, including the Mini-Mental State
Examination, are not designed to test frontal lobe function—they are
insensitive and not specific to frontal lobe dysfunction. A person with a Mini-
Mental State score of 26 from early Alzheimer disease may have relatively
preserved frontal lobe function, yet a patient with Pick disease with a similar
score may have profound frontal lobe dysfunction. Two validated bedside
tools that extend the cognitive screen to the frontal lobes are the Frontal
Assessment Battery (FAB) [4] and the Montreal Cognitive Assessment
(MoCA). [5] These instruments may be helpful for bedside evaluation of frontal
lobe function.
FAB was shown to be sensitive to frontal lobe damage of the right hemisphere
in stroke patients. The findings indicated that several FAB scores (including
composite and item scores) provided valid measures of right hemispheric
lateral frontal lobe dysfunction, specifically of focal lesions near the anterior
insula, in the right middle frontal gyrus, and in the right inferior frontal gyrus. [6]
Most neurologists and psychiatrists are familiar with the general principles of
evaluating frontal lobe function but a careful detailed evaluation usually
requires consultation with a neuropsychologist or cognitive (behavioral)
neurologist. Tests relatively sensitive to frontal lobe dysfunction include the
following:
 Go/No-Go task: Ask the patient to hold up one finger if the examiner
holds up two, and two fingers if the examiner holds up one. Test the
patient to ensure his or her understanding of the task. Perform 10 trials. A
failure to respond correctly (ie, echopraxia) suggests a lack of normal
response inhibition.
 Antisaccade task: After checking eye movements and visual fields, ask
the patient to move his or her eyes contralateral to the stimulus (usually a
wiggling finger). Therefore, if the left hand wiggles, the patient's eyes
should move approximately an equal distance to the right. A failure in the
task (visual grasp) may reflect dysfunction in the dorsolateral prefrontal
cortex or a lesion interrupting the pathway between this frontal region and
the superior colliculus. [7]
 Trail-making test (TMT): This test is widely used as a diagnostic tool for
eliciting shifts between cognitive sets. [8] The TMT contains two parts. In
part A (TMTA), subjects must connect 25 numbered circles, and in part B
(TMTB), numbers (1-13) and letters (A-M) must be connected in
alternating progression, from 1-A to M-13. Total score is the time in
seconds spent to complete each part. TMT requires cognitive flexibility
generated through activity in the dorsolateral and medial prefrontal
cortices. [9]
 Lexical fluency (word generation, Thurstone test): Ask the patient to
generate as many words as possible beginning with the letter F in one
minute. No proper names or derivatives are allowed. A normal score for a
native English speaker with at least a high school education is at least 8
words. Note that semantic category fluency tasks (eg, naming as many
animals or fruits in a minute as possible) localize to the temporal not
frontal lobes. [4] Therefore, such tests are not as useful as the letter
fluency task for testing frontal lobe dysfunction. Design fluency (how
many designs with four lines) has been suggested as an alternative for
aphasic patients. Although the lexical fluency test has relatively poor
localizing value, marked impairment is lateralizing to the left frontal
lobe. [10]
 Attention and concentration test: Intact attention and concentration is the
foundation on which all other cognitive tests are based. A patient who
does not attend normally cannot be tested accurately for cognitive
dysfunction. Serial 7s (ie, serial subtraction of 7 from 100 to 65) has been
proposed as a measure of attention and concentration. Spelling the
word WORLD backwards is commonly used as a substitute for patients
who cannot perform the serial 7s. Digit span is also used to measure
attention and concentration. A normal span is 6-7 digits forward and 4-5
backward. An abnormal digit span is the most common neuropsychologic
deficit in patients with head injury. Attention has a poor localizing value as
it may represent diffuse bihemispheric involvement.
 Alternating sequences task: Ask the patient to copy a segment with
alternating M s and N s. Perseveration may occur in patients with frontal
lobe lesions. Luria's three-step motor program is a sequential
 performance of three movements, usually the fist-edge–palm test, which
is making a fist, laying the hand on edge, and laying the palm of the hand
down on the table. Consider perseveration or failure to perform sequential
movements an abnormal response.
 The applause test is also a manifestation of perseveration. Patients are
asked to clap three times after demonstration by the examiner. Abnormal
outcome consists of clapping four or more times (positive applause sign).
This test has been felt highly specific for parkinsonian disorders with
frontal involvement. [11]
 Among the bedside screening tests, the FAB assesses conceptualization
(category responses, such as "in what way are a banana and an orange
are alike?"), lexical fluency, programming or motor series (Luria),
sensitivity to interference (conflicting instructions, such as "tap twice when
I tap once"), inhibitory control (Go/No-Go), and environmental autonomy
(prehension behavior, such as "do not take my hands"). For MoCA, from
the eight domains evaluated, aspects of executive functions are probed
using an alternation task adapted from the Trail-making B task, a
phonemic fluency task, and a two-item verbal abstraction task.
 Tests for nonspecific cognitive deficits: Nonspecific cognitive deficits may
be found in patients with frontal lesions. The deficits described below are
not specific to the frontal lobe and may also occur in nonfrontal lesions.
General bedside and neuropsychological testing for these deficits is
described below.
o Aphasia: Aphasia may result from lesions in and around the Broca
area (see Aphasia).
 Classic Broca-type aphasia consists of nonfluent speech,
grammatical errors, inability to repeat and to name objects and
verbs, and deep dyslexia.
 Aphasia can be assessed at the bedside by asking patients to
name and repeat both common and low-frequency words (eg,
pen and watch are considered easy, but clip, lens, and
hammock are considered difficult). The naming items on the
National Institutes of Health Stroke Scale (NIHSS) laminated
cards sold by the American Academy of Neurology (AAN)
contain six items of moderate difficulty. Repetition should include
a sentence with functor words. "No ifs, ands, or buts" is
commonly applied. Assess reading, writing, and spontaneous
speech. Deep dyslexia and spelling disorders are extremely
common in patients with Broca aphasia.
o Praxis
  As discussed in Apraxia and Related Syndromes, the engram
for skilled limb movements resides in the left inferior parietal
lobule in most right-handed people, but the engrams are
translated into motor programs by the premotor cortices.
Therefore, left frontal lesions, especially near supplementary
motor and premotor cortices, can cause limb apraxia.
 Therefore, patients with frontal lesions can be apraxic for skilled
limb movements without losing the knowledge or understanding
of the movement. Patients can also be apraxic because of
supplementary motor area lesions and convexity lesions, in
addition to parietal lesions. Asking the patient to pantomime the
use of real tools (eg, scissors, bread knife, hammer,
screwdriver) can test praxis.
 Buccofacial apraxia occurs when patients cannot perform
movements with the mouth or lips and localizes separately near
the Broca area.
 Callosal apraxia also may occur with anterior cerebral artery
strokes, causing unilateral left-limb apraxia. A curious finding is
that callosal apraxia is uncommon after surgical callosotomy but
relatively common after strokes of the anterior cerebral artery,
which also affect the gyri adjacent to the corpus callosum.
o Neglect: Neglect is most common after lesions of the right
hemisphere involving either the right parietal lobe or the right frontal
lobe. Other areas, including the thalamus and the basal ganglia, may
also be implicated. Patients with right brain lesions typically neglect
the left hemispace. Neglect can be further fractionated into motor
and sensory components, extinction, anosognosia (denial of illness),
and anosodiaphoria (minimization of illness).
o Neglect can be tested at the bedside by asking the patient to draw or
read. Patients may neglect the left half of the drawing or leave off the
left half of words (neglect dyslexia). Cancellation tasks require that
the patient cancel or cross out all the letter A s, circles, or some other
element mixed with others on a page. Patients with neglect may omit
cancelling the targets on the left half of the page. Line bisection tests
require the patient to bisect a line of sufficient length (usually 12
inches or more). Patients with neglect may bisect significantly to the
right of midline.
o Constructional apraxia: This refers to the inability to draw. On the
Mini-Mental State Examination, subjects are asked to draw
interlocking pentagons. Complex figures can be taken from the
Wechsler Adult Intelligence Scale (WAIS) or the Rey Complex Figure
 Test. Constructional apraxia localizes to the right hemisphere or to
the frontal lobes.
o Judgment, insight, and social appropriateness: No good tests exist
for these functions other than observation. Patients can score highly
on the WAIS or other cognitive tests and still be unable to behave
appropriately. Acquired sociopathy can occur with individuals with
orbitofrontal cortex injuries who may score highly on all cognitive
measures and yet are unable to hold a job, make and maintain long-
term personal relationships, and exercise judgment.
o Memory deficits: Patients with frontal-lobe injuries, especially
orbitofrontal injuries, may have deficits of declarative memory or
memory for temporal order of events. In 1935, Jacobsen
demonstrated impairments in monkeys on delayed response tasks.
o Lack of originality, inattentiveness, and inappropriate emotional
reactions: Some patients with traumatic lesions of the frontal lobes
have these qualities. Patients cannot plan, initiate, organize, or form
and maintain personal relationships. They lack insight and remain
dependent on caregivers despite normal intellect, as measured
conventionally. Witzelsucht, a term meaning facetiousness, and
moria (a form of euphoria) or lack of concern may appear. Patients
undergo personality changes. A famous 19th-century patient named
Phineas Gage was injured in the head with a tamping iron, and his
friends described a personality change after the injury, saying, "Gage
was not Gage." Many such patients have been described, and some
are characterized as pseudopsychopaths.
o Frontal release responses: Frontal release responses, including
suck, grasp, snout, and groping reflexes, may be present, as may
paratonic rigidity and abnormal gaze. Although these are not
cognitive signs of dysfunction, they certainly help in localization and
diagnosis.
o Utilization behavior: This behavior includes using, touching, or
playing with an object that most people would consider inappropriate
and may be a sign of frontal lobe dysfunction. An example would be
a patient taking a physician’s stethoscope off his desk and listening
to his heart while the physician is sitting and talking with him.
o Alien hand syndrome: This occurs when a patient’s hand assumes
complex positions that are not under the patient’s volitional control
and may also be a sign of frontal systems dysfunction.
 Gait impairment: A relatively upright posture in the setting of short-stride,
hesitant, slightly widened-base gait are characteristic of frontal lobe
disorders. Some patients, even when helped to stand up, cannot begin
 walking (ignition apraxia); others have poor balance with risk of falling
from the slightest shove or surface irregularity. Frontal gait is common in
advanced Alzheimer disease, some vascular dementias, and normal
pressure hydrocephalus. This is sometimes referred to as Bruns apraxia,
and is found in patients with bilateral frontal lobe disorders.
 Incontinence: Dysfunction of the posterior superior frontal gyri and
anterior parts of the cingulate gyrus can lead to incontinence of urine and
stool. Patients frequently have no warning of the need to urinate or
defecate, and are surprised and embarrassed when they find they have
soiled themselves.
Causes
The manifestations of a frontal lobe syndrome in any patient depend on many
factors, including baseline intelligence and education, site of the lesions,
whether the lesions developed slowly or rapidly, age, possibly sex, and
function of nonfrontal brain regions. Causes of frontal lobe dysfunction include
mental retardation, cerebrovascular disease, head trauma, brain tumors, brain
infections, neurodegenerative diseases including multiple sclerosis, and
normal pressure hydrocephalus.
Cerebrovascular disease
The anterior cerebral artery supplies the medial surface of the brain, including
the ventromedial frontal lobe, the cingulum, the premotor cortex, and the
motor strip. Bilateral anterior cerebral artery infarct is associated with a
syndrome of quadriparesis (legs worse than arms) and akinetic mutism.
Occlusion of the artery of Huebner may cause infarction of the head of the
caudate nucleus and may result in an agitated confusional state that with time
evolves to akinesia, abulia, and mutism, along with personality changes.
Language may also be affected.
The anterior branches of the upper division of the middle cerebral artery
supply parts of the lateral prefrontal and frontal cortex. Infarction of these
arteries may be characterized by planning deficits, impairment of working
memories, and apathy as well as weakness of the contralateral face and arm.
Borderzone infarctions between the distribution of the anterior and middle
cerebral arteries are characterized by wedge-shaped lesions between the
superior and middle frontal gyri and may result in the man-in-the-barrel
syndrome with proximal weakness at the shoulder and hip.
Lacunar infarcts that occur in the deep white matter of the frontal lobe,
caudate, or putamen may cause dysfunction of frontostriatal circuits.
Some patients with aneurysms and/or hemorrhage of the anterior
communicating artery develop infarctions in the basal forebrain. In addition to
the akinesia and personality changes already described, patients may develop
a striking confabulatory amnesia that is severe and permanent and that
resembles Wernicke-Korsakoff syndrome. Mild anomia may also be present.
Finally, a syndrome of affective (as opposed to apathetic) depression may
occur after strokes affecting predominantly the left frontal lobe. [12]
Tumors
A classic presentation of frontal lobe dysfunction is an olfactory groove
meningioma characterized by anosmia, loss of inhibition, memory impairment,
headaches, and visual symptoms. The frontal lobes are also common sites for
primary and metastatic brain tumors.
Traumatic lesions
Closed head injuries are often associated with unilateral or bilateral contusions of the
orbitofrontal cortex. Some patients recover completely and others sustain lifelong
impairments. The orbitofrontal cortex is susceptible to contrecoup injury when the
accelerating brain strikes against bony prominences on the nonaccelerating surface of
the anterior cranial fossa.
Prefrontal lobotomies were performed on some patients in the late 1940s and early
1950s with schizophrenia or other severe psychiatric illnesses. In these procedures,
fibers connecting the frontal lobe with the basal ganglia were cut. Although some
claimed that such patients performed normally on neuropsychological tests, studies
were incomplete and lacked appropriate tests sensitive to frontal lobe dysfunction. Many
patients performed normally on selected neuropsychological tests but were still unable
to function independently.
Other structural causes of frontal lobe dysfunction
Hydrocephalus of any cause may be associated with frontal lobe dysfunction due to
increased intracranial pressure and/or stretching of frontostriatal pathways. Normal
pressure hydrocephalus (NPH) has received substantial attention as a reversible cause
of dementia. Unfortunately, not all patients who seem to meet criteria for NPH are
helped with surgery. Core features of NPH are gait apraxia, urinary incontinence, and
frontal-predominant cognitive impairment.
Tourette syndrome, a tic disorder associated with prominent behavioral disorders such
as obsessive-compulsive disorder, is associated with alterations in frontal lobe regions
connected to the striatum. In particular, prefrontal areas and anterior cingulate gyrus are
reduced in volume compared with age- and sex-matched healthy individuals. [5, 13] In this
condition, tics are worse when the volume of the orbitofrontal and right cingulate gyrus
is less.
Frontotemporal lobar degenerations (FTLD)
These disorders include at least 4 clinically distinguishable neurocognitive syndromes
based on the location of the pathologic burden: (1) behavioral variant of frontotemporal
dementia (bvFTD), (2) primary progressive aphasia (PPA), also known as progressive
nonfluent aphasia (PNFA), (3) logopenic progressive aphasia (LPA) and (4) semantic
dementia (SD), also known as fluent PPA. These disorders are all slowly progressive
neurodegenerative disorders. [14] The bvFTD and PNFA are the only FTLDs truly
affecting the frontal lobes. Although LPA and SD are considered within the spectrum of
FTLD, they result from primary involvement of the parietal and temporal regions,
respectively.
 FTD, the behavioral variant of FTLD, results from bilateral frontal atrophy and
causes a dementia syndrome with changes in personality in the context of relative
preservation of memory and language (economical speech) but impairments in
abstraction, attention, problem solving, and planning. Echolalia, perseveration, and
stereotypical use of words may arise. Three clinical FTD phenotypes may be
defined based on the distribution of regional atrophy:
o Orbitobasal or pseudopsychopathic FTD causes disinhibition and irritability.
o Mediofrontal (anterior cingulate) FTD leads to mutism and apathy.
o Dorsolateral prefrontal or pseudodepressive FTD, probably the most common
variant, is recognized by apathy, psychomotor retardation, and executive
dysfunction, expressed as reduced learning and retrieval with decreased
problem solving and set shifting.
 PPA or PNFA, due to left frontal and temporal atrophy, causes nonfluent and
nonrepetitive speech with word-finding difficulty and agrammatism (syntactic
aphasia), progressing to stuttering, phonemic paraphasias, anomia, and mutism.
 LPA due to atrophy in the posterior portion of the left superior and middle temporal
gyri and inferior parietal lobe results in slow speech rate with long word-finding
pauses. Grammar and articulation are preserved, although phonological
paraphasias can be present. Repetition and comprehension were impaired for
sentences but preserved for single words, and naming is moderately affected. [15]
 SD or fluent PPA, due to left anterolateral temporal atrophy with relative sparing of
hippocampus (right-sided involvement causes progressive prosopagnosia), results
in a syntactically fluent but empty speech, semantic paraphasias, and shrinking
vocabulary (poor word retrieval and semantics).
Infectious causes of frontal lobe dysfunction
HIV frequently affects basal ganglia, hippocampus, and the deep white matter of the
frontal lobe. The spectrum of cognitive impairment in HIV ranges from no impairment to
HIV-dementia. Abscesses in the frontal lobe can also impair frontal lobe function.
Differential Diagnoses
 Alzheimer Disease Imaging
 Alzheimer Disease in Down Syndrome
 Anterior Circulation Stroke
 Aphasia
 Apraxia and Related Syndromes
 Cardioembolic Stroke
 Cerebral Amyloid Angiopathy
 Cerebral Aneurysms
 Glioblastoma Multiforme
 Low-Grade Astrocytoma
 Meningioma
 Pick Disease
  Primary CNS Lymphoma
 Vascular Surgery for Arteriovenous Malformations
Laboratory Studies
Choice of blood tests depends on clinical setting.
In many cases, tests of thyroid function, B-12 level, and serology for syphilis
are appropriate.
In other instances, testing for HIV or connective tissue disorders is indicated.
Imaging Studies
CT scanning is adequate to diagnose acute bleeds and ventriculomegaly
(hydrocephalus).
MRI is more sensitive and specific than CT for showing tumors, focal or
diffuse atrophy, subdural hematomas, or vascular and microvascular
pathology.
Many behavioral neurology specialists would obtain a deoxyglucose PET scan
in patients with a clinical diagnosis of frontotemporal dementia. A pattern of
decreased frontal lobe glucose utilization with preserved temporal-parietal
glucose utilization would favor the diagnosis of a frontotemporal dementia.
The opposite pattern is characteristic of Alzheimer disease. [16]
In one study, 18-fluorodeoxyglucose-positron emission tomography (18F-
FDG-PET) was able to identify nearly half of the cases of behavioral variant of
frontotemporal dementia (bvFTD) that were not detected by magnetic
resonance imaging. According to the authors, high specificity of 18F-FDG-
PET can enable exclusion of psychiatric and other neurodegenerative
disorders. The 18F-FDG-PET study was performed in 52 patients with
suspected bvFTD who lacked characteristic structural neuroimaging
results. [17]
Other Tests
Neuropsychology: Many tests are described in Physical.
EEG may be exceptionally considered if evidence of subclinical seizure
activity is suspected, particularly in rapidly progressive symptomatic cases.
Procedures
Lumbar puncture may be needed to look for signs of occult infection.
Medical Care
Medical care depends entirely on the pathology present. Physical and
occupational therapy remain an important cornerstone of motor symptom
management in FTD. Speech therapy may also help patients manage
symptoms associated with aphasia, apraxia, and dysarthria. Recent advances
in the understanding of FTLD pathophysiology and genetics have led to
development of potentially disease-modifying therapies, as well as
symptomatic therapies aimed at ameliorating social and behavioral deficits. [18]
Consultations
Consultation with a neuropsychologist and/or behavioral neurologist is
indicated to determine the nature and extent of the cognitive deficits present
and to help work with the patients and families.
Formal consultation with a neuropsychologist is often advantageous to clarify
the extent of the brain damage and to make appropriate cognitive treatment
plans. Neuropsychologists are also exceedingly helpful because of their
psychological background in dealing with patients and their families.
The patient and family frequently deny or minimize the importance of the
deficit. Consultation can help ensure that the home setting is truly appropriate
for the patient and/or family.
If a home setting is agreed on, these consultants can determine the need for
assistance. Assistants can include physical, occupational, and/or speech
therapists; home health aides; visiting nurses; respite care staff; and adult
day-care staff, who are trained to help the patient succeed in the desired
setting. Consultation with a social worker may also be helpful.
Activity
Patients with frontal lesions and deficits frequently need supervision because
of their lack of impulse control and their inability to form and follow plans and
strategies.
Medication Summary
No medications are available to help frontal injuries.
Drugs that help memory in Alzheimer dementia are rarely of benefit for frontal
lobe deficits or problems.
Further Outpatient Care
Outpatient care monitors what tasks a patient can accomplish in his home or
residential facility and what tasks are sources of difficulty for the patient and
his caregivers. Assessing how patients spend their time each day is useful.
Further Inpatient Care
Excluding rare cases in which surgical care may be indicated (eg, tumors,
subdural hematomas), most care is directed at providing a safe, secure
environment for the patient and at supporting caregivers.
Family education about the patient's deficit is essential.
Discharge planning and family meetings may be necessary if the family
remains unrealistic about the possibility of home discharge. In such a meeting,
team members, including therapists, nurses, and physicians, can elaborate on
the patient's needs and impress on the family the sometimes-unrealistic
nature of their expectations.
Services, as described in Consultations, can be arranged for patients.
Prognosis
The prognosis depends on the underlying pathology.
Patient Education
For patients in whom frontal lobe dysfunction is the result of strokes, visit
eMedicineHealth's Brain and Nervous System Center. Also, see
eMedicineHealth's patient education article Stroke.

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