Frontal Lobe Syndromes

Author: Stephen L Nelson Jr, MD, PhD, FAAP; Chief Editor: Michael Hoffmann, MBBCh,
MD, FCP(SA), FAAN, FAHA
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), prefrontal cortex (extending
from the frontal poles to the precentral cortex and including the frontal operculum,
dorsolateral, and superior mesial regions), orbitofrontal cortex (including the orbitobasal or
ventromedial and the inferior mesial regions), and superior mesial regions (containing,
primarily, the anterior cingulate gyrus). 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 aphasiaand 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 superior mesial 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 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 can't 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 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:

Mental retardation
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 mental retardation,
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 of frontal lobe predominance, frontotemporal lobar degenerations,
together with Alzheimer disease, are the most common degenerative dementias in the presenile age (younger than 65 years).
CLINICAL PRESENTATION
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 then 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 a careful developmental history, head
trauma history, and social history, 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, 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 functionthey 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 1 finger if the examiner holds up 2 and 2
fingers if the examiner holds up 1. 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 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 (Munoz and Everling, 2004).
Trail-making test (TMT): This test is widely used as a diagnostic tool for eliciting shifts
between cognitive sets. [7] The TMT contains 2 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. [8]
Lexical fluency (word generation, Thurstone test): Ask the patient to generate as many
words as possible beginning with the letter F in 1 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 dysfunction. Design fluency (how many designs with 4 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.[9]
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 7 s (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 3-step
motor program is a sequential performance of 3 movements, usually the fist-edgepalm
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 manifestation of perseveration. Patients are asked to clap 3
times after demonstration by the examiner. Abnormal outcome consists of clapping 4 or
more times (positive applause sign). This test has been felt highly specific for
parkinsonian disorders with frontal involvement.[10]
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 8 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
2-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 contain 6 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.

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 physicians 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 patients hand assumes complex positions
that are not under the patients 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.
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
o

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 cortex. Infarction of these arteries may be characterized by planning
deficits, impairment of working memories, and apathy.
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.[11]
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 or leukotomies 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 lacking 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 frontalpredominant 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, 12] 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 offrontotemporal
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.[13] 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. [14]
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
Alzheimer Disease in Individuals With Down Syndrome
Amyloid Angiopathy

Anterior Circulation Stroke

Aphasia
Apraxia and Related Syndromes
Arteriovenous Malformations
Cardioembolic Stroke
Cerebral Aneurysms
Glioblastoma Multiforme
Low-Grade Astrocytoma
Meningioma
Pick Disease
Primary CNS Lymphoma
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.[15]
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.[16]
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.[17
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
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.

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.
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.
References
1. Mesulam MM. The Human Frontal Lobes: Transcending the Default Mode through
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