eMedicine Specialties > Neurology > Behavioral Neurology and Dementia

Frontal Lobe Syndromes

Alberto J Espay, MD, MSc, Assistant Professor, Department of Neurology, University of Cincinnati
Daniel H Jacobs, MD, Associate Professor of Neurology, University of Central Florida College of Medicine

Updated: Jan 11, 2008

Introduction

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), and orbitofrontal cortex (including the orbitobasal or ventromedial and the inferior mesial regions). 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. 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 superior mesial lesions 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 (but sparing) to 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.

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. Accordingly, poor judgment and inappropriately weighting the value of past experiences often 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 impairments of working memory may have decreased capacity in working memory (eg, shortened digit span) or difficulty manipulating information in working memory (eg, impaired reverse digit span test).

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 eMedicine articles. Common causes (see also Causes) include the following:

• Mental retardation
• Traumatic brain injury (see Management and Staging of Traumatic Brain Injury and Traumatic Brain Injury: Definition, Epidemiology, Pathophysiology
• Brain tumors (see Metastatic Disease to the Brain and EEG in Brain Tumors)
• Degenerative dementias including Alzheimer disease, dementia with Lewy bodies, Parkinsonian dementias, and frontotemporal dementias
• Cerebrovascular disease
• 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. 

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. 

Clinical

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. 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 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 recently validated bedside tools that extend the cognitive screen to the frontal lobes are the Frontal Assessment Battery (FAB)³ and the Montreal Cognitive Assessment (MoCA).⁴  These instruments may be helpful for bedside evaluation of frontal lobe function.

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.⁵ 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.⁶
• 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) are less purely generative tasks and therefore partly depend on the integrity of language-related cortex. 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.⁷
• 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-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. 
• 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.
• 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 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 AmericanAcademy 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. 
• 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.
• 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).
• 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.
• 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.
• 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.
• 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.
• 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. Utilization behaviors, grasping behaviors, magnetic responses, and alien-hand syndrome refer to a group of behaviors that may be attributable to frontal dysfunction.
• Gait impairment: A stooped flexed posture, short hesitant steps, and a slightly widened base are characteristic of frontal lobe gait. 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

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.

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 frontal-predominant cognitive impairment.

Frontotemporal lobar degenerations (FTLD)

These disorders include at least 3 clinically distinguishable neurocognitive syndromes based on the location of the pathologic burden: (1) frontotemporal dementia (FTD), (2) primary progressive aphasia (PPA), and (3) semantic dementia (SD). These disorders are all slowly progressive neurodegenerative disorders. 

• FTD, the behavioral variant of FTLD, results from bilateral frontal atrophy and causes relative preservation of memory and language (economical speech) with 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:  
  • Orbitobasal or pseudopsychopathic FTD causes disinhibition and irritability.
  • Mediofrontal (anterior cingulate) FTD leads to mutism and apathy.
  • 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, 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.
• SD (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). Verbal and written comprehension represents a transcortical sensory aphasia.

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

Other Problems to Be Considered

Dementia
Trauma
Alcoholism
Stroke
Substance abuse
Developmental disorder
Alexia
Neglect
Carotid disease and stroke

Workup

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.
• MRI is more sensitive and specific than CT for showing tumors, focal or diffuse atrophy, subdural hematomas, or vascular pathology.

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.

Treatment

Medical Care

Medical care depends entirely on the pathology present.

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

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.

Follow-up

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 a source of difficulty for the patient and his caregivers. Assessing how patients spends 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 eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

Miscellaneous

Medicolegal Pitfalls

• Patients with frontal lobe injuries may have severe cognitive impairment despite good performance on standard neuropsychological tests.
• Patients may be extremely irresponsible and even exhibit dangerous behavior because of their lack of judgment and insight.
• Clinicians should consult social workers, neuropsychologists, neurologists, and psychiatrists as needed to ensure that the patient's home circumstances are safe and that necessary services are available.

Multimedia

Media file 1: 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.

References

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Keywords

frontal-lobe syndromes, mental status examinations, Mini-Mental State Examination, MMSE, Mental Status Examination, MSE, neuropsychology, precentral cortex, prefrontal cortex, orbitofrontal cortex, Alzheimer disease, amyloid angiopathy, anterior circulation stroke, aphasia, apraxia, arteriovenous malformations, cardioembolic stroke, carotid disease, cerebral aneurysms, glioblastoma multiforme, low-grade astrocytoma, meningioma, Pick disease, primary CNS lymphoma, echopraxia, antisaccade task
 
Thurstone test, semantic category fluency tasks, letter fluency task, design fluency, digit span, alternating sequences task, Luria's 3-step motor program, fist-palm-edge test, Paced Auditory Serial Addition Test, PASAT, Visual Span subtest of the Wechsler Memory Scale, Hamilton Depression Scale, Beck Depression Inventory, Zung Self-rating Depression Scale, Stroop test, classic Broca-type aphasia, National Institutes of Health Stroke Scale, NIHSS, deep dyslexia,  Controlled Oral Word Association test, FAS test, Western Aphasia Battery test, WAB test, Boston Diagnostic Aphasia Examination, BDAE, Token testpraxis, buccofacial apraxia, callosal apraxia, anterior cerebral artery strokes, anosognosia, anosodiaphoria, neglect dyslexia, motor extinction, misoplegia, dressing apraxia, constructional apraxia, Wechsler Adult Intelligence Scale, WAIS, Rey Complex Figure Test, Wisconsin Card Sorting Test, WCST, Witzelsucht, factiousness, moria, pseudopsychopaths, frontosubcortical dementia, multiple sclerosis, AIDS, Parkinson disease, progressive supranuclear palsy, depressive pseudodementia, vitamin B-12 dementia, nutrition-related whole-brain atrophy, alcohol-related whole-brain atrophy, paratonic rigidity, vascular syndromes, middle cerebral artery strokes, artery of Huebner, akinesia, abulia, mutism, confabulatory amnesia, Wernicke-Korsakoff syndrome, anomia, agitated confusional state, frontal lobe tumors, gliomatous tumors, meningioma, subdural hematoma, prefrontal lobotomy, leukotomy, normal pressure hydrocephalus, gait apraxia, cortical atrophy, Boston naming test, frontotemporal dementias

Contributor Information and Disclosures

Author

Alberto J Espay, MD, MSc, Assistant Professor, Department of Neurology, University of Cincinnati
Alberto J Espay, MD, MSc is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society
Disclosure: Boehringer-Ingelheim Consulting fee Consulting; Codman Grant/research funds Other; Medtronic Honoraria Speaking and teaching; Medtronic Grant/research funds Other; Allergan Grant/research funds Other; UCB-Schwarz Pharm Honoraria Speaking and teaching; Novartis  Speaking and teaching

Coauthor(s)

Daniel H Jacobs, MD, Associate Professor of Neurology, University of Central Florida College of Medicine
Daniel H Jacobs, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, and Society for Neuroscience
Disclosure: Teva Pharmaceutical Grant/research funds Consulting; Biogen Idex Grant/research funds Independent contractor; Serono EMD Royalty Speaking and teaching; Pfizer Royalty Speaking and teaching; Berlex Royalty Speaking and teaching

Medical Editor

Joseph Quinn, MD, Assistant Professor, Department of Neurology, Portland VA Medical Center, Oregon Health Sciences University
Joseph Quinn, MD is a member of the following medical societies: American Academy of Neurology, Society for Neuroscience, and Society for Pediatric Radiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Richard J Caselli, MD, Professor, Department of Neurology, Mayo Medical School, Rochester, MN; Chair, Department of Neurology, Mayo Clinic of Scottsdale
Richard J Caselli, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Neurological Association, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Chief Editor

Howard A Crystal, MD, Professor, Departments of Neurology and Pathology, State University of New York Downstate; Consulting Staff, Department of Neurology, University Hospital and Kings County Hospital Center
Howard A Crystal, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association
Disclosure: Pfizer Honoraria Speaking and teaching; Myriad Honoraria Consulting

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