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Frontal Lobe Syndromes

  • Author: Stephen L Nelson, Jr, MD, PhD, FAAP; Chief Editor: Jasvinder Chawla, MD, MBA  more...
Updated: Apr 11, 2016


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 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 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 trem 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.


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).




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:


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.


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 pre-senile age (younger than 65 years).

Contributor Information and Disclosures

Stephen L Nelson, Jr, MD, PhD, FAAP Section Head of Pediatric Neurology, Associate Professor of Pediatrics, Neurology, and Psychiatry, Tulane University School of Medicine

Stephen L Nelson, Jr, MD, PhD, FAAP is a member of the following medical societies: Academic Pediatric Association, American Academy of Neurology, American Academy of Pediatrics, American Medical Association, Association of Military Surgeons of the US, Child Neurology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Jasvinder Chawla, MD, MBA Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Joseph Quinn, MD, MD Assistant Professor, Department of Neurology, Portland VA Medical Center, Oregon Health Sciences University

Joseph Quinn, MD, MD is a member of the following medical societies: American Academy of Neurology, Society for Neuroscience, Society for Pediatric Radiology

Disclosure: Nothing to disclose.


Alberto J Espay, MD, MSc Associate Professor, Director of Clinical Research, Gardner Family Center for Parkinson's Disease and Movement Disorders, University of Cincinnati College of Medicine

Alberto J Espay, MD, MSc is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society

Disclosure: Abbott Consulting fee Consulting; Chelsea therapeutics Consulting fee Consulting; Novartis Honoraria Speaking and teaching; TEVA Consulting fee Consulting; NIH Grant/research funds K23 Career Development Award; Eli Lilly Consulting fee Consulting; Great Lakes Neurotechnologies Other; Michael J Fox Foundation Grant/research funds Other; Lippincott Williams & Wilkins Royalty Book; American Academy of Neurology Honoraria Speaking and teaching

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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.
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