Frontal Lobe Syndrome

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Information about Frontal Lobe Syndrome
Health & Medicine

Published on August 5, 2008

Author: shahparind



Some highlights of frontal lobe syndrome


History: What Is Frontal Lobe Syndrome? The earliest described case of "frontal lobe syndrome" dates back to 1835. However, the best-known early case is that of Phineas Gage, a man who suffered a frontal lobe injury for which the pathology and etiology were known. On Sept. 13, 1848, in New Hampshire, Phineas Gage suffered an accident while on the job as a railroad construction foreman. A tamping iron blasted through his left cheek, through his left frontal lobe, and his skull and landed far behind him. He was knocked off his feet and may have briefly been unconscious but seems to have recovered rather quickly. He was unable to return to work as a foreman. Accounts of the time referred to him as a "changed person" who drifted down socially and could only briefly sustain work as a stable hand until his death in 1860

The frontal lobes are the largest of the major cortical lobes. They contain five key areas for neuropsychiatric function (e.g., executive function, personality, intellect, working memory, speech) and motor functions. The frontal operculum contains Broca's area on the left (responsible for fluency of speech). The right frontal operculum adds emotion to speech—gesturing, prosody, and inflection

The dorsolateral prefrontal region is highly critical for focused attention, concentration, working memory, management of retrograde memory recall, and mood

a set of behaviors commonly encountered in neuropsychiatric patients, namely, disinhibition, stimulus-bound behavior, disorganization, social inappropriateness, overactivity, apathy, perseveration, and subcortical dementia . The clinical picture does not fit that of a classical psychiatric syndrome, such as mania, mood disorder, anxiety disorder, or psychosis similar presentations are seen at times in patients with traumatic brain injury, Parkinson's disease, stroke, AIDS, Alzheimer's disease, and frontotemporal dementia . Often this presentation is referred to as a "frontal lobe syndrome

Luria popularized the term in 1969, derived from studies of patients who suffered lesions in the frontal lobes . Blumer and Benson used the term "frontal lobe personality" when referring to much the same constellation of signs and symptoms . The literature contains multiple accounts of the clinical pictures of frontal lobe damage. Some use the term to describe specific neurological signs, such as frontal release or alien hand . Others refer to cognitive features, such as difficulty in planning and sequencing .

One form of progressive neurodegeneration has been called "frontotemporal dementia.“ The clinical description refers to progressive personality change and a breakdown in social contact. Some patients are said to be restless, distractible, or disinhibited. Others are apathetic, slowed, and amotivated. Many exhibit hypochondriasis, stereotyped behaviors, concrete thinking, echolalia, perseveration, and memory disturbances. It is of note that while most exhibit degeneration of the frontal lobes, many develop degeneration of the temporal lobes and/or subcortical structures

The term " frontal lobe syndrome " is no longer useful because it implies damage to a specific region of the brain. The clinical presentations involved reflect dysfunction in several parts of the brain, some of which are in the frontal lobes and some of which are not. It is best not to use an anatomical term to describe a clinical syndrome. The common theme is not anatomy but behaviors that reflect dysfunction of the executive system .

Some cases of so-called frontal lobe syndrome occur in patients who do not have obvious damage to the frontal lobes. Some examples include episodic dyscontrol after bilateral caudate nucleus lesions, disinhibited behaviors after bilateral thalamic infarcts,apathy and abulia with globus pallidus lesions,or apathy and disinhibition in multiple sclerosis . Some of these symptoms have been reported in more classical psychiatric disturbances. Some of these are major depression (apathy and mood lability), especially in old age, which has been associated with disturbances in the anterior cingulum; schizophrenia(apathy and executive disturbance), which has been associated with disruptions in the dorsolateral prefrontal cortex; attention deficit hyperactivity disorder and obsessive-compulsive disorder (repetitive, intrusive, and irresistible behaviors), which have been associated with overactivity in orbitofrontal lobe areas Understanding the functional anatomy of the frontal lobes and their linkages with key subcortical structures is critical to putting together this picture

Anatomical Organization, Internal Neurochemistry, and Known External Neurochemical Modulators of the Frontosubcortical Circuit

The DSM-IV diagnosis that best fits the disturbance is "personality change due to a general medical condition." However, the disturbance is no more a personality disturbance than would be a mood or psychotic syndrome .


Common post-TBI psychiatric comorbidities include affective, cognitive, and behavioral disorders .

Research on possible biopsychosocial risk factors and screening tools may lead to earlier identification of at-risk patients and more rapid diagnosis after TBI. Early appropriate treatment of these at-risk patients may improve outcome and prevent future adverse consequences

The prevalence of psychiatric diagnoses in these patients is much higher than in the general population, and up to 44% of patients suffer from more than one psychiatric disorder. Unfortunately, the symptoms of psychiatric conditions are often accepted as "normal" reactions to a devastating event. Without a diagnosis, TBI patients are deprived of appropriate treatment for prolonged periods. During this critical period, symptoms worsen and the consequences are compounded

personality changes commonly seen after TBI : disinhibition, impulsivity, and inadequate self-monitoring of interpersonal behavior. The manifestation of these emotional and behavioral difficulties is generally multifactorial and involves contributions from brain, premorbid personality, and environmental variables.Management of such symptoms often requires setting limits, maintaining structure, redirecting negative behavior, and reinforcing positive behavior, as well as pharmacologic approaches. Personality changes associated with TBI can be difficult to differentiate from mania or hypomania; regular follow-up and history from family regarding premorbid personality and the nature, frequency, and duration of symptoms helps to establish the diagnosis

that patients with TBI who have a change in mood and behavior undergo a thorough psychiatric evaluation for specific diagnoses; that they receive individualized treatment plans; and that they remain in active follow-up in order to refine treatment and monitor for the emergence of new disorders

A comprehensive evaluation to determine the presence of psychiatric disorders is essential for TBI patients. The detection of psychiatric phenomena affects crucial decisions that will set the pace for treatment and increase the likelihood of successful rehabilitation

Mania. Secondary mania has been described in a variety of settings involving brain damage and stimulation.The clinical features of episodic elevated mood; increase in goal-directed activity; rapid, pressured speech; and increased energy are diagnostic of mania. This aspect of his illness made diagnosis challenging and required reformulation and changes in treatment from antidepressants to mood-stabilizers such as lithium and divalproex

In addition to pharmacological approaches to up- or down-regulation of circuit activity, surgical approaches in key areas might be used to affect circuit activity

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