Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 13)

The prefrontal network plays an important role in behaviors that require an integration of thought with emotion and motivation. There is no simple formula for summarizing the diverse functional affiliations of the prefrontal network. Its integrity appears important for the simultaneous awareness of context, options, consequences, relevance, and emotional impact so as to allow the formulation of adaptive inferences, decisions, and actions. Damage to this part of the brain impairs mental flexibility, reasoning, hypothesis formation, abstract thinking, foresight, judgment, the online (attentive) holding of information, and the ability to inhibit inappropriate responses. Behaviors impaired by prefrontal cortex lesions, especially...
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Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 13) Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 13) The prefrontal network plays an important role in behaviors that require anintegration of thought with emotion and motivation. There is no simple formulafor summarizing the diverse functional affiliations of the prefrontal network. Itsintegrity appears important for the simultaneous awareness of context, options,consequences, relevance, and emotional impact so as to allow the formulation ofadaptive inferences, decisions, and actions. Damage to this part of the brainimpairs mental flexibility, reasoning, hypothesis formation, abstract thinking,foresight, judgment, the online (attentive) holding of information, and the abilityto inhibit inappropriate responses. Behaviors impaired by prefrontal cortex lesions,especially those related to the manipulation of mental content, are often referred toas executive functions. Even very large bilateral prefrontal lesions may leave all sensory, motor,and basic cognitive functions intact while leading to isolated but dramaticalterations of personality and behavior. The most common clinical manifestationsof damage to the prefrontal network take the form of two relatively distinctsyndromes. In the frontal abulic syndrome, the patient shows a loss of initiative,creativity, and curiosity and displays a pervasive emotional blandness and apathy.In the frontal disinhibition syndrome, the patient becomes socially disinhibited andshows severe impairments of judgment, insight, and foresight. The dissociationbetween intact cognitive function and a total lack of even rudimentary commonsense is striking. Despite the preservation of all essential memory functions, thepatient cannot learn from experience and continues to display inappropriatebehaviors without appearing to feel emotional pain, guilt, or regret when suchbehaviors repeatedly lead to disastrous consequences. The impairments mayemerge only in real-life situations when behavior is under minimal externalcontrol and may not be apparent within the structured environment of the medicaloffice. Testing judgment by asking patients what they would do if they detected afire in a theater or found a stamped and addressed envelope on the road is not veryinformative since patients who answer these questions wisely in the office maystill act very foolishly in the more complex real-life setting. The physician musttherefore be prepared to make a diagnosis of frontal lobe disease on the basis ofhistoric information alone even when the office examination of mental state maybe quite intact. The abulic syndrome tends to be associated with damage to the dorsolateralprefrontal cortex, and the disinhibition syndrome with the medial prefrontal ororbitofrontal cortex. These syndromes tend to arise almost exclusively afterbilateral lesions, most frequently in the setting of head trauma, stroke, rupturedaneurysms, hydrocephalus, tumors (including metastases, glioblastoma, and falxor olfactory groove meningiomas), or focal degenerative diseases. Unilaterallesions confined to the prefrontal cortex may remain silent until the pathologyspreads to the other side. The emergence of developmentally primitive reflexes,also known as frontal release signs, such as grasping (elicited by stroking thepalm) and sucking (elicited by stroking the lips) are seen primarily in patients withlarge structural lesions that extend into the premotor components of the frontallobes or in the context of metabolic encephalopathies. The vast majority ofpatients with prefrontal lesions and frontal lobe behavioral syndromes do notdisplay these reflexes. Damage to the frontal lobe disrupts a variety of attention-related functionsincluding working memory (the transient online holding of information),concentration span, the scanning and retrieval of stored information, the inhibitionof immediate but inappropriate responses, and mental flexibility. The capacity forfocusing on a trend of thought and the ability to voluntarily shift the focus ofattention from one thought or stimulus to another can become impaired. Digit span(which should be seven forward and five reverse) is decreased; the recitation ofthe months of the year in reverse order (which should take less than 15 s) isslowed; and the fluency in producing words starting with a, f, or s that can begenerated in 1 min (normally ≥12 per letter) is diminished even in nonaphasicpatients. Characteristically, there is a progressive slowing of performance as thetask proceeds; e.g., the patient asked to count backwards by 3s may say 100, 97,94, . . . 91, . . . 88, etc., and may not complete the task. In go–no-go tasks(where the instructio ...