Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 14)

Caring for the Patient with Deficits of Higher Cerebral FunctionSome of the deficits described in this chapter are so complex that they may bewilder not only the patient and family but also the physician. It is imperative to carry out a systematic clinical evaluation in order to characterize the nature of the deficits and explain them in lay terms to the patient and family. Such an explanation can allay at least some of the anxieties, address the mistaken impression that the deficit (e.g., social disinhibition or inability to recognize family members) is psychologically motivated, and lead to practical suggestions...
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Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 14) Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 14) Caring for the Patient with Deficits of Higher Cerebral Function Some of the deficits described in this chapter are so complex that they maybewilder not only the patient and family but also the physician. It is imperative tocarry out a systematic clinical evaluation in order to characterize the nature of thedeficits and explain them in lay terms to the patient and family. Such anexplanation can allay at least some of the anxieties, address the mistakenimpression that the deficit (e.g., social disinhibition or inability to recognizefamily members) is psychologically motivated, and lead to practical suggestionsfor daily living activities. The consultation of a skilled neuropsychologist may aidin the formulation of diagnosis and management. Patients with simultanagnosia,for example, may benefit from the counterintuitive instruction to stand back whenthey cannot find an item so that a greater search area falls within the immediatefield of gaze. Some patients with frontal lobe disease can be extremely irritableand abusive to spouses and yet display all the appropriate social graces during thevisit to the medical office. In such cases, the history may be more important thanthe bedside examination in charting a course of treatment. Reactive depression is common in patients with higher cerebral dysfunctionand should be treated. These patients may be sensitive to the usual doses ofantidepressants or anxiolytics and deserve a careful titration of dosage. Braindamage may cause a dissociation between feeling states and their expression, sothat a patient who may superficially appear jocular could still be suffering from anunderlying depression that deserves to be treated. In many cases, agitation may becontrolled with reassurance. In other cases, treatment with sedatingantidepressants may become necessary. The use of neuroleptics for the control ofagitation should be reserved for refractory cases since extrapyramidal side effectsare frequent in patients with coexisting brain damage. Spontaneous improvement of cognitive deficits due to acute neurologiclesions is common. It is most rapid in the first few weeks but may continue for upto 2 years, especially in young individuals with single brain lesions. Themechanisms for this recovery are incompletely understood. Some of the initialdeficits appear to arise from remote dysfunction (diaschisis) in parts of the brainthat are interconnected with the site of initial injury. Improvement in these patientsmay reflect, at least in part, a normalization of the remote dysfunction. Othermechanisms may involve functional reorganization in surviving neurons adjacentto the injury or the compensatory use of homologous structures, e.g., the rightsuperior temporal gyrus with recovery from Wernickes aphasia. In some patientswith large lesions involving Brocas and Wernickes areas, only Wernickes areamay show contralateral compensatory reorganization (or bilateral functionality),giving rise to a situation where a lesion that should have caused a global aphasiabecomes associated with a residual Brocas aphasia. Prognosis for recovery fromaphasia is best when Wernickes area is spared. Cognitive rehabilitationprocedures have been used in the treatment of higher cortical deficits. There arefew controlled studies, but some do show a benefit of rehabilitation in the recoveryfrom hemispatial neglect and aphasia. Some types of deficits may be more proneto recovery than others. For example, patients with nonfluent aphasias are morelikely to benefit from speech therapy than patients with fluent aphasias andcomprehension deficits. In general, lesions that lead to a denial of illness (e.g.,anosognosia) are associated with cognitive deficits that are more resistant torehabilitation. The recovery from higher cortical dysfunction is rarely complete.Periodic neuropsychological assessment is necessary for quantifying the pace ofthe improvement and for generating specific recommendations for cognitiverehabilitation, modifications in the home environment, and the timetable forreturning to school or work. In general medical practice, most patients with deficits in higher cognitivefunctions will be suffering from dementia. There is a mistaken belief thatdementias are anatomically diffuse and that they cause global cognitiveimpairments. This is only true at the terminal stages. During most of the clinicalcourse, dementias are exquisitely selective with respect to anatomy and cognitivepattern. Alzheimers disease, for example, causes the greatest destruction in medialtemporal areas b ...