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

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 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
for daily living activities. The consultation of a skilled neuropsychologist may aid
in the formulation of diagnosis and management. Patients with simultanagnosia,
for example, may benefit from the counterintuitive instruction to stand back when
they cannot find an item so that a greater search area falls within the immediate
field of gaze. Some patients with frontal lobe disease can be extremely irritable
and abusive to spouses and yet display all the appropriate social graces during the
visit to the medical office. In such cases, the history may be more important than
the bedside examination in charting a course of treatment.
Reactive depression is common in patients with higher cerebral dysfunction
and should be treated. These patients may be sensitive to the usual doses of
antidepressants or anxiolytics and deserve a careful titration of dosage. Brain
damage may cause a dissociation between feeling states and their expression, so
that a patient who may superficially appear jocular could still be suffering from an
underlying depression that deserves to be treated. In many cases, agitation may be
controlled with reassurance. In other cases, treatment with sedating
antidepressants may become necessary. The use of neuroleptics for the control of
agitation should be reserved for refractory cases since extrapyramidal side effects
are frequent in patients with coexisting brain damage.
Spontaneous improvement of cognitive deficits due to acute neurologic

lesions is common. It is most rapid in the first few weeks but may continue for up
to 2 years, especially in young individuals with single brain lesions. The
mechanisms for this recovery are incompletely understood. Some of the initial
deficits appear to arise from remote dysfunction (diaschisis) in parts of the brain
that are interconnected with the site of initial injury. Improvement in these patients
may reflect, at least in part, a normalization of the remote dysfunction. Other
mechanisms may involve functional reorganization in surviving neurons adjacent
to the injury or the compensatory use of homologous structures, e.g., the right
superior temporal gyrus with recovery from Wernicke's aphasia. In some patients
with large lesions involving Broca's and Wernicke's areas, only Wernicke's area
may show contralateral compensatory reorganization (or bilateral functionality),
giving rise to a situation where a lesion that should have caused a global aphasia
becomes associated with a residual Broca's aphasia. Prognosis for recovery from
aphasia is best when Wernicke's area is spared. Cognitive rehabilitation
procedures have been used in the treatment of higher cortical deficits. There are
few controlled studies, but some do show a benefit of rehabilitation in the recovery
from hemispatial neglect and aphasia. Some types of deficits may be more prone
to recovery than others. For example, patients with nonfluent aphasias are more
likely to benefit from speech therapy than patients with fluent aphasias and
comprehension deficits. In general, lesions that lead to a denial of illness (e.g.,
anosognosia) are associated with cognitive deficits that are more resistant to
rehabilitation. The recovery from higher cortical dysfunction is rarely complete.
Periodic neuropsychological assessment is necessary for quantifying the pace of
the improvement and for generating specific recommendations for cognitive
rehabilitation, modifications in the home environment, and the timetable for
returning to school or work.
In general medical practice, most patients with deficits in higher cognitive
functions will be suffering from dementia. There is a mistaken belief that
dementias are anatomically diffuse and that they cause global cognitive
impairments. This is only true at the terminal stages. During most of the clinical

course, dementias are exquisitely selective with respect to anatomy and cognitive
pattern. Alzheimer's disease, for example, causes the greatest destruction in medial
temporal areas belonging to the memory network and is clinically characterized by
a correspondingly severe amnesia. There are other dementias where memory is
intact. Frontal lobe dementia results from a selective degeneration of the frontal
lobe and leads to a gradual dissolution of behavior and complex attention. Primary
progressive aphasia is characterized by a gradual atrophy of the left perisylvian
language network and leads to a progressive dissolution of language that can
remain isolated for up to 10 years. An enlightened approach to the differential
diagnosis and treatment of these patients requires an understanding of the
principles that link neural networks to higher cerebral functions.
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