Signs of Central Nervous System Disorders

Signs of Damage of the Dominant, Nondominant, or Both Cerebral Hemispheres

Although hemiparesis, hemisensory loss, homonymous hemianopsia, and focal seizures may result from lesions of either cerebral hemisphere, several neuropsychologic deficits are related to either the dominant or nondominant hemisphere. Neurologists usually ask a patient’s handedness when taking a history, but if this information is unavailable, because approximately 85% of people are right-handed, they assume that the left hemisphere is dominant.

Lesions of the dominant hemisphere may cause language impairment, aphasia , a prominent and frequently occurring neuropsychologic deficit (see Chapter 8 ). Because the corticospinal tract sits adjacent to the language centers, right hemiparesis often accompanies aphasia (see Fig. 8.1 ).

Lesions of the nondominant parietal lobe tend to produce one or more striking neuropsychologic disturbances (see Chapter 8 ). For example, patients may neglect or ignore left-sided visual and tactile stimuli (hemi-inattention) . They may fail to use their left arm and leg because they neglect their limbs rather than because of paresis. When they have left hemiparesis, patients may not appreciate it (anosognosia) . Many patients with nondominant lesions lose their ability to arrange matchsticks into certain patterns or copy simple forms ( constructional apraxia , Fig. 2.8 ).

As opposed to signs resulting from unilateral cerebral hemisphere damage, bilateral cerebral hemisphere damage produces several important disturbances that psychiatrists are likely to encounter in their patients. One of them, pseudobulbar palsy , best known for producing emotional lability, results from bilateral corticobulbar tract damage (see Chapter 4 ). The corticobulbar tract, like its counterpart, the corticospinal tract, originates in the motor cortex of the posterior portion of the frontal lobe. It innervates the brainstem motor nuclei, which in turn innervate the head and neck muscles. Traumatic brain injury (TBI), multiple cerebral infarctions (strokes), multiple sclerosis (MS), and neurodegenerative conditions, including frontotemporal dementia (see Chapter 7 ), are apt to strike the corticobulbar tract along with the surrounding frontal lobes and thereby cause pseudobulbar palsy.

Damage of both cerebral hemispheres—from large or multiple discrete lesions, degenerative diseases, or metabolic abnormalities—also causes dementia (see Chapter 7 ). In addition, because CNS damage that causes dementia must be extensive and severe, it usually also produces at least subtle physical neurologic findings, such as hyperactive DTRs, Babinski signs, mild gait impairment, and frontal lobe release reflexes. However, many neurodegenerative illnesses that cause dementia, particularly Alzheimer disease, do not cause “hard” findings such as hemiparesis.

While certainly not peculiar to cerebral lesions, and even typically absent in early Alzheimer disease, gait impairment is a crucial neurologic finding. Because walking requires intact and well-integrated strength, sensation, and coordination, testing the patient’s gait is the single most reliable assessment of a patient’s noncognitive neurologic function. Gait impairment constitutes the primary physical component of the subcortical dementias, such as vascular dementia, dementia with Lewy body disease, and Parkinson disease dementia (see Chapter 7 ). Several distinct gait abnormalities are clues to specific neurologic disorders, such as normal pressure hydrocephalus (see Table 2.1 ). As a general rule, slow gait speed, that is, 0.7 m/s, is associated with an increased risk of dementia, stroke, falls, disability, hospitalization, and death.