Cerebral. Many portions of the cerebral examination are of considerable value in helping localize lesions associated with speech and language disorders.
When speech alterations are due to bilateral involvement of corticobulbar tracts, a special type of affect is observed in which the patient experiences emotional incontinence (spasmodic crying and laughing). This is part of the pseudobulbar syndrome, which is described in the next section. These patients typically also have evidence of psychomotor slowing.
Language disturbances can be associated with other types of cognitive dysfunction, such as impaired memory, abstraction, visuospatial function, and praxis, as well as changes in personality (decreased inhibition), irritability, apathy, and agitation, which may indicate the presence of widespread dysfunction such as that encountered in degenerative dementing diseases. Evaluation for apraxia (which is defined as failure to carry out a maneuver on command, excluding any primary motor, sensory, or comprehension disorder) is important because ideomotor and buccofacial apraxia are often associated with nonfluent aphasias and conduction aphasia.
Cranial Nerves. Speech disorders could be associated with lower motor neuron pathology including abnormalities of the neuromuscular junction. Therefore, it is important to search for any weakness, atrophy, and fasciculation in the facial musculature, the tongue, and the palate. Also, the cranial nerves must be assessed. Ptosis, ophthalmoplegia, and fatigability should be observed and tested. The gag reflex should be examined because it may be depressed in dysarthria of the lower motor neuron type and increased in dysarthria of the upper motor neuron type. A masked or inexpressive face and decreased blinking may be clues to the presence of an extrapyramidal cause of dysarthria.
Right homonymous hemianopia or quadrantanopia is helpful in localizing the site of pathology associated with language disorders. Anterior aphasias have little or no involvement of the visual fields compared with more posterior aphasic syndromes. The cranial nerves should also be assessed for the presence of a central type of facial muscle weakness on the right side. Occasionally, patients with acute onset of anterior aphasia have a conjugate gaze deviation to the left (see CMpieiJ.., ).
Motor/Reflex Cerebellar/Gait. Speech abnormalities in the presence of a significant spastic paralysis involving the entire side of the body suggest a deep-lying lesion involving the contralateral internal capsule. This type of lesion typically gives rise to spastic speech. When weakness is bilateral or unilateral but is associated with cranial nerve deficits on the opposite side, a brain stem lesion is suspected. Dysarthria associated with this type of insult is either flaccid or spastic, depending on the involvement of either the motor nuclei controlling the speech apparatus or their supranuclear pathways. Bradykinesia, rigidity, resting tremor, chorea, and dystonia are all signs suggestive of extrapyramidal disease and are usually associated with hypokinetic or hyperkinetic dysarthrias. Upper motor neuron signs including spasticity and hyper-reflexia should be sought as well as lower motor neuron signs including atrophy, fasciculation, and hyporeflexia and areflexia. These signs are helpful in distinguishing lesions producing spastic dysarthria from those causing flaccid dysarthria. Cerebellar findings include ataxia, dysmetria on finger-to-nose and heel-to-shin testing as well as gaze-evoked nystagmus, dysmetric saccades, and rebound nystagmus. These findings are often associated with ataxic dysarthria.
Weakness involving only one limb with or without facial weakness is most suggestive of cortical pathology. Brachiofacial involvement suggests infarction of the territory of the middle cerebral artery and is usually associated with perisylvian aphasias; crural weakness without involvement of the arm and face suggests infarction in the territory of the anterior cerebral artery and is usually associated with transcortical motor aphasia. Greater weakness of proximal musculature in contrast to distal musculature is suggestive of involvement in the border zone vascular areas and can be associated with extrasylvian aphasias (transcortical aphasias). Testing for ideomotor apraxia is helpful to localize pathology further within the left hemisphere. Language disturbances are not usually associated with cerebellar disease.
Sensory. Intact perception of light touch and proprioception with impaired sensation of pain and temperature occurring in an alternate pattern affecting one side of the face and the opposite side of the body helps localize pathology to the lateral brain stem. This type of lesion could also affect lower cranial nerves such as cranial nerves IX and X and create a flaccid dysarthria.
Cortical sensory loss (astereognosia, impaired two-point discrimination, agraphesthesia) indicates involvement of the parietal cortex and can be associated with more posterior aphasia-producing lesions. Pseudothalamic pain that begins months after the onset of the sensory abnormality is seen after lesions affecting the white matter just deep to the supramarginal gyrus and can be associated with conduction aphasia. y
Neurovascular. The presence of significant bilateral vascular bruits on neurovascular examination is an important risk factor for stroke. Stroke patients could present with spastic dysarthria or pseudobulbar palsy secondary to single or multiple cerebral infarcts, respectively.
As for speech disorders, abnormal neurovascular examination suggests the presence of cerebrovascular disease. Multiple language disturbances and syndromes are caused by strokes. Transcortical aphasia occurs following watershed zone infarction in patients with severe carotid stenosis during a hypotensive episode.
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