Cerebral. Cognitive function and abilities with language should be examined, as the clinician seeks impaired attention or concentration, slurred speech, dysarthria, or aphasia. Affect and emotions should be noted, looking for personality changes, apathy, inappropriate crying, or emotional outbursts. Memory should be assessed for deficits. Subfluent aphasia occurs in the context of a right central CN VII lesion, whereas cerebellar speech deficits may be found with peripheral disorders of CN VII, especially if the cerebellopontine angle is involved.
Cranial Nerves. The optic discs should be visualized for signs of increased intracranial pressure or stigmata of systemic conditions like hypertension or diabetes. Direct and consensual pupillary reflexes and extraocular movements, especially abduction of the globe (CN VI), should be evaluated. Facial sensation in the three divisions, as well as motor function of the muscles of mastication, should be checked to assess if CN V is also involved, as in a cerebellopontine lesion. Audition should be evaluated with tuning forks, looking for ipsilateral sensorineural or conductive hearing loss. If nystagmus is present, its direction and other characteristics should be documented. Unilateral vestibular weakness should be tested with the Mittelmeyer test (the patient marches in place with eyes closed and hands outstretched; there is a tendency to turn toward the side of vestibular weakness). Palatal sensation and movement, vocal cord motion, trapezial strength, and tongue function should be evaluated.
Motor/Reflexes/Cerebellar/Gait. Hemiparesis ipsilateral to the facial paralysis suggests a cortical or subcortical lesion, whereas contralateral hemiparesis suggests a pontine lesion near the facial motor nucleus. Reflexes should be checked for increased function, as is seen with a central nervous system lesion, or decreased function, as is seen in various neuropathies. The existence of flaccidity, atrophy, and fasciculations should be noted, which are indicative of a neuropathic process. Involuntary movements of the face in the form of synkinesis may suggest an old lesion with reinnervation. In patients with facial diplegia, ascending diffuse distal weakness with loss of reflexes suggests Guillain-Barre(c) syndrome, whereas facial diplegia with diffuse proximal muscle weakness is seen more often in myopathies. When associated with facial weakness, the complex of ataxia, incoordination, and other signs of cerebellar disease suggest a brain stem or cerebellopontine angle lesion.
Sensory. A loss of sensation to pinprick, temperature, light touch, or vibration of the face or body (contralateral or ipsilateral) suggests lateral brain stem involvement or a cerebellopontine angle lesion. With ischemic damage from mid-pons to lower medulla, there is a loss of pain, temperature, and corneal reflex from the ipsilateral side of the face (descending tract of CN V), combined with pain and temperature loss from the contralateral side of the body (spinothalamic tract). Patients with lower brain stem lesions usually have intact proprioception and other signs of lateral medullary damage (Wallenberg's syndrome), whereas those
with upper brain stem injury have impaired proprioception. In addition, those with upper pontine lesions have sensory loss from the contralateral side of the face and body.
Neurovascular. Because it is both a risk factor for and cause of intracranial vascular disorders, the presence of hypertension should be evaluated by both blood pressure determination and systemic examination (e.g., retinal vessel evaluation). Bruits and other evidence of carotid artery disease may point to thromboembolic disease as an etiology. A tender and enlarged temporal artery, especially with an elevated erythrocyte sedimentation rate, suggests temporal arteritis.
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