Associated Neurological Findings

Cerebral. With regard to CN XI or XII, bihemispherical lesions may result in significant weakness of the SCM, trapezeii, or extrinsic tongue muscles. Other features that confirm the presence of bihemispherical lesions are urinary incontinence, gait apraxia, pseudobulbar palsy (i.e., dysarthria, dysphagia, and emotional incontinence), cognitive deficits, and alterations in personality.

Cranial Nerves. Dysfunction of neck or tongue musculature may be the result of lesions in the brain stem affecting supranuclear, nuclear, or nerve fibers of CN XI or CN XII. Other features of a brain stem lesion are facial numbness (CN V), weakness of the palate (CN X), or autonomic dysfunction, indicating involvement of cranial nerve nuclei or sympathetic fibers in close proximity to the nuclei of CN XI or XII. Additionally, although supranuclear lesions may result in both head and eye deviation (due to connections between the accessory nucleus and the medial longitudinal fasciculus), a peripheral lesion of the spinal accessory nerve should not be accompanied by eye deviation.

Motor/Reflexes/Cerebellar/Gait. When examining a patient with a suspected lesion of CN XI or XII, it is important to perform a thorough motor examination. The examiner should note any primitive reflexes (e.g., suck, snout, glabellar) or paratonic rigidity (gegenhalten). These signs, along with pseudobulbar palsy, may be indicative of bilateral frontal lobe lesions. In addition, weakness in other ipsilateral muscles in the face, arm or leg, accompanied by hypertonia, hyperreflexia, or extensor plantar responses, are suggestive of an upper motor neuron lesion, y whereas weakness with atrophy, loss of reflexes, or fasciculations are signs of either a lower motor neuron lesion or neuronopathy. The supranuclear fibers for the sternal head of the SCM muscle probably decussate twice: once in the midbrain or pons and a second time in the medulla or cervical spinal cord. y Hence, a lesion in the right side of the pons may result in (1) left-sided weakness (involvement of corticospinal tract fibers before their decussation in the medulla); and (2) weakness of the left SCM muscle and deviation of the head to the left (i.e., the same side as the hemiparesis) because of involvement of the supranuclear input to the left SCM muscle after the first but before the second decussation. In contrast, a lesion in the right cerebral hemisphere or right internal capsule or high in the right midbrain, before the initial decussation of the supranuclear fibers to the SCM, may result in (1) left-sided weakness due to involvement of the corticospinal tract fibers before their decussation; and (2) weakness of the right SCM muscle and deviation of the head to the right (i.e., the side opposite the hemiparesis). y

When dysfunction of CN XI or XII is present, it is also important to perform a thorough examination of coordination and gait. The presence of cerebellar signs ipsilateral to CN XI or XII deficits may be indicative of involvement of the inferior cerebellar peduncle, which is consistent with a lesion in the region of the medulla.

Sensory. The sensory examination is especially im- portant in assessing brain stem dysfunction because of the distinctive pattern of findings seen only with damage to this structure. The nucleus ambiguus is situated just medial to the spinothalamic and trigeminothalamic tracts in the medulla. Contralateral loss of pain and temperature in the body and ipsilateral loss of pain and temperature in the face confirm a lesion in the medulla in the region of the nucleus ambiguus. The medial lemniscus is located in the medial medulla, ventral to the hypoglossal nucleus, and tongue weakness with simultaneous loss of position and vibratory sense implies a lesion in this area (i.e., Dejerine's syndrome or anterior spinal artery syndrome of the medulla). M , y

Autonomic Nervous System. Lesions of the brain stem may sometimes involve autonomic pathways. An examination of the autonomic nervous system involves assessment of: pulse rate, blood pressure in different positions (lying, seated, and standing), changes in skin color and texture, changes in hair and nails, decreased or excessive perspiration (e.g., anhidrosis in Horner's syndrome), and reflexes (e.g., pupillary, oculocardiac).

Neurovascular. Carotid dissection as well as brain stem stroke are etiologies of lower cranial nerve dysfunction, and the patency of the carotid artery may be preliminarily assessed at the bedside. Auscultation may reveal a bruit (i.e., partial occlusion). Palpation of the carotid pulse may reveal unilateral or even bilateral diminished pulsation, indicative of partial or complete occlusion of this blood vessel.


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