Location of Lesion Pattern of Weakness Reflexes and Associated Signs

Bilateral cerebral Tetraparesis, spastic dysarthria, dysphagia with hyperreactive jaw and facial jerks (pseudobulbar palsy), decorticate posturing (large hemispheres acute lesions)

Midbrain

Tetraparesis, coma, mid-size poorly reactive pupils, decerebrate posturing

Basis pontis

"Locked-in" syndrome; tetraparesis, paralysis of horizontal eye movements, jaw, face, pharynx, and tongue muscles; preservation of eye blink, vertical eye movements, consciousness

Cervicomedullary junction

Tetraparesis with or without weakness of pharynx and tongue

High cervical

Tetraparesis, no cranial nerve palsies, normal jaw and facial jerks

Mid cervical

Tetraparesis with preservation of shoulder movements

to involvement of the corticobulbar fibers to the lower cranial nerves, and occasionally his horizontal eye movements are impaired owing to bilateral involvement of the fascicle of the sixth cranial nerve as it exits the pons. Because the patient cannot move or speak, he may initially appear to be in a coma. However, because the tegmentum of the pons is spared, the reticular formation is intact, and the patient is awake. Vertical eye movements and blinking are still intact, and the patient is able to communicate via eye blinks.

Hemorrhages in the pons that produce tetraplegia owing to destruction of the basis pontis usually also affect the dorsal tegmentum, producing sudden coma, pinpoint pupils, ophthalmoplegia, hyperthermia, and progression to death. A more restricted hemorrhage may occur in the lateral tegmentum of the pontomesencephalic junction, producing a more restricted syndrome that includes small reactive pupils with the smaller pupil ipsilateral to the lesion, ipsilateral conjugate palsy due to involvement of the paramedian pontine reticular formation, ipsilateral ataxia due to involvement of cerebellar connections, and contralateral hemiparesis and hemisensory deficits. Occasionally, the ocular motor abnormality is an ipsilateral skew deviation or internuclear ophthalmoplegia caused by involvement of the medial longitudinal fasciculus.

Although we often refer to the corticospinal tract as the

pyramidal tract and to weakness from a lesion as a pyramidal weakness, weakness resulting from lesions of the pyramids in the medulla is very seldom seen. The medullary pyramids are supplied by the paramedian arteries branching off the vertebral artery and, more inferiorly, from the interior spinal artery. Occlusion of these arteries can produce infarction of the ipsilateral pyramid, medial lemniscus, and hypoglossal nerve and nucleus, producing a contralateral hemiplegia with sparing of the face and ipsilateral paresis and atrophy of the tongue. Occasionally, there is a contralateral loss of position of vibratory sensation due to involvement of the medial lemniscus. Because the more dorsolateral spinothalamic tract is unaffected, pain and temperature sensation are spared. However, infarction of the medulla occurs much more commonly in the vascular supply of the lateral medulla, producing the Wallenberg or lateral medullary syndrome, which spares the pyramids (see Chapters 13 , 14 , 22 , and 45 ).

Developmental malformations of the brain stem such as the Chiari malformations or tumors in the foramen magnum at the cervical medullary junction more commonly produce weakness by involvement of the medullary pyramids and the upper cervical cord at the place where they decussate into the corticospinal tracts of the lateral and ventral funiculi of the spinal cord. A spastic tetraparesis (generally the legs are more involved than the arms) occurs in varying combinations with weakness of the tongue and pharynx, nystagmus (due to involvement of the inferior cerebellar peduncle), and facial hypalgesia (due to involvement of the descending tract of the trigeminal nerve) (see Table 15-10 ). A syringomyelic syndrome occurs if central cavitation of the cord is present. This characteristically produces a loss of pain and temperature sensation over the shoulders and a lower motor neuron syndrome of the upper extremities with weakness, atrophy, fasciculations, and loss of reflex. The distribution of the weakness and loss of reflex depends on which segments of the cervical spinal cord are involved.

The characteristic pattern of weakness seen in patients with upper motor neuron lesions of the spinal cord is weakness combined with appropriate reflex changes on both sides of the body with no signs of cerebral, cortical, or brain stem dysfunction. The level of the lesion is defined by whether the arms are involved (cervical cord) or just the legs (thoracic cord). More exact definition of the level of the lesion is made by noting the distribution of lower motor neuron involvement if the lesion is in the cervical cord or by noting the sensory level resulting from involvement of the ascending sensory tracts with lesions in either the thoracic or cervical cord. These characteristic clinical syndromes are described in more detail in the later section on combined upper and lower motor neuron lesions (see Table 15-7 ).

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