Less often, occlusion of the vertebral artery or one of its medial branches produces an infarct that involves the medullary pyramid, the medial lemniscus, and the emergent hypoglossal fibers; the resultant syndrome consists of a contralateral paralysis of arm and leg (with sparing of the face), contralateral loss of position and vibration sense, and ipsilateral paralysis and later atrophy of the tongue. This is the medial medullary syndrome (Fig. 33-13). A more limited lesion, from occlusion of one spinal artery arising from the vertebral artery, gives rise to a contralateral hemiplegia (rarely a quadriplegia) that spares the face. When the vertebral branch to the anterior spinal artery is blocked, flow from the other (corresponding) branch is usually sufficient to prevent infarction of the cervical cord, but we and others have described solely pyramidal infarction with hemiplegia or quadriplegia that spares the face (Ropper et al).
Known also as the Wallenberg syndrome (who described a case in 1895), this common stroke is produced by infarction of a wedge of lateral medulla lying posterior to the inferior olivary nucleus (see Figs. 33-2, 33-12, and 33-13). The complete syndrome, as outlined by Fisher and colleagues (1961) comprises (a) symptoms derived from the vestibular nuclei (vertigo, nystagmus, oscillopsia, vomiting); (b) spinothalamic tract (contralateral or, less often, ipsilateral impairment of pain and thermal sense over half the body); (c) descending sympathetic tract (ipsilateral Horner syndrome—miosis, ptosis, decreased sweating); (d) issuing fibers of the ninth and tenth nerves (hoarseness, dysphagia, hiccough, ipsilateral paralysis of the palate and vocal cord, diminished gag reflex); (e) utricular nucleus (vertical diplopia and illusion of tilting of vision and rotation of the vertical meridian, rarely so severe as to produce upside down vision); (f) olivocerebellar, spinocerebellar fibers, restiform body and inferior cerebellum (ipsilateral ataxia of limbs, falling or toppling to the ipsilateral side, and the sensation of lateropulsion); (g) descending tract and nucleus of the fifth nerve (pain, burning, and impaired sensation over ipsilateral half of the face); (h) nucleus and tractus solitarius (loss of taste); and rarely, (i) cuneate and gracile nuclei (numbness of ipsilateral limbs). Fragmentary syndromes are more frequent, especially at the onset of the stroke. These subsyndromes consist mainly of vertigo but may include and ptosis, toppling and vertical diplopia, hoarseness and disequilibrium, or other combinations short of the entire syndrome. While vertigo is the most frequent feature, it alone, is not usually an indication of lateral medullary infarction. The smallest infarctions we have encountered gave rise only to symptoms of lateropulsion and mild ipsilateral limb ataxia and in one case with a very small region of pontomedullary infarction on MRI, vertigo, and associated gait difficulty.
The eye signs of lateral medullary infarction are also varied and quite interesting. Nystagmus is almost invariable. Direction-changing nystagmus (with different positions of gaze) is a useful feature that suggests brainstem forms of nystagmus (see Chap. 13). There may be a fragment of an internuclear ophthalmoplegia or a skew deviation (hypotropia on the side of the stroke). There may be hypometric saccades toward the side of the lesion and hypermetric saccades in the opposite direction.