LATERAL MEDULLARY SYNDROME
Occlusion of the Posterior Inferior Cerebellar Artery (PICA)
The PICA supplies the dorsal lateral medullary plate and portions of the posterior medial cerebellum (uvula, nodulus and probably portions of the paraflocculus). Occlusion of its distal cerebellar branches can produce a syndrome very difficult to distinguish from a peripheral labyrinthine disorder, with vertigo, dysequilibrium and spontaneous nystagmus (medial pica syndrome, distal pica infarct). Careful examination may show more evidence of ocular motor involvement (gaze-holding difficulties, vertical positional nystagmus, pursuit defects) than one normally finds with peripheral lesions, but one can not always confidently distinguish between a peripheral and a central cause. Recall that the labyrinth has direct monosynaptic projections to the cerebellar nodulus, so it is not surprising that similar syndromes may occur with lesions in both places.
When the PICA is occluded at its origin Wallenberg's syndrome results with a characteristic neuroophthalmologic and neurootologic manifestations including
Otolith syndrome (involvement of caudal vestibular complex)
Skew deviation -- eye lower on the side of the lesion
Head tilt -- to the side of the lesion
Ocular counterroll -- both eyes roll (top of eye) toward the side of the lesion
Disordered perceptions of verticality
Pulsion of the body (vestibulospinal) toward the side of the lesion
Saccade syndrome (interruption of inferior cerebellar peduncle (and climbing fibers) causing a functional inhibition of ipsilateral fastigial nucleus)
Lateropulsion of saccades (ipsipulsion)
Vertical saccades deviate toward the side of the lesion
Steady-state deviation of the eyes toward the side of the lesion under closed lids
Other vascular syndromes to keep in mind in the differential diagnosis of the patient with acute vertigo include the vestibular-masseter syndrome, due a branch occlusion (AICA or PICA) involving the vestibular afferents on their way to the vestibular nuclei as they pass the motor nucleus of the V nerve. Such patients have acute vertigo with weakness or deviation of the jaw. Occlusions of branches of the superior cerebellar artery involving the superior cerebellar peduncle may also cause vertigo as well as contrapulsion of saccades (due to involvement of fastigial nucleus outflow projection (which courses through the uncinate fasciculus of Hook) just after it crosses the midline to reach the contralateral brainstem). Cerebellar hemorrhages and swollen cerebellar hemispheres due to cerebellar ischemic infarction may also simulate an acute peripheral vestibulopathy with vertigo, ataxia and nausea and vomiting. In patients above the age of 45 who develop acute vertigo, dysequilibrium without hearing symptoms, and are seen in the ER, it is often prudent to obtain a CT scan, especially if the patient has any vascular risk factors, to look for hemorrhage or swelling.