Vertigo of cerebellar origin is exceptional in this respect in that it may rarely be the sole manifestation of cerebellar infarction or hemorrhage, as described earlier in the introductory sections of the chapter and in Chap. 33. It follows that isolated vertigo may be the result of occlusion of the posterior inferior cerebellar artery or its parent vertebral artery although most often, there are additional features related to damage to the lateral medulla. In instances of isolated vertigo, one seeks confirmation that there are no features pointing to a central origin or conversely, if there are signs such as nystagmus in more than one direction of gaze with a single position of the head, or vertical nystagmus, there is concern for ischemia of the brainstem. The nystagmus and ataxia of gait (more of a propelling, or pulsion, to one side) that accompany acute cerebellar lesions are toward the same side (the side of the lesion), while in acute vestibulopathies, nystagmus beats away from the side of the lesion and pulsion is still toward the affected side.
Multiple sclerosis may be the explanation of persistent vertigo in an adolescent or young adult, sometimes with little or no nystagmus. In most cases, there are other characteristic features of multiple sclerosis (e.g., internuclear ophthalmoplegia) but rarely, a demyelinating plaque in the vicinity of the vestibular nuclei simulates a peripheral vestibular disorder.
The relationship of migraine to vertigo was mentioned earlier. This refers to otherwise mundane migraine in which the vertigo is perhaps an aura, or to episodes of paroxysmal vertigo in adults that are considered to be migraine equivalents. In addition, attacks of vertigo followed by an intense unilateral and often suboccipital headache and vomiting are the characteristic features of basilar artery migraine. The prodromal visual symptoms take the form of blindness or of photopsia that occupies all of the visual fields. Between headaches, tests of cochlear and vestibular function in these patients are normal. Some authorities have stated that most cases of recurrent vertigo without hearing loss over many years can be attributed to migraine and not to Ménière disease. An instructive series of such cases has been published by Dieterich and Brandt.
Finally, mention should be made of a familial vestibulocerebellar syndrome, beginning in childhood or early adult life and characterized by recurrent episodes of vertigo and imbalance. Diplopia and dysarthria complicate some attacks, which seem to be precipitated by extreme exertion and emotion. Repeated attacks are followed by a mild, persistent ataxia, mainly of the trunk. This disorder was first described by Farmer and Mustian and more recently by Baloh and Winder, who have pointed out that both the episodic vertigo and ataxia are markedly reduced or abolished by the administration of acetazolamide. This process is most likely related to the inherited acetazolamide-responsive ataxic channelopathy syndrome described in Chap. 5. A form that is kinesigenic, that is, brought on by activity, has a similar appearance.
In summary, the nature of the nystagmus, instability of the eyes during the head impulse test, and the other features of the neurologic examination allow a distinction to be made between central and peripheral cases of vertigo. Associated hearing loss favors a vestibular cause of vertigo. Tables 14-2 and 14-3 summarize the features of the various vertiginous syndromes.
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