The fact that vertigo may constitute the aura of an epileptic seizure supports the view that this symptom may have a cerebrocortical origin. Indeed, electrical stimulation of the cerebral cortex in an unanesthetized patient, either of the posterolateral aspects of the temporal lobe or the inferior parietal lobule adjacent to the sylvian fissure, may evoke intense vertigo. The occurrence of vertigo as the initial symptom of a seizure is, however, infrequent. In such cases, a sensation of movement—either of the body away from the side of the lesion or of the environment in the opposite direction—lasts for a few seconds before being submerged in other seizure activity. Vertiginous epilepsy of this type should be differentiated from vestibulogenic seizures, in which an excessive vestibular discharge serves as the stimulus for a seizure. The latter is a rare form of reflex epilepsy, in which tests that induce vertigo may provoke the seizure (see Chap. 16).
The issue of migraine as a cause of vertigo has occasioned much discussion. Several authoritative clinicians attribute many instances of otherwise unexplained dizziness and vertigo to migraine with aura, but it is not entirely clear whether they are referring to an attack of basilar migraine, usually in children (migrainous vertigo), or to episodes of vague disequilibrium or vertigo at various times in migraineurs, which has been more typical in our experience. A survey by Neuhauser and colleagues found that 7 to 9 percent of patients had conventional migrainous symptoms during or before a vertiginous attack, and in half of those the vertigo was regularly associated with migraine.
Lesions of the cerebellum produce vertigo depending on which part of this structure is involved. Large, destructive processes in the cerebellar hemispheres and vermis, such as cerebellar hemorrhage may, or at times may not, cause vertigo. However, strokes in the territory of the medial branch of the posterior inferior cerebellar artery (which arises distal to the branches to the medulla, and therefore does not involve the lateral medulla) causes intense vertigo and vomiting that is indistinguishable from that caused by labyrinthine disorder. In two such pathologically studied cases, a large zone of infarction extended to the midline and involved the flocculonodular lobe (Duncan et al). Falling in these cases was toward the side of the lesion; nystagmus was present on gaze to each side but was more prominent on gaze to the side of the infarct. These findings have been confirmed by CT and MRI (Amarenco et al). Early in the course of an acute attack of vertigo, when it may be difficult to assess the gait and the quality of nystagmus, it may be necessary to exclude a cerebellar infarct or hemorrhage by use of imaging procedures.
Labyrinthine disease, on the other hand, causes predominantly unidirectional nystagmus with the fast phase opposite to the side of the impaired labyrinth, and swaying or falling toward the involved side—that is, the direction of the nystagmus is opposite to that of the falling and past pointing (the latter referring to overshooting a target by the patient’s finger with eyes closed, as originally described by Bárány [1921]). Ataxia and dysarthria are, of course, typical of many forms of cerebellar disease but may be minimal or absent in cerebellar hemorrhage and some infarctions as well as being lacking in all forms of vestibular disease.
The topic of vertigo with fluctuating ischemia in the territory of the basilar and vertebral arteries (transient ischemic attack [TIA]) and the problem of subclavian steal syndrome are discussed further on under “Vertigo of Brainstem Origin” and in Chap. 33. Also common in practice is vertigo caused by the demyelinating lesions of multiple sclerosis, as noted in the later section.