Labyrinthine infarction can be a component of the stroke syndrome from occlusion of the anterior inferior cerebellar artery (AICA). In the complete syndrome there is hearing loss, cerebellar ataxia, and sometimes “screaming tinnitus” or lesser degrees of tonal tinnitus. Also reported is a clinical syndrome of unknown nature consisting of a single abrupt attack of severe vertigo, nausea, and vomiting without tinnitus or hearing loss but with permanent ablation of labyrinthine function on one side. It has been suggested that this syndrome is a result of occlusion of the labyrinthine division of the internal auditory artery, but so far, anatomic confirmation has not been obtained. Labyrinthine hemorrhage has been demonstrated by MRI in some of these patients; others are attributed, speculatively, to viral infection.
Basser described a particular form of paroxysmal vertigo that occurs in childhood. The attacks occur in a setting of good health and are of sudden onset and brief duration. Pallor, sweating, and immobility are prominent manifestations; occasionally, vomiting and nystagmus occur. No relation to posture or movement has been observed. The attacks are recurrent but tend to cease spontaneously after a period of several months or years. The outstanding abnormality is demonstrated by caloric testing, which shows impairment or loss of vestibular function, bilaterally or unilaterally, frequently persisting after the attacks have ceased. Cochlear function is unimpaired. The pathologic basis of this disorder has not been determined, and a suggested connection with migraine is tenuous. The special case of basilar artery migraine is discussed below.
Cogan has described an infrequent syndrome in young adults in which a nonsyphilitic interstitial keratitis is associated with vertigo, tinnitus, nystagmus, and rapidly progressive deafness. The prognosis for vision is good, but the deafness and loss of vestibular function are usually permanent. The cause and pathogenesis of this syndrome are unknown, although approximately half of the patients later develop aortic insufficiency or a systemic vasculitis that resembles polyarteritis nodosa. These vascular complications proved fatal in 7 of 78 cases reviewed by Vollertsen and colleagues.
There are many other causes of aural vertigo, such as purulent labyrinthitis complicating mastoiditis or meningitis; serous labyrinthitis caused by infection of the middle ear; “toxic labyrinthitis” caused by intoxication with alcohol, quinine, or salicylates; motion sickness; and hemorrhage into the inner ear. Bárány (1911) was the first to draw attention to the nystagmus and positional vertigo, worse on closing the eyes that occurs at a certain level of intoxication with alcohol and lasts a few hours. Such an episode of alcohol-induced vertigo tends to last longer than a vertiginous attack of Ménière disease, but in other respects, the symptoms (excepting tinnitus) are similar.
Vertigo with varying degrees of spontaneous or positional nystagmus and reduced vestibular responses is a frequent complication of cranial trauma. Vertigo, often of the nonrotatory, to-and-fro type, may follow cerebral concussion or whiplash injury, in which the head has not been impacted. Brandt has attributed this syndrome to a loosening or dislodgement of the otoconia in the otoliths. The vertigo in these circumstances usually improves in a few days or weeks and is rarely accompanied by impairment of hearing—in distinction to the vertigo that follows fractures of the temporal bones (as described earlier in this chapter in the discussion of deafness). Dizziness is also a prominent complaint as part of the syndrome of a postconcussion syndrome as described in Chap. 35, but usually this proves to be ill-defined giddiness rather than true vertigo.