Peripheral vestibular disorders

Purpose of review First, to update the diagnosis, pathophysiology, and treatment of the most frequent peripheral vestibular disorders. Second, to identify those disorders for which the diagnostic criteria are still deficient and treatment trials are still lacking. Recent findings Bilateral vestibulopathy can be reliably diagnosed by the head-impulse test, caloric irrigation, and vestibular-evoked myogenic potentials. A new frequent subtype has been described: cerebellar ataxia, neuropathy, and vestibular areflexia syndrome. Benign paroxysmal positioning vertigo can be easily diagnosed and effectively treated. Vestibular neuritis is most likely caused by the reactivation of a herpes simplex type 1 infection; the inferior vestibular nerve subtype is now well established. More evidence is needed that the recovery can be improved by corticosteroids. Endolymphatic hydrops in Meniere's disease can be depicted by high-resolution MRI after transtympanic gadolinium injection; a high-dosage and long-term prophylactic treatment with betahistine is evidently effective. Its mechanism of action is most likely an increase in the inner-ear blood flow. Vestibular paroxysmia is now a well established entity; carbamazepine is the treatment of first choice. Superior canal dehiscence syndrome can be reliably diagnosed; the best current treatment option is canal plugging. Summary Although progress has been made in the diagnosis and treatment of most peripheral vestibular disorders, more state-of-the-art trials are needed on the treatment of bilateral vestibulopathy to prove the efficacy of balance training, of vestibular neuritis (in terms of recovery of peripheral vestibular function and central compensation), of vestibular paroxysmia to prove the effects of carbamazepine, and of Meniere's disease to find the optimal dosage of betahistine