Vestibular paroxysmia: a systematic review.

Abstract

The key symptoms of vestibular paroxysmia (VP) due to neurovascular cross-compression (classical VP) or compression of the eighth nerve by space-occupying cerebellar-pontine angle processes (secondary VP) are frequent short attacks of vertigo and dizziness with unsteadiness which last seconds to minutes. They can be accompanied by unilateral auditory symptoms such as tinnitus or hyperacusis. Head movements and hyperventilation can induce nystagmus and VP attacks that most often occur spontaneously. VP is diagnosed in 3% of patients in a tertiary vertigo care center and very rarely affects children. The mean age of first appearance is 47 to 51 years with equal sex distribution. A combination of high-resolution MRI sequences (with constructive interference in steady-state/fast imaging employing steady-state, 3D-CISS/ FIESTA) of the cerebello-pontine may support the diagnosis although the beneficial treatment with sodium channel blockers is the most reliable clinical sign for classical VP, secondary VP and idiopathic VP (without verification of a causative pathology). Because of the frequency, shortness, and audiovestibular symptomatology of the attacks, the differential diagnosis to other conditions such as paroxysmal brainstem attacks, vestibular epilepsy, rotational vertebral artery compression syndrome or "near"-narrowed internal auditory canal syndrome is only relevant in exceptional cases. However, imaging of the posterior fossa including the inner ear is mandatory to distinguish between classical, secondary and idiopathic VP forms. Randomized controlled trials for medical treatment are still needed. Practical therapy of choice is medical treatment with sodium channel blockers (carbamazepine, oxcarbazepine, lacosamide). A microsurgical decompression is effective in secondary VP but is the ultimate therapy in cases with classical or idiopathic VP when medication is not tolerated.