A scoping review of vestibular paroxysmia: An acute disabling clinical entity

Abstract

The pathogenesis of vestibular paroxysmia (VP) is the neurovascular cross-compression of cranial nerve VIII with short episodes of vertigo as the common symptom. The exact etiological and clinical profiles of the patients with VP are uncertainly reported in literature. It is general thought that loop of the anterior inferior cerebellar artery and posterior inferior cerebellar artery (less commonly), vertebral artery, or a vein is involved in compressing cranial nerve VIII. Ephaptic neural discharges at the proximal end of cranial nerve VIII, which is covered by oligodendrocytes, are thought to be the mechanism for VP. Patients with VP often suffer from brief vertiginous attacks of several episodes in a single day, and nystagmus is seen during the vertiginous episodes. Cranial magnetic resonance imaging could reveal the arterial compression of cranial nerve VIII. The important differential diagnosis of VP includes vestibular migraine, Meniere’s disease, benign paroxysmal positional vertigo, superior canal dehiscence syndrome, epileptic vertebral aura, paroxysmal brainstem attacks (in multiple sclerosis or after brainstem stroke), transient ischemic attacks and panic attacks. The vertiginous attacks can be ceased by administration of a low dose of carbamazepine. Carbamazepine or oxcarbazepine, even in low doses, can be efficient to relieve VP, and they have the same efficiency both in adults and in children.