Abstract
Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vertigo and is characterized by brief attacks of rotatory vertigo associated with positional and/or positioning nystagmus, which are elicited by specific head positions or changes in head position relative to gravity. The pathophysiology of BPPV is canalolithiasis comprising free-floating otoconial debris within the endolymph of a semicircular canal, or cupulolithiasis comprising otoconial debris adherent to the cupula. In the canalolithiasis theory, when patients with BPPV move their head, free-floating otoconial debris in the canal creates the endolymph flow, the flow of the fluid causes deflection of the cupula of the canal, and as a result, the canal is stimulated or inhibited and nystagmus and vertigo are induced. In the cupulolithiasis theory, when patients with BPPV move their head, the cupula, with its adherent otoconial debris, deviates in the direction of gravity, and as a result, the canal is stimulated or inhibited and nystagmus and vertigo are induced.
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