Benign paroxysmal positional vertigo: a clinician's perspective

Abstract

The pathogenesis and epidemiology of benign paroxysmal positional vertigo are still not well defined. Treatment protocols have emerged along with complementary hypotheses regarding pathogenesis. Ultrastructural studies suggest a multistep process of otoconia metabolism responsible for forming the otolith membrane. A defect in otoconia metabolism leads to an excess of otoconia within the utricular sac (utriculolithiasis). Gravitational forces cause the entrapment of otoconia within the semicircular canal system (canalolithiasis). Localization of these otoconia within the semicircular canal system is deducted by combining the gravitational orientation of the canal involved with the vestibular neurophysiology of the resulting nystagmus recorded during testing and throughout treatment. New terminology is required to differentiate short-arm from long-arm canalolithiasis. Evidence from digital videonystagmography recordings of nystagmus is coupled with principles of gravitational fluid mechanics to explain the mechanisms of disease development and treatment. These observations lead to important questions that define future directions in research.