Current view of the mechanism of benign paroxysmal positioning vertigo: cupulolithiasis or canalolithiasis?

Abstract

Theoretical evidence is presented that all the typical features of BPPV (benign paroxysmal positioning vertigo) cannot be explained by cupulolithiasis in that otoconial debris become settled on the cupula of the posterior semicircular canal. A free floating clot of inorganic particles (heavier than endolymph) in the ampullofugal branch of the posterior semicircular canal is more likely to cause the syndrome. The clot always gravitates to the most dependent part of the canal as soon as the patient's head is moved in a way that alters the angle between the canal's plane and the gravity vector. As compared to a plunger (depending on the direction it moves) the clot produces push or pull forces on the cupula, thereby eliciting the BPPV attack. This clot-induced endolymph flow mechanism is compatible with all features of BPPV such as latency, limited duration, fatigability, change in direction of the induced nystagmus, and the efficacy of physical therapy in both posterior and horizontal semicircular canal BPPV. The floating clot is only activated by changes in position of the head relative to the gravitational vector (positioning vertigo) but not by prolonged static positions of the head (positional vertigo), which fits clinical experience. Therefore, canalolithiasis rather than cupulolithiasis provides a better definition of the underlying mechanism in BPPV.