Clinical Implications of a Mathematical Model of Benign Paroxysmal Positional Vertigo

Abstract

Benign paroxysmal positional vertigo (BPPV) is the most commonly diagnosed vertigo syndrome. It is caused by movement of detached otoconia within the inner ear (canalithiasis) or otoconia adherent to the cupula (cupulolithiasis). A mathematical model incorporating fluid dynamics of BPPV, which results in the following insights, has been developed recently: (1) The characteristic latency of BPPV is explained by movement of detached otoconia through the ampulla, as pressure caused by moving otoconia is negligible until otoconia enter the narrow duct of the semicircular canal. Typical otoconia move at a rate of 0.2 mm/s, or about 1% of the circumference of the canal each second. (2) Particle-wall interactions can account for the considerable variability in duration and latency of BPPV. (3) Dispersion of a clump of otoconia creates more rather than less nystagmus. Thus, dispersion is not a viable explanation of fatigability. (4) Cupulolithiasis is predicted to cause a far weaker nystagmus than canalithiasis. (5) Inertial effects of treatment maneuvers cause negligible movement of otoconia.