Benign Paroxysmal Positional Vertigo (BPPV) is a mechanical disorder of the
vestibular system in which calcite particles called otoconia interfere with the
mechanical functioning of the fluid-filled semicircular canals normally used to
sense rotation. Using hydrodynamic models, we examine the two mechanisms
proposed by the medical community for BPPV: cupulolithiasis, in which otoconia
attach directly to the cupula (a sensory membrane), and canalithiasis, in which
otoconia settle through the canals and exert a fluid pressure across the
cupula. We utilize known hydrodynamic calculations and make reasonable
geometric and physical approximations to derive an expression for the
transcupular pressure ΔPc exerted by a settling solid particle in
canalithiasis. By tracking settling otoconia in a two-dimensional model
geometry, the cupular volume displacement and associated eye response
(nystagmus) can be calculated quantitatively. Several important features
emerge: 1) A pressure amplification occurs as otoconia enter a narrowing duct;
2) An average-sized otoconium requires approximately five seconds to settle
through the wide ampulla, where ΔPc is not amplified, which suggests a
mechanism for the observed latency of BPPV; and 3) An average-sized otoconium
beginning below the center of the cupula can cause a volumetric cupular
displacement on the order of 30 pL, with nystagmus of order 2∘/s, which
is approximately the threshold for sensation. Larger cupular volume
displacement and nystagmus could result from larger and/or multiple otoconia.Comment: 15 pages, 5 Figures updated, to be published in J. Biomechanic