2003/05/31 by Todd M. Squires, Michael S. Weidman, Timothy C. Hain +1
Physics and Astronomy · Biochemistry, Genetics and Molecular Biology · #physics.flu-dyn #physics.med-ph #q-bio
paper · pdf · doi:10.1016/j.jbiomech.2003.12.014
published as J. Biomech. 37 (2004)1137 --1146 · 15 pages, 5 Figures updated, to be published in J. Biomechanics
arxiv created 2004/01/17 · arxiv updated 2009/12/01
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.