Abstract
Canalolithiasis and cupulolithiasis have been proposed to be causative mechanisms of BPPV. Anatomical and physiological features of otoconia are reviewed. Three layers, the columnar fibers, gelatin membrane, and otolithic membrane, are known as overlaying structures on the macular sensory epithelia. The supporting cell plays an essential role in otoconial formation. It secretes granules containing calcium as a precursor of otoconia. A number of proteins are involved in the production and growth of otoconia, such as Otoconin-90 and CB-D28K. Alterations of the endolymphatic environment, ototoxic drugs, carbonic anhydrase, hormones, aging, or gene mutation lead to degeneration or deformity of otoconia. Hydrodynamic and physiological features of otoconia existing within the semicircular canal or attaching to the cupula have been studied using mathematical models and amphibian semicircular canals. These studies showed that canalolithiasis is potentially the most relevant mechanism of BPPV in terms of the long latency and short duration of nystagmus. Human temporal bone sections had been studied to demonstrate deposits on the cupula or within the canal lumen. Otoconia were also found in the posterior canal lumen that was opened during canal plugging surgery. Clarification of the basic characters of otoconia is essential for elucidating the clinical picture of BPPV.
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