KAREN H.CALHOUNMDRONALD B.KUPPERSMITHMD
Otolith repositioning, if properly performed, is nearly always effective in relieving symptoms of benign paroxysmal positional vertigo (BPPV).
It is generally agreed that BPPV results from dysfunction of the posterior semicircular canal (PSCC). The characteristic rotary nystagmus seen in BPPV can be reproduced by electrical stimulation of the PSCC and eliminated by deafferentation of the PSCC. Two theories have been advanced to explain the pathophysiological characteristics of BPPV; these are cupulolithiasis and canalithiasis. The former is Schuknecht's original theory of a substance adherent to the cupula, while the latter presumes the presence of free-floating debris within the posterior canal.1 Temporal bone studies may not be able to provide sufficient evidence to differentiate between the 2 theories. Moriarty et al2 showed that deposits are present on all of the semicircular canal ampullae, although the PSCC is most commonly involved. Supportive evidence for the canalithiasis theory is provided by surgeons who have noted freely moving particles within the semicircular canals during the translabyrinthine approach to the cerebellopontine angle and when performing posterior canal occlusion.
Vrabec JT. Benign Paroxysmal Positional Vertigo and Otolith Repositioning. Arch Otolaryngol Head Neck Surg. 1998;124(2):223–225. doi:10.1001/archotol.124.2.223
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