27:T519,

While most studies have demonstrated damage to the cochlear and vestibular endorgan as the primary site of aminoglycoside toxicity, the effect on the primary afferent neurons of the vestibular ganglion remains to be determined. This study used the unbiased stereology-optical fractionator method to obtain estimates of the vestibular ganglion neuronal number. Archival temporal bone specimens from seven subjects with a history of gentamicin (n = 3) and streptomycin (n = 4) aminoglycoside ototoxicity were used. The post-ototoxicity survival time ranged from two months to 8 years, with an average of 2.2 years. Seven archival human temporal bone specimens from age-matched subjects with no history of audiovestibular symptoms or ototoxicity served as controls. Group means were compared using unpaired, two-tailed student's t test. The average vestibular ganglion neuronal number in the aminoglycoside ototoxicity group was 20, 733 neurons (CV = 0.073), which was significantly lower (p < 0.005) than the average number in the age-matched control group of 24, 902 neurons (CV = 0.109). These findings may be consistent with either retrograde degeneration or a direct neurotoxic effect of the aminoglycosides on the vestibular ganglion neuron.

28:T48a,

Horizontal canal (HC) benign paroxysmal positional vertigo (HC-BPPV) is a vestibular disorder characterized by bouts of horizontal ocular nystagmus induced during reorientation of the head relative to gravity. The present report addresses the application of a morphologically descriptive 3-canal biomechanical model of the human membranous labyrinth to study gravity-dependent semicircular canal responses during this condition. The model estimates dynamic cupular and endolymph displacements elicited during HC-BPPV provocative diagnostic maneuvers and canalith repositioning procedures (CRPs). The activation latencies in response to an HC-BPPV provocative diagnostic test were predicted to vary depending upon the initial location of the canalith debris (e.g. within the HC lumen vs. in the ampulla). Results may explain why the onset latency of ocular nystagmus evoked by the Dix-Hallpike provocative maneuver for posterior canal BPPV are typically longer than the latencies evoked by analogous tests for HC-BPPV. The model was further applied to assess the efficacy of a 360°-rotation CRP for the treatment of canalithiasis HC-BPPV.

29:T60c,