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J Assoc Res Otolaryngol. Dec 2002; 3(4): 430–443.
Published online Mar 26, 2002. doi:  10.1007/s101620010053
PMCID: PMC3202443
Changes in the Three-Dimensional Angular Vestibulo-Ocular Reflex following Intratympanic Gentamicin for Ménière's Disease
John P. Carey, Lloyd B. Minor, Grace C.Y. Peng, Charles C. Della Santina, Phillip D. Cremer, and Thomas Haslwanter
Department of Otolaryngology–Head and Neck Surgery, Johns Hopkins University, Baltimore, MD 21287, USA, , , , US
Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205, USA, , , , US
Department of Neuroscience, Johns Hopkins University, Baltimore, MD 21205, USA, , , , US
Department of Neurology, Johns Hopkins University, Baltimore, MD 21287, USA, , , , US
Department of Biomedical Engineering, Catholic University of America, Washington, DC 20064, USA, , , , US
Eye and Ear Research Unit, Institute of Clinical Neurosciences, Royal Prince Alfred Hospital, Sydney, Australia, , , , AU
Department of Neurology, Zürich University Hospital, Zürich, Switzerland, , , , CH
Received June 19, 2000; Accepted January 21, 2002.
Abstract
The 3-dimensional angular vestibulo-ocular reflexes (AVOR) elicited by rapid rotary head thrusts were studied in 17 subjects with unilateral Ménière's disease before and 2–10 weeks after treatment with intratympanic gentamicin and in 13 subjects after surgical unilateral vestibular destruction (SUVD). Each head thrust was in the horizontal plane or in either diagonal plane of the vertical semicircular canals, so that each head thrust effectively stimulated only one pair of canals. The AVOR gains (eye velocity/head velocity during the 30 ms before peak head velocity) for the head thrusts exciting each individual canal were averaged and taken as a measure of the function of that canal. Prior to intratympanic gentamicin, gains for head thrusts that excited canals on the affected side were 0.91 ± 0.20 (horizontal canal, HC), 0.78 ± 0.20 (anterior canal, AC), and 0.83 ± 0.10 (posterior canal, PC). The asymmetries between these gain values and those for head thrusts that excited the contralateral canals were <2%. In contrast, caloric asymmetries averaged 40% ± 32%. Intratympanic gentamicin resulted in decreased gains attributable to each canal on the treated side: 0.40 ± 0.12 (HC), 0.35 ± 0.14 (AC), 0.31 ± 0.14 (PC) (p <0.01). However, the gains attributable to contralateral canals dropped only slightly, resulting in marked asymmetries between gains for excitation of ipsilateral canals versus their contralateral mates: HC: 34% ± 12%, AC: 24% ± 25%, and PC: 42% ± 13%. There was no difference in the AVOR gain for excitation of the ipsilateral HC after gentamicin in patients who received a single intratympanic injection (0.39 ± 0.11, n = 12) in comparison to those who received 2–3 injections (0.42 ± 0.15, n = 5, p = 0.7). Gain decreases attributed to the gentamicin-treated HC and AC were not as severe as those observed after SUVD. This finding suggests that intratympanic gentamicin causes a partial vestibular lesion that may involve preservation of spontaneous discharge and/or rotational sensitivity of afferents.
Articles from JARO: Journal of the Association for Research in Otolaryngology are provided here courtesy of
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