Changes in the Three-Dimensional Angular Vestibulo-Ocular Reflex following Intratympanic Gentamicin for Ménière's Disease

Abstract

The 3-dimensional angular vestibulo-ocular re¯exes (AVOR) elicited by rapid rotary head thrusts were studied in 17 subjects with unilateral Me Ânie Áre'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 gentamicintreated HC and AC were not as severe as those observed after SUVD. This ®nding suggests that intratympanic gentamicin causes a partial vestibular lesion that may involve preservation of spontaneous discharge and/or rotational sensitivity of afferents.

The Effects of Cochlear Implantation on Vestibular Function

“…"Severe-to-profound" hypofunction was defined as VOR gains that were <0.40, <0.52, and <0.36 for horizontal, anterior, and posterior SCCs, respectively. By these definitions, "mild-to-moderate" hypofunction is comparable to VOR performance observed in ears treated with intratympanic gentamicin for Ménière's disease (26), and "severe-to-profound" hypofunction is comparable to VOR performance observed in ears after ipsilateral labyrinthectomy (36).…”

“…Individual and mean ± standard deviation VOR gains for qHIT data for 28 subjects. These data are compared to normal, gentamicin-treated (Post-Gent), and surgically deafferented (SUVD) ears' qHIT results for each SCC from prior studies (26,34). The bolded lines represent the only subject with significantly decreased vestibular function in all 3 SCCs of the implanted ear.…”

Longitudinal Results With Intratympanic Dexamethasone in the Treatment of Ménière's Disease

“…The IT gentamicin titration protocol would appear to have an advantage over IT dexamethasone treatment in clustering mutiple injections at the time of initial treatment and decreasing the probability for needing subsequent injections. However, IT gentamicin treatment carries the risks of worsening the hearing loss in the treated ear and of causing disequilibrium (1,2) because a reduction in vestibular function is likely the mechanism by which gentamicin achieves vertigo control (19,20).…”

Regeneration of Vestibular Otolith Afferents after Ototoxic Damage

“…Trauma, disease, or toxicity can produce damage to the vestibular receptor system, with immediate functional disabilities resulting. For example, ototoxic antibiotics produce vestibular sensory cell death and receptor denervation (Berg, 1951;Wersäll and Hawkins, 1962;Lindeman, 1969a,b), followed by severe dysfunction (Wersäll and Hawkins, 1962;Carey et al, 1996Carey et al, , 2002Goode et al, 1999;Hirvonen et al, 2005). It is now firmly established that cochlear and vestibular sensory hair cells spontaneously regenerate after damage in fish, amphibians, and birds (Corwin and Cotanche, 1988;Rubel, 1992, 1993;Baird et al, 1993), and these regenerated hair cells are contacted by new afferent and efferent terminals (Ryals and Westbrook, 1994;Masetto and Correia, 1997b;Hennig and Cotanche, 1998).…”