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: 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.

This paper describes our analysis of the complex head-neck system using a combination of experimental and modeling approaches. Dynamical analysis of head movements and EMG activation elicited by perturbation of trunk position has examined functional contributions of biomechanically and neurally generated forces in lumped systems with greatly simplified kinematics. This has revealed that visual and voluntary control of neck muscles and the dynamic and static vestibulocollic and cervicocollic reflexes preferentially govern head-neck system state in different frequency domains. It also documents redundant control, which allows the system to compensate for lesions and creates a potential for substantial variability within and between subjects. Kinematic studies have indicated the existence of reciprocal and co-contraction strategies for voluntary force generation, of a vestibulocollic strategy for stabilizing the head during body perturbations and of at least two strategies for voluntary head tracking. Each strategy appears to be executed by a specific muscle synergy that is presumably optimized to efficiently meet the demands of the task.