Mechanisms of vibration-induced nystagmus in normal subjects and patients with vestibular neuritis
- PMID: 17259708
- DOI: 10.1159/000099023
Mechanisms of vibration-induced nystagmus in normal subjects and patients with vestibular neuritis
Abstract
It has been reported that vibration applied either on the mastoid or on the sternocleidomastoid (SCM) muscles induces nystagmus in normal subjects or patients after unilateral vestibular neuritis (VN). The aims of the study were to characterize vibration-induced nystagmus (VIN) in normal and patient groups and to propose the mechanism of VIN. We recorded eye movements during unilateral 100-Hz vibration on the mastoid bone and SCM muscles in 22 normal subjects and 19 patients with unilateral VN. In normal subjects, the direction of slow-phase velocity (SPV) tended to be toward the vibrated side. Vibration on the right/left SCM muscles induced mean SPV of 1.7 degrees/s, -1.9 degrees/s toward the stimulated side in all normal subjects. Vibration on the right/left mastoid bone induced mean SPV of 1.5 degrees/s, -0.4 degrees/s toward the stimulated side in most of the normal subjects. Positive value means SPV to the right side. This directional preponderance to the vibrated side was statistically significant. Among the patients with VN, the slow phase of the VIN was directed towards the lesioned side, irrespective of whether vibration was applied on the lesioned or intact side. Vibration on the right/left mastoid bone induced mean SPV of -10.4 degrees/s, -10.8 degrees/s toward the lesioned side. Vibration on the right/left SCM induced mean SPV of -7.9 degrees/s, -10.5 degrees/s toward the lesioned side. The amplitude of SPV showed a significant correlation with the unilateral weakness of caloric test. Our results suggest that the proprioceptive stimulation plays a major role in producing VIN in normal subjects, while VIN is generated mostly by the vestibular stimulation in patients with unilateral VN, which helps us localize the lesion side. Vibration tests on the SCM muscles as well as on the mastoid are recommended and our hypothetic mechanisms of VIN are presented.
Copyright 2007 S. Karger AG, Basel.
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