Brain, Vol. 126, No. 4, 956-964,
April 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg091
Vibration-induced ocular torsion and nystagmus after unilateral vestibular deafferentation
1 Neuro-otology Department, Royal Prince Alfred Hospital, 2 Department of Psychology, University of Sydney, Sydney, Australia and 3 Department of Oto-rhino-laryngology, Head and Neck Surgery, Lund University Hospital, Lund, Sweden
Correspondence to: Dr Mikael Karlberg, Department of Oto-rhino-laryngology, Head and Neck Surgery, Lund University Hospital, SE-221 85 Lund, Sweden E-mail: mikael.karlberg{at}onh.lu.se
Vibration is an excitatory stimulus for both vestibular and proprioceptive afferents. Vibration applied either to the skull or to the neck muscles of subjects after unilateral vestibular deafferentation induces nystagmus and a shift of the subjective visual horizontal. Previous studies have ascribed these effects to vibratory stimulation of neck muscle proprioceptors. Using scleral search coils, we recorded three-dimensional eye movements during unilateral 92 Hz vibration of the mastoid bone or of the sternocleidomastoid (SCM) muscle in 18 subjects with chronic unilateral vestibular deficits after vestibular neurectomy or neuro-labyrinthitis. Nine subjects had lost function of all three semicircular canals (SSCs) on one side, and the other nine had lost function of only the anterior and lateral SSCs. Vibration of the mastoid bone or of the SCM muscle on either side induced an ipsilesional tonic shift of torsional eye position of up to 6.5° during visual fixation, as well as a nystagmus with horizontal, vertical and torsional components in darkness. Subjects who had lost function of all three SSCs on one side showed a larger shift in ocular torsion in response to SCM vibration than did subjects who had lost function of only two SSCs. The difference between ocular torsion produced by ipsilesional muscle or bone vibration was not significantly different from that produced by contralesional bone or muscle vibration. The vibration-induced nystagmus rotation axis tended to align with the pitch (y) axis of the head in subjects who had lost only anterior and lateral SSC function, and with the roll (x) axis of the head in subjects who had lost function of all three SSCs. We propose that the previously described vibration-induced shift of the subjective visual horizontal can be explained by the vibration-induced ocular torsion, and that the magnitude of ocular torsion is related to the extent of the unilateral vestibular deficit. While altered proprioceptive inputs from neck muscles might be important in the mechanism of vibration-induced ocular torsion and nystagmus after unilateral vestibular deafferentation, vibratory stimulation of vestibular receptors in the intact labyrinth also appears to have an important role.
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