骨传导刺激产生的前庭诱发眼外电位

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Objective: To investigate the origin, whether ocular or extraocular, of the short latency frontal potential (N15) reported by Todd et al. (2003) following vestibular stimulation. Methods: Fourteen subjects with low VEMP thresholds (VT) and 9 patients with vestibular or ocular disorders were stimulated at the mastoid with bone-conducted tone bursts (500 Hz, 8 ms) above vestibular threshold, using a B71 bone vibrator. Surface potentials were recorded from Fpz and around the eyes and referred to linked earlobes. Results: The N15 was present at Fpz,but was largest around the eyes (mean amplitude 2.6 μV, peak latency 13.4 ms, with stimulation at +18 dB above threshold) and was generally in phase above and below the eyes. The response was vestibular-dependent and modulated by alteration of gaze direction. The potentials were delayed in a patient with Miller Fisher syndrome and were larger in patients with superior canal dehiscence than in controls. Conclusions: We report a new vestibular-evoked extraocular potential. Its properties are not consistent with an eye movement. It is likely to be produced, mainly or exclusively, by synchronous activity in extraocular muscles (i.e. a myogenic potential). Significance: Vestibularevoked extraocular potentials extend the range of vestibular pathways that can be assessed electrophysiologically, and may be a useful additional test of vestibular function. Methods: Fourteen subjects with low VEMP thresholds (VT) and 9 patients with vestibular (N15) reported by Todd et al. or ocular disorders were stimulated at the mastoid with bone-conducted tone bursts (500 Hz, 8 ms) above vestibular threshold, using a B71 bone vibrator. Surface potentials were recorded from Fpz and around the eyes and referred to linked earlobes. N15 was present at Fpz, but was largest around the eyes (mean amplitude 2.6 μV, peak latency 13.4 ms, with stimulation at +18 dB above threshold) and was generally in phase above and below the eyes. The response was vestibular-dependent and modulated by alteration of gaze direction. The potentials were delayed in a patient with Miller Fisher syndrome and were larger in patients with superior canal dehiscence than in controls. Conclusions: We report a new vestibular-ev Its properties are not consistent with an eye movement. It is likely to be produced, mainly or exclusively, by synchronous activity in extraocular muscles (ie a myogenic potential). Significance: Vestibularevoked extraocular potentials extend the range of vestibular pathways that can be ordered electrophysiologically, and may be a useful additional test of vestibular function.
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