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Objective: To examine the properties and potential clinical uses of myogenic potentials to bone conducted sound. Methods: Myogenic potentials were recorded from normal volunteers, using bone conducted tone bursts of 7 ms duration and 250–2000 Hz frequencies delivered over the mastoid processes by a B 71 clinical bone vibrator. Biphasic positive–negative (p1n1) responses were recorded from both sternocleidomastoid (SCM) muscles using averaged unrectified EMG. The best location for stimulus delivery, optimum stimulus frequency, stimulus thresholds, and the effect of aging on evoked response amplitudes and thresholds were systematically examined. Subjects with specific lesions were studied. Vestibular evoked myogenic potentials (VEMP) to air conducted 0.1 ms clicks, 7 ms/250–2000 Hz tones, and forehead taps were measured for comparison. Results: Bone conducted sound evoked short latency p1n1 responses in both SCM muscles. Ipsilateral responses occurred earlier and were usually larger. Mean (SD) p1 and n1 latencies were 13.6 (1.8) and 22.3 (1.2) ms ipsilaterally and 14.9 (2.1) and 23.7 (2.7) ms contralaterally. Stimuli of 250 Hz delivered over the mastoid process, posterosuperior to the external acoustic meatus, yielded the largest amplitude responses. Like VEMP in response to air conducted clicks and tones, p1n1 responses were absent ipsilaterally in subjects with selective vestibular neurectomy and preserved in those with severe sensorineural hearing loss. However, p1n1 responses were preserved in conductive hearing loss, whereas VEMP to air conducted sound were abolished or attenuated. Bone conducted response thresholds were 97.5 (3.9) dB SPL/30.5 dB HL, significantly lower than thresholds to air conducted clicks (131.7 (4.9) dB SPL/86.7 dB HL) and tones (114.0 (5.3) dB SPL/106 dB HL). Conclusions: Bone conducted sound evokes p1n1 responses (bone conducted VEMP) which are a useful measure of vestibular function, especially in the presence of conductive hearing loss. For a given perceptual intensity, bone conducted sound activates the vestibular apparatus more effectively than air conducted sound.

Background: Spontaneous nystagmus caused by dorsolateral medullary infarction may be of vestibular origin. Objectives: To test if imbalance of the central pathways of the semicircular canals contributes to spontaneous nystagmus in dorsolateral medullary syndrome. Methods: We examined four patients with dorsolateral medullary syndrome and recorded spontaneous nystagmus binocularly at gaze straight ahead with the three-dimensional search coil technique. The median slow phase velocity of the nystagmus was analysed in the light and in the dark, and the normalised velocity axes were compared with the rotation axes as predicted from anatomical data of the semicircular canal. Results: The slow phase rotation axes of all patients aligned best with the rotation axes resulting from stimulation of the contralesional posterior and horizontal semicircular canals. This alignment cannot be explained by pure otolith imbalance. Conclusion: We propose that vestibular imbalance caused by an ipsilesional lesion of the central semicircular canal pathways of the horizontal and anterior semicircular canals largely accounts for spontaneous nystagmus in dorsolateral medullary syndrome.