The effect of noise exposure in the presence of canal fenestration on the amplitude of short-latency vestibular evoked potentials.

Abstract

Exposure to high-intensity noise causes little, if any, reduction in vestibular function in normal animals as shown by short-latency vestibular evoked potentials (VsEPs). To investigate the effect of noise exposure on VsEPs following fenestration of the horizontal semicircular canal. Psammomys obesus (fat sand rat) underwent labyrinthectomy in 1 ear, while the lateral semicircular canal in the other ear was fenestrated. Control VsEPs to linear acceleration (approximately 3g; rise time, approximately 1-2 milliseconds) were recorded immediately after the operation. The experimental group animals were then subjected to loud white noise (113-dB sound pressure level) for 1 hour. Immediately after the noise exposure in the experimental group animals, VsEPs were once more recorded. The VsEPs in the experimental group animals were significantly reduced immediately following the noise exposure, while there was no change in the recordings from the control group animals (fenestrated but not noise exposed; noise exposed but not fenestrated), even though the noise exposure induced a mean 47-dB threshold elevation of the auditory brainstem response. The presence of the fenestration caused the vestibular end organs to become vulnerable to noise exposure. The fenestration may create a pathway enabling pressure release through the vestibular end organs during noise exposure, thus increasing the possibility of damage to the vestibular end organs. This did not occur in the intact, nonfenestrated animals.