Abstract

Exposure to 120 dB sound pressure level (SPL) band-limited noise results in delayed onset latency and reduced vestibular short-latency evoked potential (VsEP) responses. These changes are still present 4 wk after noise overstimulation. Noise-induced hearing loss (NIHL) has been shown to vary in extent and duration based on the noise intensity. This study investigated whether noise-induced peripheral vestibular hypofunction (NPVH) would also decrease in extent and/or duration with less intense noise exposure. In the present study, rats were exposed to a less intense noise (110 dB SPL) but for the same duration (6 h) and frequency range (500-4,000 Hz) as used in previous studies. The VsEP was assessed 1, 3, 7, 14, 21, and 28 days after noise exposure. In contrast to 120 dB SPL noise exposure, the 110 dB SPL noise exposures produced smaller deficits in VsEP responses that fully recovered in 62% (13/21) of animals within 1 wk. These findings suggest that NPVH, a loss or attenuation of VsEP responses with a requirement for elevated stimulus intensity to elicit measurable responses, is similar to NIHL, that is, lower sound levels produce a smaller or transient deficit. These results show that it will be important to determine the extent and duration of vestibular hypofunction for different noise exposure conditions and their impact on balance.NEW & NOTEWORTHY This is the first study to show a temporary noise-induced peripheral vestibular hypofunction that recovers following exposure to continuous noise.

Highlights

  • Multiple characteristics of noise exposure, for example, frequency bandwidth, sound level, exposure duration, and time course, are likely to determine the extent of peripheral damage

  • Peripheral vestibular hypofunction was characterized by threshold shifts in the stimulus intensity required to elicit measurable vestibular short-latency evoked potential (VsEP) responses, reduced VsEP amplitudes, and increased VsEP latencies

  • This study examined the effect of continuous noise exposure on auditory brainstem response (ABR) and VsEP responses in rats using a sound level 10 dB less than used in our previous studies [2, 18]

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Summary

Introduction

Multiple characteristics of noise exposure, for example, frequency bandwidth, sound level, exposure duration, and time course, are likely to determine the extent of peripheral damage (for review, see Ref. 1). Intense noise exposure causes attenuated and delayed vestibular short-latency evoked potential (VsEP) responses to head jerks, indicating peripheral vestibular hypofunction. Tamura et al [3] reported functional motor deficits related to vestibular loss in mice for 4 wk after 1-mo continuous 70 dB sound pressure level (SPL) low- but not high-frequency noise exposure. Hsu et al [4] reported recovery of vestibular evoked myogenic potential (VEMP) responses and auditory brainstem response (ABR) thresholds in guinea pigs after brief (30 min) noise exposure (115 dB SPL broadband noise). They reported normal saccular morphology in guinea pigs with

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