Abstract

Despite our understanding of the impact of noise-induced damage to the auditory system, much less is known about the impact of noise exposure on the vestibular system. In this article, we review the anatomical, physiological, and functional evidence for noise-induced damage to peripheral and central vestibular structures. Morphological studies in several animal models have demonstrated cellular damage throughout the peripheral vestibular system and particularly in the otolith organs; however, there is a paucity of data on the effect of noise exposure on human vestibular end organs. Physiological studies have corroborated morphological studies by demonstrating disruption across vestibular pathways with otolith-mediated pathways impacted more than semicircular canal-mediated pathways. Similar to the temporary threshold shifts observed in the auditory system, physiological studies in animals have suggested a capacity for recovery following noise-induced vestibular damage. Human studies have demonstrated that diminished sacculo-collic responses are related to the severity of noise-induced hearing loss, and dose-dependent vestibular deficits following noise exposure have been corroborated in animal models. Further work is needed to better understand the physiological and functional consequences of noise-induced vestibular impairment in animals and humans.

Highlights

  • It is well-established that noise overstimulation has the potential to cause temporary or permanent damage to sensory cells in the cochlea and the afferent neurons innervating them, resulting in temporary or permanent loss of hearing [for review see: [1, 2]]

  • Continuous noise occurs over an extended period of time, whereas impulse noise occurs rapidly, and generally at a considerably higher sound pressure level (SPL)

  • This study suggests that intermittent noise exposure is less damaging to the vestibular system than continuous noise exposure

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Summary

Introduction

It is well-established that noise overstimulation has the potential to cause temporary or permanent damage to sensory cells in the cochlea and the afferent neurons innervating them, resulting in temporary or permanent loss of hearing [for review see: [1, 2]]. Similar to the auditory system, animal models of continuous noise exposure have revealed that damage to the vestibular periphery is dependent on characteristics of the noise, including: duration, frequency, level, and time course.

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