The effect of noise exposure on vestibular function

Damage to the auditory mechanism in the inner ear due to noise is well established. However, exactly how noise affects the human vestibular system is still unclear. Therefore, this thesis examines the effect of noise exposure on the human vestibular system, particularly saccular function. This was achieved by proposing several hypotheses, tested via a series of studies and described in separate chapters. The literature suggests that the saccule is the potential site of noise damage in the vestibular system. To date, the only available clinical tool to evaluate the saccule is cervical vestibular evoked myogenic potential (cVEMP). Although cVEMP data have been widely published, cVEMP methodology is still being explored. First of all, cVEMP optimal methodology using head rotation-sitting (HR-S) as a sternocleidomastoid (SCM) muscle activation procedure was established before going on to investigate the effect of noise exposure on vestibular function. The optimal cVEMP protocol (HR-S as a muscle activation procedure, blood pressure manometer as a biofeedback method and amplitude normalization as a data analysis technique), pure tone audiometry and distortion product otoacoustic emissions (DPOAE) were used to investigate the effects of noise exposure on the audio-saccular function of adults working in potentially noisy environments. The lifetime cumulative noise exposure levels for participants were estimated based on their self-reported noise exposure data. Overall thesis findings support the existence of cochlear and saccular dysfunction in noise-exposed workers with and without hearing loss. Results indicate that noise exposure may alter saccular function and result in symptoms before noise-induced cochlear damage is detected by routine clinical testing. Findings suggest that combining cVEMP findings with self-reported data along with findings obtained from other noise sensitive diagnostic procedures like DPOAE may help to identify people at risk of developing noise-induced saccular dysfunction