Noise Exposure, Self-Reported Speech-in-Noise Percpetion, and the Auditory Brainstem Response in Normal-Hearing Human Ears

Abstract

Difficulty understanding speech-in-noise (SIN) is a common complaint among many listeners. There is emerging evidence that noise exposure is associated with difficulties in speech discrimination and temporal processing despite normal audiometric thresholds. At present, evidence linking temporary noise-induced hearing loss and selective loss of low spontaneous rate fibers in human ears is limited and inconsistent. Likewise, results of SIN measures in relation to noise-induced cochlear synaptopathy varied across studies. The goals of this study are to further our understanding of the effects of noise exposure on the auditory system and to investigate novel approaches for detecting early noise-induced auditory damage. Data were collected from 30 normal-hearing subjects (18-35 years old) with varying amounts of noise exposure. Auditory brainstem responses (ABR) were recorded to both a click (measure of auditory nerve function) and speech stimulus (/da/; measure of temporal processing). The speech hearing subscale of the Speech, Spatial and Qualities of Hearing Scale (SSQ) was also administered to quantify individual self-reported SIN abilities. The data resulted in mixed findings. Overall click-ABR wave I results provided no evidence for noise-induced synaptopathy in this cohort. However, differences in the wave I amplitude between males and females were observed suggesting noise effects may vary between sexes. Transient components of the speech-ABR showed no evidence of neural slowing but revealed enhanced neural responses in individuals with greater amounts of noise exposure. This later finding may be a manifestation of either musical training or increased central neural gain as a result of pathology. Lastly, individuals with greater amounts of noise exposure reported experiencing more difficulties hearing SIN (as per the SSQ) but ABR data did not show the predicted physiologic evidence to explain the self-perceived SIN deficit.