RESUMO
A current initiative in auditory neuroscience research is to better understand why some listeners struggle to perceive speech-in-noise (SIN) despite having normal hearing sensitivity. Various hypotheses regarding the physiologic bases of this disorder have been proposed. Notably, recent work has suggested that the site of lesion underlying SIN deficits in normal hearing listeners may be either in "sub-clinical" outer hair cell damage or synaptopathic degeneration at the inner hair cell-auditory nerve fiber synapse. In this study, we present a retrospective investigation of these peripheral sources and their relationship with SIN performance variability in one of the largest datasets of young normal-hearing listeners presented to date. 194 participants completed detailed case history questionnaires assessing noise exposure, SIN complaints, tinnitus, and hyperacusis. Standard and extended high frequency audiograms, distortion product otoacoustic emissions, click-evoked auditory brainstem responses, and SIN performance measures were also collected. We found that: 1) the prevalence of SIN deficits in normal hearing listeners was 42% when based on subjective report and 8% when based on SIN performance, 2) hearing complaints and hyperacusis were more common in listeners with self-reported noise exposure histories than controls, 3) neither extended high frequency thresholds nor compound action potential amplitudes differed between noise-exposed and control groups, 4) extended high frequency hearing thresholds and compound action potential amplitudes were not predictive of SIN performance. These results suggest an association between noise exposure and hearing complaints in young, normal hearing listeners; however, SIN performance variability is not explained by peripheral auditory function to the extent that these measures capture subtle physiologic differences between participants.