Abstract

Threshold audiometry is currently the foundation of clinical audiology. Yet, many individuals with normal hearing thresholds (NHTs) have difficulty communicating in noisy settings. We previously documented that even among listeners with NHTs and no hearing complaints, large individual differences exist in the ability to perceive subtle temporal features of clearly audible sounds, and to selectively process target speech in the presence of competing sounds. Critically, we find that these suprathreshold differences in individual perceptual sensitivity correlate with physiological measures from the brainstem and auditory nerve. These measures, including brainstem envelope-following responses, auditory brainstem responses, and the middle-ear muscle reflex, show that some perceptually relevant physiological differences arise very early along the auditory pathway. Cochlear synaptopathy—a loss of afferent synapses and nerve terminals innervating the cochlea—is well documented in noise-exposed and aging animals (Kujawa & Liberman, Hear. Res. 2015). Cochlear synaptopathy in humans may account for both large individual differences and hearing difficulties in human listeners with NHTs. This presentation will summarize updated human evidence consistent with cochlear synaptopathy, discuss some of the challenges that remain with this interpretation, and review the search for clinical markers of such damage.

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