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INSPECTSYN

Speech-in-noise Intelligibility Deficits: Designing Psychophysical and Electrophysiological Markers of Spectral Shape-Coding Sensitive to Cochlear Synaptopathy
Funder: French National Research Agency (ANR)Project code: ANR-22-CE28-0010
Funder Contribution: 226,990 EUR

INSPECTSYN

Description

At present, it is estimated that over 10% of individuals with clinically-normal audiograms have significant difficulty understanding speech-in-noise (SPiN). In particular, synaptopathy - the loss of synapses connecting the cochlea to the auditory nerve, caused by aging or noise exposure - is thought to be an important factor contributing to this problem. Yet, recent attempts to assess synaptopathy in humans have produced mixed results. Because of its pivotal role for SPiN understanding, we hypothesize that addressing temporal fine-structure (TFS) coding fidelity should provide a more direct estimate of the impact of synaptopathy on these deficits. The INSPECTSYN project will thus focus on the coding of signals with different spectral shapes, such as vowels, to develop and test new tools to assess the contribution of synaptopathy to TFS coding. This project relies on an integrated multidisciplinary approach combining computational modelling, psychophysics and electrophysiology. In Axis #1, we will use state-of-the-art physiological models to deepen our theoretical understanding of how the peripheral auditory system encodes spectral shapes, and disentangle specific distortions caused by outer-hair-cell loss vs. synaptopathy on neural representations. In Axis #2, we will conduct psychoacoustical and electrophysiological measurements based on stimuli specifically designed to be sensitive to the impact of synaptopathy on TFS coding in various groups of listeners, young/old, with/without sensorineural hearing-loss. In Axis #3, we will study how these measurements account for SPiN intelligibility differences across listeners. Overall, this project will provide novel audiological tools to better characterize hidden hearing deficits in humans.

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