Sensory Inhibition Is Related to Variable Speech Perception in Noise in Adults With Normal Hearing

Purpose Speech perception in noise (SPiN) varies widely in individuals with normal hearing, which may be attributed to factors that are not reflected in the audiogram, such as inhibition. However, inhibition is involved at both sensory and cognitive stages of auditory perception, and while inhibition at the cognitive level has been shown to be a significant factor in SPiN processes, it is unknown whether sensory inhibition may also contribute to SPiN variability. Therefore, the goal of this study was to evaluate sensory inhibition in adults with normal hearing and mild SPiN impairment. Method Cortical auditory evoked potentials (CAEPs) were recorded in 49 adults via high-density electroencephalography using an auditory gating paradigm. Participants were categorized according to a median signal-to-noise ratio (SNR) loss of 1.5 dB: typical SNR loss ≤ 1.5 dB (n = 32), mild SNR loss > 1.5 dB (n = 17). CAEP gating responses were compared and correlated with SNR loss and extended high-frequency thresholds. Current density reconstructions were performed to qualitatively observe underlying cortical inhibitory networks in each group. Results In comparison to adults with typical SPiN ability, adults with mild SPiN impairment showed an absence of the gating response. A CAEP gating component (P2) reflected decreased sensory inhibition and correlated with increased SNR loss. Extended high-frequency thresholds were also found to correlate with SNR loss, but not gating function. An atypical cortical inhibitory network was observed in the mild SNR loss group, with reduced frontal and absent prefrontal activation. Conclusion Sensory inhibition appears to be atypical and related to SPiN deficits in adults with mild impairment. In addition, cortical inhibitory networks appear to be incomplete, with a possible compensatory parietal network. Further research is needed to delineate between types or levels of central inhibitory mechanisms and their contribution to SPiN processes.