Many individuals struggle to understand speech in listening scenarios that include reverberation and background noise. An individual's ability to understand speech arises from a combination of peripheral auditory function, central auditory function, and general cognitive abilities. The interaction of these factors complicates the prescription of treatment or therapy to improve hearing function. Damage to the auditory periphery can be studied in animals; however, this method alone is not enough to understand the impact of hearing loss on speech perception. Computational auditory models bridge the gap between animal studies and human speech perception. Perturbations to the modeled auditory systems can permit mechanism-based investigations into observed human behavior. In this study, we propose a computational model that accounts for the complex interactions between different hearing damage mechanisms and simulates human speech-in-noise perception. The model performs a digit classification task as a human would, with only acoustic sound pressure as input. Thus, we can use the model's performance as a proxy for human performance. This two-stage model consists of a biophysical cochlear-nerve spike generator followed by a deep neural network (DNN) classifier. We hypothesize that sudden damage to the periphery affects speech perception and that central nervous system adaptation over time may compensate for peripheral hearing damage. Our model achieved human-like performance across signal-to-noise ratios (SNRs) under normal-hearing (NH) cochlear settings, achieving 50% digit recognition accuracy at −20.7 dB SNR. Results were comparable to eight NH participants on the same task who achieved 50% behavioral performance at −22 dB SNR. We also simulated medial olivocochlear reflex (MOCR) and auditory nerve fiber (ANF) loss, which worsened digit-recognition accuracy at lower SNRs compared to higher SNRs. Our simulated performance following ANF loss is consistent with the hypothesis that cochlear synaptopathy impacts communication in background noise more so than in quiet. Following the insult of various cochlear degradations, we implemented extreme and conservative adaptation through the DNN. At the lowest SNRs (<0 dB), both adapted models were unable to fully recover NH performance, even with hundreds of thousands of training samples. This implies a limit on performance recovery following peripheral damage in our human-inspired DNN architecture.
Temporal contrast effects in human speech perception are immune to selective attention