The healthy auditory system enables communication in challenging situations with high levels of background noise. Yet, despite normal sensitivity to pure tones, many listeners complain about having difficulties in such situations. Recent animal studies demonstrated that noise overexposure that produces temporary threshold shifts can cause the loss of auditory nerve (AN) fiber synapses (i.e., cochlear synaptopathy, CS), which appears to predominantly affect medium- and low-spontaneous rate (SR) fibers. In the present study, envelope following response (EFR) magnitude-level functions were recorded in normal hearing (NH) threshold and mildly hearing-impaired (HI) listeners with thresholds elevated above 2 kHz. EFRs were elicited by sinusoidally amplitude modulated (SAM) tones presented in quiet with a carrier frequency of 2 kHz, modulated at 93 Hz, and modulation depths of 0.85 (deep) and 0.25 (shallow). While EFR magnitude-level functions for deeply modulated tones were similar for all listeners, EFR magnitudes for shallowly modulated tones were reduced at medium stimulation levels in some NH threshold listeners and saturated in all HI listeners for the whole level range. A phenomenological model of the AN was used to investigate the extent to which hair-cell dysfunction and/or CS could explain the trends observed in the EFR data. Hair-cell dysfunction alone, including postulated elevated hearing thresholds at extended high frequencies (EHF) beyond 8 kHz, could not account for the recorded EFR data. Postulated CS led to simulations generally consistent with the recorded data, but a loss of all types of AN fibers was required within the model framework. The effects of off-frequency contributions (i.e., away from the characteristic place of the stimulus) and the differential loss of different AN fiber types on EFR magnitude-level functions were analyzed. When using SAM tones in quiet as the stimulus, model simulations suggested that (1) EFRs are dominated by the activity of high-SR fibers at all stimulus intensities, and (2) EFRs at medium-to-high stimulus levels are dominated by off-frequency contributions.

A model of the cochlea was used to bridge the gap between model approaches commonly used to investigate phenomena related to otoacoustic emissions and more filter-based model approaches often used in psychoacoustics. In the present study, a nonlinear and active one-dimensional transmission line model was developed that accounts for several aspects of physiological data with a single fixed parameter set. The model shows plausible excitation patterns and an input-output function similar to the linear-compressive-linear function as hypothesized in psychoacoustics. The model shows realistic results in a two-tone suppression paradigm and a plausible growth function of the 2f1−f2 component of distortion product otoacoustic emissions. Finestructure was found in simulated stimulus-frequency otoacoustic emissions (SFOAE) with realistic levels and rapid phase rotation. A plausible “threshold in quiet” including finestructure and spontaneous otoacoustic emissions (SOAE) could be simulated. It is further shown that psychoacoustical data of modulation detection near threshold can be explained by the mechanical dynamics of the modeled healthy cochlea. It is discussed that such a model can be used to investigate the representation of acoustic signals in healthy and impaired cochleae at this early stage of the auditory pathway for both, physiological as well as psychoacoustical paradigms.

A computational model of cat auditory nerve fiber (ANF) responses to electrical stimulation is presented. The model assumes that (1) there exist at least two sites of spike generation along the ANF and (2) both an anodic (positive) and a cathodic (negative) charge in isolation can evoke a spike. A single ANF is modeled as a network of two exponential integrate-and-fire point-neuron models, referred to as peripheral and central axons of the ANF. The peripheral axon is excited by the cathodic charge, inhibited by the anodic charge, and exhibits longer spike latencies than the central axon; the central axon is excited by the anodic charge, inhibited by the cathodic charge, and exhibits shorter spike latencies than the peripheral axon. The model also includes subthreshold and suprathreshold adaptive feedback loops which continuously modify the membrane potential and can account for effects of facilitation, accommodation, refractoriness, and spike-rate adaptation in ANF. Although the model is parameterized using data for either single or paired pulse stimulation with monophasic rectangular pulses, it correctly predicts effects of various stimulus pulse shapes, stimulation pulse rates, and level on the neural response statistics. The model may serve as a framework to explore the effects of different stimulus parameters on psychophysical performance measured in cochlear implant listeners.

A keyword spotting algorithm implemented on an embedded system using a depthwise separable convolutional neural network classifier is reported. The proposed system was derived from a high-complexity system with the goal to reduce complexity and to increase efficiency. In order to meet the requirements set by hardware resource constraints, a limited hyper-parameter grid search was performed, which showed that network complexity could be drastically reduced with little effect on classification accuracy. It was furthermore found that quantization of pre-trained networks using mixed and dynamic fixed point principles could reduce the memory footprint and computational requirements without lowering classification accuracy. Data augmentation techniques were used to increase network robustness in unseen acoustic conditions by mixing training data with realistic noise recordings. Finally, the system’s ability to detect keywords in a continuous audio stream was successfully demonstrated.

Recent auditory brain stem response measurements in tinnitus subjects with normal audiograms indicate the presence of hidden hearing loss that manifests as reduced neural output from the cochlea at high sound intensities, and results from mice suggest a link to deafferentation of auditory nerve fibers. As deafferentation would lead to deficits in hearing performance, the present study investigates whether tinnitus patients with normal hearing thresholds show impairment in intensity discrimination compared to an audiometrically matched control group. Intensity discrimination thresholds were significantly increased in the tinnitus frequency range, consistent with the hypothesis that auditory nerve fiber deafferentation is associated with tinnitus.