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. Electronic supplementary material The online version of this article (10.1007/s10162-019-00721-7) contains supplementary material, which is available to authorized users.

Different attempts have been made to directly measure frequency specific basilar membrane ͑BM͒ delays in animals, e.g., laser velocimetry of BM vibrations and auditory nerve fiber recordings. The present study uses otoacoustic emissions ͑OAEs͒ and auditory brainstem responses ͑ABRs͒ to estimate BM delay non-invasively in normal-hearing humans. Tone bursts at nine frequencies from 0.5 to 8 kHz served as stimuli, with care taken to quantify possible bias due to the use of tone bursts with different rise times. BM delays are estimated from the ABR latency estimates by subtracting the neural and synaptic delays. This allows a comparison between individual OAE and BM delays over a large frequency range in the same subjects, and offers support to the theory that OAEs are reflected from a tonotopic place and carried back to the cochlear base via a reverse traveling wave.

A quantitative model is presented that describes the formation of auditory brainstem responses (ABRs) to tone pulses, clicks, and rising chirps as a function of stimulation level. The model computes the convolution of the instantaneous discharge rates using the "humanized" nonlinear auditory-nerve model of Zilany and Bruce [J. Acoust. Soc. Am. 122, 402-417 (2007)] and an empirically derived unitary response function which is assumed to reflect contributions from different cell populations within the auditory brainstem, recorded at a given pair of electrodes on the scalp. It is shown that the model accounts for the decrease of tone-pulse evoked wave-V latency with frequency but underestimates the level dependency of the tone-pulse as well as click-evoked latency values. Furthermore, the model correctly predicts the nonlinear wave-V amplitude behavior in response to the chirp stimulation both as a function of chirp sweeping rate and level. Overall, the results support the hypothesis that the pattern of ABR generation is strongly affected by the nonlinear and dispersive processes in the cochlea.

Objective hearing threshold estimation based on ear-EEG can be integrated into hearing aids, thereby allowing hearing assessment to be performed by the hearing instrument on a regular basis.

To understand speech, the slowly varying outline, or envelope, of the acoustic stimulus is used to distinguish words. A small amount of information about the envelope is sufficient for speech recognition, but the mechanism used by the auditory system to extract the envelope is not known. Several different theories have been proposed, including envelope detection by auditory nerve dendrites as well as various mechanisms involving the sensory hair cells. We used recordings from human and animal inner ears to show that the dominant mechanism for envelope detection is distortion introduced by mechanoelectrical transduction channels. This electrical distortion, which is not apparent in the sound-evoked vibrations of the basilar membrane, tracks the envelope, excites the auditory nerve, and transmits information about the shape of the envelope to the brain.