Investigating the Effect of Cochlear Synaptopathy on Envelope Following Responses Using a Model of the Auditory Nerve

Gerard Encina-Llamas,Torsten Dau,James M Harte,Barbara Shinn-Cunningham,Bastian Epp

doi:10.1007/s10162-019-00721-7

Abstract

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.

Highlights

It is well known that noise overexposure can impair the auditory system by producing a sensorineural hearing loss, seen in a permanent elevation of puretone detection thresholds
envelope following response (EFR) magnitude-level functions recorded from a group of young normal hearing (NH) threshold listeners showed individual differences for deeply and shallowly modulated tones, indicating differences in neural supra-threshold encoding of envelope modulations
Similar differences for mild HI listeners measured at an audiometrically normal center frequency supported the idea of coexisting hearing loss due to hair-cell dysfunction and supra-threshold deficits at frequencies of normal sensitivity

Summary

Introduction

It is well known that noise overexposure can impair the auditory system by producing a sensorineural hearing loss, seen in a permanent elevation of puretone detection thresholds. Recent animal studies have shown that noise overexposure producing TTS can lead to the loss of AN fiber synapses, without damaging the sensitive hair cells in the cochlea Kujawa and Liberman (2009). As this neuronal degeneration does not result in a PTS, it has been termed “hidden” hearing loss (Schaette and McAlpine 2011). It was further shown that the magnitude-level function of distortion-product otoacoustic emissions (DPOAE) remained unaffected in the same mice These results indicate that the outer hair cells (OHC) were not damaged due to the noise exposure. Many hypotheses about CS in humans (including this study) start with an assumption that low-SR fibers are more affected than other fibers and that the spiking rate of the high-SR fibers saturates at supra-threshold levels (e.g., Bharadwaj et al 2015; Mehraei et al 2016; Paul et al 2017; Valero et al 2018)

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