The electrical signal recorded at the round window was used to estimate the location of missing outer hair cells. The cochlear response was recorded to a low frequency tone embedded in high-pass filtered noise conditions. Cochlear damage was created by either overexposure to frequency-specific tones or laser light. In animals with continuous damage along the partition, the amplitude of the cochlear response increased as the high-pass cutoff frequency increased, eventually reaching a plateau. The cochlear distance at the onset of the plateau correlated with the anatomical onset of outer hair cell loss. A mathematical model replicated the physiologic data but was limited to cases with continuous hair cell loss in the middle and basal turns. The neural contribution to the cochlear response was determined by recording the response before and after application of Ouabain. Application of Ouabain eliminated or reduced auditory neural activity from approximately two turns of the cochlea. The amplitude of the cochlear response was reduced for moderate signal levels with a limited effect at higher levels, indicating that the cochlear response was dominated by outer hair cell currents at high signal levels and neural potentials at low to moderate signal levels.

Purpose The aim of this study was to quantify the portion of variance in several measures suggested to be indicative of peripheral noise-induced cochlear synaptopathy and hidden hearing disorder that can be attributed to individual cognitive capacity. Method Regression and relative importance analysis was used to model several behavioral and physiological measures of hearing in 32 adults ranging in age from 20 to 74 years. Predictors for the model were hearing sensitivity and performance on a number of cognitive tasks. Results There was a significant influence of cognitive capacity on several measures of cochlear synaptopathy and hidden hearing disorder. These measures include frequency modulation detection threshold, time-compressed word recognition in quiet and reverberation, and the strength of the frequency-following response of the speech-evoked auditory brainstem response. Conclusions Measures of hearing that involve temporal processing are significantly influenced by cognitive abilities, specifically, short-term and working memory capacity, executive function, and attention. Research using measures of temporal processing to diagnose peripheral disorders, such as noise-induced synaptopathy, need to consider cognitive influence even in a young, healthy population.

The consequences of noise exposure on the auditory system are not entirely understood. In animals, noise exposure causes selective synaptopathy-an uncoupling of auditory nerve fibers from sensory cells-mostly in fibers that respond to high sound levels. Synaptopathy can be measured physiologically in animals, but a direct relationship between noise exposure and synaptopathy in humans has yet to be proven. Sources of variability, such as age, indirect measures of noise exposure, and comorbid auditory disorders, obfuscate attempts to find concrete relationships between noise exposure, synaptopathy, and perceptual consequences. This study adds to the ongoing effort by examining relationships between noise exposure, auditory brainstem response (ABR) amplitudes, and speech perception in adults of various ages and audiometric thresholds and a subset of younger adults with clinically normal hearing. Regression models including noise exposure, age, hearing thresholds, and sex as covariates were compared to find a best-fitting model of toneburst ABR wave I amplitude at two frequencies and word recognition performance in three listening conditions: background noise, time compression, and time compression with reverberation. The data suggest the possibility of detecting synaptopathy in younger adults using physiological measures, but that age and comorbid hearing disorders may hinder attempts to assess noise-induced synaptopathy.

Objectives: Recent animal studies have shown that noise exposure can cause cochlear synaptopathy without permanent threshold shift. Because the noise exposure preferentially damaged auditory nerve fibers that processed suprathreshold sounds (low-spontaneous rate fibers), it has been suggested that synaptopathy may underlie suprathreshold hearing deficits in humans. Recently, several researchers have suggested measures to identify the pathology or pathologies underlying suprathreshold hearing deficits in humans based on results from animal studies; however, the reliability of some of these measures have not been assessed. The purpose of this study was to assess the test–retest reliability of measures that may have the potential to relate suprathreshold hearing deficits to site(s)-of-lesion along the peripheral auditory system in humans. Design: Adults with audiometric normal hearing were tested on a battery of behavioral and physiologic measures that included (1) thresholds in quiet (TIQ), (2) thresholds in noise (TIN), (3) frequency-modulation detection threshold (FMDT), (4) word recognition in four listening conditions, (5) distortion-product otoacoustic emissions (DPOAE), (6) middle ear muscle reflex (MEMR), (7) tone burst-elicited auditory brainstem response (tbABR), and (8) speech-evoked ABR (sABR). Data collection for each measure was repeated over two visits separated by at least one week. The residuals of the correlation between the suprathreshold measures and TIQ serve as functional and quantitative proxies for threshold-independent hearing disorders because they represent the portion of the raw measures that is not dependent on TIQ. Reliability of the residual measures was assessed using intraclass correlation (ICC). Results: Reliability for the residual measures was good (ICC ≥ 0.75) for FMDT, DPOAEs, and MEMR. Residual measures showing moderate reliability (0.5 ≤ ICC < 0.75) were tbABR wave I amplitude, TIN, and word recognition in quiet, noise, and time-compressed speech with reverberation. Wave V of the tbABR, waves of the sABR, and recognition of time-compressed words had poor test–retest reliability (ICC < 0.5). Conclusions: Reliability of residual measures was mixed, suggesting that care should be taken when selecting measures for diagnostic tests of threshold-independent hearing disorders. Quantifying hidden hearing loss as the variance in suprathreshold measures of auditory function that is not due to TIQ may provide a reliable estimate of threshold-independent hearing disorders in humans.