Hearing research
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Hearing-in-noise (HIN) is a primary complaint of both the hearing impaired and the hearing aid user. Both auditory nerve (AN) function and outer hair cell (OHC) function are thought to contribute to HIN, but their relative contributions are still being elucidated. OHCs play a critical role in HIN by fine tuning the motion of the basilar membrane. Further, animal studies suggest that cochlear (auditory) synaptopathy, which is the loss of synaptic contact between hair cells and the AN, may be another cause of HIN difficulty. While there is evidence that cochlear synaptopathy occurs in animal models, there is debate as to whether cochlear synaptopathy is clinically significant in humans, which may be due to disparate methods of measuring noise exposure in humans and our high variability in susceptibility to noise damage. Rather than use self-reported noise exposure to define synaptopathic groups, this paper assumes that the general population exhibits a range of noise exposures and resulting otopathologies and defines cochlear synaptopathy "operationally" as low CAP amplitude accompanied by normal DPOAE levels in persons with low pure tone averages. The first question is whether the standard audiogram detects AN dysfunction and OHC dysfunction? The second question is whether HIN performance is primarily dependent on AN function, OHC function, or both functions? ⋯ The results of this study suggest the following: (1) persons hearing within normal limits may exhibit HIN difficulties; (2) persons hearing within normal limits may exhibit undetected otopathologies, namely AN dysfunction and OHC dysfunction; (3) AN untuning secondary to OHC dysfunction occurs in subjects with Mild-Moderate SNHL; (4) HIN performance is primarily governed by OHC function rather than AN function.