Abstract

Tinnitus—the phantom ringing of the ears—is thought arise from neuroplastic changes in the central auditory system in response to peripheral hearing damage. However, a minority of tinnitus sufferers have clinically normal hearing thresholds. One explanation of these cases is that auditory nerve fibers with low firing thresholds (LT-ANFs) are intact, but ANFs with high thresholds (HT-ANFs) are not. HT-ANF damage would be “hidden” to the audiogram but evident in suprathreshold tests. To test this hypothesis, we measured the ability of tinnitus and control subjects with normal audiograms to detect amplitude modulation (AM) in a 5 kHz, suprathreshold tone in a narrowband noise. We also recorded by 32-channel EEG the “envelope following response” (EFR, generated subcortically) to the same AM tone in conditions of noise and no noise. Tinnitus subjects had worse AM detection thresholds and had smaller EFRs compared to controls. Simulations of ANF responses from the model of Zilany et al. (2014) found that in addition to ~100% loss of HT ANFs, a further ~30% loss of LT fibers was needed to account for the reduced EFRs of tinnitus subjects. ~30% of LT ANFs would not have been expected to affect hearing thresholds. [Work supported by NSERC of Canada.]

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