Cochlear neuropathy : detection using envelope following responses and Impacts on central auditory coding

Abstract

Nearly all information about the acoustic environment is conveyed to the brain by auditory nerve (AN) fibers. While essential for hearing, these fibers may also be the most vulnerable link in the auditory pathway: moderate noise exposure can cause loss of AN fibers without causing hair cell damage or permanent threshold shift. This neuropathy is undetectable by standard clinical examination, but post-mortem evidence suggests that it is widespread in humans. Its impact on suprathreshold hearing ability is likely profound, but is not well understood. An essential tool for evaluating the impact of neuropathy is a non-invasive test useable in humans. Since noise-induced neuropathy is selective for high-threshold AN fibers, where phase locking to envelopes is particularly strong, we hypothesized that the envelope following response (EFR) might be a more sensitive measure of neuropathy than the more traditional auditory brainstem response (ABR). We compared ABRs and EFRs in mice following a neuropathic noise exposure. Changes to EFRs were more robust: the variance was smaller, thus inter-group differences were clearer. Neuropathy may be the root cause of a number of deficits that can occur in listeners with normal audiograms, such as speech discrimination in noise and ability to use envelope cues. We searched for neural correlates of these deficits in the mouse auditory midbrain following exposure. Consistent with reductions in EFRs, synchronization to envelopes was impaired. Neural detectability of tones in background noise was impaired, but only for cases when noise level changed every 600 milliseconds. When noise level changed every minute, responses were equal to those of unexposed mice, implicating changes to adaptation. In quiet, tone-evoked rate-level functions were steeper, indicating that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis. In sum, we found compensatory effects on coding in the midbrain beyond the simple direct effects expected by peripheral neuropathy.