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

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.

Department dc:contributor.department

Harvard--MIT Program in Health Sciences and Technology.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2016

Author dc:creator

• Shaheen, Luke A

Advisor dc:contributor.advisor

• M. Charles Liberman.

• Harvard--MIT Program in Health Sciences and Technology.

Statement dc:rights

• MIT theses are protected by copyright. They may be viewed, downloaded, or printed from this source but further reproduction or distribution in any format is prohibited without written permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/107340

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/107340