Auditory brainstem response latency in noise as a marker of cochlear synaptopathy

Communication in environments with multiple competing sound sources can be challenging, even for listeners with normal hearing thresholds (NHT). This difficulty in "normal" listeners is thought to arise from central sites of the auditory system with the assumption that sound encoding at the auditory nerve (AN) is robust. Despite this assumption, growing evidence from animal and human studies suggests that acoustic exposure, too modest to elevate hearing thresholds, can nonetheless cause "hidden hearing loss" that interferes with coding of supra-threshold sound. In animal studies, such noise exposure leads to cochlear synaptopathy (death of auditory nerve fibers or ANFs); however, there is no clinical test of synaptopathy in humans. In animals, synaptopathy reduces the amplitude of auditory brainstem response (ABR) wave-I. Unfortunately, ABR wave-I is difficult to measure in humans, limiting its clinical use. Here, using behavioral, otoacoustic, and electrophysiological measures in humans and mice in conjunction with computational models of sound processing by the auditory periphery and brainstem, we show that the effect of masking noise on the latency of the more robust ABR wave-V mirrors changes in ABR wave-I amplitude. In our human cohort, the effect of noise on wave-V latency predicts perceptual temporal sensitivity. Further, we show evidence that ABR wave-V latency in forward masking may be affected by ANF loss and is predictive of a listener's performance in a perceptual task related to speech intelligibility in noise. Our results suggest that measures of the effects of masking on ABR wave-V latency can be used to diagnose ANF survival in humans.

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

• Mehraei, Golbarg

Advisor dc:contributor.advisor

• Barbara Shinn-Cunningham.

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

Statement dc:rights

• M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about 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/1721.1/103440

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/103440