Citation

Amanipour RM, Frisina RD, Cresoe SA, Parsons TJ, Zhu X, Borlongan CV, Walton JP, Amanipour RM, Frisina RD, Cresoe SA, Parsons TJ, Xiaoxia Zhu, Borlongan CV, Walton JP, Frisina RD, Borlongan CV, Amanipour RM, Zhu X, Cresoe SA, Walton JP, Parsons TJ. Conf. Proc. IEEE Eng. Med. Biol. Soc. 2016; 2016: 1854-1857.

Copyright

(Copyright © 2016, IEEE (Institute of Electrical and Electronics Engineers))

DOI

10.1109/EMBC.2016.7591081

PMID

28226874

Abstract

The auditory brainstem response (ABR) is an electrophysiological test that examines the functionality of the auditory nerve and brainstem. Traumatic brain injury (TBI) can be detected if prolonged peak latency is observed in ABR measurements, since latency measures the neural conduction time in the brainstem, and an increase in latency can be a sign of pathological lesion at the auditory brainstem level. The ABR is elicited by brief sounds that can be used to measure hearing sensitivity as well as temporal processing. Reduction in peak amplitudes and increases in latency are indicative of dysfunction in the auditory nerve and/or central auditory pathways. In this study we used sixteen young adult mice that were divided into two groups: sham and mild traumatic brain injury (mTBI), with ABR measurements obtained prior to, and at 2, 6, and 14 weeks after injury. Abnormal ABRs were observed for the nine TBI cases as early as two weeks after injury and the deficits lasted for fourteen weeks after injury.

RESULTS indicated a significant reduction in the Peak 1 (P1) and Peak 4 (P4) amplitudes to the first noise burst, as well as an increase in latency response for P1 and P4 following mTBI. These results are the first to demonstrate auditory sound processing deficits in a rodent model of mild TBI.

Language: en