Auditory Brainstem Response Latency in Noise As a Marker of Cochlear Synaptopathy
The Journal of Neuroscience, March 30, 2016 • 36(13):3755–3764 • 3755 Systems/Circuits Auditory Brainstem Response Latency in Noise as a Marker of Cochlear Synaptopathy X Golbarg Mehraei,1,2 XAnn E. Hickox,1,4 X Hari M. Bharadwaj,2,7 Hannah Goldberg,1 Sarah Verhulst,2,6 M. Charles Liberman,1,4,5 and XBarbara G. Shinn-Cunningham2,3 1Program in Speech and Hearing Bioscience and Technology, Harvard University/Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, 2Center for Computational Neuroscience and Neural Technology, Boston University, Boston, Massachusetts 02215, 3Department of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, 4Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114, 5Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02114, 6Cluster of Excellence Hearing4All and Medical Physics, Department of Medical Physics and Acoustics, Oldenburg University, 26129 Oldenburg, Germany, 7Martinos Center for Biomedical Imaging, Department of Neurology, Massachusetts General Hospital/Harvard Medical School, Charlestown, Massachusetts 02129 Evidence from animal and human studies suggests that moderate acoustic exposure, causing only transient threshold elevation, can nonetheless cause “hidden hearing loss” that interferes with coding of suprathreshold sound. Such noise exposure destroys synaptic connections between cochlear hair cells and auditory nerve fibers; however, there is no clinical test of this 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 analogous measurements in humans and mice, 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.
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