TY - JOUR
T1 - Tinnitus with a normal audiogram
T2 - Physiological evidence for hidden hearing loss and computational model
AU - Schaette, Roland
AU - McAlpine, David
PY - 2011/9/21
Y1 - 2011/9/21
N2 - Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.
AB - Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.
UR - http://www.scopus.com/inward/record.url?scp=80053003469&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.2156-11.2011
DO - 10.1523/JNEUROSCI.2156-11.2011
M3 - Article
C2 - 21940438
AN - SCOPUS:80053003469
SN - 0270-6474
VL - 31
SP - 13452
EP - 13457
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 38
ER -