Author(s): Weisz N, Voss S, Berg P, Elbert T
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Abstract BACKGROUND: Tinnitus is an auditory sensation frequently following hearing loss. After cochlear injury, deafferented neurons become sensitive to neighbouring intact edge-frequencies, guiding an enhanced central representation of these frequencies. As psychoacoustical data 123 indicate enhanced frequency discrimination ability for edge-frequencies that may be related to a reorganization within the auditory cortex, the aim of the present study was twofold: 1) to search for abnormal auditory mismatch responses in tinnitus sufferers and 2) relate these to subjective indicators of tinnitus. RESULTS: Using EEG-mismatch negativity, we demonstrate abnormalities (N = 15) in tinnitus sufferers that are specific to frequencies located at the audiometrically normal lesion-edge as compared to normal hearing controls (N = 15). Groups also differed with respect to the cortical locations of mismatch responsiveness. Sources in the 90-135 ms latency window were generated in more anterior brain regions in the tinnitus group. Both measures of abnormality correlated with emotional-cognitive distress related to tinnitus (r approximately .76). While these two physiological variables were uncorrelated in the control group, they were correlated in the tinnitus group (r =.72). Concerning relationships with parameters of hearing loss (depth and slope), slope turned out to be an important variable. Generally, the steeper the hearing loss is the less distress related to tinnitus was reported. The associations between slope and the relevant neurophysiological variables are in agreement with this finding. CONCLUSIONS: The present study is the first to show near-to-complete separation of tinnitus sufferers from a normal hearing control group based on neurophysiological variables. The finding of lesion-edge specific effects and associations with slope of hearing loss corroborates the assumption that hearing loss is the basis for tinnitus development. It is likely that some central reorganization follow a damage to hearing receptors, even though the paradoxical results indicate that they most likely are somewhat different than originally assumed (see Background). One partial explanation might lie in the involvement of top-down (presumably frontal-lobe) controlled processes. A better comprehension of the exact mechanisms leading to the present results could have a broad impact on the understanding and perhaps treatment of tinnitus.
This article was published in BMC Neurosci
and referenced in Journal of Phonetics & Audiology