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dc.contributor.authorSong, Jae Jinen_US
dc.contributor.authorVanneste, Svenen_US
dc.contributor.authorDe Ridder, Dirken_US
dc.description.abstractBackground Peripheral auditory deafferentation and central compensation have been regarded as the main culprits of tinnitus generation. However, patient-to-patient discrepancy in the range of the percentage of daytime in which tinnitus is perceived (tinnitus awareness percentage, 0 - 100%), is not fully explicable only by peripheral deafferentation, considering that the deafferentation is a stable persisting phenomenon but tinnitus is intermittently perceived in most patients. Consequently, the involvement of a dysfunctional noise cancellation mechanism has recently been suggested with regard to the individual differences in reported tinnitus awareness. By correlating the tinnitus awareness percentage with resting-state source-localized electroencephalography findings, we may be able to retrieve the cortical area that is negatively correlated with tinnitus awareness percentage, and then the area may be regarded as the core of the noise cancelling system that is defective in patients with tinnitus. Methods and Findings Using resting-state cortical oscillation, we investigated 80 tinnitus patients by correlating the tinnitus awareness percentage with their source-localized cortical oscillatory activity and functional connectivity. The activity of bilateral rostral anterior cingulate cortices (ACCs), left dorsal-and pregenual ACCs for the delta band, bilateral rostral/pregenual/subgenual ACCs for the theta band, and left rostral/pregenual ACC for the beta 1 band displayed significantly negative correlations with tinnitus awareness percentage. Also, the connectivity between the left primary auditory cortex (A1) and the rostral ACC, as well as between the left A1 and the subgenual ACC for the beta 1 band, were negatively correlated with tinnitus awareness percentage. Conclusions These results may designate the role of the rostral ACC as the core of the descending noise cancellation system, and thus dysfunction of the rostral ACC may result in perception of tinnitus. The present study also opens a possibility of tinnitus modulation by neuromodulatory approaches targeting the rostral ACC.en_US
dc.description.sponsorship"This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (No. 2014002619) and the Seoul National University Bundang Hospital Research Fund 14-2014-019."en_US
dc.publisherPublic Library of Scienceen_US
dc.rightsCC BY 4.0 (Attribution)en_US
dc.rights©2015 The Authorsen_US
dc.subjectAuditory perceptionen_US
dc.subjectSensorineural Hearing Lossen_US
dc.subjectLate Onseten_US
dc.subjectPrefrontal cortexen_US
dc.subjectNeural mechanismsen_US
dc.titleDysfunctional Noise Cancelling of the Rostral Anterior Cingulate Cortex in Tinnitus Patientsen_US
dc.identifier.bibliographicCitationSong, Jae Jin, Sven Vanneste, and Dirk De Ridder. 2015. "Dysfunctional Noise Cancelling of the Rostral Anterior Cingulate Cortex in Tinnitus Patients." Plos One 10(4) doi:10.1371/journal.pone.0123538.en_US
dc.source.journalPLOS Oneen_US

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