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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0123538
Abstract
Background
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.
tinnitus is frequently associated with auditory deafferentation in cases of sensorineural hearing loss [3–5], a notion supported by transient phantom sound perception after experimentally induced partial and complete auditory deprivation in normal subjects [6,7]. Previous researchers have suggested the auditory deafferentation and resultant compensatory changes in the central auditory system as the main culprit of tinnitus generation, and thus an up-regulation of spontaneous firing rates [8], tonotopic map reorganization and increased neural synchrony [9], increased central noise [10], synchronous neuronal activity of cell assemblies within the auditory cortex [11], and a loss of lateral inhibition [12] have been proposed to be associated with tinnitus generation. Nevertheless, tinnitus perception is not entirely explainable by the changes in the central auditory system in that only a subset of hearing loss accompanies tinnitus [13] and neuroimaging studies have consistently shown limbic system involvement in tinnitus [14–17]. Based on these observations, a "dysfunctional noise cancelling mechanism" has recently been conceptualized [18,19]. According to this concept, patients become aware of tinnitus only if the noise (tinnitus) cancellation system fails to suppress the tinnitus signal generated by auditory cortical changes. For the noise cancellation system, the ventromedial prefrontal cortex (vmPFC) [18] has been suggested to be one of the core regions, and this was confirmed by structural [20] and functional [21] imaging studies in patients with chronic tinnitus, but other structural imaging studies failed to find vmPFC as the core region [22,23]. Meanwhile, because fluctuations of activity in the anterior cingulate cortex (ACC) and anterior insula determine whether a near threshold pain stimulus is consciously perceived or not [24], the ACC and anterior insula, also known as the components of "salience network" that relate to interoceptive-autonomic processing [25], have been suggested to be another core network for the noise cancelling system, based on the similarity of pain and tinnitus pathways
Note the funding:
Funding: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (No. 2014002619) (http://www.nrf.re.kr/nrf_eng_cms/) and the Seoul National University Bundang Hospital Research Fund 14-2014-019. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0123538
Abstract
Background
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.
tinnitus is frequently associated with auditory deafferentation in cases of sensorineural hearing loss [3–5], a notion supported by transient phantom sound perception after experimentally induced partial and complete auditory deprivation in normal subjects [6,7]. Previous researchers have suggested the auditory deafferentation and resultant compensatory changes in the central auditory system as the main culprit of tinnitus generation, and thus an up-regulation of spontaneous firing rates [8], tonotopic map reorganization and increased neural synchrony [9], increased central noise [10], synchronous neuronal activity of cell assemblies within the auditory cortex [11], and a loss of lateral inhibition [12] have been proposed to be associated with tinnitus generation. Nevertheless, tinnitus perception is not entirely explainable by the changes in the central auditory system in that only a subset of hearing loss accompanies tinnitus [13] and neuroimaging studies have consistently shown limbic system involvement in tinnitus [14–17]. Based on these observations, a "dysfunctional noise cancelling mechanism" has recently been conceptualized [18,19]. According to this concept, patients become aware of tinnitus only if the noise (tinnitus) cancellation system fails to suppress the tinnitus signal generated by auditory cortical changes. For the noise cancellation system, the ventromedial prefrontal cortex (vmPFC) [18] has been suggested to be one of the core regions, and this was confirmed by structural [20] and functional [21] imaging studies in patients with chronic tinnitus, but other structural imaging studies failed to find vmPFC as the core region [22,23]. Meanwhile, because fluctuations of activity in the anterior cingulate cortex (ACC) and anterior insula determine whether a near threshold pain stimulus is consciously perceived or not [24], the ACC and anterior insula, also known as the components of "salience network" that relate to interoceptive-autonomic processing [25], have been suggested to be another core network for the noise cancelling system, based on the similarity of pain and tinnitus pathways
Note the funding:
Funding: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (No. 2014002619) (http://www.nrf.re.kr/nrf_eng_cms/) and the Seoul National University Bundang Hospital Research Fund 14-2014-019. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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