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@ARTICLE{Silchenko:133852,
      author       = {Silchenko, Alexander and Adamchic, Ilya and Hauptmann,
                      Christian and Tass, Peter A.},
      title        = {{I}mpact of acoustic coordinated reset neuromodulation on
                      effective connectivity in a neural network of phantom sound},
      journal      = {NeuroImage},
      volume       = {77},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {FZJ-2013-02243},
      pages        = {133 - 147},
      year         = {2013},
      abstract     = {Chronic subjective tinnitus is an auditory phantom
                      phenomenon characterized by abnormal neuronal synchrony in
                      the central auditory system. As recently shown in a proof of
                      concept clinical trial, acoustic coordinated reset (CR)
                      neuromodulation causes a significant relief of tinnitus
                      symptoms combined with a significant decrease of
                      pathological oscillatory activity in a network comprising
                      auditory and non-auditory brain areas. The objective of the
                      present study was to analyze whether CR therapy caused an
                      alteration of the effective connectivity in a tinnitus
                      related network of localized EEG brain sources. To determine
                      which connections matter, in a first step, we considered a
                      larger network of brain sources previously associated with
                      tinnitus. To that network we applied a data-driven approach,
                      combining empirical mode decomposition and partial directed
                      coherence analysis, in patients with bilateral tinnitus
                      before and after 12weeks of CR therapy as well as in healthy
                      controls. To increase the signal-to-noise ratio, we focused
                      on the good responders, classified by a
                      reliable-change-index (RCI). Prior to CR therapy and
                      compared to the healthy controls, the good responders showed
                      a significantly increased connectivity between the left
                      primary cortex auditory cortex and the posterior cingulate
                      cortex in the gamma and delta bands together with a
                      significantly decreased effective connectivity between the
                      right primary auditory cortex and the dorsolateral
                      prefrontal cortex in the alpha band. Intriguingly, after
                      12weeks of CR therapy most of the pathological interactions
                      were gone, so that the connectivity patterns of good
                      responders and healthy controls became statistically
                      indistinguishable. In addition, we used dynamic causal
                      modeling (DCM) to examine the types of interactions which
                      were altered by CR therapy. Our DCM results show that CR
                      therapy specifically counteracted the imbalance of
                      excitation and inhibition. CR significantly weakened the
                      excitatory connection between posterior cingulate cortex and
                      primary auditory cortex and significantly strengthened
                      inhibitory connections between auditory cortices and the
                      dorsolateral prefrontal cortex. The overall impact of CR
                      therapy on the entire tinnitus-related network showed up as
                      a qualitative transformation of its spectral response, in
                      terms of a drastic change of the shape of its averaged
                      transfer function. Based on our findings we hypothesize that
                      CR therapy restores a silence based cognitive auditory
                      comparator function of the posterior cingulate cortex.},
      cin          = {INM-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406},
      pnm          = {333 - Pathophysiological Mechanisms of Neurological and
                      Psychiatric Diseases (POF2-333)},
      pid          = {G:(DE-HGF)POF2-333},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000320073900013},
      pubmed       = {pmid:23528923},
      doi          = {10.1016/j.neuroimage.2013.03.013},
      url          = {https://juser.fz-juelich.de/record/133852},
}