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@ARTICLE{Eggermont:281689,
      author       = {Eggermont, Jos J. and Tass, Peter A.},
      title        = {{M}aladaptive {N}eural {S}ynchrony in {T}innitus: {O}rigin
                      and {R}estoration},
      journal      = {Frontiers in neurology},
      volume       = {6},
      issn         = {1664-2295},
      publisher    = {Frontiers Research Foundation},
      reportid     = {FZJ-2016-01377},
      pages        = {29},
      year         = {2015},
      abstract     = {Tinnitus is the conscious perception of sound heard in the
                      absence of physical sound sources external or internal to
                      the body, reflected in aberrant neural synchrony of
                      spontaneous or resting-state brain activity. Neural
                      synchrony is generated by the nearly simultaneous firing of
                      individual neurons, of the synchronization of
                      membrane-potential changes in local neural groups as
                      reflected in the local field potentials, resulting in the
                      presence of oscillatory brain waves in the EEG.
                      Noise-induced hearing loss, often resulting in tinnitus,
                      causes a reorganization of the tonotopic map in auditory
                      cortex and increased spontaneous firing rates and neural
                      synchrony. Spontaneous brain rhythms rely on neural
                      synchrony. Abnormal neural synchrony in tinnitus appears to
                      be confined to specific frequency bands of brain rhythms.
                      Increases in delta-band activity are generated by
                      deafferented/deprived neuronal networks resulting from
                      hearing loss. Coordinated reset (CR) stimulation was
                      developed in order to specifically counteract such abnormal
                      neuronal synchrony by desynchronization. The goal of
                      acoustic CR neuromodulation is to desynchronize
                      tinnitus-related abnormal delta-band oscillations. CR
                      neuromodulation does not require permanent stimulus delivery
                      in order to achieve long-lasting desynchronization or even a
                      full-blown anti-kindling but may have cumulative effects,
                      i.e., the effect of different CR epochs separated by pauses
                      may accumulate. Unlike other approaches, acoustic CR
                      neuromodulation does not intend to reduce tinnitus-related
                      neuronal activity by employing lateral inhibition. The
                      potential efficacy of acoustic CR modulation was shown in a
                      clinical proof of concept trial, where effects achieved in
                      12 weeks of treatment delivered 4-6 h/day persisted
                      through a preplanned 4-week therapy pause and showed
                      sustained long-term effects after 10 months of therapy,
                      leading to $75\%$ responders.},
      cin          = {INM-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406},
      pnm          = {89573 - Neuroimaging (POF2-89573)},
      pid          = {G:(DE-HGF)POF2-89573},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000363758800001},
      pubmed       = {pmid:25741316},
      doi          = {10.3389/fneur.2015.00029},
      url          = {https://juser.fz-juelich.de/record/281689},
}