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@ARTICLE{Tscherpel:1030861,
      author       = {Tscherpel, Caroline and Mustin, Maike and Massimini,
                      Marcello and Paul, Theresa and Ziemann, Ulf and Fink, Gereon
                      R. and Grefkes, Christian},
      title        = {{L}ocal neuronal sleep after stroke: {T}he role of cortical
                      bistability in brain reorganization},
      journal      = {Brain stimulation},
      volume       = {17},
      number       = {4},
      issn         = {1935-861X},
      address      = {New York, NY [u.a.]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2024-05470},
      pages        = {836 - 846},
      year         = {2024},
      abstract     = {Background: Acute cerebral ischemia triggers a number of
                      cellular mechanisms not only leading to excitotoxic cell
                      death but also to enhanced neuroplasticity, facilitating
                      neuronal reorganization and functional recovery.Objective:
                      Transferring these cellular mechanisms to neurophysiological
                      correlates adaptable to patients is crucial to promote
                      recovery post-stroke. The combination of TMS and EEG
                      constitutes a promising readout of neuronal network activity
                      in stroke patients.Methods: We used the combination of TMS
                      and EEG to investigate the development of local signal
                      processing and global network alterations in 40 stroke
                      patients with motor deficits alongside neural reorganization
                      from the acute to the chronic phase.Results: We show that
                      the TMS-EEG response reflects information about
                      reorganization and signal alterations associated with
                      persistent motor deficits throughout the entire post-stroke
                      period. In the early post-stroke phase and in a subgroup of
                      patients with severe motor deficits, TMS applied to the
                      lesioned motor cortex evoked a sleep-like slow wave response
                      associated with a cortical off-period, a manifestation of
                      cortical bistability, as well as a rapid disruption of the
                      TMS-induced formation of causal network effects.
                      Mechanistically, these phenomena were linked to lesions
                      affecting ascending activating brainstem fibers. Of note,
                      slow waves invariably vanished in the chronic phase, but
                      were highly indicative of a poor functional
                      outcome.Conclusion: In summary, we found evidence that
                      transient effects of sleep-like slow waves and cortical
                      bistability within ipsilesional M1 resulting in excessive
                      inhibition may interfere with functional reorganization,
                      leading to a less favorable functional outcome post-stroke,
                      pointing to a new therapeutic target to improve recovery of
                      function.Keywords: Neuromodulation; Neurorehabilitation;
                      Plasticity; Sleep-like cortical off-period; Slow waves;
                      Stroke lesion; TMS-EEG.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525) / DFG
                      project 431549029 - SFB 1451: Schlüsselmechanismen normaler
                      und krankheitsbedingt gestörter motorischer Kontrolle
                      (431549029)},
      pid          = {G:(DE-HGF)POF4-5252 / G:(GEPRIS)431549029},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {39019396},
      UT           = {WOS:001274661900001},
      doi          = {10.1016/j.brs.2024.07.008},
      url          = {https://juser.fz-juelich.de/record/1030861},
}