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@ARTICLE{Annen:1021985,
      author       = {Annen, Jitka and Frasso, Gianluca and van der Lande, Glenn
                      J. M. and Bonin, Estelle A. C. and Vitello, Marie M. and
                      Panda, Rajanikant and Sala, Arianna and Cavaliere, Carlo and
                      Raimondo, Federico and Bahri, Mohamed Ali and Schiff,
                      Nicholas D. and Gosseries, Olivia and Thibaut, Aurore and
                      Laureys, Steven},
      title        = {{C}erebral electrometabolic coupling in disordered and
                      normal states of consciousness},
      journal      = {Cell reports},
      volume       = {42},
      number       = {8},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2024-01124},
      pages        = {112854 -},
      year         = {2023},
      abstract     = {We assess cerebral integrity with cortical and subcortical
                      FDG-PET and cortical electroencephalography (EEG) within the
                      mesocircuit model framework in patients with disorders of
                      consciousness (DoCs). The mesocircuit hypothesis proposes
                      that subcortical activation facilitates cortical function.
                      We find that the metabolic balance of subcortical
                      mesocircuit areas is informative for diagnosis and is
                      associated with four EEG-based power spectral density
                      patterns, cortical metabolism, and α power in healthy
                      controls and patients with a DoC. Last, regional
                      electrometabolic coupling at the cortical level can be
                      identified in the θ and α ranges, showing positive and
                      negative relations with glucose uptake, respectively. This
                      relation is inverted in patients with a DoC, potentially
                      related to altered orchestration of neural activity, and may
                      underlie suboptimal excitability states in patients with a
                      DoC. By understanding the neurobiological basis of the
                      pathophysiology underlying DoCs, we foresee translational
                      value for diagnosis and treatment of patients with a DoC.},
      cin          = {INM-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5252},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37498745},
      UT           = {WOS:001050983200001},
      doi          = {10.1016/j.celrep.2023.112854},
      url          = {https://juser.fz-juelich.de/record/1021985},
}