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@ARTICLE{Forsyth:904404,
      author       = {Forsyth, Anna E. M. and McMillan, Rebecca and Dukart,
                      Juergen and Hipp, Jörg F. and Muthukumaraswamy, Suresh D.},
      title        = {{E}ffects of {K}etamine and {M}idazolam on {S}imultaneous
                      {EEG}/f{MRI} {D}ata {D}uring {W}orking {M}emory {P}rocesses},
      journal      = {Brain topography},
      volume       = {34},
      number       = {6},
      issn         = {0896-0267},
      address      = {Dordrecht [u.a.]},
      publisher    = {Springer Science + Business Media B.V},
      reportid     = {FZJ-2021-05974},
      pages        = {863 - 880},
      year         = {2021},
      abstract     = {Reliable measures of cognitive brain activity from
                      functional neuroimaging techniques may provide early
                      indications of efficacy in clinical trials. Functional
                      magnetic resonance imaging and electroencephalography
                      provide complementary spatiotemporal information and
                      simultaneous recording of these two modalities can remove
                      inter-session drug response and environment variability. We
                      sought to assess the effects of ketamine and midazolam on
                      simultaneous electrophysiological and hemodynamic recordings
                      during working memory (WM) processes. Thirty participants
                      were included in a placebo-controlled, three-way crossover
                      design with ketamine and midazolam. Compared to placebo,
                      ketamine administration attenuated theta power increases and
                      alpha power decreases and midazolam attenuated low beta band
                      decreases to increasing WM load. Additionally, ketamine
                      caused larger blood-oxygen-dependent (BOLD) signal increases
                      in the supplementary motor area and angular gyrus, and
                      weaker deactivations of the default mode network (DMN),
                      whereas no difference was found between midazolam and
                      placebo. Ketamine administration caused positive temporal
                      correlations between frontal-midline theta (fm-theta) power
                      and the BOLD signal to disappear and attenuated negative
                      correlations. However, the relationship between fm-theta and
                      the BOLD signal from DMN areas was maintained in some
                      participants during ketamine administration, as increasing
                      theta strength was associated with stronger BOLD signal
                      reductions in these areas. The presence of, and ability to
                      manipulate, both positive and negative associations between
                      the BOLD signal and fm-theta suggest the presence of
                      multiple fm-theta components involved in WM processes, with
                      ketamine administration disrupting one or more of these
                      theta-linked WM strategies.},
      cin          = {INM-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5251},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34642836},
      UT           = {WOS:000706573000001},
      doi          = {10.1007/s10548-021-00876-8},
      url          = {https://juser.fz-juelich.de/record/904404},
}