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@ARTICLE{Forsyth:867722,
      author       = {Forsyth, Anna and McMillan, Rebecca and Campbell, Doug and
                      Malpas, Gemma and Maxwell, Elizabeth and Sleigh, Jamie and
                      Dukart, Juergen and Hipp, Jörg and Muthukumaraswamy, Suresh
                      D.},
      title        = {{M}odulation of simultaneously collected hemodynamic and
                      electrophysiological functional connectivity by ketamine and
                      midazolam},
      journal      = {Human brain mapping},
      volume       = {41},
      number       = {6},
      issn         = {1097-0193},
      address      = {New York, NY},
      publisher    = {Wiley-Liss},
      reportid     = {FZJ-2019-06337},
      pages        = {1472-1494},
      year         = {2020},
      note         = {This work was funded by F Hoffman La Roche Ltd.},
      abstract     = {The pharmacological modulation of functional connectivity
                      in the brain may under-lie therapeutic efficacy for several
                      neurological and psychiatric disorders. Functionalmagnetic
                      resonance imaging (fMRI) provides a noninvasive method of
                      assessing thismodulation, however, the indirect nature of
                      the blood-oxygen level dependent sig-nal restricts the
                      discrimination of neural from physiological contributions.
                      Here wefollowed two approaches to assess the validity of
                      fMRI functional connectivity indeveloping drug biomarkers,
                      using simultaneous electroencephalography (EEG)/fMRI in a
                      placebo-controlled, three-way crossover design with ketamine
                      andmidazolam. First, we compared seven different
                      preprocessing pipelines to deter-mine their impact on the
                      connectivity of common resting-state networks. Indepen-dent
                      components analysis (ICA)-denoising resulted in stronger
                      reductions inconnectivity after ketamine, and weaker
                      increases after midazolam, than pipelinesemploying
                      physiological noise modelling or averaged signals from
                      cerebrospinalfluid or white matter. This suggests that
                      pipeline decisions should reflect a drug'sunique noise
                      structure, and if this is unknown then accepting possible
                      signal losswhen choosing extensive ICA denoising pipelines
                      could engender more confidencein the remaining results. We
                      then compared the temporal correlation structure offMRI to
                      that derived from two connectivity metrics of EEG, which
                      provides a directmeasure of neural activity. While
                      electrophysiological estimates based on thepower envelope
                      were more closely aligned to BOLD signal connectivity than
                      thosebased on phase consistency, no significant relationship
                      between the change in electrophysiological and hemodynamic
                      correlation structures was found, implyingcaution should be
                      used when making cross-modal comparisons of
                      pharmacologically-modulated functional connectivity.},
      cin          = {INM-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31808268},
      UT           = {WOS:000500765600001},
      doi          = {10.1002/hbm.24889},
      url          = {https://juser.fz-juelich.de/record/867722},
}