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@ARTICLE{Wang:12585,
      author       = {Wang, L.E. and Fink, G. R. and Diekhoff, S. and Rehmke,
                      A.K. and Eickhoff, S. B. and Grefkes, C.},
      title        = {{N}oradrenergic enhancement improves motor network
                      connectivity in stroke patients},
      journal      = {Annals of neurology},
      volume       = {69},
      issn         = {0364-5134},
      address      = {Hoboken, NJ},
      publisher    = {Wiley-Blackwell},
      reportid     = {PreJuSER-12585},
      pages        = {375 - 388},
      year         = {2011},
      note         = {This research was supported by a grant from the Human Brain
                      Project (R01-MH074457-01A1 to S.B.E.) and the Initiative and
                      Networking Fund of the Helmholtz Association within the
                      Helmholtz Alliance on Systems Biology (Human Brain Model to
                      S.B.E.).},
      abstract     = {Both animal and human data suggest that noradrenergic
                      stimulation may enhance motor performance after brain
                      damage. We conducted a placebo-controlled, double-blind and
                      crossover design study to investigate the effects of
                      noradrenergic stimulation on the cortical motor system in
                      hemiparetic stroke patients.Stroke patients (n = 11) in the
                      subacute or chronic stage with mild-to-moderate hand paresis
                      received a single oral dose of 6 mg reboxetine (RBX), a
                      selective noradrenaline reuptake inhibitor. We used
                      functional magnetic resonance imaging and dynamic causal
                      modeling to assess changes in neural activity and
                      interregional effective connectivity while patients moved
                      their paretic hand.RBX stimulation significantly increased
                      maximum grip power and index finger-tapping frequency of the
                      paretic hand. Enhanced motor performance was associated with
                      a reduction of cortical "hyperactivity" toward physiological
                      levels as observed in healthy control subjects, especially
                      in the ipsilesional ventral premotor cortex (vPMC) and
                      supplementary motor area (SMA), but also in the
                      temporoparietal junction and prefrontal cortex. Connectivity
                      analyses revealed that in stroke patients neural coupling
                      with SMA or vPMC was significantly reduced compared with
                      healthy controls. This "hypoconnectivity" was partially
                      normalized when patients received RBX, especially for the
                      coupling of ipsilesional SMA with primary motor cortex.The
                      data suggest that noradrenergic stimulation by RBX may help
                      to modulate the pathologically altered motor network
                      architecture in stroke patients, resulting in increased
                      coupling of ipsilesional motor areas and thereby improved
                      motor function.},
      keywords     = {Adrenergic Uptake Inhibitors: therapeutic use / Adult /
                      Aged / Cross-Over Studies / Double-Blind Method / Hand
                      Strength: physiology / Humans / Magnetic Resonance Imaging /
                      Male / Middle Aged / Morpholines: therapeutic use / Motor
                      Cortex: drug effects / Motor Cortex: physiopathology /
                      Paresis: drug therapy / Paresis: etiology / Paresis:
                      physiopathology / Psychomotor Performance: drug effects /
                      Recovery of Function: drug effects / Stroke: complications /
                      Stroke: drug therapy / Stroke: physiopathology / Adrenergic
                      Uptake Inhibitors (NLM Chemicals) / Morpholines (NLM
                      Chemicals) / reboxetine (NLM Chemicals) / J (WoSType)},
      cin          = {INM-2 / INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406 / I:(DE-Juel1)INM-3-20090406},
      pnm          = {Funktion und Dysfunktion des Nervensystems (FUEK409) /
                      89572 - (Dys-)function and Plasticity (POF2-89572)},
      pid          = {G:(DE-Juel1)FUEK409 / G:(DE-HGF)POF2-89572},
      shelfmark    = {Clinical Neurology / Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21387380},
      UT           = {WOS:000288284900020},
      doi          = {10.1002/ana.22237},
      url          = {https://juser.fz-juelich.de/record/12585},
}