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@ARTICLE{Kusch:851757,
      author       = {Kusch, M. and Schmidt, Claudia and Göden, L. and
                      Tscherpel, C. and Stahl, J. and Saliger, J. and Karbe, H.
                      and Fink, G. R. and Weiss, P. H.},
      title        = {{R}ecovery from apraxic deficits and its neural correlate},
      journal      = {Restorative neurology and neuroscience},
      volume       = {36},
      number       = {6},
      issn         = {0922-6028},
      address      = {Amsterdam},
      publisher    = {IOS Press},
      reportid     = {FZJ-2018-05281},
      pages        = {669–678},
      year         = {2018},
      abstract     = {Background and Objective: Apraxia is a deficit of motor
                      cognition leading to difficulties in actual tool use,
                      imitation of gestures, and pantomiming object use. To date,
                      little data exist regarding the recovery from apraxic
                      deficits after stroke, and no statistical lesion mapping
                      study investigated the neural correlate of recovery from
                      apraxia. Accordingly, we here examined recovery from apraxic
                      deficits, differential associations of apraxia task
                      (imitation vs. pantomime) and effector (bucco-facial vs.
                      limb apraxia) with recovery, and the underlying neural
                      correlates. Methods: We assessed apraxia in 39 patients with
                      left hemisphere (LH) stroke both at admission and
                      approximately 11 days later. Furthermore, we collected
                      clinical imaging data to identify brain regions associated
                      with recovery from apraxic deficits using voxel-based
                      lesion-symptom mapping (VLSM). Results:Between the two
                      assessments, a significant recovery from apraxic deficits
                      was observed with a tendency of enhanced recovery of limb
                      compared to bucco-facial apraxia. VLSM analyses revealed
                      that within the lesion pattern initially associated with
                      apraxia, lesions of the left insula were associated with
                      remission of apraxic deficits, whereas lesions to the
                      (inferior) parietal lobe (IPL; supramarginal and angular
                      gyrus) and the superior longitudinal fasciculus (SLF) were
                      associated with persistent apraxic deficits. Conclusions:
                      Data suggest that lesions affecting the core regions (and
                      white matter) of the fronto-parietal network cause more
                      persistent apraxic deficits than lesions affecting other
                      regions (here: the left insula) that also contribute to
                      motor cognition and apraxic deficits.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30282379},
      UT           = {WOS:000451336100001},
      doi          = {10.3233/RNN-180815},
      url          = {https://juser.fz-juelich.de/record/851757},
}