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@ARTICLE{Perlova:1050024,
      author       = {Perlova, Ksenia and Schmidt, Claudia C. and Fink, Gereon R.
                      and Weiss-Blankenhorn, Peter},
      title        = {{T}he role of the left primary motor cortex in apraxia},
      journal      = {Neurological research and practice},
      volume       = {7},
      number       = {1},
      issn         = {2524-3489},
      address      = {[London]},
      publisher    = {BioMed Central},
      reportid     = {FZJ-2025-05738},
      pages        = {2},
      year         = {2025},
      note         = {FundingOpen Access funding enabled and organized by Projekt
                      DEAL. Funded by the German Research Foundation
                      (DFG)—Project-ID 431549029 (CRC/SFB 1451).},
      abstract     = {Background: Apraxia is a motor-cognitive disorder that
                      primary sensorimotor deficits cannot solely explain.
                      Previous research in stroke patients has focused on damage
                      to the fronto-parietal praxis networks in the left
                      hemisphere (LH) as the cause of apraxic deficits. In
                      contrast, the potential role of the (left) primary motor
                      cortex (M1) has largely been neglected. However, recent
                      brain stimulation and lesion-mapping studies suggest an
                      involvement of left M1 in motor cognitive processes-over and
                      above its role in motor execution. Therefore, this study
                      explored whether the left M1 plays a specific role in
                      apraxia.Methods: We identified 157 right-handed patients
                      with first-ever unilateral LH stroke in the sub-acute phase
                      (< 90 days post-stroke), for whom apraxia assessments
                      performed with the ipsilesional left hand and lesion maps
                      were available. Utilizing the maximum probability map of
                      Brodmann area 4 (representing M1) provided by the JuBrain
                      Anatomy Toolbox in SPM, patients were subdivided into two
                      groups depending on whether their lesions involved (n = 40)
                      or spared (n = 117) left M1. We applied a mixed model ANCOVA
                      with repeated measures to compare apraxic deficits between
                      the two patient groups, considering the factors "body part"
                      and "gesture meaning". Furthermore, we explored potential
                      differential effects of the anterior (4a) and posterior (4p)
                      parts of Brodmann area 4 by correlation analyses.Results:
                      Patients with and without M1 involvement did not differ in
                      age and time post-stroke but in lesion size. When
                      controlling for lesion size, the total apraxia scores did
                      not differ significantly between groups. However, the mixed
                      model ANCOVA showed that LH stroke patients with lesions
                      involving left M1 performed differentially worse when
                      imitating meaningless finger gestures. This effect was
                      primarily driven by lesions affecting Brodmann area
                      4p.Conclusions: Even though many current definitions of
                      apraxia disregard a relevant role of (left) M1, the observed
                      differential effect of M1 lesions, specifically involving
                      subarea 4p, on the imitation of meaningless finger gestures
                      in the current sample of LH stroke patients suggests a
                      specific role of left M1 in imitation when high amounts of
                      (motor) attention and sensorimotor integration are
                      required.Keywords: Body-part specificity; Finger gestures;
                      Gesture meaning; Imitation; Limb-kinetic apraxia; Motor
                      cognition},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525) / DFG project G:(GEPRIS)431549029 - SFB 1451:
                      Schlüsselmechanismen normaler und krankheitsbedingt
                      gestörter motorischer Kontrolle (431549029)},
      pid          = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1186/s42466-024-00359-8},
      url          = {https://juser.fz-juelich.de/record/1050024},
}