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@ARTICLE{Paul:911401,
      author       = {Paul, Theresa and Cieslak, Matthew and Hensel, Lukas and
                      Wiemer, Valerie M and Grefkes, Christian and Grafton, Scott
                      T and Fink, Gereon R and Volz, Lukas J},
      title        = {{T}he role of corticospinal and extrapyramidal pathways in
                      motor impairment after stroke},
      journal      = {Brain communications},
      volume       = {5},
      number       = {1},
      issn         = {2632-1297},
      address      = {[Großbritannien]},
      publisher    = {Guarantors of Brain},
      reportid     = {FZJ-2022-04684},
      pages        = {fcac301},
      year         = {2023},
      abstract     = {Anisotropy of descending motor pathways has repeatedly been
                      linked to the severity of motor impairment following
                      stroke-related damage to the corticospinal tract (CST).
                      Despite promising findings consistently tying anisotropy of
                      the ipsilesional CST to motor outcome, anisotropy is not yet
                      utilized as a biomarker for motor recovery in clinical
                      practice as a conclusive understanding of degenerative
                      processes in the ipsilesional CST and compensatory roles of
                      other descending motor pathways is hindered by
                      methodological constraints such as estimating anisotropy in
                      voxels with multiple fiber directions, sampling biases, and
                      confounds due to aging-related atrophy. The present study
                      addressed these issues by combining diffusion spectrum
                      imaging (DSI) with a novel compartmentwise analysis approach
                      differentiating voxels with one dominant fiber direction
                      (one-directional voxels) from voxels with multiple fiber
                      directions. Compartmentwise anisotropy for bihemispheric CST
                      and extrapyramidal tracts was compared between chronic
                      stroke patients (N=25), age-matched controls (N=22), and
                      young controls (N=24) and its associations with motor
                      performance of the upper and lower limbs were assessed. Our
                      results provide direct evidence for Wallerian degenration
                      along the entire length of the ipsilesional CST reflected by
                      decreased anisotropy in descending fibers compared to
                      age-matched controls, while aging-related atrophy was
                      observed more ubiquitously across compartments. Anisotropy
                      of descending ipsilesional CST voxels showed a highly robust
                      correlation with various aspects of upper and lower limb
                      motor impairment, highlighting the behavioral relevance of
                      Wallerian degeneration. Moreover, anisotropy measures of
                      two-directional voxels within bihemispheric rubrospinal and
                      reticulospinal tracts were linked to lower limb deficits,
                      while anisotropy of two-directional contralesional
                      rubrospinal voxels explained gross motor performance of the
                      affected hand. Of note, the relevant extrapyramidal
                      structures contained fibers crossing the midline, fibers
                      potentially mitigating output from brain stem nuclei, and
                      fibers transferring signals between the extrapyramidal
                      system and the cerebellum. Thus, specific parts of
                      extrapyramidal pathways seem to compensate for impaired
                      gross arm and leg movements incurred through stroke-related
                      CST lesions, while fine motor control of the paretic hand
                      critically relies on ipsilesional CST integrity.
                      Importantly, our findings suggest that the extrapyramidal
                      system may serve as a compensatory structural reserve
                      independent of post-stroke reorganization of extrapyramidal
                      tracts. In summary, compartment-specific anisotropy of
                      ipsilesional CST and extrapyramidal tracts explained
                      distinct aspects of motor impairment, with both systems
                      representing different pathophysiological mechanisms
                      contributing to motor control post-stroke. Considering both
                      systems in concert may help develop diffusion imaging
                      biomarkers for specific motor functions after stroke.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525) / DFG
                      project 431549029 - SFB 1451: Schlüsselmechanismen normaler
                      und krankheitsbedingt gestörter motorischer Kontrolle
                      (431549029)},
      pid          = {G:(DE-HGF)POF4-5252 / G:(GEPRIS)431549029},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {36601620},
      UT           = {WOS:000905773200002},
      doi          = {10.1093/braincomms/fcac301},
      url          = {https://juser.fz-juelich.de/record/911401},
}