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@ARTICLE{Wieters:892060,
      author       = {Wieters, Frederique and Weiss Lucas, Carolin and Gruhn,
                      Matthias and Büschges, Ansgar and Fink, Gereon R. and
                      Aswendt, Markus},
      title        = {{I}ntroduction to spasticity and related mouse models},
      journal      = {Experimental neurology},
      volume       = {335},
      issn         = {0014-4886},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {FZJ-2021-01911},
      pages        = {113491 -},
      year         = {2021},
      abstract     = {Although spasticity is one of the most common causes of
                      motor disability worldwide, its precise definition and
                      pathophysiology remain elusive, which to date renders its
                      experimental targeting tricky. At least in part, this
                      difficulty is caused by heterogeneous phenotypes of
                      spasticity-causing neurological disorders, all causing
                      spasticity by involving upper motor neurons. The most common
                      clinical symptoms are a series of rapid muscle contractions
                      (clonus), an increased muscle tone (hypertonia), and
                      augmented tendon reflex activity (hyperreflexia). This
                      muscle overactivity is due to disturbed inhibition of spinal
                      reflexes following upper motor neuron dysfunction. Despite a
                      range of physical and pharmacological therapies ameliorating
                      the symptoms, their targeted application remains difficult.
                      Therefore, to date, spasticity impacts rehabilitative
                      therapy, and no therapy exists that reverses the pathology
                      completely. In contrast to the incidence and importance of
                      spasticity, only very little pre-clinical work in animal
                      models exists, and this research is focused on the cat or
                      the rat spastic tail model to decipher altered reflexes and
                      excitability of the motor neurons in the spinal cord.
                      Meanwhile, the characterization of spasticity in clinically
                      more relevant mouse models of neurological disorders, such
                      as stroke, remains understudied. Here, we provide a brief
                      introduction into the clinical knowledge and therapy of
                      spasticity and an in-depth review of pre-clinical studies of
                      spasticity in mice including the current experimental
                      challenges for clinical translation.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {525 - Decoding Brain Organization and Dysfunction
                      (POF4-525)},
      pid          = {G:(DE-HGF)POF4-525},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33007294},
      UT           = {WOS:000600689300007},
      doi          = {10.1016/j.expneurol.2020.113491},
      url          = {https://juser.fz-juelich.de/record/892060},
}