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[Spasticity: from pathophysiology to treatment].

D A Iskra1, A P Kovalenko1, M A Koshkarev1

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Zhurnal Nevrologii I Psikhiatrii Imeni S.S. Korsakova
|December 1, 2018
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Summary

This review details the pathophysiology of spasticity following upper motor neuron damage. It highlights neuroplasticity, pathogenesis, and current treatments like botulinum neurotoxin type A (BoNT) for rehabilitation.

Keywords:
botulinumpathophysiologyrehabilitationspasticityspasticity patternupper motor neuron damage syndrome

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Area of Science:

  • Neurology
  • Rehabilitation Medicine
  • Neuroscience

Background:

  • Spasticity is a common, disabling outcome of upper motor neuron (UMN) damage.
  • Understanding the pathophysiology of spasticity is crucial for effective management.
  • Existing definitions and clinical presentations of spasticity require comprehensive analysis.

Purpose of the Study:

  • To present modern perspectives on spasticity pathophysiology.
  • To analyze the morphological and functional changes post-UMN damage.
  • To review current diagnostic techniques and treatment strategies for spasticity.

Main Methods:

  • Review of existing literature on spasticity pathophysiology and treatment.
  • Analysis of neuroplasticity, pathogenesis, and sanogenesis in spasticity development.
  • Comparison of pathogenetic mechanisms with clinical symptoms and diagnostic methods.

Main Results:

  • Spasticity involves complex pathobiological processes in muscles, tendons, and joints.
  • Botulinum neurotoxin type A (BoNT) and muscle relaxants are key treatments.
  • BoNT is an integral component of comprehensive spasticity rehabilitation programs.

Conclusions:

  • Effective spasticity management requires understanding its pathophysiological basis.
  • Integrated treatment approaches, including BoNT, are essential for rehabilitation.
  • Further research into diagnostic and therapeutic advancements is warranted.