Pathophysiology of spasticity in stroke

Neurology. 2013 Jan 15;80(3 Suppl 2):S20-6. doi: 10.1212/WNL.0b013e31827624a7.

Abstract

Spasticity is defined clinically by increased muscle tone and tendon jerk hyperreflexia in patients who are at rest. However, the excitability of spinal circuits changes during movement, and this definition provides no insight into the extent to which spasticity and associated motor disturbances cause disability. Only a few spinal circuits have been shown to underlie the abnormalities of patients at rest. Movement can be restrained by pathologically enhanced muscle tone, and there is defective control of the feedback to active motoneurons through virtually all spinal reflex pathways. Spasticity does not necessarily require treatment: in fact, some patients rely on the increased muscle tone to help support otherwise weak muscle contractions for stance and locomotion. In addition, much of the increase in muscle tone arises from changes in muscle and motor units, independent of reflex mechanisms. Managing a patient with impairment after a stroke requires therapy tailored to that particular patient because the mechanisms contributing to the disability experienced by one patient may differ from those affecting another.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Motor Neurons
  • Movement
  • Muscle Contraction*
  • Muscle Hypertonia / etiology
  • Muscle Hypertonia / physiopathology
  • Muscle Spasticity / etiology*
  • Muscle Spasticity / physiopathology*
  • Muscle Tonus
  • Muscle Weakness
  • Muscle, Skeletal / physiopathology*
  • Neural Conduction
  • Neural Inhibition
  • Reflex, Abnormal
  • Spinal Cord / physiopathology
  • Stroke / complications*
  • Stroke / physiopathology*
  • Synaptic Transmission