What are the pathophysiologic mechanisms of spasticity?

Updated: Jun 28, 2019
  • Author: Krupa Pandey, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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The pathophysiologic mechanisms causing the increase in stretch reflexes in spasticity also are not well understood. Unlike healthy subjects, in whom rapid muscle stretch does not elicit reflex muscle activity beyond the normal short-latency tendon reflex, patients with spasticity experience prolonged muscle contraction when spastic muscles are stretched. After an acute injury, the ease with which muscle activity is evoked by stretch increases in the first month of spasticity; then, the threshold remains stable until declining after a year.

During the development of spasticity, the spinal cord undergoes neurophysiologic changes in the excitability of motor neurons, interneuronal connections, and local reflex pathways. The excitability of alpha motor neurons is increased, as is suggested by enhanced H-M ratios [8] and F-wave amplitudes. [9] Judged by recordings from Ia spindle afferents, muscle spindle sensitivity is not increased in human spasticity.

Local anesthetic injections into spastic muscles in man can diminish spasticity through an effect on gamma motor neurons. Renshaw cells receive inputs from descending motor pathways, and recurrent collateral axons from motor neurons activate Renshaw cells, which inhibit gamma motor neurons. Renshaw cell activity is not reduced significantly in spasticity.

Reciprocal inhibition between antagonist muscles is mediated by the Ia inhibitory interneuron, which also receives input from descending pathways. Altered activity in Ia pathways has been shown in spasticity. Inhibitory interneurons acting on primary afferent terminals of the alpha motor neuron also influence the local circuitry.

Finally, plasticity and the formation of new aberrant connections in the central nervous system (CNS) is another theoretical explanation for some of the events in spasticity.

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