Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

Authors

  • Jean-Michel Gracies MD, PhD

    Corresponding author
    1. Department of Neurology, Mount Sinai Medical Center, One Gustave L Levy Place, Annenberg 2/Box 1052, New York, New York 10029-6574, USA
    • Department of Neurology, Mount Sinai Medical Center, One Gustave L Levy Place, Annenberg 2/Box 1052, New York, New York 10029-6574, USA
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Abstract

Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis–disuse–paresis and the contracture in soft tissues. Muscle Nerve, 2005

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