Pathophysiology of spastic paresis. II: Emergence of muscle overactivity

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

In the subacute and chronic stages of spastic paresis, stretch-sensitive (spastic) muscle overactivity emerges as a third fundamental mechanism of motor impairment, along with paresis and soft tissue contracture. Part II of this review primarily addresses the pathophysiology of the various forms of spastic overactivity. It is argued that muscle contracture is one of the factors that cause excessive responsiveness to stretch, which in turn aggravates contracture. Excessive responsiveness to stretch also impedes voluntary motor neuron recruitment, a concept termed stretch-sensitive paresis. None of the three mechanisms of impairment (paresis, contracture, and spastic overactivity) is symmetrically distributed between agonists and antagonists, which generates torque imbalance around joints and limb deformities. Thus, each may be best treated focally on an individual muscle-by-muscle basis. Intensive motor training of the less overactive muscles should disrupt the cycle of paresis–disuse–paresis, and concomitant use of aggressive stretch and focal weakening agents in their more overactive and shortened antagonists should break the cycle of overactivity–contracture–overactivity. Muscle Nerve, 2005

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