Gracies Jean-Michel
Department of Neurology, Mount Sinai Medical Center, One Gustave L Levy Place, Annenberg 2/Box 1052, New York, New York 10029-6574, USA.
Muscle Nerve. 2005 May;31(5):535-51. doi: 10.1002/mus.20284.
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.
痉挛性轻瘫是由于中枢对意志性指令的执行长期中断所致。随着时间的推移，痉挛性轻瘫患者的运动功能会受到三种基本损害，其中后两种是可以避免的：（1）神经损伤本身，它导致轻瘫，即随意运动单位募集减少；（2）通常由当前护理环境造成的瘫痪身体部位的相对固定，这会导致处于缩短位置的肌肉适应性缩短和关节挛缩；（3）瘫痪身体部位的长期废用，在大多数患者中这通常是自我造成的。长期废用会导致高级中枢发生可塑性重排，进一步降低随意募集运动单位的能力，即加重基线轻瘫。本综述的第一部分重点关注导致痉挛性轻瘫运动障碍的前两个因素的病理生理学：轻瘫-废用-轻瘫的恶性循环以及软组织挛缩。
