Physiological effects of botulinum toxin in spasticity
Physiological effects of botulinum toxin in spasticity
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DOI：
10.1002/mds.20065
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发表时间：
2004-03-01
影响因子：
8.6
通讯作者：
Gracies, JM
中科院分区：
文献类型：
--
作者：
Gracies, JM
有相当多的证据表明，将肉毒毒素（BTX）注射到痉挛过度活动的肌肉中，会降低被注射肌肉供应的关节对被动运动的抵抗力。迄今为止，对麻痹肢体活动能力改善的证明只是轶事，这代表了BTX治疗痉挛性瘫痪研究中最困难的挑战。本文回顾了BTX的一些神经生理作用，除了阻断神经肌肉末端的乙酰胆碱释放：对中枢神经系统的影响，包括轴突逆行运输，降低运动神经元的兴奋性，对中枢突触的作用，如Renshaw抑制降低和突触前抑制增加；对运动神经元末梢的作用；对大多数有源终端的作用；BTX向邻近肌肉扩散；BTX效应扩散到远端肌肉其中一些神经生理作用可能有助于改善主动运动，因为它们可能对抗痉挛性麻痹患者功能损害的主要机制：无力、痉挛性收缩、痉挛性肌张力障碍和肌肉缩短。我们回顾了BTX注射后肌肉及其拮抗剂痉挛收缩减少的证据，以及拮抗剂无力的改善。肌内BTX减少痉挛性肌张力障碍和延长缩短肌肉的能力也根据先前的文献进行了讨论。当注射到关节周围一对过度活跃的痉挛拮抗剂时，BTX应该影响所有主要机制，损害关节周围的活跃功能。(C) 2004运动障碍学会。
There is considerable evidence that injection of botulinum toxin (BTX) into muscles with spastic overactivity reduces resistance to passive movement in joints supplied by the injected muscles. The demonstration of improvement in active performance of the paretic limbs has been only anecdotal to date, and represents the most difficult challenge in research on BTX therapy in spastic paralysis. Data are reviewed that indicate several neurophysiological actions of BTX, other than the blocking of acetylcholine release at the neuromuscular ending: effects on the central nervous system, including retrograde axonal transport, reduced motoneuronal excitability, action on central synapses such as decreased Renshaw inhibition and increased presynaptic inhibition; action on gamma motoneuronal endings; action on most active terminals; spread of BTX to neighboring muscles; spread of BTX effects to remote muscles. Several of these neurophysiological actions are likely to contribute to improvement in active movements, as they may antagonize the primary mechanisms of functional impairment in patients with spastic paralysis: weakness, spastic cocontraction, spastic dystonia, and muscle shortening. We review the evidence for reduction of spastic cocontraction in both the injected muscle and its antagonist, and for improvement of antagonist weakness after BTX injection. The capacity of intramuscular BTX to reduce spastic dystonia and lengthen shortened muscles is also discussed based on prior literature. When injected into the more overactive of a pair of spastic antagonists around a joint, BTX should affect all the main mechanisms impairing active function around the joint. (C) 2004 Movement Disorder Society.