Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
Neurorehabil Neural Repair. 2010 Jan;24(1):23-33. doi: 10.1177/1545968309343213. Epub 2009 Sep 1.
Spasticity, resulting in involuntary and sustained contractions of muscles, may evolve in patients with stroke, cerebral palsy, multiple sclerosis, brain injury, and spinal cord injury (SCI). The authors critically review the neural mechanisms that may contribute to spasticity after SCI and assess their likely degree of involvement and relative significance to its pathophysiology. Experimental data from patients and animal models of spasticity as well as computer simulations are evaluated. The current clinical methods used for the management of spasticity and the pharmacological actions of drugs are discussed in relation to their effects on spinal mechanisms. Critical assessment of experimental findings indicates that increased excitability of both motoneurons and interneurons plays a crucial role in pathophysiology of spasticity. New interventions, including forms of spinal electrical stimulation to suppress increased neuronal excitability, may reduce the severity of spasticity and its complications.
痉挛是一种肌肉不自主的持续收缩,可能发生在脑卒中、脑瘫、多发性硬化、脑损伤和脊髓损伤(SCI)患者中。作者批判性地回顾了可能导致 SCI 后痉挛的神经机制,并评估了它们的可能参与程度及其对其病理生理学的相对重要性。评估了痉挛患者的实验数据和动物模型以及计算机模拟。讨论了目前用于管理痉挛的临床方法以及药物的药理作用与其对脊髓机制的影响。对实验结果的批判性评估表明,运动神经元和中间神经元兴奋性的增加在痉挛的病理生理学中起着至关重要的作用。新的干预措施,包括抑制神经元兴奋性增加的脊髓电刺激形式,可能会降低痉挛的严重程度及其并发症。