中国康复理论与实践
中國康複理論與實踐
중국강복이론여실천
CHINESE JOURNAL OF REHABILITATION THEORY & PRACTICE
2015年
8期
913-916
,共4页
脑卒中%强制性运动疗法%康复%肢体功能%综述
腦卒中%彊製性運動療法%康複%肢體功能%綜述
뇌졸중%강제성운동요법%강복%지체공능%종술
stroke%constraint induced movement therapy%rehabilitation%limb motor function%review
本文主要综述强制性运动疗法(CIMT)对脑卒中后肢体运动能力恢复的起效机制。CIMT可促进侧脑室室管膜下区神经元的新生,并促进缺血半暗带区新生神经元的存活和分化;还可促进来自健侧大脑的皮质脊髓束纤维在脊髓颈段向患肢侧的交叉,进而对神经传导通路产生可塑性影响。生长抑制蛋白勿动蛋白(Nogo-A)可因CIMT训练而下调,从而减弱神经损伤后对纤维生长的抑制。除此之外,CIMT还可通过影响脑源性神经营养因子(BDNF)、Rho激酶等的表达而发挥治疗作用。尽管如此,CIMT所引起的神经系统结构重塑是否在肢体功能支配过程中真正发挥作用还有待进一步证实,分子机制的研究也多缺乏必要的相关分子抑制与促进效应的论证。
本文主要綜述彊製性運動療法(CIMT)對腦卒中後肢體運動能力恢複的起效機製。CIMT可促進側腦室室管膜下區神經元的新生,併促進缺血半暗帶區新生神經元的存活和分化;還可促進來自健側大腦的皮質脊髓束纖維在脊髓頸段嚮患肢側的交扠,進而對神經傳導通路產生可塑性影響。生長抑製蛋白勿動蛋白(Nogo-A)可因CIMT訓練而下調,從而減弱神經損傷後對纖維生長的抑製。除此之外,CIMT還可通過影響腦源性神經營養因子(BDNF)、Rho激酶等的錶達而髮揮治療作用。儘管如此,CIMT所引起的神經繫統結構重塑是否在肢體功能支配過程中真正髮揮作用還有待進一步證實,分子機製的研究也多缺乏必要的相關分子抑製與促進效應的論證。
본문주요종술강제성운동요법(CIMT)대뇌졸중후지체운동능력회복적기효궤제。CIMT가촉진측뇌실실관막하구신경원적신생,병촉진결혈반암대구신생신경원적존활화분화;환가촉진래자건측대뇌적피질척수속섬유재척수경단향환지측적교차,진이대신경전도통로산생가소성영향。생장억제단백물동단백(Nogo-A)가인CIMT훈련이하조,종이감약신경손상후대섬유생장적억제。제차지외,CIMT환가통과영향뇌원성신경영양인자(BDNF)、Rho격매등적표체이발휘치료작용。진관여차,CIMT소인기적신경계통결구중소시부재지체공능지배과정중진정발휘작용환유대진일보증실,분자궤제적연구야다결핍필요적상관분자억제여촉진효응적론증。
Constraint induced movement therapy (CIMT) is considered to be effective in restoring the impaired limb motor function in patients after stroke. CIMT enhanced neurogenesis in sub-ventricular zone and promoted the proliferation and long-term survival of the new-born neurons in the ischemic penumbra region. CIMT also enhanced the midline-crossing phenomenon, which means the midline crossing of the contralesional corticospinal tract originated nerve fibers to the denervated side in the cervical spinal cord. CIMT down-regulated the expression of Neurite outgrowth inhibitor-A (Nogo-A) as well as regulated other molecules to promote the growth of nerve fibers. In addi-tion, CIMT ajusted the expression of brain-derived neurotrophic factor and Rho kinsase. Nevertheless, whether the structural plasticity caused by CIMT really participated in limb function remains unknown. And many studies on molecular mechanisms lack the evidence of necessary promotion and inhibition of the related molecule.