课题基金 / 基金详情

SPASTICITY MECHANISMS AND QUANTIFICATION

SPASTICITY MECHANISMS AND QUANTIFICATION
痉挛机制和量化
批准号:
3399386
负责人:
WILLIAM Zev RYMER
金额:
$16.43万
依托单位国家:
美国
项目类别:
财政年份:
1983
资助国家:
美国
项目状态:
已结题
起止时间:
1983-04-01 至 1994-11-30

项目摘要

项目成果

WILLIAM Zev RYMER的其他基金

相关文献

中文摘要
翻译
描述(研究者摘要):三个具体目标将是 这项关于中风引起的运动障碍的持续研究的重点是 痉挛性偏瘫 第一个具体目标将试图区分两种可能的机制 肌肉选择的空间模式的干扰, 偏瘫性中风 这两个是解剖学上的限制 残余腹内侧脊髓通路的分支模式,或增加 屈曲反射中神经元间通路的敏感性。 这两 将使用皮肤刺激检查替代品,皮肤刺激 麻醉和单运动单位记录技术。 有限或不存在 肌电空间模式的修改,以响应操纵 皮肤的输入会支持卓越的脊髓上的作用。 第二个目标将是描述自愿性干扰的特征。 运动在痉挛性瘫痪肢体通过评估空间 运动到水平面中不同位置的特性, 同时记录运动速度、加速度和肢体阻尼 特色 这些研究的结果应允许自愿 运动和自主运动的阻尼是否部分负责 偏瘫性中风的残疾。 第三个目的是确定中风时的肌无力是否是 至少部分由运动单位募集障碍介导, 在个别肌肉内的速率调节。 这些异常很容易 在痉挛性轻瘫的动物模型中很明显, 脊髓运动神经元的神经调质输入紊乱。 单个 运动单位记录技术将用于比较招募, 特征和运动单位的同步性,在匹配的肌肉上, 同一个偏瘫患者的偏瘫侧和对侧。 总之,这些研究应该促进我们对 脑卒中偏瘫运动障碍的机制 为临床合理诊断和治疗提供指导 干预
英文摘要
DESCRIPTION (Investigator's Abstract): Three specific aims will be the focus of this continuing study of motor disability in stroke-induced spastic hemiparesis. The first specific aim will attempt to distinguish two possible mechanisms underlying the disturbance in spatial patterns of muscle selection in hemiparetic stroke. These two are the anatomical constraints imposed by branching patterns of residual ventromedial spinal pathways, or increased sensitivity of interneuronal pathways in the flexion-reflex. These two alternatives will be examined using cutaneous stimuli, cutaneous anesthesia, and single motor unit recording techniques. Limited or absent modification of EMG spatial pattern in response to manipulation of cutaneous input would argue for a pre-eminent supraspinal role. The second aim will be to characterize the disturbances in voluntary movement in the spastic paretic limbs by evaluating the spatial characteristics of movement to different locations in the horizontal plane, while recording movement velocity, acceleration and limb damping characteristics. The results of these studies should allow to voluntary motion and whether damping of voluntary motion is in part responsible for the disability of hemiparetic stroke. The third aim is to determine whether muscular weakness in stroke is mediated, at least in part, by disturbances of motor unit recruitment and rate modulation within individual muscles. These abnormalities are readily apparent in animal models of spastic paresis, where they appear to reflect disturbances in neuromodulator input to the spinal motoneurons. Single motor unit recording techniques will be used to compare recruitment, rate characteristics, and synchrony of motor units in matched muscles on the paretic and contralateral sides of the same hemiparetic subject. Taken together, these studies should advance our knowledge of the mechanisms underlying the disturbances of movement in hemiparetic stroke and should help provide guidelines for rational diagnosis and therapeutic intervention.
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