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帕金森病中缩短反应和拉伸诱导抑制对僵直的贡献的区分。

Differentiation between the contributions of shortening reaction and stretch-induced inhibition to rigidity in Parkinson's disease.

机构信息

Rehabilitation Science Research Laboratory, Department of Physical Therapy, Creighton University, Omaha, NE 68178, USA.

出版信息

Exp Brain Res. 2011 Apr;209(4):609-18. doi: 10.1007/s00221-011-2594-2. Epub 2011 Feb 24.

DOI:10.1007/s00221-011-2594-2
PMID:21347660
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3142787/
Abstract

Parkinsonian rigidity is characterized by an increased resistance of a joint to externally imposed motion that remains uniform with changing joint angle. Two candidate mechanisms are proposed for the uniformity of rigidity, involving neural-mediated excitation of shortening muscles, i.e., shortening reaction (SR), or inhibition of stretched muscles, i.e., stretch-induced inhibition (SII). To date, no study has addressed the roles of these two phenomena in rigidity. The purpose of this study was to differentiate these two phenomena, and to quantify the potential contribution of each to wrist joint moment in 17 patients with parkinsonian rigidity, in both Off- and On-medication states. Joint position, torque, and EMGs of selected muscles were collected during externally imposed flexion and extension motions. Moments of shortened and stretched muscles were estimated using a biomechanical model. Slopes of the estimated torque-angle curve were calculated for shortened and stretched muscles, separately. A mixed model ANOVA was performed to compare the contribution between the two mechanisms. During flexion, slopes were significantly (P = 0.003) smaller for SR than for SII, whereas during extension, slopes for SII were significantly (P = 0.003) smaller. Results showed that both SR and SII contributed to rigidity. Which mechanism predominates appeared to be associated with the direction of movement. The findings provide new insights into the biomechanical underpinnings of this common symptom in Parkinson's disease.

摘要

帕金森病僵硬的特点是关节对外加运动的阻力增加,且随着关节角度的变化而保持均匀。有两种候选机制被提出用于解释僵硬的均匀性,涉及到神经介导的缩短肌肉兴奋,即缩短反应(SR),或伸展肌肉的抑制,即伸展诱导抑制(SII)。迄今为止,尚无研究探讨这两种现象在僵硬中的作用。本研究旨在区分这两种现象,并量化每个现象对 17 名帕金森病僵硬患者腕关节力矩的潜在贡献,包括 Off- 和 On-药物状态。在外部施加的屈伸运动过程中,记录关节位置、扭矩和选定肌肉的肌电图。使用生物力学模型估计缩短和伸展肌肉的力矩。分别计算缩短和伸展肌肉的估计扭矩-角度曲线的斜率。采用混合模型方差分析比较两种机制的贡献。在屈曲时,SR 的斜率显著(P=0.003)小于 SII,而在伸展时,SII 的斜率显著(P=0.003)小于 SII。结果表明,SR 和 SII 都对僵硬有贡献。哪种机制占主导地位似乎与运动方向有关。这些发现为帕金森病这一常见症状的生物力学基础提供了新的见解。

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