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痉挛和强直状态下步态的电生理研究。肌肉力学特性改变导致张力亢进的证据。

Electrophysiological studies of gait in spasticity and rigidity. Evidence that altered mechanical properties of muscle contribute to hypertonia.

作者信息

Dietz V, Quintern J, Berger W

出版信息

Brain. 1981 Sep;104(3):431-49. doi: 10.1093/brain/104.3.431.

DOI:10.1093/brain/104.3.431
PMID:7272709
Abstract

The surface electromyogram (EMG) of mm. tibialis anterior and triceps surae was recorded in 10 patients with spasticity, 10 patients with rigidity and 20 normal subjects and correlated with the changes in ankle joint angle during the different phases of the gait cycle. While the strength and timing of EMG activity recorded from triceps surae during the stance phase of gait did not differ from that of normal subjects, the EMG of tibialis anterior was significantly stronger during the swing phase in both groups of patients. Although the reciprocally organized innervation pattern of the leg muscles was preserved, spastic patients could hardly lift up the affected foot during the swing phase despite the enhanced activity of tibialis anterior. There was no coactivation of the calf muscles during the hyperactivity of tibialis anterior. Therefore, no electrophysiological explanation could be found for the increased muscle tone in either group of patients. The possibilities of reduced force development by the muscle fibres of tibialis anterior or of some mechanical obstruction in the ankle joint were largely excluded as alternative explanations underlying the impeded elevation of the foot. We suppose that in both diseases the muscle fibres undergo changes which are responsible for increased muscle tone in spasticity and rigidity. The pathophysiological mechanism of these changes remains unknown.

摘要

记录了10例痉挛患者、10例强直患者和20名正常受试者的胫前肌和小腿三头肌的表面肌电图(EMG),并将其与步态周期不同阶段踝关节角度的变化相关联。虽然在步态站立期从小腿三头肌记录的肌电图活动的强度和时间与正常受试者没有差异,但两组患者在摆动期胫前肌的肌电图明显更强。尽管腿部肌肉相互组织的神经支配模式得以保留,但痉挛患者在摆动期尽管胫前肌活动增强,却几乎无法抬起患足。在胫前肌活动亢进时,小腿肌肉没有共同激活。因此,在两组患者中均未找到肌张力增加的电生理解释。胫前肌肌纤维力量发展降低或踝关节存在某种机械性梗阻的可能性在很大程度上被排除,因为它们是足部抬高受阻的潜在替代解释。我们推测,在这两种疾病中,肌纤维都会发生变化,这些变化导致了痉挛和强直时肌张力增加。这些变化的病理生理机制仍然未知。

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