ELECTRO-PHYSIOLOGICAL STUDIES OF GAIT IN SPASTICITY AND RIGIDITY - EVIDENCE THAT ALTERED MECHANICAL-PROPERTIES OF MUSCLE CONTRIBUTE TO HYPERTONIA

ELECTRO-PHYSIOLOGICAL STUDIES OF GAIT IN SPASTICITY AND RIGIDITY - EVIDENCE THAT ALTERED MECHANICAL-PROPERTIES OF MUSCLE CONTRIBUTE TO HYPERTONIA
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DOI:
10.1093/brain/104.3.431
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发表时间:
1981-01-01
期刊:
影响因子:
14.5
通讯作者:
BERGER, W
BERGER, W
中科院分区:
医学1区
文献类型:
--
作者:
DIETZ, V;QUINTERN, J;BERGER, W

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本文记录了10例痉挛型、10例强直型和20例正常人的胫前肌和小腿三头肌的表面肌电(EMG),并与步态周期各时相踝关节角的变化进行了相关分析。虽然小腿三头肌在步态站立阶段记录的肌电图活动的强度和时间与正常受试者没有差异,但两组患者在摆动阶段的胫骨前肌肌电图明显更强。虽然保留了腿部肌肉的神经支配模式,但痉挛患者在摆动阶段几乎无法抬起患足,尽管胫骨前肌的活动增强。胫骨前肌过度活动时,小腿肌肉无协同激活。因此,在两组患者中均未发现肌张力增加的电生理学解释。胫骨前肌纤维的力量发展减少或踝关节中的一些机械性障碍的可能性在很大程度上被排除作为足部抬高受阻的替代解释。我们认为,在这两种疾病中,肌纤维发生了变化,这些变化是导致痉挛和僵硬状态下肌张力增加的原因。这些变化的病理生理机制仍然未知。
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.