Abstract：
OBJECTIVE: Motor neuron pool activity is high in spasticity. The effect of inhibitory kinesiotaping (KT) on spasticity is unclear. The aim of this study is to investigate the effect of inhibitory KT on spasticity after stroke.
METHODS: Fifty stroke patients with ankle plantarflexor spasticity were randomised to intervention (27) and control (23) groups. Inhibitory KT was applied to the triceps surae muscle in the intervention group and sham KT to the Achilles tendon in the control group. Inhibitory and sham KT were applied for 72 h with a combined conventional rehabilitation programme. Spasticity was assessed at baseline and 72 h after KT using three instruments: Modified Ashworth Scale (MAS), Homosynaptic Post-Activation Depression (HPAD) reflecting the level of motor neuron pool activity, and joint torque as a measure of resistance to passive ankle dorsiflexion.
RESULTS: The baseline MAS score, HPAD levels and dorsiflexion torque of the two groups were not significantly different. The change in MAS score was -3.7 ± 17.5 (p = 0.180) in the intervention group and 3.6 ± 33.3 (p = 0.655) in the control group. The change in dorsiflexion torque was -0.3 ± 16.1 kg m (p = 0.539) in the intervention group and 8.0 ± 24.1 kg m (p = 0.167) in the control group. The change in mean HPAD was 8.7 ± 34.7 (p = 0.911) in the intervention group and 10.1 ± 41.6 (p = 0.609) in the control group.
CONCLUSIONS: The present study showed that inhibitory KT has no antispastic effect in stroke patients.
METHODS: Fifty stroke patients with ankle plantarflexor spasticity were randomised to intervention (27) and control (23) groups. Inhibitory KT was applied to the triceps surae muscle in the intervention group and sham KT to the Achilles tendon in the control group. Inhibitory and sham KT were applied for 72 h with a combined conventional rehabilitation programme. Spasticity was assessed at baseline and 72 h after KT using three instruments: Modified Ashworth Scale (MAS), Homosynaptic Post-Activation Depression (HPAD) reflecting the level of motor neuron pool activity, and joint torque as a measure of resistance to passive ankle dorsiflexion.
RESULTS: The baseline MAS score, HPAD levels and dorsiflexion torque of the two groups were not significantly different. The change in MAS score was -3.7 ± 17.5 (p = 0.180) in the intervention group and 3.6 ± 33.3 (p = 0.655) in the control group. The change in dorsiflexion torque was -0.3 ± 16.1 kg m (p = 0.539) in the intervention group and 8.0 ± 24.1 kg m (p = 0.167) in the control group. The change in mean HPAD was 8.7 ± 34.7 (p = 0.911) in the intervention group and 10.1 ± 41.6 (p = 0.609) in the control group.
CONCLUSIONS: The present study showed that inhibitory KT has no antispastic effect in stroke patients.
摘要：
目的：运动神经元池活动在痉挛状态下很高。抑制动力学分析（KT）对痉挛的影响尚不清楚。这项研究的目的是研究抑制性KT对中风后痉挛的影响。
方法：将50例踝屈肌痉挛的卒中患者随机分为干预组（27例）和对照组（23例）。干预组的腓肠三头肌应用抑制性KT，对照组的跟腱应用假KT。抑制和假KT应用72小时，并结合常规康复计划。使用三种仪器在基线和KT后72小时评估痉挛：改良的Ashworth量表（MAS），同突触激活后抑郁（HPAD）反映运动神经元池活动的水平，和关节扭矩作为抵抗被动踝关节背屈的量度。
结果：基线MAS评分，两组的HPAD水平和背屈扭矩无明显差异。干预组MAS评分变化为-3.7±17.5(p=0.180),对照组为3.6±33.3(p=0.655)。干预组的背屈力矩变化为-0.3±16.1kgm（p=0.539），对照组为8.0±24.1kgm（p=0.167）。干预组平均HPAD变化为8.7±34.7（p=0.911），对照组为10.1±41.6（p=0.609）。
结论：本研究表明，抑制性KT对中风患者没有抗痉挛作用。
方法：将50例踝屈肌痉挛的卒中患者随机分为干预组（27例）和对照组（23例）。干预组的腓肠三头肌应用抑制性KT，对照组的跟腱应用假KT。抑制和假KT应用72小时，并结合常规康复计划。使用三种仪器在基线和KT后72小时评估痉挛：改良的Ashworth量表（MAS），同突触激活后抑郁（HPAD）反映运动神经元池活动的水平，和关节扭矩作为抵抗被动踝关节背屈的量度。
结果：基线MAS评分，两组的HPAD水平和背屈扭矩无明显差异。干预组MAS评分变化为-3.7±17.5(p=0.180),对照组为3.6±33.3(p=0.655)。干预组的背屈力矩变化为-0.3±16.1kgm（p=0.539），对照组为8.0±24.1kgm（p=0.167）。干预组平均HPAD变化为8.7±34.7（p=0.911），对照组为10.1±41.6（p=0.609）。
结论：本研究表明，抑制性KT对中风患者没有抗痉挛作用。
