正常人同侧足部机械压力对同侧和对侧H反射的调节。

A Bastani, M R Hadian, S Talebian, H Bagheri, G R Olyaie
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引用次数: 0

摘要

目的:足底的机械感受器可能参与反射调节。因此,我们假设重复低阈传入刺激对比目鱼h反射有抑制作用。方法:16名正常受试者自愿参与研究,随机分配。受试者保持俯卧位。皮肤机械压力(CMP等于腿部和足部重量的50%)通过设计的仪器通过方形钢板(30 x 30 mm)施加于同侧外侧和内侧足底表面。H反射作为运动神经元兴奋性的指标,在应用CMP前后双侧被激发。估计h反射参数。结果:机械压力显著降低了所有受试者同侧和对侧足比目鱼h反射的兴奋性。结论:对足底施加压力导致h反射兴奋性降低,这表明反射兴奋性的变化是一种共同的脊柱机制的结果。结果强调了传入神经的自然刺激对反射兴奋性的调节作用。意义:放置一个小平板,以便对足底隆起施加压力,可能有助于调节肌肉张力。此外,这些发现可能有助于减少痉挛;因为痉挛至少部分是由运动神经元池的过度兴奋性引起的。
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Modulation of the ipsilateral and contralateral H reflexes following ipsilateral mechanical pressure of the foot in normal subjects.

Objective: Mechanoreceptors from the foot sole likely contribute in the reflex regulations. Therefore, it was hypothesized that repetitive low threshold afferents stimulation would have an inhibitory effect on the soleus H-reflexes.

Methods: Sixteen normal subjects voluntarily, participated in the study and were randomly allocated. Subjects were remained in prone position. The Cutaneous Mechanical Pressure (CMP equal to 50% of leg and foot weight) was applied to the ipsilateral lateral and Medial plantar surface by a designed instrument through a square plate (30 x 30 mm). H reflex as an indicator for excitability of motoneurones was bilaterally elicited before and after the application of the CMP. The H-reflex parameters were estimated.

Results: Mechanical pressure significantly depressed soleus H-reflex excitability in ipsilateral and contralateral feet in all subjects.

Conclusion: The demonstration of a decrease in H-reflex excitability as a result of applied pressure to the foot sole suggests that the change in reflex excitability is the result of a common spinal mechanism. The results highlight the modulatory effects that natural stimulation of afferents can have on reflex excitability.

Significance: The placement of a small flat plate, in order to apply pressure to the plantar eminence, may be useful for modulation of muscle tone. In addition, these findings might be useful for reducing spasticity; because spasticity is at least partially caused by hyperexcitability of the motorneuron pool.

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