Leonard Charles T, Sandholdt Daniel Y, McMillan James A, Queen Susan
Physical Therapy Department, The Motor Control Research Laboratory, The University of Montana, Missoula, MT 59812, USA.
J Child Neurol. 2006 Mar;21(3):240-6. doi: 10.2310/7010.2006.00068.
Deficits in reciprocal inhibition likely contribute to excessive antagonist muscle cocontraction during voluntary movements of individuals with cerebral palsy. This study examined neural contributions to reciprocal inhibition of the soleus motoneurons of individuals with spastic, diplegic cerebral palsy and nondisabled individuals during various levels of voluntary tibialis anterior contraction. A condition-test H-reflex paradigm examined short- and long-latency contributions to reciprocal inhibition of soleus neural pools during changing levels of voluntary tibialis anterior contraction. Electrically induced short- and long-latency inhibition was similar between healthy, neurologically intact control subjects and subjects with cerebral palsy during rest. With increasing levels of tibialis anterior contraction, control subjects experienced increasing levels of soleus motoneuron inhibition, especially of long-latency inhibitory responses. In contrast, there was no evidence of modulation of short- or long-latency inhibition with increasing levels of tibialis anterior contraction among subjects with cerebral palsy. Deficits in long-latency (presynaptic) inhibition appear to contribute prominently to voluntary movement impairment of individuals with cerebral palsy.
交互抑制功能缺陷可能导致脑瘫患者在自主运动过程中拮抗肌过度共同收缩。本研究探讨了痉挛型双侧瘫脑瘫患者和非残疾个体在不同程度的自主胫骨前肌收缩过程中，对比目鱼肌运动神经元交互抑制的神经作用。一种条件测试H反射范式研究了在自主胫骨前肌收缩水平变化时，对比目鱼肌神经池交互抑制的短潜伏期和长潜伏期作用。在静息状态下，健康的神经功能正常的对照受试者和脑瘫受试者之间，电诱发的短潜伏期和长潜伏期抑制相似。随着胫骨前肌收缩水平的增加，对照受试者的比目鱼肌运动神经元抑制水平增加，尤其是长潜伏期抑制反应。相比之下，在脑瘫受试者中，没有证据表明随着胫骨前肌收缩水平的增加，短潜伏期或长潜伏期抑制会发生调节。长潜伏期（突触前）抑制功能缺陷似乎是导致脑瘫患者自主运动障碍的主要原因。
