Morita H, Crone C, Christenhuis D, Petersen N T, Nielsen J B
Division of Neurophysiology, Department of Medical Physiology, The Panum Institute, Copenhagen University, Blegdamsvej, Copenhagen, Denmark.
Brain. 2001 Apr;124(Pt 4):826-37. doi: 10.1093/brain/124.4.826.
The aim of the study was to investigate whether impaired control of transmission in spinal inhibitory pathways contributes to the functional disability of patients with spasticity. To this end, transmission in the pathways mediating disynaptic reciprocal Ia inhibition and presynaptic inhibition was investigated in 23 healthy subjects and 20 patients with spastic multiple sclerosis during ankle dorsiflexion and plantar flexion. In healthy subjects, but not in spastic patients, the soleus H reflex was depressed at the onset of dorsiflexion (300 ms rise time, 20% of maximal voluntary effort). At the onset of plantar flexion, the soleus H reflex was more facilitated in the healthy subjects than in the patients. The H reflex increased more with increasing level of tonic plantar flexion and decreased more with dorsiflexion in the healthy subjects than in the spastic patients. Transmission in the disynaptic Ia reciprocal inhibitory pathway from ankle dorsiflexors to plantar flexors was investigated by conditioning the soleus H reflex by previous stimulation of the common peroneal nerve (conditioning-test interval 2-3 ms; stimulation intensity 1.05 times the motor response threshold). At the onset of dorsiflexion, stimulation of the common peroneal nerve evoked a significantly larger inhibition than at rest in the healthy subjects but not in the spastic patients. At the onset of plantar flexion the inhibition decreased in the healthy subjects, but because only weak inhibition was observed at rest in the patients it was not possible to determine whether a similar decrease occurred in this group. There were no differences in the modulation of inhibition during tonic plantar flexion and dorsiflexion in the two populations. Presynaptic inhibition of Ia afferents terminating on soleus motor neurones was evaluated from the monosynaptic Ia facilitation of the soleus H reflex evoked by femoral nerve stimulation. Femoral nerve facilitation was decreased at the onset of dorsiflexion and increased at the onset of plantar flexion in the healthy subjects and patients, but the changes were significantly greater in the healthy subjects. There was no difference between the two populations in the modulation of presynaptic inhibition during tonic plantar flexion and dorsiflexion. It is suggested that the abnormal regulation of disynaptic reciprocal inhibition and presynaptic inhibition in patients with spasticity is responsible for the abnormal modulation of stretch reflexes in relation to voluntary movement in these patients. Lack of an increase in reciprocal inhibition and presynaptic inhibition at the onset of dorsiflexion may be responsible for the tendency to elicitation of unwanted stretch reflex activity and co-contraction of antagonistic muscles in patients with spasticity.
本研究的目的是调查脊髓抑制通路中传递控制受损是否导致痉挛患者的功能障碍。为此，在23名健康受试者和20名痉挛性多发性硬化症患者进行踝关节背屈和跖屈时，研究了介导双突触交互性Ia抑制和突触前抑制的通路中的传递情况。在健康受试者中，而非痉挛患者中，在背屈开始时（上升时间300毫秒，最大自主用力的20%）比目鱼肌H反射受到抑制。在跖屈开始时，健康受试者比目鱼肌H反射比患者更容易受到易化。与痉挛患者相比，在健康受试者中，随着强直性跖屈程度增加，H反射增加得更多，随着背屈增加，H反射减少得更多。通过先前刺激腓总神经来条件化比目鱼肌H反射（条件-测试间隔2-3毫秒；刺激强度为运动反应阈值的1.05倍），研究从踝关节背屈肌到跖屈肌的双突触Ia交互抑制通路中的传递情况。在背屈开始时，刺激腓总神经在健康受试者中诱发的抑制比静息时显著更大，但在痉挛患者中则不然。在跖屈开始时，健康受试者中的抑制减弱，但由于在患者静息时仅观察到微弱抑制，因此无法确定该组是否发生了类似的减弱。在这两个人群中，强直性跖屈和背屈期间抑制的调制没有差异。通过股神经刺激诱发的比目鱼肌H反射的单突触Ia易化来评估终止于比目鱼肌运动神经元的Ia传入纤维的突触前抑制。在健康受试者和患者中，股神经易化在背屈开始时降低，在跖屈开始时增加，但健康受试者中的变化显著更大。在强直性跖屈和背屈期间，这两个人群在突触前抑制的调制方面没有差异。提示痉挛患者中双突触交互抑制和突触前抑制的异常调节是这些患者中与随意运动相关的牵张反射异常调制的原因。在背屈开始时交互抑制和突触前抑制缺乏增加可能是痉挛患者中诱发不必要的牵张反射活动和拮抗肌共同收缩倾向的原因。
