Nielsen J, Petersen N, Crone C
Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.
Brain. 1995 Aug;118 ( Pt 4):995-1004. doi: 10.1093/brain/118.4.995.
The transmission across synapses of Ia afferents on spinal motor neurons was investigated in 30 healthy subjects and 25 spastic multiple sclerosis patients. Slow passive stretch (17 degrees/s of the soleus muscle evoked a pronounced depression of the soleus Hoffmann reflex (H-reflex) lasting for more than 10 s in the healthy subjects. This depression was less pronounced and had a shorter duration in the spastic patients. A tap applied to the biceps femoris tendon also produced an inhibition of the soleus H-reflex, which was larger in the healthy subjects than in the spastic patients. This inhibition only lasted for 300-400 ms. Finally, stimulation of the femoral nerve (FN) produced a facilitation of the soleus H-reflex, which was larger in the spastic patients than in the healthy subjects. The inhibition of the H-reflex evoked by the biceps femoris tendon tap is known to be caused by presynaptic inhibition of the Ia afferents, which mediate the reflex. The facilitation of the soleus H-reflex produced by FN stimulation has also been shown to be influenced by changes in presynaptic inhibition. The increased facilitation from the FN and the decreased inhibition from the biceps femoris tendon tap onto the soleus H-reflex in spastic patients are thus both compatible with a deficient presynaptic inhibition in these subjects. The long lasting depression of the reflex evoked by a previous slow stretch of the soleus muscle is most likely caused by a decrease of the probability of transmitter release from the Ia afferents. The decrease of this depression in spastic patients suggests that mechanisms other than presynaptic inhibition may contribute to changes in the efficiency of transmission across the synapses of Ia afferents in spastic patients and thus contribute to the exaggeration of stretch reflexes seen in these patients.
在30名健康受试者和25名痉挛性多发性硬化症患者中，研究了Ia传入神经在脊髓运动神经元上的突触传递。在健康受试者中，比目鱼肌缓慢被动拉伸（17度/秒）会引起比目鱼肌霍夫曼反射（H反射）明显抑制，持续超过10秒。这种抑制在痉挛性患者中不太明显，持续时间较短。轻敲股二头肌肌腱也会抑制比目鱼肌H反射，健康受试者中的这种抑制作用比痉挛性患者更大。这种抑制仅持续300 - 400毫秒。最后，刺激股神经（FN）会促进比目鱼肌H反射，痉挛性患者中的促进作用比健康受试者更大。已知股二头肌肌腱轻敲引起的H反射抑制是由介导该反射的Ia传入神经的突触前抑制引起的。FN刺激产生的比目鱼肌H反射促进作用也已被证明受突触前抑制变化的影响。因此，痉挛性患者中FN促进作用增加以及股二头肌肌腱轻敲对比目鱼肌H反射的抑制作用降低，都与这些受试者突触前抑制不足相符。比目鱼肌先前缓慢拉伸引起的反射的长期抑制很可能是由于Ia传入神经递质释放概率降低所致。痉挛性患者中这种抑制作用的减弱表明，除突触前抑制外的其他机制可能导致痉挛性患者中Ia传入神经突触传递效率的变化，从而导致这些患者中看到的牵张反射亢进。
