Delwaide P J, Pepin J L, Maertens de Noordhout A
University Department of Neurology, Hôpital de la Citadelle, Liege, Belgium.
Ann Neurol. 1991 Jul;30(1):83-9. doi: 10.1002/ana.410300115.
The spinal Ib interneuron efficacy has been compared in 11 control subjects and 19 patients with parkinsonian rigidity. In normal subjects, gastrocnemius medialis nerve stimulation induces an inhibition of the soleus H reflex for 3 to 8 msec with a peak at 5 msec of 83.72 +/- 7.28% of the control value of H reflex. In parkinsonian patients, inhibition is reduced or even replaced by facilitation, which also peaks at 5 msec. The departures from normal values correlate with rigidity intensity assessed by the Webster scale. Increase in rigidity is associated, first, with a reduction of inhibition and, from a score of 2 or more, with facilitation replacing the normal inhibition. In addition to providing an electrophysiological index of rigidity, reduction in autogenic inhibition might be one of the neurophysiological mechanisms underlying rigidity. In association with the known hyperactivity of the Ia inhibitory interneuron in Parkinson's disease, reduction of activity of Ib interneuron could be explained by an increased activity in the reticularis gigantocellularis nucleus; its efferent tracts both inhibit Ib interneurons and activate Ia interneurons.
对11名对照受试者和19名帕金森病僵硬患者的脊髓Ib中间神经元效能进行了比较。在正常受试者中，刺激腓肠内侧神经会导致比目鱼肌H反射被抑制3至8毫秒，在5毫秒时达到峰值，为H反射对照值的83.72±7.28%。在帕金森病患者中，抑制作用减弱甚至被易化作用取代，易化作用也在5毫秒时达到峰值。与正常值的偏差与用韦伯斯特量表评估的僵硬强度相关。僵硬程度增加首先与抑制作用减弱有关，当分数达到2分或更高时，则与易化作用取代正常抑制作用有关。除了提供僵硬的电生理指标外，自生抑制作用的降低可能是僵硬背后的神经生理机制之一。与帕金森病中已知的Ia抑制性中间神经元活动亢进相关，Ib中间神经元活动的降低可以通过巨细胞网状核活动增加来解释；其传出纤维既抑制Ib中间神经元，又激活Ia中间神经元。
