Baldissera F, Cavallari P, Dworzak F
Istituto di Fisiologia Umana II, Università di Milano, Italy.
Brain. 1994 Oct;117 ( Pt 5):929-39. doi: 10.1093/brain/117.5.929.
In three patients suffering from chronic muscle cramps, spasms and myokymia, these involuntary contractions were triggered in the triceps surae, quadriceps, flexor carpi radialis or flexor digitorum by means of single or short-train stimulation of homonymous Ia afferents, elicited by electrical means or tendon taps. In some cases cramp was induced by the first afferent volleys; more often, however, continued stimulation produced stepwise recruitment of motor units (whose rhythmic firing was visible as myokymia in the muscle) until cramp developed. Cramps and myokymic discharges could usually be terminated by a single maximal stimulus to the motor axons (producing antidromic invasion and Renshaw inhibition of the motor neurons), or by short trains of volleys in inhibitory pathways from the skin. The fact that it was possible to induce myokymia and cramps by brief synaptic excitation and terminate them by antidromic invasion or synaptic inhibition, suggests that the mechanism generating these disturbances is intrinsic to alpha-motor neuron somata. Similar on-off switching of self-sustained motor discharges has been observed in the decerebrate cat and is known to depend on 'bistability' of the motor neuron membrane. We propose that a similar mechanism is responsible for discharges that produce cramp.
在三名患有慢性肌肉痉挛、抽搐和肌束震颤的患者中，通过对同名Ia传入神经进行单次或短串刺激（通过电刺激或轻叩肌腱引发），在腓肠肌、股四头肌、桡侧腕屈肌或指屈肌中引发了这些不自主收缩。在某些情况下，第一次传入冲动就诱发了痉挛；然而，更常见的是，持续刺激会逐步募集运动单位（其节律性放电在肌肉中表现为肌束震颤），直到痉挛发作。痉挛和肌束震颤放电通常可以通过对运动轴突的单次最大刺激（产生逆行性侵入并对运动神经元产生闰绍抑制），或通过来自皮肤的抑制性通路中的短串冲动来终止。通过短暂的突触兴奋能够诱发肌束震颤和痉挛，并通过逆行性侵入或突触抑制来终止它们，这一事实表明，产生这些紊乱的机制是α运动神经元胞体所固有的。在去大脑猫中也观察到了类似的自维持运动放电的开-关切换，并且已知这取决于运动神经元膜的“双稳态”。我们提出，类似的机制导致了产生痉挛的放电。
