Brown J C
J Neurol Neurosurg Psychiatry. 1974 Dec;37(12):1336-42. doi: 10.1136/jnnp.37.12.1336.
Changes in amplitude of the evoked muscle action potential (MAP) have been observed in four patients with myotonia congenita and two with dystrophia myotonica. A fade in the response occurred in every case with stimulus frequencies of 10 per second or less, provided that the muscle was in a rested state and that long enough stimulus trains were used. Intramuscular stimulation and recording techniques show that the myotonic muscle fibre is the site of this defect. The MAP fade is thought to represent the transient weakness from which such patients may suffer, particularly after rest. Since neither this weakness nor the fade was related to the severity of the myotonia, nor were they significantly influenced by cooling or hydantoins, they may well be due to a separate defect in the myotonic muscle from that which causes the hyperexcitability of the fibre membrane.
在4例先天性肌强直患者和2例强直性肌营养不良患者中观察到诱发性肌肉动作电位(MAP)振幅的变化。只要肌肉处于静息状态且使用足够长的刺激序列,在每秒10次或更低的刺激频率下,每例患者的反应都会出现衰减。肌内刺激和记录技术表明,肌强直肌纤维是该缺陷的部位。MAP衰减被认为代表了这些患者可能遭受的短暂性肌无力,尤其是在休息后。由于这种肌无力和衰减既与肌强直的严重程度无关,也不受冷却或苯妥英的显著影响,它们很可能是由肌强直肌肉中与导致纤维膜过度兴奋的缺陷不同的另一种缺陷引起的。