MacKinnon C D, Rothwell J C
MRC Human Movement and Balance Unit, Institute of Neurology, Queen Square, London WC1N 3BG, UK.
J Physiol. 2000 Nov 1;528(Pt 3):633-45. doi: 10.1111/j.1469-7793.2000.00633.x.
Nine healthy subjects performed single rapid wrist movements from neutral to targets at 20 deg of flexion or extension in response to an auditory cue. Surface EMG was recorded from the wrist flexors and extensors together with wrist position. Movements in both directions were characterised by the usual triphasic pattern of EMG activity in agonist (AG1), antagonist (ANTAG) and again in agonist (AG2) muscles. Single pulses of transcranial magnetic stimulation (TMS) were applied over the motor cortex at an intensity of 80 % of resting threshold at random times between 80 and 380 ms after the cue. We measured the peak-to-peak amplitude of the evoked motor potential (MEP) and the integrated EMG (IEMG) activity that preceded the MEP. In a separate set of experiments H reflexes were elicited in the wrist flexors instead of MEPs. MEP amplitudes in the agonist muscle increased by an average of 10 +/- 8 ms (range -1 to 23 ms) prior to the onset of the AG1 burst and were associated with an increase of over sevenfold in the MEP:IEMG ratio, irrespective of movement direction. Agonist H reflex amplitudes were linearly related to, and increased at the same time as, changes in agonist IEMG. The principal ANTAG burst was not preceded by an increase in the antagonist muscle MEP:IEMG ratio. No relationship was found between the amplitude of the antagonist H reflexes and the preceding antagonist IEMG. Five subjects showed an increase in the MEP:IEMG ratio preceding and during the initial part of the AG2 burst. Our method of analysis shows that changes in motor cortical excitability mediating the initiation of movement occur much closer to the onset of EMG activity (less than 23 ms) than the 80-100 ms lead time previously reported. The lack of such changes before the onset of the ANTAG burst suggests that this may be initiated by a different, perhaps subcortical, mechanism.
九名健康受试者在听到听觉提示后,从自然状态进行单次快速腕部运动,分别向20度屈曲或伸展的目标位置移动。同时记录腕部屈肌和伸肌的表面肌电图以及腕部位置。两个方向的运动均表现出激动肌(AG1)、拮抗肌(ANTAG)以及再次激动肌(AG2)中常见的三相肌电图活动模式。在提示音后80至380毫秒之间的随机时间,以静息阈值的80%强度对运动皮层施加单脉冲经颅磁刺激(TMS)。我们测量了诱发运动电位(MEP)的峰峰值幅度以及MEP之前的积分肌电图(IEMG)活动。在另一组实验中,在腕部屈肌中诱发H反射而非MEP。激动肌中的MEP幅度在AG1爆发开始前平均增加了10±8毫秒(范围为-1至23毫秒),并且与MEP:IEMG比值增加超过七倍相关,与运动方向无关。激动肌的H反射幅度与激动肌IEMG的变化呈线性相关且同时增加。拮抗肌的主要爆发之前,拮抗肌MEP:IEMG比值没有增加。未发现拮抗肌H反射幅度与之前的拮抗肌IEMG之间存在关系。五名受试者在AG2爆发之前及初始阶段,MEP:IEMG比值增加。我们的分析方法表明,介导运动起始的运动皮层兴奋性变化发生的时间比之前报道的80 - 100毫秒的提前时间更接近肌电图活动的起始(小于23毫秒)。在ANTAG爆发开始之前缺乏这种变化表明,这可能是由不同的、也许是皮层下的机制启动的。