McNulty P A, Macefield V G, Taylor J L, Hallett M
Prince of Wales Medical Research Institute and University of New South Wales, Sydney, NSW, Australia.
J Physiol. 2002 Jan 1;538(Pt 1):279-88. doi: 10.1113/jphysiol.2001.013200.
Reorganisation of the motor cortex may occur after limb amputation or spinal cord injury. In humans, transcranial magnetic stimulation (TMS) shows expansion of motor cortical representations of muscles proximal to the injury. Similarly, ischaemic block of the hand can increase acutely the representation of the biceps muscle, measured by increased biceps motor potentials evoked by TMS. It is thought that this increase occurs at the expense of the cortical representation of the paralysed and deafferented hand muscles but this has never been investigated. To study what changes occur in the cortical representation of the hand muscles during ischaemic block, a tungsten microelectrode was inserted into the ulnar or median nerve above the elbow and the size of the neural potential elicited by TMS in fascicles supplying the hand was measured in seven subjects. Prior to ischaemia, TMS evoked EMG responses in the intrinsic hand muscles. In the nerve, a brief motor potential preceded the response in the muscle and was followed by a contraction-induced sensory potential. During 40 min of ischaemia produced by a blood pressure cuff inflated around the forearm to 210 mmHg, the EMG response to TMS and the sensory potential from the hand were progressively blocked. However, the motor neural evoked potential showed a significant increase in amplitude during the ischaemic period (30.5 %, P = 0.005). The increase in the neural potential suggests that output to the hand evoked from the cortex by TMS was not decreased by ischaemic block. Thus, we conclude that the increased response of biceps to TMS during distal ischaemia is not accompanied by a corresponding decrease in the motor cortical representation of the hand.
肢体截肢或脊髓损伤后,运动皮层可能会发生重组。在人类中,经颅磁刺激(TMS)显示损伤近端肌肉的运动皮层表征会扩大。同样,手部缺血性阻滞可使肱二头肌的表征急性增加,这通过TMS诱发的肱二头肌运动电位增加来衡量。据认为,这种增加是以瘫痪和去传入的手部肌肉的皮层表征为代价发生的,但这从未得到过研究。为了研究缺血性阻滞期间手部肌肉的皮层表征会发生什么变化,将一根钨微电极插入肘部上方的尺神经或正中神经,并在7名受试者中测量了TMS在供应手部的神经束中诱发的神经电位大小。在缺血之前,TMS在手内肌中诱发肌电图反应。在神经中,一个短暂的运动电位先于肌肉中的反应出现,随后是收缩诱发的感觉电位。在前臂周围用血压袖带充气至210 mmHg产生40分钟缺血期间,对TMS的肌电图反应和来自手部的感觉电位逐渐被阻断。然而,运动神经诱发电位在缺血期间幅度显著增加(30.5%,P = 0.005)。神经电位的增加表明,TMS从皮层诱发的对手部的输出并未因缺血性阻滞而减少。因此,我们得出结论,远端缺血期间肱二头肌对TMS的反应增加并未伴随着手部运动皮层表征的相应减少。