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正常受试者重复磁刺激后皮质水平电活动的传播

Spread of electrical activity at cortical level after repetitive magnetic stimulation in normal subjects.

作者信息

Lorenzano C, Gilio F, Inghilleri M, Conte A, Fofi L, Manfredi M, Berardelli A

机构信息

Dipartimento Scienze Neurologiche, Università di Roma La Sapienza, Viale dell'Università, 30, 00185 Rome, Italy.

出版信息

Exp Brain Res. 2002 Nov;147(2):186-92. doi: 10.1007/s00221-002-1237-z. Epub 2002 Sep 20.

DOI:10.1007/s00221-002-1237-z
PMID:12410333
Abstract

In normal subjects, focal repetitive transcranial magnetic stimulation (rTMS) of the hand motor area evokes muscle potentials (MEPs) from muscles in the hand (target muscles) and the arm (non-target muscles). In this study we investigated the mechanisms underlying the spread of MEPs induced by focal rTMS in non-target muscles. rTMS was delivered with a Magstim stimulator and a figure-of-eight coil placed over the first dorsal interosseus (FDI) motor area of the left hemisphere. Trains of 10 stimuli were given at a suprathreshold intensity (120% of motor threshold) and at frequencies of 5, 10 and 20 Hz at rest. Electromyographic (EMG) activity was recorded simultaneously from the FDI (target muscle) and the contralateral biceps muscle and from the FDI muscle ipsilateral to the side of stimulation (non-target muscle). rTMS delivered in trains to the FDI motor area of the left hemisphere elicited MEPs in the contralateral FDI (target muscle) that gradually increased in amplitude over the course of the train. Focal rTMS trains also induced MEPs in the contralateral biceps (non-target muscle) but did so only after the second or third stimulus; like target-muscle MEPs, in non-target muscle MEPs progressively increased in amplitude during the train. At no frequency did rTMS elicit MEPs in the FDI muscle ipsilateral to the site of stimulation. rTMS left the latency of EMG responses in the FDI and biceps muscles unchanged during the trains of stimuli. The latency of biceps MEPs was longer after rTMS than after a single TMS pulse. In conditioning-test experiments designed to investigate the cortical origin of the spread, a single TMS pulse delivered over the left hemisphere at an interstimulus interval (ISI) of 50, 100 and 150 ms reduced the amplitude of the test MEP evoked by a single TMS pulse delivered over the right hemisphere; and a conditioning rTMS train delivered over the left hemisphere increased the amplitude of the test MEP evoked by a single TMS pulse over the right hemisphere. A conditioning rTMS train delivered over the left hemisphere and paired magnetic shocks (test stimulus) at 3 and 13 ms ISIs over the right hemisphere reduced MEP inhibition at the 3-ms ISI but left the MEP facilitation at 13 ms unchanged. Using a control MEP size matched with that observed after a conditioning contralateral rTMS, we found that paired-pulse inhibition remained unchanged. Yet a single TMS conditioning pulse sufficiently strong to evoke a MEP in the contralateral FDI and biceps muscles simultaneously (as rTMS did) left paired-pulse inhibition unchanged. We conclude that the spread of EMG activity to non-target muscles depends on cortical mechanisms, mainly including changes in the excitability of the interneurones mediating intracortical inhibition.

摘要

在正常受试者中,对手部运动区进行局灶性重复经颅磁刺激(rTMS)可诱发手部(目标肌肉)和手臂(非目标肌肉)肌肉的肌电图(MEP)。在本研究中,我们调查了局灶性rTMS在非目标肌肉中诱发MEP传播的潜在机制。使用Magstim刺激器和放置在左半球第一背侧骨间肌(FDI)运动区的八字形线圈进行rTMS。在静息状态下,以阈上强度(运动阈值的120%)和5、10和20Hz的频率给予10次刺激的序列。同时从FDI(目标肌肉)、对侧肱二头肌以及刺激侧同侧的FDI肌肉(非目标肌肉)记录肌电图(EMG)活动。对左半球FDI运动区进行序列rTMS可在对侧FDI(目标肌肉)中诱发MEP,其幅度在序列过程中逐渐增加。局灶性rTMS序列也可在对侧肱二头肌(非目标肌肉)中诱发MEP,但仅在第二次或第三次刺激后才出现;与目标肌肉MEP一样,非目标肌肉MEP在序列过程中幅度逐渐增加。在刺激部位同侧的FDI肌肉中,rTMS在任何频率下均未诱发MEP。在刺激序列期间,rTMS未改变FDI和肱二头肌中EMG反应的潜伏期。rTMS后肱二头肌MEP的潜伏期比单次经颅磁刺激(TMS)脉冲后更长。在旨在研究传播的皮层起源的条件-测试实验中,在左半球以50、100和150ms的刺激间隔(ISI)给予单个TMS脉冲,可降低右半球单个TMS脉冲诱发的测试MEP的幅度;在左半球给予条件性rTMS序列可增加右半球单个TMS脉冲诱发的测试MEP的幅度。在左半球给予条件性rTMS序列,并在右半球以3和13ms的ISI给予配对磁刺激(测试刺激),可减少3ms ISI时的MEP抑制,但13ms时的MEP易化不变。使用与对侧条件性rTMS后观察到的MEP大小匹配的对照MEP大小,我们发现配对脉冲抑制保持不变。然而,单个TMS条件性脉冲强度足以同时在对侧FDI和肱二头肌中诱发MEP(如rTMS那样)时,配对脉冲抑制不变。我们得出结论,EMG活动向非目标肌肉的传播取决于皮层机制,主要包括介导皮层内抑制的中间神经元兴奋性的变化。

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