Physiology of modulation of motor cortex excitability by low-frequency suprathreshold repetitive transcranial magnetic stimulation
Physiology of modulation of motor cortex excitability by low-frequency suprathreshold repetitive transcranial magnetic stimulation
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DOI：
10.1007/s00221-005-0262-0
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发表时间：
2006-05-01
影响因子：
2
通讯作者：
Ziemann, U.
中科院分区：
文献类型：
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作者：
Heide, G.;Witte, O. W.;Ziemann, U.
许多研究一致表明，重复经颅磁刺激（rTMS）的频率为1 Hz，强度高于静息运动阈值（RMT）进行了几分钟以上的初级运动皮层（M1）导致皮质兴奋性的抑制。此外，大多数研究都同意促进非刺激对侧M1。然而，人们对这些影响背后的生理机制知之甚少。在11名健康志愿者中，我们用115%RMT的1Hz-rTMS刺激左侧M1 15分钟。在rTMS训练前、训练后即刻和训练后30 min，我们采用已建立的配对脉冲方案检查短间期皮质内抑制（SICI;刺激间间期（ISI）为2和4 ms）、皮质内易化（ICF; ISI 10 ms）和短间期皮质内易化（SICF; ISI 1.5 ms）。平均非条件运动诱发电位（MEP）的幅度和RMT也进行了测量。两个阶段至少间隔1周进行，在一个刺激的M1的兴奋性进行了测试，在另一个非刺激的M1的兴奋性。rTMS导致预期的MEP幅度的刺激M1，这是显着的，只有立即后rTMS列车。rTMS增加MEP振幅的非刺激的M1，持续至少30分钟。RMT，SICI，ICF和SICF没有显示任何显着的变化，无论是M1，除了一个长期持续增加的SICF在非刺激的M1。总之，MEP增加在非刺激M1持续时间长于MEP减少刺激M1。只有持久的MEP增加与皮质内兴奋性的特定变化（SICF增加）相关。运动皮层抑制的调制没有发挥作用，在解释rTMS引起的MEP幅度的变化。
Many studies show consistently that repetitive transcranial magnetic stimulation (rTMS) with a frequency of 1 Hz and an intensity above the resting motor threshold (RMT) performed for several minutes over the primary motor cortex (M1) leads to a depression of cortical excitability. Furthermore, most studies concur on a facilitation of the non-stimulated contralateral M1. Little is known, however, about the physiological mechanisms underlying these effects. In 11 healthy volunteers, we stimulated the left M1 for 15 min with 1 Hz-rTMS of 115% RMT. Before, immediately after, and 30 min after the rTMS train, we examined short-interval intracortical inhibition (SICI; interstimulus interval (ISI) of 2 and 4 ms), intracortical facilitation (ICF; ISI 10 ms), and short-interval intracortical facilitation (SICF; ISI 1.5 ms) with established paired-pulse protocols. Mean unconditioned motor evoked potential (MEP) amplitudes and RMT were also measured. Two sessions were run at least 1 week apart, in one excitability of the stimulated M1 was tested, in the other one excitability of the non-stimulated M1. rTMS led to the expected reduction of MEP amplitude of the stimulated M1, which was significant only immediately after the rTMS train. rTMS increased MEP amplitude of the non-stimulated M1, which lasted for at least 30 min. RMT, SICI, ICF and SICF did not show any significant change in either M1, except for a long lasting increase of SICF in the non-stimulated M1. In conclusion, the MEP increase in the non-stimulated M1 lasted longer than the MEP decrease in the stimulated M1. Only the long-lasting MEP increase was associated with a specific change in intracortical excitability (increase in SICF). Modulation of motor cortical inhibition did not play a role in explaining the rTMS induced changes in MEP amplitude.