Oscillatory beta activity mediates neuroplastic effects of motor cortex stimulation in humans.
Oscillatory beta activity mediates neuroplastic effects of motor cortex stimulation in humans.
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DOI：
10.1523/jneurosci.5624-12.2013
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发表时间：
2013-05-01
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影响因子：
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通讯作者：
Hall SD
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作者：
McAllister CJ;Rönnqvist KC;Stanford IM;Woodhall GL;Furlong PL;Hall SD
连续θ突发刺激（cTBS）是一种重复经颅磁刺激方案，可抑制人类运动皮层（M1）兴奋性并损害运动≤1小时。虽然这些神经塑性效应为大脑功能和潜在治疗益处提供了宝贵的见解，但个体之间差异很大。这种变异性的来源以及抑制性后遗症的电生理机制在很大程度上尚不清楚。在这方面，β频率（15-35 Hz）的振荡活动特别令人感兴趣，因为它在帕金森病等运动障碍中会升高，并在运动产生过程中受到调节。在这里，我们使用源级脑磁图方法来研究以下假设：cTBS 后神经塑性效应的存在与振荡 M1 β 活性的同时变化相关。 M1 皮质通过视觉提示食指运动的合成孔径磁力波束形成分析进行定位。使用虚拟电极分析重建 cTBS 之前和之后 10 至 45 分钟双边 M1 皮质的自发和运动相关振荡活动。我们证明，对 8/16 名参与者的左侧 M1 施加 40 秒的 cTBS 降低了右侧食指的皮质脊髓兴奋性。仅在这些响应者参与者中，cTBS 增加了受刺激 M1 中自发 β 振荡的功率，并延迟了对侧食指的反应时间。与运动相关的β振荡的潜伏期或功率没有观察到进一步的变化。这些数据提供了对 cTBS 介导的运动功能损伤背后的电生理机制的见解，并证明了 M1 自发振荡 β 活性与运动功能抑制之间的关联。
Continuous theta burst stimulation (cTBS) is a repetitive transcranial magnetic stimulation protocol that can inhibit human motor cortex (M1) excitability and impair movement for ≤1 h. While offering valuable insights into brain function and potential therapeutic benefits, these neuroplastic effects are highly variable between individuals. The source of this variability, and the electrophysiological mechanisms underlying the inhibitory after-effects, are largely unknown. In this regard, oscillatory activity at beta frequency (15–35 Hz) is of particular interest as it is elevated in motor disorders such as Parkinson’s disease and modulated during the generation of movements. Here, we used a source-level magnetoencephalography approach to investigate the hypothesis that the presence of neuroplastic effects following cTBS is associated with concurrent changes in oscillatory M1 beta activity. M1 cortices were localized with a synthetic aperture magnetometry beamforming analysis of visually cued index finger movements. Virtual electrode analysis was used to reconstruct the spontaneous and movement-related oscillatory activity in bilateral M1 cortices, before and from 10 to 45 min after cTBS. We demonstrate that 40 s of cTBS applied over left M1 reduced corticospinal excitability in the right index finger of 8/16 participants. In these responder participants only, cTBS increased the power of the spontaneous beta oscillations in stimulated M1 and delayed reaction times in the contralateral index finger. No further changes were observed in the latency or power of movement-related beta oscillations. These data provide insights into the electrophysiological mechanisms underlying cTBS-mediated impairment of motor function and demonstrate the association between spontaneous oscillatory beta activity in M1 and the inhibition of motor function.