Department of Neurology, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany; Medical Faculty, University of Cologne, and Department of Neurology, University Hospital Cologne, Cologne, Germany; Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Centre Jülich, Jülich, Germany.
Medical Faculty, University of Cologne, and Department of Neurology, University Hospital Cologne, Cologne, Germany.
Brain Stimul. 2024 Jul-Aug;17(4):836-846. doi: 10.1016/j.brs.2024.07.008. Epub 2024 Jul 15.
Acute cerebral ischemia triggers a number of cellular mechanisms not only leading to excitotoxic cell death but also to enhanced neuroplasticity, facilitating neuronal reorganization and functional recovery.
Transferring these cellular mechanisms to neurophysiological correlates adaptable to patients is crucial to promote recovery post-stroke. The combination of TMS and EEG constitutes a promising readout of neuronal network activity in stroke patients.
We used the combination of TMS and EEG to investigate the development of local signal processing and global network alterations in 40 stroke patients with motor deficits alongside neural reorganization from the acute to the chronic phase.
We show that the TMS-EEG response reflects information about reorganization and signal alterations associated with persistent motor deficits throughout the entire post-stroke period. In the early post-stroke phase and in a subgroup of patients with severe motor deficits, TMS applied to the lesioned motor cortex evoked a sleep-like slow wave response associated with a cortical off-period, a manifestation of cortical bistability, as well as a rapid disruption of the TMS-induced formation of causal network effects. Mechanistically, these phenomena were linked to lesions affecting ascending activating brainstem fibers. Of note, slow waves invariably vanished in the chronic phase, but were highly indicative of a poor functional outcome.
In summary, we found evidence that transient effects of sleep-like slow waves and cortical bistability within ipsilesional M1 resulting in excessive inhibition may interfere with functional reorganization, leading to a less favorable functional outcome post-stroke, pointing to a new therapeutic target to improve recovery of function.
急性脑缺血不仅会引发一系列细胞机制，导致兴奋性细胞死亡，还会增强神经可塑性，促进神经元重组和功能恢复。
将这些细胞机制转化为适应患者的神经生理学相关性对于促进中风后恢复至关重要。TMS 和 EEG 的结合为中风患者的神经元网络活动提供了一种很有前途的读出方式。
我们使用 TMS 和 EEG 的组合来研究 40 名运动功能障碍的中风患者从急性期到慢性期的局部信号处理和全局网络变化的发展，以及神经重组。
我们表明，TMS-EEG 反应反映了与持续运动功能障碍相关的重组和信号变化的信息，贯穿整个中风后期间。在中风后的早期阶段和一部分运动功能严重障碍的患者中，应用于损伤运动皮层的 TMS 会引起类似睡眠的慢波反应，与皮层关闭期相关，这是皮层双稳态的表现，以及 TMS 诱导的因果网络效应形成的快速中断。从机制上讲，这些现象与影响上行激活脑干纤维的病变有关。值得注意的是，慢波在慢性期总是消失，但高度提示预后不良。
总之，我们发现证据表明，同侧 M1 中类似睡眠的慢波和皮质双稳态的短暂效应导致过度抑制，可能会干扰功能重组，导致中风后功能恢复不佳，为改善功能恢复指明了新的治疗靶点。
