Cortical mechanisms of loss of consciousness: insight from TMS/EEG studies
Cortical mechanisms of loss of consciousness: insight from TMS/EEG studies
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DOI：
10.4449/aib.v150i2.1361
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发表时间：
2012-06-01
影响因子：
1
通讯作者：
Tononi, G.
中科院分区：
文献类型：
--
作者：
Massimini, M.;Ferrarelli, F.;Tononi, G.
在最近的一系列实验中，我们通过结合经颅磁刺激 (TMS) 和高密度脑电图 (hd-EEG) 记录了人类在清醒、非快速眼动睡眠、快速眼动睡眠和麻醉期间对直接皮质刺激的脑电图 (EEG) 反应。 TMS/hd-EEG 测量表明，在清醒和快速眼动睡眠期间，大脑能够维持长期特定的激活模式，而在非快速眼动睡眠和咪达唑仑诱导的麻醉期间，当意识消退时，这种能力就会丧失：丘脑皮层系统尽管处于活跃和反应状态，但要么在因果独立的模块中崩溃（产生局部慢波），要么爆发成爆炸性和非特异性的。 反应（产生全球脑电图慢波）。我们假设，与自发睡眠慢波一样，TMS 在睡眠和麻醉期间触发的慢波是由于丘脑皮质回路中上状态和下状态之间的双稳态造成的。在这种情况下，初始激活后不可避免地会出现沉默、低落状态，这会损害丘脑皮质回路维持远程、差异化激活模式的能力，而这是意识的理论上的必要条件。根据动物实验和计算机模拟，丘脑皮质双稳定性可能是由于 K 电流增加、兴奋和抑制之间平衡的改变以及部分皮质传入神经阻滞造成的。我们假设这些因素可能在决定脑损伤受试者意识丧失和恢复方面发挥重要作用。如果是这种情况，某些类型的大脑损伤可能会通过诱导丘脑皮质系统中原本健康的部分的双稳态，从而损害信息传输，而不仅仅是相关的解剖学断开。
In a recent series of experiments we recorded the electroencephalogram (EEG) response to a direct cortical stimulation in humans during wakefulness, NREM sleep, REM sleep and anesthesia by means of a combination of transcranial magnetic stimulation (TMS) and high-density EEG (hd-EEG). TMS/hd-EEG measurements showed that, while during wakefulness and REM sleep the brain is able to sustain long-range specific patterns of activation, during NREM sleep and Midazolam-induced anesthesia, when consciousness fades, this ability is lost: the thalamocortical system, despite being active and reactive, either breaks down in causally independent modules (producing a local slow wave), or it bursts into an explosive and non-specific response (producing a global EEG slow wave). We hypothesize that, like spontaneous sleep slow waves, the slow waves triggered by TMS during sleep and anaesthesia are due to bistability between up- and down-states in thalamocortical circuits. In this condition, the inescapable occurrence of a silent, down state after an initial activation impairs the ability of thalamocortical circuits to sustain long-range, differentiated patterns of activation, a theoretical requisite for consciousness. According to animal experiments and computer simulations, thalamocortical bistability may result from increased K-currents, from alterations of the balance between excitation and inhibition and from partial cortical de-afferentation. We hypothesize that these factors may play an important role in determining loss, and recovery, of consciousness also in brain-injured subjects. If this is the case, some types of brain lesions may impair information transmission, above and beyond the associated anatomical disconnection, by inducing bistability in portions of the thalamocortical system that are otherwise healthy.