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 lot: 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 upand 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 factor 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.

中文翻译：

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失去知觉的皮质机制：TMS / EEG研究的见解。

在最近的一系列实验中，我们结合经颅磁刺激（TMS）和高密度脑电图（hd），记录了人在清醒，NREM睡眠，REM睡眠和麻醉期间对人类直接皮层刺激的脑电图（EEG）反应-EEG）。TMS / hd-EEG测量显示，尽管在清醒和REM睡眠期间，大脑能够维持长期的特定激活模式，但在NREM睡眠和咪达唑仑诱导的麻醉期间，当意识消失时，这种能力非常强大：丘脑皮质系统尽管是活跃的和反应性的，要么分解成因果独立的模块（产生局部慢波），要么爆发成爆炸性和非特定性的响应（产生整体EEG慢波）。我们假设，就像自发的睡眠慢波一样，TMS在睡眠和麻醉过程中触发的慢波是由于丘脑皮层回路的上下状态之间的双稳态引起的。在这种情况下，初始激活后不可避免地会出现无声的向下状态，这削弱了丘脑皮层回路维持远距离的，不同的激活模式的能力，这是意识的理论要求。根据动物实验和计算机模拟，丘脑皮层的双稳态可能是由于K电流增加，激发和抑制之间的平衡改变以及部分皮层脱除咖啡因而引起的。我们假设这些因素可能在确定脑部受伤者的意识丧失和恢复中起重要作用。如果是这种情况，某些类型的脑部病变可能会损害信息传输，