Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston MA, USA.
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston MA, USA.
Brain. 2020 Mar 1;143(3):833-843. doi: 10.1093/brain/awaa017.
How the brain recovers from general anaesthesia is poorly understood. Neurocognitive problems during anaesthesia recovery are associated with an increase in morbidity and mortality in patients. We studied intracortical neuronal dynamics during transitions from propofol-induced unconsciousness into consciousness by directly recording local field potentials and single neuron activity in a functionally and anatomically interconnecting somatosensory (S1, S2) and ventral premotor (PMv) network in primates. Macaque monkeys were trained for a behavioural task designed to determine trial-by-trial alertness and neuronal response to tactile and auditory stimulation. We found that neuronal dynamics were dissociated between S1 and higher-order PMv prior to return of consciousness. The return of consciousness was distinguishable by a distinctive return of interregionally coherent beta oscillations and disruption of the slow-delta oscillations. Clustering analysis demonstrated that these state transitions between wakefulness and unconsciousness were rapid and unstable. In contrast, return of pre-anaesthetic task performance was observed with a gradual increase in the coherent beta oscillations. We also found that recovery end points significantly varied intra-individually across sessions, as compared to a rather consistent loss of consciousness time. Recovery of single neuron multisensory responses appeared to be associated with the time of full performance recovery rather than the length of recovery time. Similar to loss of consciousness, return of consciousness was identified with an abrupt shift of dynamics and the regions were dissociated temporarily during the transition. However, the actual dynamics change during return of consciousness is not simply an inverse of loss of consciousness, suggesting a unique process.
大脑如何从全身麻醉中恢复尚不清楚。麻醉恢复期间的神经认知问题与患者的发病率和死亡率增加有关。我们通过直接记录局部场电位和在灵长类动物中功能和解剖上相互连接的体感（S1、S2）和腹侧运动前（PMv）网络中的单个神经元活动，研究了从异丙酚诱导的无意识到意识的转变过程中的皮质内神经元动力学。猕猴接受了一项行为任务的训练，旨在确定逐次试验的警觉性以及对触觉和听觉刺激的神经元反应。我们发现，在意识恢复之前，S1 和更高阶的 PMv 之间的神经元动力学是分离的。意识的恢复可以通过区域间相干β振荡的独特恢复和慢δ振荡的破坏来区分。聚类分析表明，这些清醒和无意识之间的状态转变是快速和不稳定的。相比之下，在相干β振荡逐渐增加的情况下，观察到麻醉前任务性能的恢复。我们还发现，与相对一致的意识丧失时间相比，个体间的恢复终点在各次试验中差异很大。多感觉反应的单个神经元恢复似乎与完全恢复性能的时间有关，而不是恢复时间的长短有关。与意识丧失相似，意识的恢复是通过动力学的突然转变来识别的，并且在过渡期间区域暂时分离。然而，意识恢复期间实际的动力学变化并不简单地是意识丧失的逆过程，这表明存在一个独特的过程。
