Coma Science Group, Cyclotron Research Centre and Neurology Department, University of Liège and Sart Tilman Hospital, 4000 Liège, Belgium.
J Neurosci. 2012 May 16;32(20):7082-90. doi: 10.1523/JNEUROSCI.3769-11.2012.
The mechanisms underlying anesthesia-induced loss of consciousness remain a matter of debate. Recent electrophysiological reports suggest that while initial propofol infusion provokes an increase in fast rhythms (from beta to gamma range), slow activity (from delta to alpha range) rises selectively during loss of consciousness. Dynamic causal modeling was used to investigate the neural mechanisms mediating these changes in spectral power in humans. We analyzed source-reconstructed data from frontal and parietal cortices during normal wakefulness, propofol-induced mild sedation, and loss of consciousness. Bayesian model selection revealed that the best model for explaining spectral changes across the three states involved changes in corticothalamic interactions. Compared with wakefulness, mild sedation was accounted for by an increase in thalamic excitability, which did not further increase during loss of consciousness. In contrast, loss of consciousness per se was accompanied by a decrease in backward corticocortical connectivity from frontal to parietal cortices, while thalamocortical connectivity remained unchanged. These results emphasize the importance of recurrent corticocortical communication in the maintenance of consciousness and suggest a direct effect of propofol on cortical dynamics.
麻醉诱导意识丧失的机制仍存在争议。最近的电生理学报告表明，虽然初始异丙酚输注会引起快节律（从β波到γ波范围）增加，但在意识丧失期间，慢波活动（从δ波到α波范围）选择性增加。动态因果建模用于研究介导这些人类光谱功率变化的神经机制。我们分析了正常清醒、异丙酚诱导的轻度镇静和意识丧失期间额皮质和顶皮质的源重建数据。贝叶斯模型选择表明，解释三个状态之间光谱变化的最佳模型涉及皮质丘脑相互作用的变化。与清醒相比，轻度镇静是由于丘脑兴奋性增加引起的，而在意识丧失期间并没有进一步增加。相比之下，意识丧失本身伴随着从前额皮质到顶皮质的皮质间向后连接的减少，而丘脑皮质连接保持不变。这些结果强调了在意识维持中反复皮质间通讯的重要性，并提示异丙酚对皮质动力学的直接影响。
