Wang Haidong, Zhang Yun, Cheng Huanhuan, Yan Fei, Song Dawei, Wang Qiang, Cai Suping, Wang Yubo, Huang Liyu
School of Life Science and Technology, Xidian University, No. 2 South Taibai Road, Xi'an, 710071 China.
Department of Anesthesiology & Center for Brain Science, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 West Yanta Road, Xi'an, 710061 China.
Cogn Neurodyn. 2022 Oct;16(5):1029-1043. doi: 10.1007/s11571-021-09775-x. Epub 2022 Jan 26.
We comprehensively studied directional feedback and feedforward connectivity to explore potential connectivity changes that underlie propofol-induced deep sedation. We further investigated the corticocortical connectivity patterns within and between hemispheres. Sixty-channel electroencephalographic data were collected from 19 healthy volunteers in a resting wakefulness state and propofol-induced deep unconsciousness state defined by a bispectral index value of 40. A source analysis was employed to locate cortical activity. The Desikan-Killiany atlas was used to partition cortices, and directional functional connectivity was assessed by normalized symbolic transfer entropy between higher-order (prefrontal and frontal) and lower-order (auditory, sensorimotor and visual) cortices and between hot-spot frontal and parietal cortices. We found that propofol significantly suppressed feedforward connectivity from the left parietal to right frontal cortex and bidirectional connectivity between the left frontal and left parietal cortex, between the frontal and auditory cortex, and between the frontal and sensorimotor cortex. However, there were no significant changes in either feedforward or feedback connectivity between the prefrontal and all the lower-order cortices and between the frontal and visual cortices or in feedback connectivity from the frontal to parietal cortex. Propofol anesthetic selectively decreased the unidirectional interaction between higher-order frontoparietal cortices and bidirectional interactions between the higher-order frontal cortex and lower-order auditory and sensorimotor cortices, which indicated that both feedback and feedforward connectivity were suppressed under propofol-induced deep sedation. Our findings provide critical insights into the connectivity changes underlying the top-down mechanism of propofol anesthesia at deep sedation.
The online version contains supplementary material available at 10.1007/s11571-021-09775-x.
我们全面研究了定向反馈和前馈连接性，以探索丙泊酚诱导深度镇静背后潜在的连接性变化。我们进一步研究了半球内和半球间的皮质皮质连接模式。从19名健康志愿者身上收集了60通道脑电图数据，这些志愿者处于静息清醒状态以及由脑电双频指数值为40定义的丙泊酚诱导深度无意识状态。采用源分析来定位皮质活动。使用Desikan-Killiany图谱对皮质进行划分，并通过高阶（前额叶和额叶）与低阶（听觉、感觉运动和视觉）皮质之间以及热点额叶和顶叶皮质之间的归一化符号转移熵来评估定向功能连接性。我们发现，丙泊酚显著抑制了从左顶叶到右额叶皮质的前馈连接性以及左额叶与左顶叶皮质之间、额叶与听觉皮质之间以及额叶与感觉运动皮质之间的双向连接性。然而，前额叶与所有低阶皮质之间以及额叶与视觉皮质之间的前馈或反馈连接性均无显著变化，额叶到顶叶皮质的反馈连接性也无显著变化。丙泊酚麻醉选择性地降低了高阶额顶叶皮质之间的单向相互作用以及高阶额叶皮质与低阶听觉和感觉运动皮质之间的双向相互作用，这表明在丙泊酚诱导的深度镇静下，反馈和前馈连接性均受到抑制。我们的研究结果为丙泊酚麻醉深度镇静下自上而下机制背后的连接性变化提供了关键见解。
在线版本包含可在10.1007/s11571-021-09775-x获取的补充材料。
