GIGA-Consciousness, Coma Science Group, Pain and Hypnosis, and Anesthesia and Intensive Care laboratories, GIGA Research, University and CHU University Hospital of Liège, Liège, Belgium.
Department of Algology and Palliative Care, CHU University Hospital of Liège, Liège, Belgium.
Br J Anaesth. 2017 Oct 1;119(4):674-684. doi: 10.1093/bja/aex257.
BACKGROUND: We used functional connectivity measures from brain resting state functional magnetic resonance imaging to identify human neural correlates of sedation with dexmedetomidine or propofol and their similarities with natural sleep. METHODS: Connectivity within the resting state networks that are proposed to sustain consciousness generation was compared between deep non-rapid-eye-movement (N3) sleep, dexmedetomidine sedation, and propofol sedation in volunteers who became unresponsive to verbal command. A newly acquired dexmedetomidine dataset was compared with our previously published propofol and N3 sleep datasets. RESULTS: In all three unresponsive states (dexmedetomidine sedation, propofol sedation, and N3 sleep), within-network functional connectivity, including thalamic functional connectivity in the higher-order (default mode, executive control, and salience) networks, was significantly reduced as compared with the wake state. Thalamic functional connectivity was not reduced for unresponsive states within lower-order (auditory, sensorimotor, and visual) networks. Voxel-wise statistical comparisons between the different unresponsive states revealed that thalamic functional connectivity with the medial prefrontal/anterior cingulate cortex and with the mesopontine area was reduced least during dexmedetomidine-induced unresponsiveness and most during propofol-induced unresponsiveness. The reduction seen during N3 sleep was intermediate between those of dexmedetomidine and propofol. CONCLUSIONS: Thalamic connectivity with key nodes of arousal and saliency detection networks was relatively preserved during N3 sleep and dexmedetomidine-induced unresponsiveness as compared to propofol. These network effects may explain the rapid recovery of oriented responsiveness to external stimulation seen under dexmedetomidine sedation. TRIAL REGISTRY NUMBER: Committee number: 'Comité d'Ethique Hospitalo-Facultaire Universitaire de Liège' (707); EudraCT number: 2012-003562-40; internal reference: 20121/135; accepted on August 31, 2012; Chair: Prof G. Rorive. As it was considered a phase I clinical trial, this protocol does not appear on the EudraCT public website.
背景：我们使用脑静息态功能磁共振成像的功能连接测量来识别右美托咪定或丙泊酚镇静的人类神经相关性，并研究其与自然睡眠的相似性。
方法：在对言语命令无反应的志愿者中，比较深度非快速眼动（N3）睡眠、右美托咪定镇静和丙泊酚镇静时，被认为维持意识产生的静息态网络内的连接。一个新获得的右美托咪定数据集与我们之前发表的丙泊酚和 N3 睡眠数据集进行了比较。
结果：在所有三种无反应状态（右美托咪定镇静、丙泊酚镇静和 N3 睡眠）中，与清醒状态相比，网络内功能连接（包括高级（默认模式、执行控制和突显）网络中的丘脑功能连接）均显著降低。在较低阶（听觉、感觉运动和视觉）网络中，无反应状态的丘脑功能连接并未降低。不同无反应状态之间的体素统计比较显示，在右美托咪定诱导的无反应状态下，与内侧前额叶/前扣带回和中脑区域的丘脑功能连接减少最少，而在丙泊酚诱导的无反应状态下减少最多。N3 睡眠期间的减少介于右美托咪定和丙泊酚之间。
结论：与丙泊酚相比，在 N3 睡眠和右美托咪定诱导的无反应状态下，与觉醒和突显检测网络关键节点的丘脑连接相对保留。这些网络效应可能解释了在右美托咪定镇静下快速恢复对外界刺激的定向反应能力。
注册号：委员会编号：“Liège 大学医院伦理委员会”（707）；EudraCT 编号：2012-003562-40；内部参考号：20121/135；2012 年 8 月 31 日接受；主席：G. Rorive 教授。由于它被认为是一项 I 期临床试验，因此该方案未出现在 EudraCT 公共网站上。
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