Vlisides Phillip E, Bel-Bahar Tarik, Lee UnCheol, Li Duan, Kim Hyoungkyu, Janke Ellen, Tarnal Vijay, Pichurko Adrian B, McKinney Amy M, Kunkler Bryan S, Picton Paul, Mashour George A
From the Department of Anesthesiology (P.E.V., T.B.-B., U.L., D.L., H.K., E.J., V.T., A.M.M., B.S.K., P.P., G.A.M.), Center for Consciousness Science (P.E.V., T.B.-B., U.L., D.L., H.K., G.A.M.), and Neuroscience Graduate Program (G.A.M.), University of Michigan Medical School, Ann Arbor, Michigan; and the Department of Anesthesiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois (A.B.P.).
Anesthesiology. 2017 Jul;127(1):58-69. doi: 10.1097/ALN.0000000000001671.
Previous studies have demonstrated inconsistent neurophysiologic effects of ketamine, although discrepant findings might relate to differences in doses studied, brain regions analyzed, coadministration of other anesthetic medications, and resolution of the electroencephalograph. The objective of this study was to characterize the dose-dependent effects of ketamine on cortical oscillations and functional connectivity.
Ten healthy human volunteers were recruited for study participation. The data were recorded using a 128-channel electroencephalograph during baseline consciousness, subanesthetic dosing (0.5 mg/kg over 40 min), anesthetic dosing (1.5 mg/kg bolus), and recovery. No other sedative or anesthetic medications were administered. Spectrograms, topomaps, and functional connectivity (weighted and directed phase lag index) were computed and analyzed.
Frontal theta bandwidth power increased most dramatically during ketamine anesthesia (mean power ± SD, 4.25 ± 1.90 dB) compared to the baseline (0.64 ± 0.28 dB), subanesthetic (0.60 ± 0.30 dB), and recovery (0.68 ± 0.41 dB) states; P < 0.001. Gamma power also increased during ketamine anesthesia. Weighted phase lag index demonstrated theta phase locking within anterior regions (0.2349 ± 0.1170, P < 0.001) and between anterior and posterior regions (0.2159 ± 0.1538, P < 0.01) during ketamine anesthesia. Alpha power gradually decreased with subanesthetic ketamine, and anterior-to-posterior directed connectivity was maximally reduced (0.0282 ± 0.0772) during ketamine anesthesia compared to all other states (P < 0.05).
Ketamine anesthesia correlates most clearly with distinct changes in the theta bandwidth, including increased power and functional connectivity. Anterior-to-posterior connectivity in the alpha bandwidth becomes maximally depressed with anesthetic ketamine administration, suggesting a dose-dependent effect.
先前的研究表明氯胺酮的神经生理效应不一致,尽管不同的研究结果可能与所研究的剂量、分析的脑区、其他麻醉药物的联合使用以及脑电图的分辨率差异有关。本研究的目的是描述氯胺酮对皮质振荡和功能连接的剂量依赖性效应。
招募10名健康人类志愿者参与研究。在基线清醒、亚麻醉剂量给药(40分钟内给予0.5mg/kg)、麻醉剂量给药(1.5mg/kg静脉推注)和恢复期间,使用128通道脑电图记录数据。未给予其他镇静或麻醉药物。计算并分析频谱图、脑电地形图和功能连接(加权和定向相位滞后指数)。
与基线(0.64±0.28dB)、亚麻醉(0.60±0.30dB)和恢复(0.68±0.41dB)状态相比,氯胺酮麻醉期间额叶θ频段带宽功率增加最为显著(平均功率±标准差,4.25±1.90dB);P<0.001。氯胺酮麻醉期间γ功率也增加。加权相位滞后指数显示,氯胺酮麻醉期间,前部区域内(0.2349±0.1170,P<0.001)以及前部和后部区域之间(0.2159±0.1538,P<0.01)存在θ相位锁定。亚麻醉剂量氯胺酮使α功率逐渐降低,与所有其他状态相比,氯胺酮麻醉期间前后部定向连接性最大程度降低(0.0282±0.0772)(P<0.05)。
氯胺酮麻醉与θ频段带宽的明显变化最密切相关,包括功率增加和功能连接增强。麻醉剂量氯胺酮给药后,α频段的前后部连接性最大程度降低,提示存在剂量依赖性效应。