Blain-Moraes Stefanie, Lee UnCheol, Ku SeungWoo, Noh GyuJeong, Mashour George A
Department of Anesthesiology, Center for Consciousness Science, University of Michigan Medical School Ann Arbor, MI, USA.
Department of Anesthesiology, Asan Medical Center, University of Ulsan College of Medicine Seoul, South Korea.
Front Syst Neurosci. 2014 Jul 1;8:114. doi: 10.3389/fnsys.2014.00114. eCollection 2014.
Recent studies of propofol-induced unconsciousness have identified characteristic properties of electroencephalographic alpha rhythms that may be mediated by drug activity at γ-aminobutyric acid (GABA) receptors in the thalamus. However, the effect of ketamine (a primarily non-GABAergic anesthetic drug) on alpha oscillations has not been systematically evaluated. We analyzed the electroencephalogram of 28 surgical patients during consciousness and ketamine-induced unconsciousness with a focus on frontal power, frontal cross-frequency coupling, frontal-parietal functional connectivity (measured by coherence and phase lag index), and frontal-to-parietal directional connectivity (measured by directed phase lag index) in the alpha bandwidth. Unlike past studies of propofol, ketamine-induced unconsciousness was not associated with increases in the power of frontal alpha rhythms, characteristic cross-frequency coupling patterns of frontal alpha power and slow-oscillation phase, or decreases in coherence in the alpha bandwidth. Like past studies of propofol using undirected and directed phase lag index, ketamine reduced frontal-parietal (functional) and frontal-to-parietal (directional) connectivity in the alpha bandwidth. These results suggest that directional connectivity changes in the alpha bandwidth may be state-related markers of unconsciousness induced by both GABAergic and non-GABAergic anesthetics.
近期关于丙泊酚诱导意识丧失的研究已经确定了脑电图α节律的特征属性,这些属性可能由丘脑γ-氨基丁酸(GABA)受体处的药物活性介导。然而,氯胺酮(一种主要非GABA能的麻醉药物)对α振荡的影响尚未得到系统评估。我们分析了28名外科手术患者在清醒状态和氯胺酮诱导的意识丧失状态下的脑电图,重点关注α频段的额叶功率、额叶交叉频率耦合、额顶叶功能连接(通过相干性和相位滞后指数测量)以及额顶叶方向连接(通过定向相位滞后指数测量)。与以往关于丙泊酚的研究不同,氯胺酮诱导的意识丧失与额叶α节律功率增加、额叶α功率和慢振荡相位的特征性交叉频率耦合模式无关,也与α频段相干性降低无关。与以往使用无向和定向相位滞后指数对丙泊酚的研究一样,氯胺酮降低了α频段的额顶叶(功能)和额顶叶(方向)连接。这些结果表明,α频段的方向连接变化可能是GABA能和非GABA能麻醉药诱导意识丧失的状态相关标志物。