From the Turku PET Centre, University of Turku and the Hospital District of Southwest Finland, Turku, Finland (A.S., K.K., J.L., A.M., H.S.) the Department of Perioperative Services, Intensive Care and Pain Medicine, Turku University Hospital, Turku, Finland (A.S., R.E.K., M.K., A.M., H.S.) the Department of Psychology and Speech-Language Pathology, and Turku Brain and Mind Center (R.E.K., K.V., A.R.) the Department of Pharmacology, Drug Development and Therapeutics (H.S.) University of Turku, Turku, Finland; the Department of Anesthesiology, Center for Consciousness Science, University of Michigan Medical School, Ann Arbor, Michigan (D.L., G.A.M.) the Department of Anesthesiology and Intensive Care, Oulu University Hospital, Oulu, Finland (K.K.) the Department of Intensive Care, Tampere University Hospital, Tampere, Finland (J.L.) the Department of Clinical Medicine, Biostatistics, University of Turku and Turku University Hospital, Turku, Finland (T.V.) the Department of Cognitive Neuroscience and Philosophy, School of Bioscience, University of Skövde, Skövde, Sweden (K.V., A.R.).
Anesthesiology. 2018 Jul;129(1):22-36. doi: 10.1097/ALN.0000000000002192.
Differentiating drug-related changes and state-related changes on the electroencephalogram during anesthetic-induced unconsciousness has remained a challenge. To distinguish these, we designed a rigorous experimental protocol with two drugs known to have distinct molecular mechanisms of action. We hypothesized that drug- and state-related changes can be separated.
Forty-seven healthy participants were randomized to receive dexmedetomidine (n = 23) or propofol (n = 24) as target-controlled infusions until loss of responsiveness. Then, an attempt was made to arouse the participant to regain responsiveness while keeping the drug infusion constant. Finally, the concentration was increased 1.5-fold to achieve presumable loss of consciousness. We conducted statistical comparisons between the drugs and different states of consciousness for spectral bandwidths, and observed how drug-induced electroencephalogram patterns reversed upon awakening. Cross-frequency coupling was also analyzed between slow-wave phase and alpha power.
Eighteen (78%) and 10 (42%) subjects were arousable during the constant drug infusion in the dexmedetomidine and propofol groups, respectively (P = 0.011 between the drugs). Corresponding with deepening anesthetic level, slow-wave power increased, and a state-dependent alpha anteriorization was detected with both drugs, especially with propofol. The slow-wave and frontal alpha activities were momentarily disrupted as the subjects regained responsiveness at awakening. Negative phase-amplitude coupling before and during loss of responsiveness frontally and positive coupling during the highest drug concentration posteriorly were observed in the propofol but not in the dexmedetomidine group.
Electroencephalogram effects of dexmedetomidine and propofol are strongly drug- and state-dependent. Changes in slow-wave and alpha activity seemed to best detect different states of consciousness.
在麻醉诱导的无意识状态下，区分与药物相关的变化和与状态相关的变化一直是一个挑战。为了区分这些变化，我们设计了一个严格的实验方案，使用两种已知具有不同作用机制的药物。我们假设可以区分药物相关和状态相关的变化。
47 名健康参与者被随机分为接受右美托咪定（n = 23）或异丙酚（n = 24）作为靶控输注，直到失去反应性。然后，尝试唤醒参与者以恢复反应性，同时保持药物输注不变。最后，将浓度增加 1.5 倍以达到可能的意识丧失。我们对药物和不同意识状态的光谱带宽进行了统计比较，并观察了药物诱导的脑电图模式在唤醒时如何逆转。还分析了慢波相位和α功率之间的跨频耦合。
在右美托咪定和异丙酚组中，分别有 18 名（78%）和 10 名（42%）受试者在药物输注不变时可被唤醒（药物之间 P = 0.011）。随着麻醉深度的加深，慢波功率增加，两种药物都检测到与状态相关的α前移位，异丙酚尤其明显。当受试者在唤醒时恢复反应性时，慢波和额部α活动暂时中断。在异丙酚但不在右美托咪定组中，观察到在前额和失响应期间的负相位-振幅耦合以及在后部最高药物浓度期间的正耦合。
右美托咪定和异丙酚的脑电图效应强烈依赖于药物和状态。慢波和α活动的变化似乎最能检测不同的意识状态。
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