无意识
氯胺酮
脑电图
麻醉
麻醉剂
NMDA受体
医学
神经科学
心理学
内科学
受体
作者
Oluwaseun Akeju,Andrew H. Song,Allison E. Hamilos,Kara J. Pavone,Francisco Flores,Emery N. Brown,Patrick L. Purdon
标识
DOI:10.1016/j.clinph.2016.03.005
摘要
Ketamine is an N-methyl-d-aspartate (NMDA) receptor antagonist commonly administered as a general anesthetic. However, neural circuit mechanisms to explain ketamine anesthesia-induced unconsciousness in humans are yet to be clearly defined. Disruption of frontal–parietal network connectivity has been proposed as a mechanism to explain this brain state. However, this mechanism was recently demonstrated at subanesthetic doses of ketamine in awake-patients. Therefore, we investigated whether there is an electroencephalogram (EEG) signature specific for ketamine anesthesia-induced unconsciousness. We retrospectively studied the EEG in 12 patients who received ketamine for the induction of general anesthesia. We analyzed the EEG dynamics using power spectral and coherence methods. Following the administration of a bolus dose of ketamine to induce unconsciousness, we observed a “gamma burst” EEG pattern that consisted of alternating slow-delta (0.1–4 Hz) and gamma (∼27–40 Hz) oscillations. This pattern was also associated with increased theta oscillations (∼4–8 Hz) and decreased alpha/beta oscillations (∼10–24 Hz). Ketamine anesthesia-induced unconsciousness is associated with a gamma burst EEG pattern. The EEG signature of ketamine anesthesia-induced unconsciousness may offer new insights into NMDA circuit mechanisms for unconsciousness.
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