Journal
CLINICAL NEUROPHYSIOLOGY
Volume 127, Issue 6, Pages 2414-2422Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.clinph.2016.03.005
Keywords
EEG; Unconsciousness; Ketamine; Anesthesia; Slow oscillations; Gamma oscillations
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Funding
- National Institutes of Health, Bethesda, Maryland [DP2-OD006454, DP1-OD003646, TR01-GM104948]
- Foundation of Anesthesia Education and Research, Rochester, Minnesota
- Massachusetts General Hospital Faculty Development Award, Boston, MA
- Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA
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Objectives: 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. Methods: 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. Results: 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 (similar to 27-40 Hz) oscillations. This pattern was also associated with increased theta oscillations (similar to 4-8 Hz) and decreased alpha/beta oscillations (similar to 10-24 Hz). Conclusions: Ketamine anesthesia-induced unconsciousness is associated with a gamma burst EEG pattern. Significance: The EEG signature of ketamine anesthesia-induced unconsciousness may offer new insights into NMDA circuit mechanisms for unconsciousness. (C) 2016 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
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