Oluwaseun Akeju1, Andrew H Song2, Allison E Hamilos3, Kara J Pavone4, Francisco J Flores5, Emery N Brown6, Patrick L Purdon5. 1. Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA. Electronic address: oluwaseun.akeju@mgh.harvard.edu. 2. Department of Brain and Cognitive Science, Massachusetts Institute of Technology, Cambridge, MA, USA. 3. Harvard Medical School, Boston, MA, USA; Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA, USA; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. 4. Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA. 5. Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Department of Brain and Cognitive Science, Massachusetts Institute of Technology, Cambridge, MA, USA. 6. Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Department of Brain and Cognitive Science, Massachusetts Institute of Technology, Cambridge, MA, USA; Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA, USA; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
Abstract
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 (0.1-4Hz) and gamma (∼27-40Hz) oscillations. This pattern was also associated with increased theta oscillations (∼4-8Hz) and decreased alpha/beta oscillations (∼10-24Hz). 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.
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 (0.1-4Hz) and gamma (∼27-40Hz) oscillations. This pattern was also associated with increased theta oscillations (∼4-8Hz) and decreased alpha/beta oscillations (∼10-24Hz). 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.
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