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Clin Neurophysiol. 2016 Jun;127(6):2414-22. doi: 10.1016/j.clinph.2016.03.005. Epub 2016 Mar 16.

Electroencephalogram signatures of ketamine anesthesia-induced unconsciousness.

Author information

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.

KEYWORDS:

Anesthesia; EEG; Gamma oscillations; Ketamine; Slow oscillations; Unconsciousness

PMID:
27178861
PMCID:
PMC4871620
DOI:
10.1016/j.clinph.2016.03.005
[Indexed for MEDLINE]
Free PMC Article

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