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Front Syst Neurosci. 2014 Jul 1;8:114. doi: 10.3389/fnsys.2014.00114. eCollection 2014.

Electroencephalographic effects of ketamine on power, cross-frequency coupling, and connectivity in the alpha bandwidth.

Author information

1
Department of Anesthesiology, Center for Consciousness Science, University of Michigan Medical School Ann Arbor, MI, USA.
2
Department of Anesthesiology, Asan Medical Center, University of Ulsan College of Medicine Seoul, South Korea.
3
Department of Anesthesiology, Center for Consciousness Science, University of Michigan Medical School Ann Arbor, MI, USA ; Neuroscience Graduate Program, University of Michigan Medical School Ann Arbor, MI, USA.

Abstract

Recent studies of propofol-induced unconsciousness have identified characteristic properties of electroencephalographic alpha rhythms that may be mediated by drug activity at γ-aminobutyric acid (GABA) receptors in the thalamus. However, the effect of ketamine (a primarily non-GABAergic anesthetic drug) on alpha oscillations has not been systematically evaluated. We analyzed the electroencephalogram of 28 surgical patients during consciousness and ketamine-induced unconsciousness with a focus on frontal power, frontal cross-frequency coupling, frontal-parietal functional connectivity (measured by coherence and phase lag index), and frontal-to-parietal directional connectivity (measured by directed phase lag index) in the alpha bandwidth. Unlike past studies of propofol, ketamine-induced unconsciousness was not associated with increases in the power of frontal alpha rhythms, characteristic cross-frequency coupling patterns of frontal alpha power and slow-oscillation phase, or decreases in coherence in the alpha bandwidth. Like past studies of propofol using undirected and directed phase lag index, ketamine reduced frontal-parietal (functional) and frontal-to-parietal (directional) connectivity in the alpha bandwidth. These results suggest that directional connectivity changes in the alpha bandwidth may be state-related markers of unconsciousness induced by both GABAergic and non-GABAergic anesthetics.

KEYWORDS:

anesthetic mechanisms; anesthetic-induced unconsciousness; consciousness; general anesthesia; ketamine

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