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.
Highlights
Ketamine is an anesthetic drug that was introduced into clinical practice in the 1960s (Corssen and Domino, 1966) and is currently used for the induction of unconsciousness and, at subanesthetic doses, the prevention of acute pain or the treatment of depression
Directed Phase Lag Index: To determine the direction of KETAMINE-INDUCED UNCONSCIOUSNESS IS NOT CHARACTERIZED BY INCREASES IN FRONTAL ALPHA POWER OR BY PHASE-AMPLITUDE COUPLING PATTERNS The group-level spectrogram of the electroencephalogram recorded from frontal channels demonstrates a decrease in alpha power upon ketamine-induced unconsciousness (Figure 1)
These patterns are in contrast to those observed with propofol, where loss of consciousness is associated with a trough-max coupling pattern (Mukamel et al, 2014)
Summary
Ketamine is an anesthetic drug that was introduced into clinical practice in the 1960s (Corssen and Domino, 1966) and is currently used for the induction of unconsciousness and, at subanesthetic doses, the prevention of acute pain or the treatment of depression. Ketamine is unique in the class of general anesthetics for a number of reasons. Ketamine is unique because it increases cortical acetylcholine levels and appears to depend on noradrenergic signaling for its effects, in contrast to a number of GABAergic anesthetics (Kikuchi et al, 1997; Kushikata et al, 2011). In contrast to virtually all other anesthetic and sedative drugs, ketamine does not appear to metabolically depress the thalamus (Långsjö et al, 2005). At the neurophysiologic level, ketamine tends to increase the power of high-frequency electroencephalographic activity, whereas most anesthetics depress this bandwidth (Maksimow et al, 2006). Ketamine fails to conform to virtually all mechanistic frameworks of anesthetic-induced unconsciousness
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