Neurophysiological correlates of sevoflurane-induced unconsciousness
Stefanie Blain-Moraes1, Vijay Tarnal, Giancarlo Vanini
1From the Department of Anesthesiology (S.B.-M., V.T., G.V., A.A., D.R., B.S., E.J., G.A.M.) and Neuroscience Graduate Program (G.A.M.), Center for Consciousness Science, University of Michigan Medical School, Ann Arbor, Michigan.
Background:
Recent studies of anesthetic-induced unconsciousness in humans have focused predominantly on the intravenous drug propofol and have identified anterior dominance of alpha rhythms and frontal phase-amplitude coupling patterns as neurophysiological markers. However, it is unclear whether the correlates of propofol-induced unconsciousness are generalizable to inhaled anesthetics, which have distinct molecular targets and which are used more commonly in clinical practice.
Methods:
The authors recorded 64-channel electroencephalograms in healthy human participants during consciousness, sevoflurane-induced unconsciousness, and recovery (n = 10; n = 7 suitable for analysis). Spectrograms and scalp distributions of low-frequency (1 Hz) and alpha (10 Hz) power were analyzed, and phase-amplitude modulation between these two frequencies was calculated in frontal and parietal regions. Phase lag index was used to assess phase relationships across the cortex.
Results:
At concentrations sufficient for unconsciousness, sevoflurane did not result in a consistent anteriorization of alpha power; the relationship between low-frequency phase and alpha amplitude in the frontal cortex did not undergo characteristic transitions. By contrast, there was significant cross-frequency coupling in the parietal region during consciousness that was not observed after loss of consciousness. Furthermore, a reversible disruption of anterior-posterior phase relationships in the alpha bandwidth was identified as a correlate of sevoflurane-induced unconsciousness.
Conclusion:
In humans, sevoflurane-induced unconsciousness is not correlated with anteriorization of alpha and related cross-frequency patterns, but rather by a disruption of phase-amplitude coupling in the parietal region and phase-phase relationships across the cortex.
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