• Mélanie Boly, Rosalyn Moran, Michael Murphy, Pierre Boveroux, Marie-Aurélie Bruno, Quentin Noirhomme, Didier Ledoux, Vincent Bonhomme, Jean-François Brichant, Giulio Tononi, Steven Laureys, and Karl Friston.
• Coma Science Group, Cyclotron Research Centre and Neurology Department, University of Liège and Sart Tilman Hospital, 4000 Liège, Belgium. mboly@ulg.ac.be
• J. Neurosci. 2012 May 16;32(20):7082-90.

AbstractThe mechanisms underlying anesthesia-induced loss of consciousness remain a matter of debate. Recent electrophysiological reports suggest that while initial propofol infusion provokes an increase in fast rhythms (from beta to gamma range), slow activity (from delta to alpha range) rises selectively during loss of consciousness. Dynamic causal modeling was used to investigate the neural mechanisms mediating these changes in spectral power in humans. We analyzed source-reconstructed data from frontal and parietal cortices during normal wakefulness, propofol-induced mild sedation, and loss of consciousness. Bayesian model selection revealed that the best model for explaining spectral changes across the three states involved changes in corticothalamic interactions. Compared with wakefulness, mild sedation was accounted for by an increase in thalamic excitability, which did not further increase during loss of consciousness. In contrast, loss of consciousness per se was accompanied by a decrease in backward corticocortical connectivity from frontal to parietal cortices, while thalamocortical connectivity remained unchanged. These results emphasize the importance of recurrent corticocortical communication in the maintenance of consciousness and suggest a direct effect of propofol on cortical dynamics.

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