title: Connectivity changes underlying spectral EEG changes during propofol-induced loss of consciousness.
abstract: The 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.
authors.affiliation: Coma Science Group, Cyclotron Research Centre and Neurology Department, University of Liège and Sart Tilman Hospital, 4000 Liège, Belgium. mboly@ulg.ac.be
authors.forename: Mélanie
authors.initials: M
authors.lastname: Boly
authors.forename: Rosalyn
authors.initials: R
authors.lastname: Moran
authors.forename: Michael
authors.initials: M
authors.lastname: Murphy
authors.forename: Pierre
authors.initials: P
authors.lastname: Boveroux
authors.forename: Marie-Aurélie
authors.initials: MA
authors.lastname: Bruno
authors.forename: Quentin
authors.initials: Q
authors.lastname: Noirhomme
authors.forename: Didier
authors.initials: D
authors.lastname: Ledoux
authors.forename: Vincent
authors.initials: V
authors.lastname: Bonhomme
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Brichant
authors.forename: Giulio
authors.initials: G
authors.lastname: Tononi
authors.forename: Steven
authors.initials: S
authors.lastname: Laureys
authors.forename: Karl
authors.initials: K
authors.lastname: Friston
mesh_terms: D000328:Adult; D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D001499:Bayes Theorem; D058256:Brain Waves / Q000187:drug effects / Q000502:physiology*; D016292:Procedural Sedation; D004569:Electroencephalography / Q000379:methods; D005260:Female; D005625:Frontal Lobe / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006993:Hypnotics and Sedatives / Q000494:pharmacology; D008297:Male; D008959:Models, Neurological; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D010296:Parietal Lobe / Q000187:drug effects / Q000502:physiology*; D015742:Propofol / Q000494:pharmacology*; D013788:Thalamus / Q000187:drug effects / Q000502:physiology*; D014474:Unconsciousness / Q000139:chemically induced / Q000503:physiopathology*; D014851:Wakefulness / Q000502:physiology
chemical_list: D018686:Anesthetics, Intravenous; D006993:Hypnotics and Sedatives; D015742:Propofol