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Brain functional integration decreases during propofol-induced loss of consciousness.

Jessica Schrouff, Vincent Perlbarg, Melanie Boly, Guillaume Marrelec, Pierre Boveroux, Audrey Vanhaudenhuyse, Marie-Aurélie Bruno, Steven Laureys, Christophe Phillips, Mélanie Pélégrini‐Issac, Pierre Maquet, Habib Benali

Neuroimage April 16, 2011 DOI: 10.1016/j.neuroimage.2011.04.020 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Observational within-subject fMRI study Peer reviewed
Sample size 18
Population Healthy adult volunteers
Intervention Propofol
Keywords Brain Neural pathways Humans Unconsciousness Propofol Anesthetics, intravenous Image interpretation, computer-assisted Magnetic resonance imaging Female Young adult
Key findings Total brain integration was significantly reduced from resting wakefulness to propofol-induced deep sedation, both across the whole brain and within and between its constituent networks, with the ventral attentional network still interacting with most other networks. The authors argue this breakdown in integration is the neural correlate of propofol-induced loss of consciousness and highlight parietal and frontal areas.

Abstract

Consciousness has been related to the amount of integrated information that the brain is able to generate. In this paper, we tested the hypothesis that the loss of consciousness caused by propofol anesthesia is associated with a significant reduction in the capacity of the brain to integrate information. To assess the functional structure of the whole brain, functional integration and partial correlations were computed from fMRI data acquired from 18 healthy volunteers during resting wakefulness and propofol-induced deep sedation. Total integration was significantly reduced from wakefulness to deep sedation in the whole brain as well as within and between its constituent networks (or systems). Integration was systematically reduced within each system (i.e., brain or networks), as well as between networks. However, the ventral attentional network maintained interactions with most other networks during deep sedation. Partial correlations further suggested that functional connectivity was particularly affected between parietal areas and frontal or temporal regions during deep sedation. Our findings suggest that the breakdown in brain integration is the neural correlate of the loss of consciousness induced by propofol. They stress the important role played by parietal and frontal areas in the generation of consciousness.

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