• Heonsoo Lee, George A Mashour, Gyu-Jeong Noh, Seunghwan Kim, and UnCheol Lee.
• Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan; Doctoral Candidate, Department of Physics, POSTECH, Pohang, Korea.
• Anesthesiology. 2013 Dec 1;119(6):1347-59.

IntroductionGeneral anesthesia induces unconsciousness along with functional changes in brain networks. Considering the essential role of hub structures for efficient information transmission, the authors hypothesized that anesthetics have an effect on the hub structure of functional brain networks.MethodsGraph theoretical network analysis was carried out to study the network properties of 21-channel electroencephalogram data from 10 human volunteers anesthetized on two occasions. The functional brain network was defined by Phase Lag Index, a coherence measure, for three states: wakefulness, loss of consciousness induced by the anesthetic propofol, and recovery of consciousness. The hub nodes were determined by the largest centralities. The correlation between the altered hub organization and the phase relationship between electroencephalographic channels was investigated.ResultsTopology rather than connection strength of functional networks correlated with states of consciousness. The average path length, clustering coefficient, and modularity significantly increased after administration of propofol, which disrupted long-range connections. In particular, the strength of hub nodes significantly decreased. The primary hub location shifted from the parietal to frontal region, in association with propofol-induced unconsciousness. The phase lead of frontal to parietal regions in the α frequency band (8-13 Hz) observed during wakefulness reversed direction after propofol and returned during recovery.ConclusionsPropofol reconfigures network hub structure in the brain and reverses the phase relationship between frontal and parietal regions. Changes in network topology are more closely associated with states of consciousness than connectivity and may be the primary mechanism for the observed loss of frontal to parietal feedback during general anesthesia.

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