• Oluwaseun Akeju, Marco L Loggia, Ciprian Catana, Kara J Pavone, Rafael Vazquez, James Rhee, Violeta Contreras Ramirez, Daniel B Chonde, David Izquierdo-Garcia, Grae Arabasz, Shirley Hsu, Kathleen Habeeb, Jacob M Hooker, Vitaly Napadow, Emery N Brown, and Patrick L Purdon.
• Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, United States.
• Elife. 2014 Jan 1;3:e04499.

AbstractUnderstanding the neural basis of consciousness is fundamental to neuroscience research. Disruptions in cortico-cortical connectivity have been suggested as a primary mechanism of unconsciousness. By using a novel combination of positron emission tomography and functional magnetic resonance imaging, we studied anesthesia-induced unconsciousness and recovery using the α₂-agonist dexmedetomidine. During unconsciousness, cerebral metabolic rate of glucose and cerebral blood flow were preferentially decreased in the thalamus, the Default Mode Network (DMN), and the bilateral Frontoparietal Networks (FPNs). Cortico-cortical functional connectivity within the DMN and FPNs was preserved. However, DMN thalamo-cortical functional connectivity was disrupted. Recovery from this state was associated with sustained reduction in cerebral blood flow and restored DMN thalamo-cortical functional connectivity. We report that loss of thalamo-cortical functional connectivity is sufficient to produce unconsciousness.

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