Resting-state Network-specific Breakdown of Functional Connectivity during Ketamine Alteration of Consciousness in
Vincent Bonhomme1, Audrey Vanhaudenhuyse, Athena Demertzi
1From the University Department of Anesthesia and Intensive Care Medicine, CHR Citadelle and CHU University Hospital of Liege, Liege, Belgium (V.B., O.J.); Coma Science Group, GIGA Research, University and CHU University Hospital of Liege, Liege, Belgium (V.B., A.V., A.D., M.-A.B., M.A.B., S.L.); GIGA-Cyclotron Research Center: In Vivo Imaging, University of Liege, Liege, Belgium (A.V., A.D., M.-A.B., M.A.B., A.P., A.S., P.M., S.L.); Departments of Algology and Palliative Care (A.V.), Anesthesia and Intensive Care Medicine (V.B., O.J., P.B., J.F.B.), and Neurology (P.M., S.L.), CHU University Hospital of Liege, Liege, Belgium; Department of Neurology, University of Wisconsin, Madison, Wisconsin (M.B.); Departments of Anesthesia and Intensive Care Medicine (P.B.); Department of Physics and Astronomy, The University of Western Ontario, London, Ontario, Canada (A.S.); and Institut du Cerveau et de la Moelle épinière - ICM, Hôpital Pitié-Salpêtrière, Paris, France (A.D.).
Background:
Consciousness-altering anesthetic agents disturb connectivity between brain regions composing the resting-state consciousness networks (RSNs). The default mode network (DMn), executive control network, salience network (SALn), auditory network, sensorimotor network (SMn), and visual network sustain mentation. Ketamine modifies consciousness differently from other agents, producing psychedelic dreaming and no apparent interaction with the environment. The authors used functional magnetic resonance imaging to explore ketamine-induced changes in RSNs connectivity.
Methods:
Fourteen healthy volunteers received stepwise intravenous infusions of ketamine up to loss of responsiveness. Because of agitation, data from six subjects were excluded from analysis. RSNs connectivity was compared between absence of ketamine (wake state [W1]), light ketamine sedation, and ketamine-induced unresponsiveness (deep sedation [S2]).
Results:
Increasing the depth of ketamine sedation from W1 to S2 altered DMn and SALn connectivity and suppressed the anticorrelated activity between DMn and other brain regions. During S2, DMn connectivity, particularly between the medial prefrontal cortex and the remaining network (effect size β [95% CI]: W1 = 0.20 [0.18 to 0.22]; S2 = 0.07 [0.04 to 0.09]), and DMn anticorrelated activity (e.g., right sensory cortex: W1 = -0.07 [-0.09 to -0.04]; S2 = 0.04 [0.01 to 0.06]) were broken down. SALn connectivity was nonuniformly suppressed (e.g., left parietal operculum: W1 = 0.08 [0.06 to 0.09]; S2 = 0.05 [0.02 to 0.07]). Executive control networks, auditory network, SMn, and visual network were minimally affected.
Conclusions:
Ketamine induces specific changes in connectivity within and between RSNs. Breakdown of frontoparietal DMn connectivity and DMn anticorrelation and sensory and SMn connectivity preservation are common to ketamine and propofol-induced alterations of consciousness.
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