• Muriëlle Kirsch, Pieter Guldenmund, Ali Bahri Mohamed M, Athena Demertzi, Katherine Baquero, Lizette Heine, Vanessa Charland-Verville, Audrey Vanhaudenhuyse, Marie-Aurélie Bruno, Olivia Gosseries, Carol Di Perri, Erik Ziegler, Jean-François Brichant, Andrea Soddu, Vincent Bonhomme, and Steven Laureys.
• From the *Coma Science Group and §MoVeRe Group, Cyclotron Research Center, University of Liège, Liège, Belgium; †Department of Anesthesia and Intensive Care Medicine, CHU Sart Tilman Hospital, University of Liège, Liège, Belgium; ‡Computer Imaging and Medical Applications Laboratory, National University of Colombia, Bogotá, Colombia; ‖Department of Neurology, CHU Sart Tilman Hospital University of Liège, Liège, Belgium; ¶Department of Algology and Palliative Care, University Hospital of Liège, University of Liège, Liège, Belgium; #Center for Sleep and Consciousness and Postle Laboratory, Department of Psychiatry, University of Wisconsin, Madison, Wisconsin; **Department of Physics and Astronomy, Brain & Mind Institute, University of Western Ontario, London, Ontario, Canada; and ††Department of Anesthesia and Intensive Care Medicine, CHR Citadelle and CHU Liège, University of Liège, Liège, Belgium.
• Anesth. Analg. 2017 Feb 1; 124 (2): 588-598.

BackgroundTo reduce head movement during resting state functional magnetic resonance imaging, post-coma patients with disorders of consciousness (DOC) are frequently sedated with propofol. However, little is known about the effects of this sedation on the brain connectivity patterns in the damaged brain essential for differential diagnosis. In this study, we aimed to assess these effects.MethodsUsing resting state functional magnetic resonance imaging 3T data obtained over several years of scanning patients for diagnostic and research purposes, we employed a seed-based approach to examine resting state connectivity in higher-order (default mode, bilateral external control, and salience) and lower-order (auditory, sensorimotor, and visual) resting state networks and connectivity with the thalamus, in 20 healthy unsedated controls, 8 unsedated patients with DOC, and 8 patients with DOC sedated with propofol. The DOC groups were matched for age at onset, etiology, time spent in DOC, diagnosis, standardized behavioral assessment scores, movement intensities, and pattern of structural brain injury (as assessed with T1-based voxel-based morphometry).ResultsDOC were associated with severely impaired resting state network connectivity in all but the visual network. Thalamic connectivity to higher-order network regions was also reduced. Propofol administration to patients was associated with minor further decreases in thalamic and insular connectivity.ConclusionsOur findings indicate that connectivity decreases associated with propofol sedation, involving the thalamus and insula, are relatively small compared with those already caused by DOC-associated structural brain injury. Nonetheless, given the known importance of the thalamus in brain arousal, its disruption could well reflect the diminished movement obtained in these patients. However, more research is needed on this topic to fully address the research question.

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