Journal
BRITISH JOURNAL OF ANAESTHESIA
Volume 119, Issue 4, Pages 674-684Publisher
OXFORD UNIV PRESS
DOI: 10.1093/bja/aex257
Keywords
cerebrovascular circulation; magnetic resonance imaging; dexmedetomidine; propofol; sleep; slow-wave; anaesthesia
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Funding
- Orion Pharma [FI 19992126]
- Belgian National Funds for Scientific Research (FNRS)
- European Commission
- James McDonnell Foundation
- European Space Agency
- Mind Science Foundation
- French Speaking Community Concerted Research Action [ARC - 06/11 - 340]
- Public Utility Foundation 'Universite Europeenne du Travail'
- Fondazione Europea di Ricerca Biomedica
- University and University Hospital of Liege
- 'Plan National Cancer' of Belgium [139]
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Background. We used functional connectivity measures from brain resting state functional magnetic resonance imaging to identify human neural correlates of sedation with dexmedetomidine or propofol and their similarities with natural sleep. Methods. Connectivity within the resting state networks that are proposed to sustain consciousness generation was compared between deep non-rapid-eye-movement (N3) sleep, dexmedetomidine sedation, and propofol sedation in volunteers who became unresponsive to verbal command. A newly acquired dexmedetomidine dataset was compared with our previously published propofol and N3 sleep datasets. Results. In all three unresponsive states (dexmedetomidine sedation, propofol sedation, and N3 sleep), within-network functional connectivity, including thalamic functional connectivity in the higher-order (default mode, executive control, and salience) networks, was significantly reduced as compared with the wake state. Thalamic functional connectivity was not reduced for unresponsive states within lower-order (auditory, sensorimotor, and visual) networks. Voxel-wise statistical comparisons between the different unresponsive states revealed that thalamic functional connectivity with the medial prefrontal/anterior cingulate cortex and with the mesopontine area was reduced least during dexmedetomidine-induced unresponsiveness and most during propofol-induced unresponsiveness. The reduction seen during N3 sleep was intermediate between those of dexmedetomidine and propofol. Conclusions. Thalamic connectivity with key nodes of arousal and saliency detection networks was relatively preserved during N3 sleep and dexmedetomidine-induced unresponsiveness as compared to propofol. These network effects may explain the rapid recovery of oriented responsiveness to external stimulation seen under dexmedetomidine sedation.
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