Breakdown of within- and between-network Resting State Functional Magnetic Resonance Imaging Connectivity during Propofol-induced Loss of Consciousness
Pierre Boveroux, Audrey Vanhaudenhuyse, Marie-Aurélie Bruno, Quentin Noirhomme, Séverine Lauwick, André Luxen, Christian Degueldre, Alain Plenevaux, Caroline Schnakers, Christophe Phillips, Jean-François Brichant, Vincent Bonhomme, Pierre Maquet, Michael D. Greicius, Steven Laureys, Melanie Boly
Anesthesiology September 30, 2010 DOI: 10.1097/aln.0b013e3181f697f5 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational cohort Peer reviewed |
|---|---|
| Sample size | 19 |
| Population | Healthy volunteers |
| Intervention | Propofol |
| Topics | Default mode network |
| Keywords | Unconsciousness Wakefulness Propofol Sensory system Resting State FMRI Magnetic resonance imaging Anesthesia Electroencephalography Cognition |
| Citations | 645 |
| Key findings | Propofol-induced unconsciousness correlates with decreased corticocortical and thalamocortical connectivity in frontoparietal networks and a loss of cross-modal interactions between visual and auditory networks. |
Abstract
Background: Mechanisms of anesthesia-induced loss of consciousness remain poorly understood. Resting-state functional magnetic resonance imaging allows investigating whole-brain connectivity changes during pharmacological modulation of the level of consciousness.
Methods: Low-frequency spontaneous blood oxygen level-dependent fluctuations were measured in 19 healthy volunteers during wakefulness, mild sedation, deep sedation with clinical unconsciousness, and subsequent recovery of consciousness.
Results: Propofol-induced decrease in consciousness linearly correlates with decreased corticocortical and thalamocortical connectivity in frontoparietal networks (i.e., default- and executive-control networks). Furthermore, during propofol-induced unconsciousness, a negative correlation was identified between thalamic and cortical activity in these networks. Finally, negative correlations between default network and lateral frontoparietal cortices activity, present during wakefulness, decreased proportionally to propofol-induced loss of consciousness. In contrast, connectivity was globally preserved in low-level sensory cortices, (i.e., in auditory and visual networks across sedation stages). This was paired with preserved thalamocortical connectivity in these networks. Rather, waning of consciousness was associated with a loss of cross-modal interactions between visual and auditory networks.
Conclusions: Our results shed light on the functional significance of spontaneous brain activity fluctuations observed in functional magnetic resonance imaging. They suggest that propofol-induced unconsciousness could be linked to a breakdown of cerebral temporal architecture that modifies both within- and between-network connectivity and thus prevents communication between low-level sensory and higher-order frontoparietal cortices, thought to be necessary for perception of external stimuli. They emphasize the importance of thalamocortical connectivity in higher-order cognitive brain networks in the genesis of conscious perception.