Propofol-induced unconsciousness is linked to decreased connectivity within frontoparietal networks (the default-mode and executive-control networks) and between the thalamus and these networks, with a negative correlation between thalamic and cortical activity emerging during unconsciousness. In contrast, connectivity in low-level sensory cortices (auditory and visual networks) is preserved, including their thalamocortical connections. Loss of consciousness is associated with a breakdown of cross-modal interactions between visual and auditory networks. These findings suggest that unconsciousness results from disrupted communication between sensory and higher-order frontoparietal cortices, preventing conscious perception.
Resting brain activity reveals two anticorrelated cortical systems linked to conscious awareness: an extrinsic system (lateral fronto-parietal areas) associated with external awareness and an intrinsic system (medial brain areas) associated with internal awareness. In 31 healthy volunteers, external and internal awareness were significantly anticorrelated, with a mean switching frequency of 0.05 Hz, similar to BOLD fMRI slow oscillations. In 22 volunteers, fMRI showed that precuneus/posterior cingulate, anterior cingulate/mesiofrontal cortices, and parahippocampal areas (intrinsic system) correlated with internal awareness, while lateral fronto-parietal cortices (extrinsic system) correlated with external awareness.
Loss of consciousness from propofol sedation reduces long-range temporal correlations in frontothalamic brain activity and weakens the link between functional connectivity and anatomical structure. A model based on phase transitions in complex systems reproduces these patterns and also explains the cortex's reduced sensitivity to external stimuli during unconsciousness. The findings suggest that these neural changes are universal across different causes of unconsciousness.