Selective corticocortical connectivity suppression during propofol-induced anesthesia in healthy volunteers

We comprehensively studied directional feedback and feedforward connectivity to explore potential connectivity changes that underlie propofol-induced deep sedation. We further investigated the corticocortical connectivity patterns within and between hemispheres. Sixty-channel electroencephalographic data were collected from 19 healthy volunteers in a resting wakefulness state and propofol-induced deep unconsciousness state defined by a bispectral index value of 40. A source analysis was employed to locate cortical activity. The Desikan-Killiany atlas was used to partition cortices, and directional functional connectivity was assessed by normalized symbolic transfer entropy between higher-order (prefrontal and frontal) and lower-order (auditory, sensorimotor and visual) cortices and between hot-spot frontal and parietal cortices. We found that propofol significantly suppressed feedforward connectivity from the left parietal to right frontal cortex and bidirectional connectivity between the left frontal and left parietal cortex, between the frontal and auditory cortex, and between the frontal and sensorimotor cortex. However, there were no significant changes in either feedforward or feedback connectivity between the prefrontal and all the lower-order cortices and between the frontal and visual cortices or in feedback connectivity from the frontal to parietal cortex. Propofol anesthetic selectively decreased the unidirectional interaction between higher-order frontoparietal cortices and bidirectional interactions between the higher-order frontal cortex and lower-order auditory and sensorimotor cortices, which indicated that both feedback and feedforward connectivity were suppressed under propofol-induced deep sedation. Our findings provide critical insights into the connectivity changes underlying the top-down mechanism of propofol anesthesia at deep sedation.

The online version contains supplementary material available at 10.1007/s11571-021-09775-x.