Abstract
ObjectiveGeneral anesthesia might disrupt neuronal network communications measured by functional connectivity (FC; undirected connectivity) and directional information flow (directed connectivity). We sought to characterize the state-dependent effects of propofol on cortico-cortical undirected and directed FC. MethodsWe collected 256-channel high-density EEGs from 14 patients undergoing surgery while awake (AWA) or in propofol-induced moderate sedation (SED) or loss of consciousness (LOC) states. Using source-space EEG, we estimated neuronal oscillatory activity for 68 cortical regions of interest. FC was analyzed using the weighted phase lag index. Directed connectivity was computed using directed phase transfer entropy (dPTE) as a measure of information flow in the bilateral prefrontal, frontal, parietal, and occipital areas. ResultsFC strength evidently reduced during LOC compared with those during the AWA and SED states. The dPTE analysis showed significant propofol-induced changes in directed connectivity. In the alpha band, the prefrontal-to-frontal information flow was significantly stronger in the AWA than in the SED (p = 0.033) and LOC states (p = 0.033). The parietal-to-frontal dPTE was significantly weaker during LOC than during the AWA (p = 0.033) and SED states (p = 0.007). Finally, a loss of occipital-to-frontal connectivity occurred during LOC but not the AWA state (p = 0.001). In the beta band, the dominant occipital-to-frontal direction of information flow in the AWA state was gradually converted to a frontal-to-occipital direction during LOC. ConclusionsPropofol-induced unconsciousness is marked by a decrease in FC and posterior-to-anterior (feedforward) directed connectivity, which may be useful as a measure to discriminate different conscious states caused by propofol administration. SignificanceThe study demonstrates that propofol produces state-dependent effects on cortico-cortical undirected and directed FC, supporting the idea that propofol induces loss of consciousness may through disrupting network interactions and cortical coordination.
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