Reconfiguration of Network Hub Structure after Propofol-induced Unconsciousness

General anesthesia with propofol reconfigures the brain's functional network hub structure and reverses the phase relationship between frontal and parietal regions. Using graph theoretical analysis of 21-channel electroencephalogram data from 10 volunteers, the study found that network topology—not connection strength—correlates with states of consciousness. After propofol administration, average path length, clustering coefficient, and modularity increased, long-range connections were disrupted, and hub node strength decreased. The primary hub shifted from parietal to frontal regions. The phase lead of frontal to parietal areas in the alpha frequency band (8-13 Hz) during wakefulness reversed direction after propofol and returned during recovery. Changes in network topology may be the primary mechanism for loss of frontal to parietal feedback during anesthesia.

Study at a glance

Abstract

INTRODUCTION: General anesthesia induces unconsciousness along with functional changes in brain networks. Considering the essential role of hub structures for efficient information transmission, the authors hypothesized that anesthetics have an effect on the hub structure of functional brain networks. METHODS: Graph theoretical network analysis was carried out to study the network properties of 21-channel electroencephalogram data from 10 human volunteers anesthetized on two occasions. The functional brain network was defined by Phase Lag Index, a coherence measure, for three states: wakefulness, loss of consciousness induced by the anesthetic propofol, and recovery of consciousness. The hub nodes were determined by the largest centralities. The correlation between the altered hub organization and the phase relationship between electroencephalographic channels was investigated. RESULTS: Topology rather than connection strength of functional networks correlated with states of consciousness. The average path length, clustering coefficient, and modularity significantly increased after administration of propofol, which disrupted long-range connections. In particular, the strength of hub nodes significantly decreased. The primary hub location shifted from the parietal to frontal region, in association with propofol-induced unconsciousness. The phase lead of frontal to parietal regions in the α frequency band (8-13 Hz) observed during wakefulness reversed direction after propofol and returned during recovery. CONCLUSIONS: Propofol reconfigures network hub structure in the brain and reverses the phase relationship between frontal and parietal regions. Changes in network topology are more closely associated with states of consciousness than connectivity and may be the primary mechanism for the observed loss of frontal to parietal feedback during general anesthesia.