Reframing “Paradoxical” Excitation: Disentangling EEG Complexity and Entropy Reveals Resting State Dynamics Associated with Propofol Susceptibility

Summary

Propofol can either suppress or paradoxically excite brain activity. EEG complexity measures on the Complexity–Entropy Causal Plane distinguish these divergent neural trajectories. Both Type I and Type II complexity reflect paradoxical excitation, and baseline EEG complexity predicts susceptibility to propofol.

Study at a glance

Abstract

Background Propofol exposure can produce heterogenous neural responses, from the expected suppression to transient paradoxical excitation. EEG measures of signal complexity and entropy have emerged as reliable markers of consciousness, but different types of complexity and entropy measures are often conflated. We used Type I and II complexity measures on the Complexity–Entropy Causal Plane (CECP) to characterize divergent neural trajectories during propofol-induced loss of consciousness. We hypothesized that paradoxical excitation is reflected in both Type I and Type II complexity; that divergent trajectories on the CECP separate paradoxical excitation from suppression; and that baseline EEG complexity is associated with susceptibility to propofol.