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

Propofol anesthesia can cause either the expected suppression of brain activity or a transient paradoxical excitation. EEG measures of signal complexity and entropy, specifically Type I and Type II complexity on the Complexity–Entropy Causal Plane (CECP), distinguish these divergent neural trajectories. The findings suggest that paradoxical excitation is reflected in both types of complexity, that the CECP separates excitation from suppression, and that baseline EEG complexity is linked to how susceptible a person is to propofol.

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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.