Reframing “Paradoxical” Excitation: Disentangling EEG Complexity and Entropy Reveals Resting State Dynamics Associated with Propofol Susceptibility
Derek Newman, Charlotte Maschke, George A. Mashour, Stefanie Blain-Moraes
medRxiv Preprint Server December 16, 2025 preprint DOI: 10.64898/2025.12.16.25342405 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational study |
|---|---|
| Intervention | Propofol |
| Key findings | Paradoxical excitation during propofol-induced loss of consciousness is reflected in both Type I and Type II complexity measures on the Complexity–Entropy Causal Plane, which separates excitation from suppression, and baseline EEG complexity is associated with susceptibility to propofol. |
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.