A Turbulence-Inspired Dynamical Systems Hypothesis of Ictogenesis: Nonlinear Amplification of Perturbations Near Critical States

Seizure onset is conventionally modelled as a bifurcation: a slow variable drives the brain across a stability boundary, and the fast subsystem falls into a pathological attractor. This account predicts critical slowing before onset, yet empirical slowing signatures are inconsistent across patients. We propose an alternative framing borrowed from hydrodynamic transition to turbulence. In subcritical shear flows the laminar state remains linearly stable over a wide parameter range while becoming increasingly vulnerable to finite-amplitude perturbations of specific structure. We hypothesise that the interictal brain occupies an analogous regime: linearly stable, but subject to transient amplification that converts small structured perturbations into escape from the physiological basin. On this account, ictogenesis is not the crossing of a bifurcation point but the shrinking of a basin of attraction, and the relevant predictor is not slowing but the amplitude and structure of the minimal seizure-triggering perturbation. We derive four falsifiable consequences concerning perturbation structure, threshold scaling, episode statistics, and marker dissociation.