Epilepsy as Paroxysmal State-Space Collapse: Ictogenesis, Inhibitory Constraint Failure, and Dynamical Systems Formalization within Informational Nosology

Epilepsy is classically defined by recurrent, unprovoked seizures arising from abnormal hypersynchronous neuronal activity. While existing models successfully describe cellular hyperexcitability, synaptic failure, and network oscillations, they leave under-specified the distinctive organizational signature of the ictal transition: an abrupt, reversible collapse of high-dimensional computational capacity into a low-dimensional, stereotyped dynamical regime. Within the framework of Informational Nosology, this monograph formalizes epilepsy as Portal IV, Regime A — Paroxysmal State-Space Collapse. Seizure onset is treated as a fold bifurcation in which the system crosses a critical stability threshold θ(t)\theta(t)θ(t), resulting in the sudden contraction of the accessible state space Ωselected\Omega_{\text{selected}}Ωselected into a hypersynchronous ictal attractor Ωictal\Omega_{\text{ictal}}Ωictal. Hypersynchrony is interpreted not as informational excess but as computational annihilation: a transient erasure of degrees of freedom that temporarily evicts operational presence from the interface. Using a six-variable dynamical system aligned with the Unified Mathematical Program, the work derives the conditions for ictogenesis, the role of inhibitory constraint failure (including parvalbumin interneuron depolarization block and chloride dysregulation), and the action of an autonomous refractory operator RrefR_{\text{ref}}Rref that accounts for rapid post-ictal recovery without structural destruction of the substrate. Clear comparative demarcations are established with respect to Migraine (Regime B: Sensory Decoherence) and the gradual portals of the Informational Nosology triad. The model yields explicit, falsifiable predictions concerning pre-ictal load accumulation, critical slowing, and the recovery window, while remaining strictly non-clinical and non-displacing of established pharmacological and neuromodulatory therapies. Keywords: Epilepsy; Paroxysmal State-Space Collapse; Ictogenesis; Fold Bifurcation; Inhibitory Constraint Failure; Refractory Reset; Informational Nosology; Portal IV; Causal Conductivity; Dynamical Systems