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Epilepsy creates a persistent increase in the probability of spontaneousseizures. An ictal episode evolves due to acute disturbance of the fine-tunedbalance between excitatory vs. inhibitory inputs within a neural network infavor of excitation. The current literature that proposes theactivity-dependent disinhibition as a valid mechanism of chronic epilepsy, doesnot provide clues on why this mechanism emerges only in epileptic patients andhow the vicious circle resulting of an activity-dependent disinhibition inover-active ictogenic network would end. A new model, which presents chronicepilepsy as a disease of faulty architecture of the neural circuit, isdiscussed. Wherein; variable genetic or acquired predisposing factors driveabnormalities in the construction of multiple neural circuits resulting in anactivity-dependent positive feedback excitatory loops which transform normalneural circuits into ictal foci. Such new mechanism, for igniting anactivity-dependent unstable excitation with subsequent relatively stabledisinhibition, leads to an ictal escape rhythm. The propagation of suchbursting activity occurs either electrochemically via synaptic communication toremote susceptible circuits, or chemically via a trigger wave which recruitsthe non-connected proximal neurons. Termination occurs abruptly when theinhibitory interneurons functionally recover and reimpose their inhibitoryeffect on the ictogenic circuit to transform the escape rhythm into a normal,under-control output. The proposed model elucidates various enigmatic featuresof the disease; and illustrates both the end-result ictogenic mechanism arisingfrom the wide variety of etiologies of human spontaneous and acquired epilepsy,and the timing of episodic transitions from normal activity to seizures.

On The Ignition, Propagation and Termination Of The Neuronal Bursting Activity During Ictogenesis In Epileptic Patients