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

Epilepsy creates a persistent increase in the probability of spontaneous seizures. An ictal episode evolves due to acute disturbance of the fine-tuned balance between excitatory vs. inhibitory inputs within a neural network in favor of excitation. The current literature that proposes the activity-dependent disinhibition as a valid mechanism of chronic epilepsy, does not provide clues on why this mechanism emerges only in epileptic patients and how the vicious circle resulting of an activity-dependent disinhibition in over-active ictogenic network would end. A new model, which presents chronic epilepsy as a disease of faulty architecture of the neural circuit, is discussed. Wherein; variable genetic or acquired predisposing factors drive abnormalities in the construction of multiple neural circuits resulting in an activity-dependent positive feedback excitatory loops which transform normal neural circuits into ictal foci. Such new mechanism, for igniting an activity-dependent unstable excitation with subsequent relatively stable disinhibition, leads to an ictal escape rhythm. The propagation of such bursting activity occurs either electrochemically via synaptic communication to remote susceptible circuits, or chemically via a trigger wave which recruits the non-connected proximal neurons. Termination occurs abruptly when the inhibitory interneurons functionally recover and reimpose their inhibitory effect on the ictogenic circuit to transform the escape rhythm into a normal, under-control output. The proposed model elucidates various enigmatic features of the disease; and illustrates both the end-result ictogenic mechanism arising from the wide variety of etiologies of human spontaneous and acquired epilepsy, and the timing of episodic transitions from normal activity to seizures.

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