Genesis of epileptic interictal spikes. New knowledge of cortical feedback systems suggests a neurophysiological explanation of brief paroxysms

Abstract

A series of divers experiments in mammalian cortex and isolated neurons have yielded data suggesting a possible mechanism for the generation of the interictal epileptic spike, the simplest type of paroxysmal neuronal activity. We have outlined the hypothesis that penicillin, the most commonly used epileptogenic agent, brings about the following effects. Excitatory feedback actions in the cortex are enhanced by a decrease in the threshold for impulse initiation in neurons within these pathways and/or by an increase in the potency of excitatory synaptic actions. An increase in the gain of positive feedback systems in the cortex could lead to the production of the explosive and synchronous ‘epileptic spike’ with its cellular correlate, the ‘paroxysmal depolarizing shift’, which is believed to be an EPSP. The termination of the interictal spike has been suggested to depend, at least in part, on the delayed and enduring operation of recurrent inhibition.