The degree of epilepsy of neurons in the focus is different. Maximum epilepticized neurons are considered as pacemakers of epileptic activity. They have the ability to give almost constant stereotypical discharges at short intervals. Other neurons are less epileptic and may be involved in epileptic excitation under the influence of pacemaker neurons. At the same time, the critical mass of neurons covered by epileptic excitation may become sufficient for the occurrence of an epileptic seizure.
The construction of a conceptual mathematical model of epilepsy has shown that for the formation of an epileptic focus it is necessary
presence of 103-105 epileptic neurons (TS Stepanova, KV Grachev, 1976). The most important property of the epileptic focus is its determinantal character, that is, the ability to impose its work on other parts of the brain (Kryzhanovsky GN, 1980). Another significant feature of epileptic foci is the ability to induce the formation of secondary and even tertiary epileptic foci. The most common foci in the symmetric parts of the other hemisphere – the so-called “mirror foci”. All this is explained by the fact that the epileptic focus is a combination of not just epileptic neurons, but in a certain way organized neural ensembles.
If we talk about the pathological and pathophysiological features of epileptic
neurons, among the structural changes in neurons of the epileptic focus should be noted the absence of dendritic spines, the smoothness of the surface of the dendrites, the reduction of dendritic endings along with their varicose changes. Selective fallout of GABA-ergic synaptic terminals has also been found (Ward, Wyler, 1980).
Normally, there is mutual collateral inhibition between neighboring neurons of the cortex, which stabilizes the stimulation of the cortex. The destruction of part of the cortical neurons is accompanied by an imbalance between afferent stimulating effects and insufficient collateral inhibition with an increase in the excitatory response. An increased level of excitatory depolarization processes in the affected area leads to an increase in the level of potassium ions in the extracellular space, which, in turn, as a result of electrolyte-ion imbalance of currents through the neuronal membrane channels leads to their additional permanent depolarization. Thus, the pathological positive feedback mechanism closes, entailing a self-sustaining and increasing epilepticization process of neurons located in the epileptic focus and along its periphery.
Under normal conditions, an excess of potassium ions is absorbed by glia. However, an excessive concentration of potassium in the epileptic focus stimulates the proliferation of glia. Gliosis disrupts the normal organization of synaptic contacts on the body and dendrites, which leads to additional instability of the membrane and, accordingly, to excessive generation of the action potential. The formation of an epileptic focus, in addition to the transmission of excitation through the trans-synaptic pathway, is additionally activated by conducting it (bypassing the synapse directly from the axon or the body of one cell to the axon or the body of another). Favorable conditions are created due to partial initial depolarization of the neuron membrane due to an excess of potassium ions in the extracellular fluid when synchronously discharging a large number of epileptic neurons adjacent to the excitable.
In recent years, not only destructive disorders of neuronal systems, but also pathological neurogenesis have received increasing attention in studies of the mechanisms of epilepsy. It has been shown that repeated epileptic seizures lead to postnatal proliferation of neurons in the hippocampus with an increase in the density of mossy fibers and, accordingly, to an increase in excitation in the brain.