The common neurochemical mechanism of these processes is neurotransmitter and ionic disorders.
One of the most important links of these disorders are disorders in the glutamine system, which occupies a key position in the metabolic processes of the brain (P.М.
Sarajishvili, T.Sh. Geladze, 1977). The glutamine system produces the most important mediators for brain tissue, such as GABA and glutamate.
The most important role in epileptogenesis is played by the activation of NMDA-glutamate receptors. Excessive activation of NMDA receptors leads to an imbalance of excitation / inhibition with a predominance of excitation. Dysfunction of the glutamine system is associated with disorders in the systems of histamine and histidine, taurine, glycine, acetylcholine. Disruption of the normal ratio of these neurotransmitters contributes to the processes of epileptogenesis. When epilepsy is broken and the interaction in the system of biogenic amines – dopamine, norepinephrine and adrenaline.
It is known that even the formation of an epileptic focus is not yet epilepsy. Even in cases of electrographically recorded lesions, seizures may be absent, and the disease does not develop. On the other hand, even with a clinical manifestation of epilepsy, seizures recur only with varying frequency, in the pauses between them the epileptic focus remains blocked. Obviously, there are mechanisms that can prevent the spread of epileptic activity from the hearth and the formation of the epileptic system, that is, the mechanisms of anti-epileptic protection.
The first level of this anti-epileptic system is already observed by the example of the peak-wave electrographic phenomenon, which reflects the epileptic process. In the peak-wave complex itself, the slow wave is the result of the anti-recirculating effect of the talamocaud brake system. The second level of anti-epileptic protection is collateral braking around the nidus in the form of a perifocal braking “shaft”. The third level is the effect on the focus of the inhibitor masses: the caudate nucleus, the cerebellum, the lateral nucleus of the hypothalamus and the caudate reticular nucleus of the bridge. Activation of these structures occurs under the influence of cortico-fugal impulses, and they exert an inhibitory effect on epileptic activity by means of inhibitory effects that cause hyperpolarization of cortical neurons.
The concept of cortical “epileptogenic focus”, which plays the role of a kind of “pacemaker” in epilepsy, logically explains the pathogenesis of partial and secondary-generalized convulsive seizures. In case of primary generalized epilepsy, the issues to date are still unclear, how are both hemispheres involved in the pathological process bilaterally synchronously?
Where is the epileptic lesion in primary-generalized forms of epilepsy? Since the time of classical studies Penfleld & Jasper (1954), three main concepts have been proposed for the emergence of primary-generalized forms of epilepsy: central-encephalic (Penfleld & Jasper, 1954), cortico-reticular (Doose, 1987) and thalamocortical (Avoli & Gloor, 1990) .