In the article, in light of the hypothesis about the pathogenesis of epilepsy the author considers certain clinical manifestations of epilepsy, touches upon the neurochemistry of behavior, as well as neurotransmitter hypothesis of schizophrenia. According to the hypothesis, in epileptic patients, epileptogenic substances are permanently accumulating in the brain, which in the course of epileptic activity in the brain undergo metabolic changes requiring their removal from the organism. When the concentration of epileptogenic substances in the brain reaches a threshold value, they cause a seizure, and in lower concentrations, they cause epileptic activity typical for the interictal period. In the context of this hypothesis, there are discussed the clinical signs of epilepsy such as forced normalization, reinforcement epilepsy activity during the sleep deprivation and one of the paradoxical effect of antiepileptic drugs such as phenomen when antiepileptic drugs prescribed cause an improvement of the electroencephalographic image but the clinical deterioration and increasing frequency of seizures, and the change of antiepileptic drugs give us the opposite results: improvement of the clinical picture and the deterioration of the electroencephalographic image. According to the supplemented hypothesis, epileptogenic substances, except that, during epileptic activity in the brain undergo metabolic transformations necessary for their removal from the body; there are also alternative transformation neurochemical pathways necessary for their further removal (elimination) from the organism. The hypothesis discusses the modern principles of epilepsy treatment. It was proposed to call the phenomenon “clinical-electroencephalographic dissociation” when the anti-epileptic drugs are associated with the improved electroencephalographic pattern, but with the deterioration of the clinic and frequent seizures, and the drug change leads to the opposite—the improvement of the clinical picture and the EEG deterioration. Forced normalization is considered as one of the manifestations of epilepsy aggravation and “clinical-electroencephalographic dissociation”. When reviewing biological antagonism of schizophrenia and epilepsy the author suggests a hypothesis that if an area of the brain producing epileptogenic substances and an area of the brain producing endogenic psychogenic substances causing psychopathology coexist simultaneously, then, in the event of a generalized convulsive seizure involving the brain in full, epileptogenic as well as psychogenic substances are released. At the same time epilepsy is demonstrated, while schizophrenia is not. The same could be the mechanism of therapeutic activity (effect) of electroconvulsive therapy.