The purpose of this research was to study electric and physiological mechanisms of the achievement of the antoconvulsant effect of the new original beprodon combination together with determination of determinant brain structures – therapeutic targets.

Materials and Methods. Partial (focal) and secondary generalized convulsions were generated using the method of creation of a chronic epileptogenic focus, caused by the cobalt application on rats’ brain.

Results: it was revealed, that at the first stage of the epileptic system (ES) beprodone is targeted to cortical focuses, and at the second stage – to subcortical focuses, generating epileptic activities. Conclusion: the beprodone effect depends on the stage of the epileptic system development and is targeted to determinant focuses.

The factors of risk in relapse of febrile convulsions have been studied: age, sex, perinatal anamnesis, heredity on febrile attacks, epilepsies, neurological status, the results in analysis (EEG, MRI of the head brain), the temperature, the type of the illness, frequency of the illness, the character of febrile paroxysm. 109 children have been investigated aged from three months to five years suffering from febrile attacks. There has been held the comparison of the groups of children with different quantity of episodes of febrile bouts (with one, two, three and more). The results of the observations testify to high degree of credibility the influence of relapsing course of febrile attacks of the following factors: hereditary burden on febrile attacks, the presence of perinatal pathology, frequent acute respiratory diseases.

The article considers the peculiarities of the spatial organization of brain potentials in epileptic patients with a lesion in the right hemisphere. We identified violations of the spatial organization of brain potentials, which allow you to objectify violations of structural-functional relationships in epileptic patients with a lesion in the right hemisphere with the formation of multilevel pathological neural networks involving intact neural populations. Specific changes of hemispheric interactions characterized by a significant decrease in average levels of coherence in the occipital, parietal and anterio temporal areas in most frequency bands. The obtained data allow to suppose the specificity of the changes in alpha activity, characterized by the reciprocity of changes in the alpha rhythm in the range of 9-10 and 11-12 number`s.

SCN2A mutations are traditionally described in benign infantile seizures. We are describing rather rare case of epileptic encephalopathy associated with incertion of ctg/ctGg in SCN2A. The female child was born at term by normal delivery after non-complicated pregnancy. Seizures started when she was 3 months old as focal tonic, later on myoclonic seizures developed. They were refractory to all used antiepileptic drugs including valproic acid, topiramate, lamotrigine, ethosuximide and tetracoside. At age of two child is mentally retarded and autistic, unable to walk (because of muscular hypotonia), has no active speech and still has asymmetrical tonic and myoclonic seizures. Unspecific modest brain atrophy was revealed by MRI. Metabolic screening, including urine and serum amino acids, organic acids, lactate, was normal. Our case (alongside with others depicted in literature) confirms that spectrum of phenotypes, associated with mutations in SCN2A, is very wide – from benign infantile seizures to severe epileptic encephalopaties leading to mental retardation, motor and speech disorders.

Tics are one of the most common neuropsychiatric disorders in children. Major role in the etiology of the disease plays a lack of work dopaminergic system, which leads to impaired attention, self-control and behavioral inhibition, reduced control of motor activity and the appearance of excessive, uncontrolled movements. Under the influence of levetiracetam, probably there is a change of neurotransmitter systems with stimulation of inhibitory mechanisms, which leads to rapid clinical and neurophysiological effects.

Alpers-Huttenlocher syndrome is a rare mitochondrial disease connected with mutations in the mitochondrial DNA replicase, polymerase gamma (POLG). The reduction of the activity within mitochondrial enzymes is connected with the reduction of replications level within the mitochondrial DNA. The disease manifests itself once the replications level reaches a critical point. We can also observe the debut variability and disease progression even among patients with identical genotypes and normal children onset up to the moment of clinical presentations debut. Seizures, liver degeneration and progressive development regression are the classical clinical triad of the disease. Seizures are usually resistant to treatment and have a status flow.Liver disfunction is one of the manifestations of the disease inevitable in the terminal stages. The disease in steadily progressive and leads to the patient s death within several years. Valproic acid causes toxic fatal hepatitis developing within several months and leading to the loss of the patent. Timely diagnosis of the disease, prescription of maintenance therapy and elimination of medications containing valproic acid from the seizures therapy can certainly increase patient s lifetime.