Recent studies show that the brain gamma activity includes both the gamma rhythm (standard EEG) and high frequency (100-1000 Hz) as well as super-high (>1000 Hz) frequency oscillations, as recorded by electrocorticography. As reported in the literature, the high-frequency oscillations (80-500 Hz) are highly informative markers of an epileptic focus. In this review, we analyze features of high-frequency activity associated with the epileptiform activity, and its relation to the seizure onset range. Further study of high-frequency bioelectric activity of the brain is of interest to researchers and clinicians, and may improve the EEG differential diagnosis of epilepsy.

The objective was to study the state of vascular walls in young patients at various stages and various courses of epilepsy.

Materialsand methods. We examined 62 patients of young age with focal symptomatic and cryptogenic epilepsy for hanges in their blood vessels. Photoplethysmography combined with a non-invasive diagnostic system (“Angioscan Electronics”, Russia) were used. The patients were divided into 3 groups: 1) patients after a single (first) epileptic seizure; 2) patients with remission; 3) patients with treatment-resistant seizures.

Results. We found no structural changes in their blood vessels. However, the occlusion test showed changes in the functional state of large muscle arteries in all groups of epileptic patients. In addition, changes in microcirculatory beds were detected in patients after a single seizure and in those resistant to treatment. Patients after single epileptic seizures showed the largest changes in small resistance arteries and arterioles.

Conclusion. The results suggest that functional characteristics of vascular endothelium change in young patients suffering from epilepsy.

Aim: To determine main etiologies and clinical features of neonatal seizures (NS) in groups of newborns of different gestational age (GA).

Materials and Methods. Main etiologies of NS were evaluated in 165 newborns divided into four groups: I – 84 early preterm newborns with GA of 28 weeks or less, II – 52 newborns with 29-32 weeks GA, III – 12 newborns with 33-36 weeks GA, and IV – 17 term infants with GA between 37 and 41 wks.

Results. In the above 165 infants, the following causes of NS were found: perinatal hypoxia-ischemia – 72.1% of cases, grade III-IV intracranial hemorrhage – 6.1%, congenital infections in 9.7%, CNS infections (bacterial meningitis and viral meningoencephalitis) – 9.7%, сerebral dysgenesis – 1.2%, and inborn errors of metabolism and neurodegenerative diseases accounted for 1.2%. Intracranial hemorrhage (grade III-IV) was detected in newborns with GA less than 32 wks only. The etiological role of CNS infections was higher in term newborns (23.5%) than in the other groups.

Conclusion. In examining newborns with NS, genetic mechanisms should be taken into consideration, especially when no indications of early brain damage are apparent. This approach is important today as targeted therapies of gene-associated epileptic syndromes are becoming feasible. In the present article, the use of levetiracetam in infants with NS and early onset epilepsy is discussed.

Objective. The aim of the study was to evaluate the efficacy of treatment in patients with prolonged duration of medial temporal epilepsy (MTE).

Materials and methods. We studied cases of 93 patients with history of MTE lasted more than 10 years.

Results. This form of epilepsy is often characterized by drug resistance; therefore, patients have to try different medications before the effective one is found (in 12% of cases, patients tried 5-7 different medicines). Nevertheless, in 48.4% of patients, pharmacotherapy is ineffective. According to our findings, patients with an early MTE debut and those with an epileptogenic focus (by EEG / MRI data) in the medial temporal zone are most likely to have treatment-resistant epilepsy.

Conclusion. If the therapy is ineffective, patients should be referred to preoperational examination.

The aim of the study was to assess the course of epilepsy in patients with signs of cranio-cerebral imbalance with a low CSF-cranial index.

Materials and methods. We conducted a prospective analysis of clinical, instrumental and laboratory data from the case histories of 78 patients with epileptic seizures (cryptogenic epilepsy). Group I included 36 patients with normal reserve CSF volumes and physiological values of the CSF-cranial index; these patients received standard multicomponent therapy. Group II was comprised of 42 patients with abnormally small reserve CSF spaces and a lower than normal CSF-cranial index; patients in group II received the same treatment as did patients in group I.

Results. We found a moderate correlation between the head circumference and the values of the CSF-cranial index. A strong correlation between the seizure occurrence rate and the values of the CSF-cranial index was also found (R=0.32, p=0.0043); the seizure rate correlation with the head circumference was less obvious (R=0.11, p=0.037). Most of the patients in group I had bilateral seizures, whereas in patients of group II the seizures were of a mixed character.

Conclusion. The results of this clinical study suggest that the course of epilepsy in patients with a low CSF-cranial index is determined by the severity of anatomical reduction in the CSF dynamics; in most cases of a low CSF-cranial index, the course of epilepsy is severe. These findings should be considered at the starting and the later stages of antiepileptic therapy.

The problem of a late referral to surgical treatment in epilepsy was addressed in this study.

Objective: To elucidate whether the course of epilepsy is influenced by the duration of the disease.

Materials and Methods. A cohort of 91 patients with epilepsy who underwent surgical interventions from 2012 to 2017, were retrospectively studied. The disease dynamics (frequency and type of seizures) as well as the EEG changes were assessed.

Results. Of those patients, 77% had epilepsy more than 10 years, and 41% – more than 20 years. The temporal localization was found in 71% of cases, and the extra-temporal – in 29%. In all patients, seizures occurred at least once a month. Secondary generalized seizures were found in 58% of patients, and status epilepticus was observed in 30% of cases.

Conclusion. The course of epilepsy in the clinical and neurophysiological terms deteriorates with a long duration of the disease. The present results can be used to determine the optimal time for a referral for surgical treatment.

The article presents a clinical case of infantile cerebral palsy combined with BEDC (with no epileptic seizures) in dizygotic twins. The case supports the hypothesis of genetic nature of the BEDC patterns. The variety of EEG characteristics and clinical courses of the disease in children with cerebral palsy and BEDC are reviewed. Correct interpretation of the EEG findings provides an accurate prognosis of seizures and cognitive functions, as well as the patient management tactics. In these patients, continuous video EEG monitoring (both awake and sleeping) is recommended for a long-time follow-up.

It is well known that sudden unexpected death in epilepsy (SUDEP) is one of the most significant factors of mortality in epileptic patients. There is an increased risk of SUDEP in genetic epileptic encephalopathies (EE), partly because those syndromes are associated with mutations in the “neurocardiac” genes, which have been implicated in both epilepsy and cardiac arrhythmias. In these clinical conditions, functions of ion selective channels (sodium, potassium and etc.) are affected; for example, in children with Dravet syndrome, the risk of SUDEP is 40 times higher than that in children with common epilepsy syndromes. In a murine model of SCN1A epilepsy, a prolongation of QT interval coincided with a seizure; in addition, an excessive excitability of cultured cardiomyocytes was demonstrated. A high risk of SUDEP is characteristic for EE caused by mutation in the SCN8A gene. Other prognostic biomarkers of SUDEP may include mutations in sodium channel genes, such as SCN4A, SCN10A, and SCN11A. Our knowledge about SUDEP associated with potassium channel dysfunctions is still very limited. There are likely some mutations in other genes, that can modify (increase or decrease) the risk of SUDEP in EE. If patients with genetic EE are indeed at a high risk for SUDEP, they must be followed up by cardiologists alongside with neurologists. Provided this hypothesis is proved, any newly diagnosed arrhythmia should be carefully monitored and treated (with medications and/or interventions), in order to improve the survival rate in genetic EE.