In this review we discuss clinical significance of using evoked potentials in children with epilepsy and related disorders. This approach has been commonly adapted for practice in pediatric epileptology. In most cases, it serves a neuromonitoring tool to assess the effectiveness of a therapy program and / or its side-effects. In addition, the method of evoked potentials is helpful in testing the central inhibition and excitation balance in different forms of epilepsy. In this respect, we also take a look at the impact of epileptic activity on the function and development of brain regions. The method of evoked potentials may be used for localization of epileptic lesions in children suffering from focal epilepsy. Given the variety of existing modalities of evoked potentials, their safety, painlessness and neuromonitoring qualities, we recommend to expand the use of these techniques in pediatric patients with paroxysmal disorders.

West syndrome is an epileptic syndrome, characterized by a triad of symptoms: infantile spasms, hypsarrhythmia on interictal EEG, and a regression or delay of psycho-motoric development. According to the current concept, two of these three criteria suffice for the diagnosis. The incidence of this syndrome is 1 per 2000 newborns. This article reviews recent publications on the etiology, pathogenesis, clinical course, diagnosis, and treatment options in West syndrome. The text is supplemented with illustrations of ictal EEG at infantile spasms and variants of hypsarrhythmia. Today, in addition to classical hypsarrhythmia, five versions of modified hypsarrhythmia are proposed: synchronized version, asymmetric version, version with stable focus of spikes or acute waves, version with rhythmic flattening episodes, version with high-amplitude and asynchronous slow activity. The hormonal therapy is recommended to begin the treatment; if not effective, vigabatrin is to be used as the second choice medication.

We have conducted an experiment with valproic acid drugs (used as an example), where we have identified the determinant and dominant structures of the epileptic system. The main determinant structure is hypothalamus; it is responsible for secondary generalized seizures formation. The next strusctures in the hierarchy are contralateral and ipsilateral hippocampus, contralateral cortex. Collateral subordination of the structures and the transformation of the epileptic pathological system has been revealed. We demonstrated the advantages of the Depakin Chronosphere microgranules and effectiveness of the drug for treating children, adolescents, adults and elderly patients with epilepsy. The results of experimental studies with Nano-Phenazepam substantiate its further development as an antiepileptic drug for the treatment of secondary generalized seizures and prevention of status epilepticus. To optimize the surgical treatment of pharmacoresistant epilepsies, it is necessary to use minimally invasive functional neurosurgical techniques and/or their combination in each individual patient.

Electrical status epilepticus during slow-wave sleep (ESES) is an EEG pattern of continuous (85-100%) diffuse epileptiform activity in the sleep EEG. The morphology of the epileptiform complexes is identical to benign epileptiform discharges of childhood (BEDC). Epilepsy with ESES (or “Penelope Syndrome”) is a form of age-dependent epileptic encephalopathies with the phenomenon of continuous spike-waves during slow wave sleep. This group of epilepsies also includes Pseudo-Lennox syndrome, Landau-Kleffner syndrome, autistic epileptiform regression and some others. In most cases, the ESES pattern correlates with the severity of cognitive deficit in this population of epileptic children. The aim of this study was to evaluate the efficacy and safety of levetiracetam in children with the ESES pattern in the EEG. Materials and Methods. During the period of 2010-2016, 34 epileptic children with ESES patterns in the EEG (14 boys and 20 girls) treated with levetiracetam (33 in combined and 1 in monotherapy) were studied. Results. Twenty eight of the patients with ESES patterns in the sleep EEG were diagnosed with the ESES form of epilepsy. Among them, 7 idiopathic, 13 symptomatic, and 8 “symptomatic” cases of ESES (the latter resulted from “double pathology” of idiopathic + hypoxic-ischemic factors and these children had cerebral palsy). Among other ESES patients, 3 cases were of Pseudo-Lennox syndrome, 2 cases of Landau-Kleffner syndrome and one girl with autistic epileptiform regression. All 28 children received levetiracetam at therapeutic doses of 20-80 mg/kg/daily. Levetiracetam was highly effective in 67.6% of patients (n=23); of those, 2 children showed full clinical and electroencephalographic remission before reaching puberty, 9 children had clinical remission and 12 children had a significant decrease in seizures and epileptiform discharges. A low efficacy of levetiracetam was seen in 20.6% (n=7) of patients. Disease aggravation (seizures and epileptiform discharges) was found in 11.8% (n=4) of patients. Other negative effects were observed in only 4 (11.8%) children (3 cases of agitation and sleep disturbance and one case of allergic rash). In conclusion, levetiracetam is a highly effective medication (67.6% of cases) in combined antiepileptic therapy in children with ESES. However, the risk of exacerbation was as high as 11.8%. The most effective combinations of levetiracetam were those with valproates and ethosuximide.

The aims of this study were: (a) to elucidate the role of prolonged computerized EEG in assessing the brain function in patients with focal lesions (stroke consequences, tumor, etc.), and (b) to summarize the experience of using outpatient and inpatient EEG monitoring in neurological practice.

Materials and methods. The study included 99 patients with post-stroke and other focal lesions or with a neurological deficit (aphasia, paresis, etc.) or with focal slow-wave and paroxysmal (epileptiform) activity, or with suspected «epilepsy». The patients were monitored using the method of ECG in outpatient and / or neurological hospital settings. The diagnosis of symptomatic epilepsy was confirmed in 81 patients (86%), and not confirmed – in 13 patients (14%). The patients’ age ranged from 16 to 78 years (average 56); the male/female ratio was 37/57.

Results. The outpatient and impatient Holter EEG monitoring revealed various EEG patterns both in norm and pathology. Among those: different epileptiform signs (detected in all groups of patients) with different occurrence rates: PLEDs – rhythmic delta, frontal – FIRDA, temporal – TIRDA, spikes and complexes on the left and / or right, generalized paroxysms and photosensitivity. Examples of these EEG patterns (awake and sleep) are presented. Of special interest is the epileptiform pattern where polyspikes are combined with K complexes in the 2nd stage of sleep. Both generalized and focal patterns – mostly typical for sleep EEG – are demonstrated. The method of multiple dipole localization (MDL) was used to directly localize the sources of the abnormal EEG activity (slow-wave and paroxysmal) in the brain. In this report, combined results of EEG and MRI indicating the sources of the abnormal electrical activity are presented to compare the localization of the spike activity with that of the rhythmic slow waves. Two major causes of functional deficiency in post-stroke aphasia and plegia (and similar disorders) are proposed. Firstly, it is the presence of an ischemic focus with a decreased cerebral blood flow in this zone that results in a focal slow-wave activity (delta focus). Secondly, a loss of function can be caused by a continuous discharge activity of brain neurons. An epileptogenic focus and a continuous paroxysmal activity can lead to over-stimulation of brain neurons.

Conclusion. Monitoring and analyzing EEG indicators in outpatients significantly expand the capabilities of EEG and provide new information on the brain function. In respect to the differential diagnosis between epileptic and non-epileptic seizures, prolonged monitoring allows to obtain additional information from EEG records and better identify epilepsy-associated activities.

Temporal epilepsy is one of the most common forms of epilepsy. This form of epilepsy is diagnosed in about 25% of all epileptic patients; around 30-40% of temporal epilepsy cases are drug-resistant. Since 1945-1955, both preoperative diagnosis and surgical treatment of temporal epilepsy have been consistently improving. Indications for surgery include drug-resistance, disease progression and a decline in patient’s quality of life. Surgical treatment of temporal epilepsy results in remission or essential decrease in the seizure incidence in 60 to 85% of patients. In this report, a female patient (35 years old) diagnosed with temporal epilepsy at the age of 2, is described in terms of preoperative diagnostic procedures and subsequent surgical treatment.

The report addresses the causes and diagnostic problems of cryptogenic focal frontal epilepsy. A clinical case of a patient with cryptogenic focal frontal epilepsy is presented. In this patient, epileptic seizures have long been considered as psychogenic non-epileptic paroxysms.

Objective of the research is to evaluate the anticonvulsant effect of the new original compound GIZH-298 (4-benzoylpyridine oxime derivative) versus valproic acid (VPA) in a model of epilepsy in rats with cobalt-induced lesions.

Materials and methods. Modeling of epileptic status was performed using the technique of creating a chronic epileptogenic focus caused by the application of cobalt to the sensorimotor zone of the rat cortex, followed by intraperitoneal administration of homolecysteine thiolactone. Compounds GIZH-298 and VPA were introduced against the background of development of electrographic status with behavioral convulsive seizure manifestations.

Results. The study revealed that GIZH-298 at a dose of 60 mg/kg (i. p.) in 50 minutes after injection reduces the number of high-amplitude generalized discharges caused by homocysteine thiolactone in the ipsilateral and contralateral cortex (46-fold decrease), in the hippocampus and hypothalamus (28-fold decrease); eliminates (in 100% of the animals) the generalized tonic-clonic seizures that arise in the advanced stage of status epilepticus. VPA at a dose of 100 mg/kg (i. p.) in 3 hours after injection significantly suppresses the EpA in all evaluated structures with the maximum value in the hypothalamus (28-fold decrease), and after 5 hours in the ipsilateral and contralateral (33-fold decrease). At the same time, VPA eliminates generalized motility of status epilepticus only in 71% of the animals and protects from death 86% of the rats.

Conclusion. The compound GIZH-298 significantly earlier (for 2 hours) than the VPA (100 mg/kg) and at a lower dose (60 mg/kg) fully eliminates electrographic (in all evaluated brain structures with the greatest efficiency in the contralateral cortex and the hypothalamus) and behavioral manifestations of unfolded status epilepticus and prevents deaths in 100%.