Objective: to study the effect of blue polarizing glasses on photosensitivity in patients with photosensitive epilepsy (PSE). Materials and methods. On the backdrop of red light stimulation, EEG and daytime video EEG recordings were performed in 19 patients with epilepsy (15 women, 4 men) aged from 14 to 41 years. Among those, 8 patients had juvenile myoclonic epilepsy (JME), 2 – eyelid myoclonus with absences, 6 – generalized epilepsy, 1 – juvenile absence epilepsy (JAA), and 2 patients had unspecified (cryptogenic) focal epilepsy. All patients underwent photo-stimulation (PS) with an increasing light frequency from 1 to 31 Hz (in 3 Hz steps). The PS procedure was carried out twice: without and with the use of blue polarizing glasses with a degree of darkness of 50%. Results. In 19 patients with PSE, we observed a photo-paroxysmal response at frequencies of 10, 13, 15, 16, 19, and 21 Hz. In the same individual, this photo-paroxysmal response could have manifested either in a burst of epileptic activity without clinical symptoms or in myoclonus / myoclonia with absences. In 8 (42.1%) patients, there was a decrease in epileptic activity upon photo-stimulation: a decrease in the duration of the acute peak-slow-wave activity or a zero epileptic activity at one frequency on the backdrop of a notable epileptic activity at other frequencies. In 3 (15.8%) patients, who were using the blue glasses, there were neither seizures nor epileptic activity at all. In one case (5.3%), there was no seizure but the PS-induced epileptiform activity did occur. The disappearance of subclinical epileptic activity was noted in 2 (10.5%) cases. Conclusion. Blue polarizing glasses can be used as an additional means of non-pharmacological therapy of PSE. The protective effect may be associated with a decrease in the melatonin content in the daytime.

Classification of epilepsy is of great importance at the stages of rehabilitation when the disease is considered resolved. This is the time to address various aspects of etiology, pathogenesis, compensation and resolution of epilepsy and to decide upon further medical care. Materials and methods. Here we review clinical-neurophysiological, experimentalpsychological, and neuroimaging results of anti-epileptic treatment and its discontinuation in seizure-free patients. We also discuss the adoption of the new international classification of ILAE 2017 in the domestic epileptology and analyze clinical cases of 270 patients with epilepsy who were in control of seizures for up to 8 years. Results. The study revealed the clinical, neuropsychological and neurophysiological signs of epilepsy regression in patients with long-term control of seizures. In 85% of these patients, seizures were under control; in 45% of them, the issue of “resolution of epilepsy” was a matter of discussion. In this regard, we address the timing and indications for the discontinuation of antiepileptic drugs. Conclusion. The prolonged absence of seizures is due to an inhibition of epileptic activity at the neuronal level with a gradual restoration of the antiepileptic system during 3-5 years of seizure-free period; this mechanism is reflected in the new classification. The data obtained in the present study support the decision of the Russian League against Epilepsy to introduce the new classification of epilepsy proposed by ILAE in 2017. The new term “resolved epilepsy” has been adopted for use in patients previously referred to as “practically recovered”.

Stimulation of the vagal nerve is an effective treatment option in patients with pharmacoresistant epilepsy. Objective: to analyze the efficacy and safety of the Vagal Nerve Stimulation (VNS) procedure in patients suffering from pharmacoresistant epilepsy. Materials and Methods: The study included 13 patients with pharmacoresistant epilepsy, aged 5 to 38 years. Results: among these patients, 25% reported a decrease in the number of epileptic seizures within one-month time after the first session of VNS. The efficacy of the treatment improved with a prolonged use of the VNS-therapy. Despite the long duration of the current pharmacoresistant form of epilepsy in most patients, a decrease in the severity of epileptic seizures and post-seizure disorientation was noted. Side effects of VNS-therapy were recorded in 38.5% of patients; in those, a correction of VNS parameters was performed. This approach allowed us to maintain the effective VNS-therapy and correct the arising side effects. Conclusion: vagal stimulation is an effective non-pharmacological option in patients with pharmacoresistant therapy who have contraindications for surgical treatment. The VNS-therapy reduces the occurrence rate of epileptic seizures by >50% in 20-50% of patients. The VNS therapy has a good long-term efficacy in patients of any age. Stimulation of the vagal nerve is usually well tolerated.

The aim was to study the effect of lacosamide on epileptiform activity (EрA) and structure-function relations in the brain in the course of development of the epileptic system in rats with cobalt-induced chronic epilepsy. Materials and methods. To model chronic focal epilepsy, we used topical applications of cobalt on the sensorimotor zone of the rat cortex. The effect of lacosamide (20 mg/kg) on the cobalt-induced epileptiform activity was analyzed in parallel with with the monitoring of spectral-coherent changes in the brain during the development of the epileptic system (ES). Results. In the first 30 minutes after the administration, lacosamide briefly enhanced the EрA in the hippocampus and ipsilateral cortex, and also strengthened the cortical-hippocampal (at stage 1) and cortical-hypothalamic connections (at stage 2). Two hours after the drug administration, a decrease in EрA was observed at stages 1 and 2 of the ES development, especially in the contralateral cortex and hippocampus. At all frequency ranges, the level of the inter-center connections decreased (most pronounced in the cortical-hippocampal links). Conclusion. The effect of lacosamide on EрA in the rat brain with cobalt-induced epileptogenic focus is characterized by a decrease in EрA, two hours after the drug administration. This effect is most expressed in the cortex and hippocampus, and is accompanied by a decrease in the level of the corticalhippocampal connections.

Aim – to study the clinical and neurological manifestations in patients with drug-resistant epilepsy and optimize the therapy. Materials and methods. Fifty patients with drug-resistant epilepsy were examined. Of these, 28 were females and 22 were males; their average age was 32.6±11.4 years. All patients had true pharmacoresistant epilepsy, i. e., the seizures occurred on the background of adequate polytherapy with anticonvulsants; the use of anticonvulsants had no effect on the course of the disease. All patients underwent clinical and neurological examination. The patients were blindly divided into two therapeutic groups: the main group consisted of 25 patients who were prescribed with the combined therapy, which included a biologically active polypeptide at a dose of 10 mg/day for 20 days with a subsequent transition to hopantenic acid (500 mg twice a day for 2 months). The second group did not receive these drugs. For the anticonvulsant therapy, both groups received the combinations of valproic acid (30 mg/kg at two daily doses) and carbamazepine (5 mg/kg at three daily doses). The significance of differences was determined by the paired and unpaired Student’s t-test. The differences were considered statistically significant at p <0.05. Results. The data on the occurrence of subjective and focal neurological symptoms indicated the prevalence of complaints characteristic of general cerebral symptoms in the form of headaches, dizziness, as well as subjective symptoms of cerebral asthenia. In addition, some patients complained of short-term memory impairments. In most cases, drug-resistant epilepsy developed on the background of organic brain damage. In 87.2±6.9% of cases, we encountered a Chvostek sign indicating an increased excitability of the nervous system. Both groups of patients showed positive yet different clinical dynamics: the number of seizures decreased in 40% of patients taking the polypeptide regulator and hopantenic acid, and in 28% of patients in the comparison group (p<0.05). Conclusion. In order to optimize the anticonvulsant therapy, it is recommended to prescribe a combination of valproate and carbamazepine; to increase the efficacy of the combined therapy it is recommended to add the polypeptide regulator and hopantenic acid.

The paper addresses the relatively rare inherited neurodermal disorder – Sturge-Weber syndrome that can manifest in epileptic seizures. We describe updated concepts, epidemiology, etiology, pathogenesis, clinical manifestations, and surgical treatment of the disease. We examined medical records of 21 patients (aged from 1 to 11 years) with Sturge-Weber syndrome treated over the period of 1996-2016. After surgical treatment of 10 patients (five cases with hemispheretomy and five – with multifocal resection), positive outcomes (Engel class I, II) were found in 70% of cases, and negative (Engel class III, IV) – in 20% of cases. Оne child suddenly died during epileptic seizures. In non-operated children (age from 2 to 5 years) under our observation, an improvement was noted in six cases, no changes – in three cases, and a further progression of the disease – in three cases. In this article, we analyze two of these cases in detail.

Aim. To analyze efficacy of levetiracetam monotherapy in patients with epilepsy associated with benign epileptiform discharges of childhood (BEDC). Materials and methods. We examined 29 pediatric patients with idiopathic and symptomatic BEDC-associated epilepsy, including continuous spike-and-wave epileptiform activity during slow-wave sleep (CSWS) in the stage of clinical remission. Of those, 12 children received antiepileptic treatment with valproic acid, and 17 children received levetiracetam. The examination included passive awake EEG recordings (with functional tests) as well as daytime sleep EEG recordings (within 60 minutes). Results. Levetiracetam was no less efficient in monotherapy of BEDC-associated epilepsy (including the CSWS patterns) than the traditionally used valproic acid, especially in idiopathic forms of epilepsy. Conclusion. Levetiracetam can be recommended for the first-choice basic anti-epileptic monotherapy treatment.

The article presents a clinical case of severe infantile generalized idiopathic epilepsy with status-like seizures, muscular dystonia and developmental delay. The examination included a phenotypic analysis: the course of the perinatal period, the nature of seizures, cognitive and behavioral disorders; video electroencephalography, and brain MRI. Using the targeted exome sequencing of genes associated with epileptic encephalopathy (NGS), we detected a nucleotide heterozygous variant of the ALDH7A1 gene (previously not described). This mutation led to the appearance of a stop codon in position 82 of the protein p.Arg82Ter and the amino acid substitution in position 399 of the protein p.Glu399Gln. This clinical observation demonstrates the importance of DNA-based diagnosis involving the targeted exome sequencing to identify molecular defects, especially in severe neonatal drug-resistant seizures. In the case of confirmed mutations in the ALDH7A1 gene, the patient should be given vitamin B6 at the therapeutic doses for seizure relief.

Pharmacotherapy is the first-line treatment modality for epilepsy. However, in 20-40% of patients, epilepsy is resistant to pharmacotherapy. These numbers have not changed for decades despite the development and use of antiepileptic drugs with novel mechanisms of action. Drug-resistant epilepsy is now considered a separate pathophysiologic and clinical entity. The existing hypotheses on its pathogenesis could be divided in two groups. Firstly, drug-resistance might be caused by an abnormal pharmacokinetics or pharmacodynamics of antiepileptic drugs as a result of congenital or acquired dysfunction of the transporter or receptor proteins. Secondly, it might be a consequence of inherent features of epilepsy per se, such as the so-called “intrinsic severity” or some disorder of the connectome. Taking into account the complexity of this phenomenon, the issue of drug resistance continues to remain in the focus of the current research efforts.

Dizziness (vertigo) and migraine headache are among the most common neurological disorders. The association of dizziness and migraine in the population occurs more often than these conditions diagnosed separately. The probability of their random coincidence is about 1% among the adult population, and the prevalence of migraines combined with dizziness is 3.2%, i. e. about 3 times higher than a mere coincidence. Epidemiological studies have found that the associations between migraine and vertigo is bi-directional. On the one hand, migraine is more common among patients with dizziness, and on the other hand, dizziness is more common among patients with migraine. Moreover, such comorbidity with dizziness is more typical for migraine, and not for other forms of headache. On this background, the term “migraine-associated dizziness”, or “vestibular migraine” (VM) has been introduced. In 2001, H. Neuhauser et al. proposed a list of diagnostic criteria for VM, and this condition has been recently included in the ICDB-3 beta version as a separate nosological unit. By now, the pathophysiology of the VM is not well understood; the current hypotheses are mainly based on the pathophysiology of migraine itself. Yet, a number of recent studies have made a significant contribution to the understanding of the neurophysiological processes involved in the development of VM. There is a hypothesis that dizziness in migraine represents a migraine aura; this mechanism is based on the phenomenon of spreading cortical depression, i. e., a wave of depolarization that originates in the occipital cortex and slowly moves to the ventrally located areas. Vestibular disorders are known to be caused by the release of neuropeptides (substance P, neurokinin A, calcitonin-like peptide); these peptides stimulate the impulse activity of the sensory epithelium in the inner ear and the vestibular nuclei of the brain stem. In addition to the existence of vestibular migraine, as an independent form of headache, other migraine-associated vestibular disorders have been identified. The most commonly seen are nonspecific symptoms, e. g., motion sickness (that occurs in about 50% of patients), peripheral vestibulopathies, and subclinical vestibular disorders detected in patients with migraine by an instrumental neurovestibular examination in the interictal period. The precise mechanisms of the association between migraine and vertigo are not well understood. Clarifying the clinical and pathophysiological details of the relationship between these conditions is very important for optimal management of patients with migraine.