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A comparative analysis of two case histories showing the effects of COVID-19 and immunization with the Sputnik V vaccine on the dynamics of epilepsy is presented. The study was part of the "Epilepsy and COVID-19" research initiative in a cohort of patients with epilepsy divided into two groups: those experiencing COVID-19 and those immunized with vaccine against COVID-19. We present here a comparative analysis of two case histories: recurrence of seizures in COVID-19 in a young (male) patient and good tolerance of vaccine in an older (female) patient with comorbid pathology after surgical treatment of drug-resistant epilepsy. Patient K (age 32 years, male) had generalized genetic (idiopathic) epilepsy with remission of seizures for three years. On the background of mild COVID-19 the patient experienced recurrence of generalized tonic-clonic seizures with deterioration of electroencephalographic indicators. Patient F (age 59 years, female) had focal drug-resistant epilepsy with remission of seizures for three years following surgical treatment, with comorbid endocrine pathology. No side effects were seen on immunization with Sputnik V vaccine and clinical-electroencephalographic remission persisted. The results showed good tolerance of Sputnik V vaccine, with persisting remission of seizures after neurosurgical treatment of drug-resistant epilepsy in the older patient with comorbid pathology and the potential for recurrence of seizures in the young patient on the background of mild COVID-19. These results will help practicing physicians determine management tactics in epilepsy patients. Continuation of this research on the effects of COVID-19 disease and vaccination on the dynamics of epilepsy in a larger cohort is needed.

There is a lot of evidence that a great Russian writer and essayist Fyodor Mikhailovich Dostoevsky suffered from epilep‑ sy. Not only this disease had influence on Dostoevsky’s personality and social life, but also affected his creative work. Dostoevsky is believed to suffer from mesiobasal temporal lobe epilepsy with an ecstatic aura – a form named after him afterwards.

Abstract Current antiepileptic strategies aim to normalize the interaction of the excitatory and inhibitory systems, which is ineffective in treating patients with drug-resistant epilepsy. Neuroinflammatory processes in the epileptic focus and its perifocal area can trigger apoptosis and also contribute to the development of drug resistance. The level of pro- and anti-apoptotic proteins (p-NF-kB, TNF-α, p53, FAS, caspase-3, caspase-9) was analyzed in intraoperative biopsies of the temporal lobe gray and white matter in the brain of patients with drug-resistant epilepsy. An increased level of pro-apoptotic proteins was revealed in the cortex and perifocal area’s white matter against the background of an imbalance of protective anti-apoptotic proteins. It appears that the activation of the extrinsic pathway of apoptosis occurs in the perifocal area, while in the epileptic focus, there are proteins responsible for the activation of the anti-apoptotic survival pathways. Active neuroinflammation in the epileptic focus and perifocal area of the temporal lobe may contribute to the development of the resistance to antiepileptic drugs and the progression of neurodegeneration in such patients.

An overview of the clinical observation of a patient with the consequences of severe traumatic brain injury, with a tracheoesophageal fistula is presented. The article discusses a staged multidisciplinary approach to treatment.

To study etiopathogenesis is one of the most important tasks of modern neurology. Various types of structural changes occur in drug-resistant epilepsy (DRE); however, they are described as distinct phenomena.To provide a comprehensive characterization of structural changes in the cortex and adjacent white matter in the electrophysiological activity zone (in the epileptic focus) in patients undergoing surgery for DRE.Biopsy material of fragments of the temporal lobe and hippocampus from 16 patients aged 21 to 54 years (mean age, 25 years) with DRE were intraoperatively obtained at the Prof. A.L. Polenov Russian Research Institute of Neurosurgery. The investigators studied histological sections stained with HE, toluidine blue according to the Nissl method and the Spielmeyer method, as well as the results of immunohistochemical reactions with glial fibrillary acidic protein (GFAP), vimentin, and neurofilaments (NF) (Dako antibodies, Denmark).Histological examination revealed a set of heterogeneous changes, reflecting the complex pathogenetic interactions that developed during the formation of an epileptic focus. Structural brain damage involved both gray and white matter. Focal cortical dysplasia was diagnosed in 14 (87.5%) cases; white matter neuronal heterotopia in 100%; neuronal reactive and destructive changes in 100%; epileptic leukoencephalopathy (vascular demyelination, microcysts, sclerosis and dystonia, gliosis) in 100%, cortical atrophy in 12.5%, and hippocampal sclerosis in 20% (in 2 out of the 10 examinees).The morphopathological heterogeneity in the structure of epileptic foci reflects the complexity of etiopathogenetic interactions, the polymorphism of epileptic manifestations, and the individual nature of formation of the epileptic system, which requires an integral approach to understanding the pathogenesis and morphogenesis of formation of the epileptic system and provides a direction for a personalized approach to epilepsy treatment.Изучение этиопатогенеза является одной из важнейших задач современной неврологии. При фармакорезистентной эпилепсии (ФРЭ) встречаются различные виды структурных изменений, однако их описывают как отдельные явления.Дать комплексную характеристику структурных изменений в коре и прилегающем белом веществе в зоне электрофизиологической активности (эпилептическом очаге) у больных, оперированных по поводу ФРЭ.Биопсийный материал фрагментов височной доли и гиппокампа (ПАО РНХИ им. проф. А.Л. Поленова), полученный интраоперационно от 16 пациентов с локально обусловленной ФРЭ в возрасте от 21 года до 54 лет (средний возраст — 25 лет). Изучали гистологические срезы, окрашенные гематоксилином и эозином, толуидиновым синим по методу Ниссля, по Шпильмейеру, а также результаты иммуногистохимических реакций с глиальным фибриллярным кислым белком (GFAP), виментином (Vimentin), нейрофиламентами (NF) (антитела фирмы Dako, Дания).При гистологическом исследовании выявлен комплекс разнородных изменений, отражающий сложные патогенетические взаимодействия, развивающиеся при формировании эпилептического очага. Структурное поражение мозга захватывало как серое, так и белое вещество. Диагностирована фокальная кортикальная дисплазия в 87,5% (14) случаев, гетеротопия нейронов в белое вещество в 100%, реактивно-деструктивные изменения нейронов в 100%, эпилептическая лейкоэнцефалопатия (демиелинизация, микрокисты, склероз и дистония сосудов, глиоз) в 100%, атрофия коры в 12,5%, «склероз» гиппокампа в 20% (2 из 10 исследованных).Патоморфологическая гетерогенность структуры эпилептических очагов отражает сложность этиопатогенетических взаимодействий, полиморфность проявлений эпилепсии, а также индивидуальный характер формирования эпилептической системы, что требует интегрального подхода для понимания пато- и морфогенеза становления эпилептической системы и дает направление персонализированному подходу к лечению эпилепсии.