In the light of the development of molecular biology and pathomorphology, ideas about degenerative diseases of the nervous system are gradually changing. A clear evidence of this is the description in recent years of new forms of neurodegenerative pathology, manifested by cognitive decline and dementia. These forms include Limbic-Predominant Age-Related TDP-43 Encephalopathy (LATE); dementia associated with Quadruple Misfolded Proteins (QMP), Neuronal Intranuclear Inclusion Disease (NIID). Their appearance in a wide range of neurodegenerative diseases, characterized at the molecular and phenotypic level, raises several questions — from the introduction of new complex terms into the Russian-language scientific literature to the formation of new knowledge among specialists to identify these conditions in practice. The review examines in detail the spectrum of clinical manifestations and genetic characteristics of new forms of neurodegenerative dementia, as well as modern possibilities of their diagnosis.

One of the most common symptoms of multiple sclerosis is a cognitive impairment, which becomes severe in the late stage of disease. It is difficult to evaluate the probability of cognitive deficit development and the rate of its progression. Evaluation of neurological status and neuroimaging data in neurodegenerative diseases patients show an inconsistency in the severity of cognitive symptoms. This served as the basis for creating the concept of cognitive reserve, which reflects the brain’s ability to compensate cognitive impairment resulting from damage to brain structures. the term «cognitive reserve» has acquired several «concepts». Despite these concepts are used only for scientific researches, it has a good potential for implementation in clinical practice. This review contains information about the supposed physiological mechanisms of the cognitive reserve, role for preventing of the development of cognitive and motor deficit, methods of cognitive reserve quantitative assessment by clinical and neuroimaging methods, and possible ways of increase.

The aim of this review was to analyze domestic and foreign publications reflecting the main existing theories of tension-type headache (TTH) development and the search for common pathogenetic links of TTH with arterial hypertension (AH) as potential triggers for the development of the clinical TTH and AH phenotype.

Methods. We searched for articles in databases (eLibrary.ru, Web of Science, Scopus, PubMed, Clinical Case) by keywords. Search depth – 2006–2021.

Results. The analysis allowed us to identify the leading theories underlying the development of TTH: psychogenic, vascular, myofascial, biochemical and neurogenic. At the same time, a neurobiological theory has been considered: it combines some of the mechanisms of previously studied pathogenetic theories of TTH. In addition, there are the most important (from the clinical point of view) mechanisms of the comorbidity of TTH and AH, which underlie the development of the TTH + AH phenotype. In terms of these mechanisms, in recent years, it is of scientific interest to study the role of nitric oxide (NO) and NO-synthases, since they play an important role not only in the development of the comorbidity of two diseases simultaneously existing in one patient (phenotype «TTH and AH», but also in modulating the response to drugs for the treatment of TTH and AH. Modulators of NO and NO-synthases, which have been developed in recent years, can improve the efficacy and safety of therapy for this phenotype.

Conclusion. New approaches to predicting and disease-modifying therapy of the TTH and AH phenotype can increase the efficiency and safety of treatment, and improve the quality of life of patients, and reduce the risk of cardiovascular complications.

Introduction. Аpproximately 20% of all patients referred for coronary bypass surgery (CABG) have hemodynamically insignificant carotid artery stenoses. It is known that a decrease in the elasticity of the walls of the arteries of the brain due to atherosclerosis is a risk factor for cerebrovascular complications in cardiac surgery. The purpose of the work. Construction of prognostic models determining the probability of decompensation of chronic cerebral ischemia (CIG) and the development of early postoperative cognitive dysfunction (POCD) in patients with hemodynamically insignificant carotid artery stenosis in the hospital period of CABG performed under conditions of artificial circulation.

Material and methods. 58 patients with < 50% carotid artery stenosis were examined, age – 56.2 [52.0; 63.0] years. Neurological, neuropsychological and laboratory-instrumental examinations were performed 2–3 days before and 8–9 days after the operation. The degree of narrowing of the carotid arteries was determined by color duplex scanning. Regression and ROC analyses were performed.

Results. Decompensation of HIGM on day 8–9 of CABG was detected in 51.7%, early POCD – in 63.8% of patients. The prognostic criteria for the decompensation of the CIG and the development of early POCD were: a long history of arterial hypertension, low myocardial contractility, estimated by the preoperative index «left ventricular ejection fraction», a low average value of plasma glucose in the intraoperative period and the development of a systemic inflammatory reaction, estimated on the SOFA scale of «5 or more points» in 1–2 days after CABG.

Conclusion. With the help of the obtained prognostic models, it is possible to stratify the probability of decompensation of HIGM and the development of early POCD in order to prescribe preventive treatment in a timely manner.

Introduction. Cerebral microangiopathy (CMA), being the leading cause of vascular cognitive impairment and strokes, has a number of causes, among which chronic kidney disease (CKD) and programmed hemodialysis (HD) are the least studied.

Purpose of the study: to determine the frequency of CMA neuroimaging markers and risk factors for its development in patients receiving renal replacement therapy for a long time using the programmed HD.

Material and methods: the study involved 70 patients who had been on programmed HD for 10 months or more. Clinical neurological examination, laboratory tests and brain MRI were performed. The analysis of CMA neuroimaging markers was carried out in accordance with the STRIVE recommendations. Cerebral Small Vessel Disease Score (CSVDS) was used to quantify the overall severity of MR imaging markers of CMA.

Results. Among 70 examined (29 men and 41 women) aged 53.0 ± 14.2 years, average HD experience – 70.0 ± 39.5 months, the main clinical manifestations of CMA were cognitive impairment (82.9%, n = 58), emotional disorders (61.4%, n = 43), sleep disorders (38.6%, n = 27), pseudobulbar syndrome (17.1%, n = 12), walking disorders (8.6%, n = 6), acute lacunar syndromes (7.1%, n = 5) and pelvic dysfunction (4.3%, n = 3). CMA neuroimaging markers of varying severity were found in 100% of cases. Expansion of perivascular spaces (100%, n = 70) and white matter hyperintensities (81.4%, n = 57) prevailed in the structure of CMA imaging markers. Cortical atrophy (67%, n = 47), cerebral microbleeds (47%, n = 33), asymptomatic lacunae (35.7%, n = 25) and minor subcortical infarctions (2.9%, n = 3) were less common. Mild CMA (1–2 points on the CSVDS scale) was determined in 38 patients (54.3%), severe CMA (3–4 points on the CSVDS scale) – in 32 patients (45.7%). The presence of uncontrolled arterial hypertension (OR 1.85, p < 0.05), intradialysis hypertension (OR 2.8, p < 0.05), dialysis vegetative polyneuropathies (OR 2.75, p < 0.05), type 2 diabetes mellitus (OR 5.7, p < 0.05) and the experience of programmed HD (more than 50 months) (OR 3.1, p < 0.05) were prognostic signifi cance for the development of severe CMA in dialysis patients.

Conclusion. All patients with end-stage CKD who have been on programmed HD for a long time are shown to undergo the brain MRI in order to timely diagnose CMA imaging markers and possible correction of therapy.

A patent foramen ovale from an anatomical and physiological point of view is a normal communication between the atria, which is present in utero and allows oxygenated placental blood to reach the fetal arterial circulation. With incomplete postpartum fusion of the primary and secondary septa, a patent foramen ovale is formed. In the last two decades, clinical interest in the problem of the patent foramen ovale is dictated by the fact that its role in the development of such clinical syndromes as ischemic stroke, myocardial infarction, pulmonary embolism, migraine and decompression sickness of divers has been established, as well as the introduction of endovascular techniques for endovascular transcatheter closure of the atrial septal defect. It was found that the frequency of patent foramen ovale detection in patients with cryptogenic stroke is on average 2 times higher than in patients with an established cause of ischemic stroke and ranges from 40% to 50%.

Aim of study. Raising awareness of neurologists about the causes, pathogenetic mechanisms of development, methods of diagnosis and treatment of ischemic stroke in patients with patent foramen ovale.

Material and methods. To achieve this goal, the results of scientific research devoted to patent foramen ovale as a risk factor for cryptogenic stroke were analyzed. The literature search was carried out in electronic search engines Scopus, eLibrary, PubMed using the keywords: «ischemic stroke», «cryptogenic stroke», «patent foramen ovale», «pathogenesis of ischemic stroke». Scientific articles published between 1878 and 2021 were selected for analysis. 31% of the analyzed works are not older than 5 years.

Conclusion. The patent foramen ovale is etiologically associated with cryptogenic stroke. Possible mechanisms of ischemic stroke in patent foramen ovale patients include in situ thrombosis, paradoxical embolism, and atrial arrhythmias. Transcatheter endovascular closure of patent foramen ovale with anatomical signs of a high risk of cerebrovascular events in combination with antiplatelet therapy are indicated for patients with cryptogenic stroke aged 18 to 60 years as an optimal means of secondary prevention of ischemic stroke.

Aim: to systematize the results of studies devoted to the treatment and rehabilitation of patients with neurological consequences of «postcoid syndrome» and with vascular, post-inflammatory and traumatic lesions of the nervous system using adult stem cells.

Materials and methods. A search was carried out for literary sources including those published in peer-reviewed journals indexed in PubMed, Wos, Scopus and RSCI. We analyzed 45 articles on cell technologies and immunotherapy in neurology, of which 39 are included in this review. 72 articles devoted to cell technologies and immunotherapy in neurology were analyzed, of which 63 are included in this review.

Results. The inclusion of stem cells (SC) in rehabilitation programs for patients with various injuries and diseases of the central nervous system is a new, promising direction of research. Possible mechanisms of therapy for spinal cord injury based on the use of adult-type stem cells from the bone marrow, including CD34+, include many aspects. On the background of SC transplantation, damaged nerve cells and surrounding tissues, including neurons and glial cells, can be restored, which helps to ensure the integrity of the nerve conduction pathway and, thus, restore nerve function. SС therapy can suppress genes involved in inflammation and apoptosis, as well as activate genes with neuroprotective action, thereby protecting spinal neurons from secondary damage. The introduction of autoCD34+ SC will be performed intrathecally by spinal (lumbar) puncture performed in the L2–L3 gap, under local anesthesia with 1% lidocaine solution. The dose of autoCD34+ SC is determined by the content of CD34+ cells and is not less than 1 × 10⁶ CD34+ cells per 1 injection. Autologous hematopoietic stem cells (HSC) obtained from the patient himself do not cause immunological conflicts, and, accordingly, do not require immunosuppressive therapy, unlike donor (allogeneic) and xenogenic cells. Thus, the patient does not experience disturbances in the natural mechanisms of anti-infectious and antitumor control. At the same time, autologous HSCs are relatively easy to obtain and cultivate if necessary, and when using this type of cells, doctors do not face ethical and legislative challenges.

Conclusion. Taking into account the previously obtained data on the effectiveness of the use of autologous HSC SD34+ for the rehabilitation of patients with various types of damage to the nervous system and the universality of pathophysiological mechanisms in the central nervous system, it can be assumed that this area of cell therapy can be used to treat post-COVID-19 syndrome.

This article provides an overview of modern concepts of cerebrovascular manifestations of familial Mediterranean fever (FMV), also known as periodic disease, and describes own clinical observation. Despite the relative infrequency of cerebrovascular accidents in the structure of the clinical phenomenology of FMV, common pathogenetic aspects of these diseases indicate the need for a detailed examination of patients with suspected FMV. In addition, insufficient awareness of physicians about autoinflammatory diseases (of which FMV is a prominent member) underlines the need to include FMV in the spectrum of differential diagnosis of ischemic stroke, including taking into account national characteristics.

There is no unified management of patients with the consequences of subarachnoid hemorrhage in the long term.

Purpose of the study. To study the nature and severity of SAH, the clinical manifestation of hemorrhage, the choice of the intervention technique in the acute period of the disease for the long-term results of the treatment of aneurysms.

Materials and methods. In the long-term period, at an average time of 3.5 years after aneurysmal subarachnoid hemorrhage, 100 patients were examined who underwent microsurgical intervention (n = 48), endovascular exclusion of the aneurysm from the bloodstream (n = 14), simultaneous intervention, including microsurgical intervention and extra-intracranial vascular bypass (n = 23), as well as microsurgical intervention followed by the introduction of a fibrinolytic agent into the subarachnoid space (n = 15).

Results. Risk factors for unfavorable clinical recovery of patients, as well as the development of cognitive and mental disorders, were: intracerebral hematoma, dislocation syndrome, duration of temporary clipping more than 7 minutes, the volume of intraoperative blood loss of more than 300 ml. The best functional recovery in the long-term period was noted in patients who underwent microsurgical clipping of the aneurysm, supplemented by surgical revascularization (p = 0.003).

Conclusion. The results of our study demonstrated the persistence of the consequences of surgical intervention for the rupture of cerebral aneurysms for a long time, which necessitates long-term observation of patients, the development of individual programs of physical and psychological rehabilitation, and clinical examination of persons at high risk.

Objective. To study the efficacy of Cytoflavinum optimizing the pharmacotherapy of traumatic brain injury.

Material and methods. We examined 45 patients with mild to moderate traumatic brain injury aged 25 to 54 years. The patients were divided into two groups depending on the prescribed treatment. The first index group included 25 patients with traumatic brain injury who received complex therapy: Cytoflavinum against the background of standard therapy in accordance with clinical guidelines for the treatment of traumatic brain injury. Cytoflavinum was injected intravenously, once a day, 10 ml in 200 ml of 0.9% sodium chloride solution at a rate of 60–80 drops/min (3–4 ml/min) daily for 7 days. The second control group included 20 patients with traumatic brain injury who received only standard therapy. In accordance with the purpose of the study, laboratory blood parameters and their correlation with the parameters of the antioxidant status were determined, and the dynamics of the clinical condition of patients was assessed.

Results and conclusion. The administration of Cytoflavinum to patients contributed to a more pronounced positive dynamics of laboratory blood parameters in comparison with the control. Optimization of the pharmacotherapy of traumatic brain injury by the administration of Cytoflavinum made it possible to achieve a more pronounced regression of clinical symptoms and reduce the duration of hospitalization in comparison with the control group of patients.