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The article discusses certain aspects of the relationship between neurological diseases and metabolic disorders that are extremely relevant in connection with the pandemic spread of obesity. The pathogenesis of damage to the nervous system (NS) is considered in detail. The influence of the main metabolic factors on the development of cerebrovascular diseases (CVD), incl. neuroinflammation, changes in hemostasis, etc. is demonstrated. The problem of the development of cognitive dysfunction against the background of obesity due to the formation of atrophic processes in brain structures is highlighted. Modern possibilities of evaluation and modulation of eating behavior due to brain stimulation using functional magnetic resonance imaging (fMRI) and navigational rhythmic transcranial magnetic stimulation (rTMS) are described.The problem of cerebrometabolic health is presented as a continuum of metabolic and cerebral disturbances. The mechanisms of interaction between the two most important systems of the body allow us to consider the changes that occur in them as an integral neuroendocrine alteration.

Aim. Evaluation of various methods for determining the effectiveness of aspirin therapy and aspirin resistance in patients with cerebrovascular disease (CVD) depending on the presence of type 2 diabetes mellitus (T2DM).Materials and methods. The prospective study included 78 patients with various manifestations of CVD. All patients received acetylsalicylic acid (ASA) 75 mg daily. Along with a comprehensive clinical examination, a laboratory assessment of platelet function with the usage of Born method with aggregometer, a detailed biochemical blood test (including the determination of the small subunit of low density lipoprotein [s-LDL]), as well as therapeutic drug monitoring of salicylates were performed on a gas chromatograph-mass spectrometer.Results. In 53% of cases, the absence or insufficiency of the effect of ASA on platelet aggregation was noted. Two subgroups were separately identified: with T2DM; (n=40) and without T2DM (n=38). Insufficient effect of the drug on platelet aggregation characteristics were observed in 65% of patients with T2DM and in 38% without T2DM. The differences were revealed between the groups in triglycerides, s-LDL, glycemic and glycated hemoglobin (p

The article presents a clinical case of comorbid pathology – development of migraine against the background of systemic mastocytosis. The classification and clinical manifestations of systemic mastocytosis, a rare blood disease, are given.This clinical case illustrates an example of excessive mast cell degranulation (with the release of proinflammatory and vasodilating agents as a result of mast cell pathology). In this regard, in addition to the pathogen-specific therapy for systemic mastocytosis (including prevention of mast cell degranulation), it seems important to describe the effectiveness and the possibility of prescribing preventive and emergency therapy for migraine against the background of the underlying hematological disease – systemic mastocytosis.Treatment of cephalalgia in patients with mastocytosis is a complex clinical task, in the solution of which it is necessary to take into account serious limitations in prescription of acetylsalicylic acid and other non-steroidal anti-inflammatory drugs.

Clinical case of ataxia development associated with accidental phenobarbital overdose is presented. Clinical manifestations and differential diagnostics are described; the results of laboratory examinations for this pathology are presented. In conclusion, there is an emphasis on the importance of collecting anamnestic data.

The article discusses the results of a study of asymptomatic patientswith a severe stenosing process in the brachiocephalicarteries (in a model of carotid atherosclerosis), with emphasison determination of biochemical markers associated with variousstages of atherogenesis. The definition of a group of proatherogenicand atheroprotective biomarkers is suggested andsubstantiated. Correlations among biomarkers are described.The correlations have potential etiopathogenetic nature, whichnecessitates further validation of these pathological changes inwider groups of patients.

Intensive development of DNA analysis technologies and largescale genome-wide association studies have led to accumulation of a large array of data on the relationship between genetic factors and various phenotypic manifestations, including monogenic and polygenic hereditary diseases. This greatly has extended the capabilities of clinical diagnostics and predictive medicine in the field of socially significant diseases. For example, a role of agenetic component of the risk for such a multifactorial and polyetiologic disease as stroke is now actively explored. Large-scale studies have revealed both general and specific genetic markers associated only with a certain type and subtype of stroke. This review analyzes the current state of the problem of using genetic markers for diagnosis of stroke predisposition, complex issues associated with multiplicity of risk factors for stroke, and possible development in this area.

Metabolic syndrome (MS) is a risk factor for the developmentof acute and chronic vascular diseases of the brain. Oxidativestress developing under these conditions promotes the progressionof atherosclerotic disease of the brachiocephalic arteries,which necessitates correction of the identified pathobiochemicalabnormalities. The use of antioxidant drugs in patients withcerebrovascular diseases and MS reduces manifestations of thelatter, including insulin resistance, hypertriglyceridemia, andhyperglycemia. The article presents the results of investigationof the drug mexidol in patients with chronic cerebrovascular diseasesassociated with atherosclerosis and MS. The findings demonstratethat drugs of this group have good prospects to be usedfor comprehensive correction of various pathogenic stages of thedeveloping pathology.

The article discusses the issues related to the personalization of preventive measures for ischemic stroke, in particular those associated with resistance to one of the most common antiplatelet drugs, aspirin. A brief historical note on investigation of acetylsalicylic acid is provided. The paper addresses the issue of etiological factors and epidemiology of aspirin resistance. Ananalysis and comparison of various techniques for evaluation ofthis phenomenon are performed. Separately, a molecular genetic aspect of the pathology is considered. In conclusion, the recommendations for overcoming tolerance to aspirin therapy are provided.

In the article, basic pathogenic mechanisms of progression ofcerebral atherosclerosis leading to ischemic stroke are discussed.The ultrasound, morphological and biochemical predictorsof changes of the atherosclerotic plaque structure arepresented. A multifactorial nature of pathogenesis of progressingcerebral atherosclerosis as a key cause of ischemic strokedetermines the need for further studies of different aspects ofthis problem, from vessel and brain morphology to metabolicparameters and various blood characteristics (biochemical,lipid, conformational, and hemostatic).

Backgrounds and Purpose: Post-COVID syndrome is characterized by persistent symptoms, including fatigue and cognitive impairment. These symptoms may be experienced by up to 80% of patients. We aimed to identify possible patterns of brain activation underlying post-COVID fatigue. Methods: The study used functional MRI (Siemens MAGNETOM Prisma 3T scanner with a specially created protocol) of the brain in 30 patients with post-COVID fatigue syndrome and 20 healthy volunteers. Task functional MRI (fMRI) was performed using a cognitive paradigm (modified Stroop test). Eligible patients included adults aged 18–50 years with a >12 weeks before enrolment (less than 12 months) prior history of documented COVID-19 with symptoms of fatigue not attributable to any other cause, and with MFI-20 score > 30 and MoCA at first visit. Healthy control participants had no prior history of COVID-19 and negative tests for severe acute coronavirus respiratory syndrome with MFI-20 score < 30 and MoCA at first visit. Task fMRI data were processed using the SPM12 software package based on MATLAB R2022a. Results: Cognitive task fMRI analysis showed significantly higher activation in the post-COVID group versus healthy volunteers' group. Between-group analysis showed significant activation differences. Using a threshold of T > 3 we identified eight clusters of statistically significant activation: supramarginal gyri, posterior cingulate cortex, opercular parts of precentral gyri and cerebellum posterior lobe bilaterally. Conclusions: Post-COVID fatigue syndrome associated with subjective cognitive impairment could show changes in brain functional activity in the areas connected with information processing speed and quality. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic inflammatory disorder which remains the main cause of cardiovascular morbidity and mortality, with carotid atherosclerosis (CA) being a major cause of ischemic stroke. Epigenetic regulation plays a significant role in CA progression and stroke, yet the impact of circulating microRNA expression, associated with atherogenesis, has not been clearly defined. We included 81 patients with moderate–severe CA (mean age 67 ± 7 years, 53% male), 42% of whom had prior ipsilateral ischemic stroke (i.e., were symptomatic). A total of 24 miRs were identified and their plasma expression levels were measured. We observed that several microRNAs were up-regulated in stroke survivors, namely miR-200c-3p (30.6 vs. 29.7, p = 0.047), miR-106b-3p (31.01 vs. 30.25, p = 0.004), and miR-494-5p (39 vs. 33, p < 0.001), while others (miR183-3p [25.5 vs. 28.6, p < 0.001], miR-126-5p [35.6 vs. 37.1, p = 0.03], and miR-216-3p [12.34 vs. 16.2, p < 0.001]) had lower plasma levels in symptomatic patients. In a multivariable logistic regression model for symptomatic CA, the only miRs showing statistical significance were miR-106b-5p, miR-183-3p, miR-216-3p, and miR-494-5p. Cluster analysis demonstrated differential miR expression in CA patients depending on their stroke status. Epigenetic modulation, represented as complex interplay between circulating miRs of different atherogenic potential, may play a significant role in CA development and progression. In our study, we show possible candidates for future research regarding CA and stroke. [ABSTRACT FROM AUTHOR]

Introduction: Neurology is arguably one of the most difficult subjects to teach and study in the medical curriculum. Educational games (EG) may be a valid option to enhance motivation in neurology residents.Methods: We developed an educational board game (Neuropoly) to assist in teaching neurology. We present here an overview of the game, as well as the results of a pilot study aimed at determining: (a) the efficacy of the game in teaching certain neurological concepts; and (b) student compliance and satisfaction with the EG.Results: The pre- and post-play questionnaire scores differed significantly (3.2 ± 1.7 vs. 7.8 ± 1.6, p < 0.001). Our group of residents, showing an overwhelmingly positive response, very well received the game. The questions were rated as above average regarding difficulty.Conclusion: The “Neuropoly” educational board game has been shown to be interesting, efficient, and motivational among first- and second-year neurology residents. Novel educational methods for complex medical disciplines should be developed, with board games being a viable and inexpensive approach.

Atherosclerosis is a chronic inflammatory disease with a complex, multifactorial pathogenesis, which includes lipid metabolism alterations. miR-33a is a microRNA that plays a key role in cholesterol efflux and promotes atherosclerosis, yet its relationship with lipid markers in carotid atherosclerosis (CA) remains unclear. The objective is to evaluate possible associations between miR-33a expression and lipid biomarkers in patients with CA. This was a prospective study that included 61 patients (median age 66.0 years, 55.7% male) with evidence of CA. Lipid profile (total cholesterol, triglycerides [TG], high-density lipoprotein [HDL] and low-density lipoprotein [LDL] cholesterol) was analyzed. Extraction and quantification of miR-33a-5p/3p was performed according to protocol. Patients were further divided depending on the target LDL level (<1.8 mmol/L). Patients with CA had relatively favorable LDL levels with a median of 2.0 mmol/L. Both miR-33a-5p and miR-33a-3p levels were lower in patients with less than targeted LDL levels (37.4 and 38.3 vs. 41.8 and 42.5 respectively, p < 0.05). A significant positive correlation between expression levels of miR-33a-5p/3p and degree of carotid stenosis was found (r = 0.44 and r = 0.38 respectively, p < 0.05). In a univariate linear regression model miR-33a-3p/5p was positively associated with LDL cholesterol (p = 0.02). miR-33a up-regulation is associated with CA and may, in fact, be a key player by targeting cholesterol metabolism. A decrease in LDL cholesterol (<1.8 mmol/L) corresponded to lower levels of miR-33a, yet the direction and causality of this association remains unclear. [ABSTRACT FROM AUTHOR]

Aim: The purpose of our study was to analyze the predictive ability of the multiplicative model of genetic risk of nonlacunar ischemic stroke (IS) for independent samples from Russia. Patients & methods: A total of 181 patients and 360 healthy controls were included in this study. The discriminative accuracy of model was evaluated by the area under the receiver operating characteristic curve (AUC). Results: Classification model based on 15 single-nucleotide polymorphisms (SNPs), which are associated with a cardioembolic subtype of IS, had an AUC of 0.62 in patients with corresponding subtypes and an AUC of 0.58 for all patients. Conclusion: Risk calculation approach based on IS-associated SNPs had satisfactory performance in predicting the predisposition to the disease. [ABSTRACT FROM AUTHOR]

Polycythemia vera (PV) is a Ph-negative myeloproliferative neoplasm (MPN) which is characterized by erythrocytosis and a high incidence of thrombotic complications, including stroke. The study aimed to evaluate red blood cell (RBC) morphodynamic properties in PV patients and their possible association with stroke. We enrolled 48 patients with PV in this cross-sectional study, 13 of which have a history of ischemic stroke. The control group consisted of 90 healthy subjects. RBC deformability and aggregation analysis were performed using a laser-assisted optical rotational red cell analyzer. The following parameters were calculated: aggregation amplitude (Amp), RBC rouleaux formation time constant (Tf), time of formation of three-dimensional aggregates (Ts), aggregation index (AI), rate of complete disaggregation (y-dis), and the maximal elongation of RBC (EImax). Statistical analysis was performed with the R programming language. There were significant differences in RBCs morphodynamics features between patients with PV and the control group. Lower EImax (0.47 (0.44; 0.51) vs. 0.51 (0.47; 0.54), p < 0.001) and γ-dis (100 (100; 140) vs. 140 (106; 188) s−1, p < 0.001) along with higher amplitude (10.1 (8.6; 12.2) vs. 7.7 (6.6; 9.2), p < 0.001) was seen in patients with PV compared with control. A statistically significant difference between PV patients with and without stroke in aggregation amplitude was found (p = 0.03). A logistic regression model for stroke was built based on RBC morphodynamics which performed reasonably well (p = 0.01). RBC alterations may be associated with overt cerebrovascular disease in PV, suggesting a possible link between erythrocyte morphodynamics and increased risk of stroke. [ABSTRACT FROM AUTHOR]

Backgrounds and Purpose. Philadelphia chromosome-negative myeloproliferative disorders (Ph-negative MPD) are a rare group of hematological diseases, including three distinct pathologies: essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF). They most often manifest with thrombotic complications, including cerebrovascular events. Covert brain infarcts (CBIs) are defin ed as predominantly small ischemic cerebral lesions that are detected using magnetic resonance imaging (MRI) in the absence of clinical stroke events. The relationship between MPD and CBIs remains unclear. Methods. Included in the study were 103 patients with the diagnosis of Ph-MPD (according to WHO 2016 criteria) (median age—47 (35; 54) years; 67% female). In total, 38 patients had ET, 42 had PV, and 23 had PMF. They underwent clinical examination, routine laboratory analyses (complete blood count), brain MRI, ultrasound carotid artery, flow-mediated dilatation (as a measure of endothelial dysfunction—FMD). Results. Overall, 23 patients experienced an ischemic stroke (as per MRI and/or clinical history), of which 16 (15.5%) could be classified as CBIs. The rate of CBIs per MPD subtype was statistically non-significant between groups (p = 0.35): ET–13.2%, PV–21.4%, and PMF–8.7%. The major vascular risk factors, including arterial hypertension, carotid atherosclerosis, and prior venous thrombosis, were not associated with CBIs (p > 0.05). Age was significantly higher in patients with CBIs compared to patients without MRI ischemic lesions: 50 (43; 57) years vs. 36 (29; 48) (p = 0.002). The frequency of headaches was comparable between the two groups. CBIs were associated with endothelial dysfunction (OR - 0.71 (95% CI: 0.49–0.90; p = 0.02)) and higher hemoglobin levels (OR—1.21 (95% CI: 1.06–1.55); p =0.03). Conclusions. CBIs are common in patients with Ph-negative MPD. Arterial hypertension and carotid atherosclerosis were not associated with CBIs in this group of patients. The most significant factors in the development of CBIs were endothelial dysfunction (as measured by FMD) and high hemoglobin levels. Patients with Ph-negative MPD and CBIs were older and had more prevalent endothelial dysfunction. [ABSTRACT FROM AUTHOR]

Introduction. Philadelphia-negative myeloproliferative neoplasms (MPNs) are a rare blood disorder characterized by pancytosis and thrombohemorrhagic complications. The aim of this article is to describe clinical and neuroimaging patterns of brain changes in patients with MPN. Materials and methods. The study included 152 patients with an established diagnosis of MPN (according to WHO criteria 2008, 2016). A clinical and neurological examination, laboratory tests, and magnetic resonance imaging of the brain were performed. Results. In patients with polycythemia vera and primary myelofibrosis, neuroimaging patterns are represented by small (up to 1.5 cm) post-infarction lesions in the brainstem, cerebellum, and cortex in adjacent perfusion territories after hemorheological microocclusive stroke. In patients with essential thrombocythemia, the neuroimaging pattern is more often represented by massive post-infarction changes in cortical-subcortical brain tissue with atherosclerotic lesions of the major head arteries, which appear to be atherothrombotic. Stroke preceded hematologic diagnosis in 30% of polycythemia vera cases, 40% of essential thrombocythemia cases, and 25% of primary myelofibrosis cases.

Backgrounds and Purpose: Post-COVID syndrome is characterized by persistent symptoms, including fatigue and cognitive impairment. These symptoms may be experienced by up to 80% of patients. We aimed to identify possible patterns of brain activation underlying post-COVID fatigue. Methods: The study used functional MRI (Siemens MAGNETOM Prisma 3T scanner with a specially created protocol) of the brain in 30 patients with post-COVID fatigue syndrome and 20 healthy volunteers. Task functional MRI (fMRI) was performed using a cognitive paradigm (modified Stroop test). Eligible patients included adults aged 18–50 years with a >12 weeks before enrolment (less than 12 months) prior history of documented COVID-19 with symptoms of fatigue not attributable to any other cause, and with MFI-20 score > 30 and MoCA at first visit. Healthy control participants had no prior history of COVID-19 and negative tests for severe acute coronavirus respiratory syndrome with MFI-20 score < 30 and MoCA at first visit. Task fMRI data were processed using the SPM12 software package based on MATLAB R2022a. Results: Cognitive task fMRI analysis showed significantly higher activation in the post-COVID group versus healthy volunteers’ group. Between-group analysis showed significant activation differences. Using a threshold of T > 3 we identified eight clusters of statistically significant activation: supramarginal gyri, posterior cingulate cortex, opercular parts of precentral gyri and cerebellum posterior lobe bilaterally. Conclusions: Post-COVID fatigue syndrome associated with subjective cognitive impairment could show changes in brain functional activity in the areas connected with information processing speed and quality.

Introduction. Cardiovascular diseases are predominantly caused by atherosclerosis as a multifactorial chronic condition. Alterations in the hematological system and the blood vessel wall are considered as highly significant for onset and development of cerebrovascular disorders associated with atherosclerosis. Biomarkers as measurable indicators are to verify abnormal activity. Objective: to assess atherogenesis biomarkers in patients after carotid angioplasty and stenting (CAS) as associated with development of cerebrovascular disease. Materials and methods. We evaluated 50 individuals (50% men, 50% women; average age 65.4 6.4 years) with established cerebrovascular disease associated with brain atherosclerosis. All of them had hemodynamically significant abnormalities in the internal carotid artery (ICA) with both symptomatic (stenosis 60% and more) and asymptomatic (stenosis 70% and more) stenoses confirmed by duplex scanning of the brachiocephalic arteries. All patients underwent CAS as indicated. Before and 1 year after the intervention, we performed clinical and neurological examinations, brain magnetic resonance imaging, and laboratory tests of atherogenesis biomarkers. Results. At baseline, all the individuals demonstrated a pro-atherogenic shift in the assessed indicators, predominantly markers of extracellular matrix degradation, inflammation and atherogenesis (including osteoprotegerin and chromogranin А). Additionally, we established a direct correlation between osteoprotegerin levels and the characteristics of mostly hyperechoic atherosclerotic plaques (r = 0.29; p 0.05). A year later, no signs of restenosis were shown in follow-up ultrasound assessment of stented arteries in any patient. In 1 year post CAS, we found significant changes in the levels of osteoprotegerin (decrease to 1.765 pg/mL [1.592; 1.937]; p 0.05) and chromogranin А (elevation to 31.3 g/L [13.9; 90.7]; p 0.05). Re-assessment demonstrated association between changes in the pattern of the nitrogen oxide system, which tends to improve (NO elevation to 38.23 mol/L [32.95; 43.51]; p 0.001), and atheroprotective shift in the morphology of atherosclerotic plaques and biomarker profile. Conclusion. Prospective, 1-year long observation for patients who underwent CAS for symptomatic/asymptomatic hemodynamically significant ICA stenoses revealed favourable atheroprotective shift in both ultrasound and hematological atherogenesis biomarker ratio. This shift contributed to the absence of cerebral atherosclerosis progression during the follow-up. The process may be mediated by chromogranin А and osteoprotegerin, and their further research is needed from perspective of atherogenesis.

Introduction. Carotid atherosclerosis (CA) is one of the main causes of ischaemic stroke. MicroRNA is a relatively new group of biomarkers, some of which are associated with atherogenesis. The aim of the study was to evaluate the expression of several microRNAs in patients with cerebrovascular disease, depending on the severity of CA. Materials and methods. The study included 50 people (median age 66 [61; 71] years, 58% men) with cerebrovascular disease secondary to CA. The patients were divided into two groups: 16 patients (32%) had 70% internal carotid artery (ICA) stenosis (main group), while the remaining 34 patients had 70% stenosis and formed the comparison group. Expression of the following microRNAs was measured: miR-126-5p, miR-126-3p, miR-29-5p, miR-29-3p, miR-33a-5p, miR-33a-3p, miR-21-5p and miR-21-3p. Results. Compared to the comparison group, patients with a high degree of CA had reduced expression of miR-126-5p/-3p (4.8 and 5.9 vs. 8.5 and 7.6, respectively; p 0.001) and miR-29-3p (7.6 vs. 10.3; p 0.001), while miR-33a-5p expression was elevated (46.3 vs. 40.0; p 0.05). Cluster analysis confirmed typical expression patterns of these microRNAs in patients with varying degrees of ICA stenosis. Significant negative correlations were also found between the degree of stenosis and expression of miR-126-5p ( = 0.83; р 0.05), miR-126-3p ( = 0.64; р 0.05) and miR-29-3p ( = 0.62; р 0.05). Conclusion. Based on an analysis of patients with cerebral atherosclerosis, the studied microRNAs can be divided into proatherogenic (miR-33a-5p/-3p) and atheroprotective (miR-126-5p/-3p, miR-29-3p, and mir-21-5p/-3p). These biomarkers can be diagnostically useful in predicting the risk of both CA progression and acute cerebrovascular accidents, yet prospective studies are required.

This review deals with research on the effect of board games on the prevention of cognitive disorders in the older population. It is known that activities using board games significantly enhance educational and intellectual abilities in children. However, data on the effect of such interventions in older patients (including those at risk for developing dementia) are few and equivocal. In the Bronx Aging Study, reading, board games, playing musical instruments, and dancing were associated with a reduced risk of cognitive disorders. The MoVIES study assessed the cognitive status of 942 participants aged 65 years and older, and a lower risk of dementia was found in those who devoted more than 1 hour per day to 'recreational activities'. The French study of the PAQUID cohort showed that those who regularly played board games had a 15% lower risk of developing dementia than those who did not. This review attempts to systematize the known data (including functional MRI data) on how playing board games influences changes in cognitive function. The article covers memory mechanisms that are necessary components of cognitive health. Structures that are directly involved in long-term memory formation, especially explicit memory, including the hippocampus, parahippocampal gyrus, and entorhinal cortex, are described. The article includes studies covering not only geographical, economic and social status, age, gender, and level of cognitive load, but also the different assessments measuring the effect board games have on the brain. Different assessment methods and functional MRI data have demonstrated the potential effectiveness of using board games in the prevention of both age-related and pathological intellectual ageing.

Research Center of Neurology, Moscow, Russia The novel coronavirus pandemic presents one of the most significant challenges to modern healthcare, which involves all medical specialties. The current review encompasses the neurologic manifestations of COVID-19 a yet to be defined problem. L. Mao et al. have found a third of COVID-19 patients to exhibit neurological symptoms the latter divided into three categories: central nervous system involvement (vertigo, headache, altered consciousness, acute cerebrovascular pathology, ataxia, and seizures) in 24.8% of patients, peripheral nervous system involvement (smell and taste disorders, neuropathy) 8.9%, and muscle pathology (muscle pain, associated with creatine kinase increase) 10,7%. Cerebrovascular pathology in 221 patients, described by Y. Li et al. occurred in 5.9% of cases the majority was comprised by ischemic stroke, and as a whole it was associated with a more severe disease course. T. Oxley et al. described 5 patients (less than 50 years of age) with a large-vessel stroke occurring as a result of COVID-19. It has been shown that meningoencephalitis may be linked to COVID-19 this review addresses several described cases. A case series of Guillain-Barre syndrome n patients with SARAS-CoV-2 infection is also described. Apart from that, it is well established that SARS-CoV-2 may lead to deterioration of concurrent somatic and (or) neurological diseases, worsening the prognosis.

Obesity is a pathological condition caused by overweight and requiring medical intervention. The clinical and scientific experience gained over the past decades has allowed researchers to consider this problem as an independent disease with its own pathophysiological features, prevalence, incidence, approaches to therapy and prevention. One of the most important factors in the pathogenesis of obesity is disordered eating behavior, the central regulation of which is carried out with the active participation of the prefrontal cortex. Impact on this area (for example, using non-invasive brain stimulation) may be one of the promising ways to modulate eating behavior. The article describes clinical cases of treatment of morbid obesity using navigated rhythmic transcranial magnetic stimulation (rTMS). Different patterns of dorsolateral prefrontal cortex (DLPFC) activation before and after rTMS are demonstrated. Possible mechanisms of the influence of DLPFC on the formation of eating behavior are also considered. These data underline the important role of DLPFC dysregulation in obesity, as well as show potentially effective neuromodulation techniques.

Ischaemic stroke (IS) is one of the leading causes of death and disability in the world. The consequences of IS manifest as severe and persistent neurological symptoms. The currently used methods for the management of IS are insufficient, partly because of incomplete understanding of the molecular mechanisms that occur in IS. Long noncoding RNA (lncRNAs) are noncoding RNAs that are longer than 200 nucleotides. It has been shown that lncRNAs control many processes: transcription, translation, regulation of gene expression, cell cycle regulation, apoptosis, cell proliferation, and differentiation. There is plenty of evidence that lncRNAs play a direct role in the pathogenesis of many human diseases, including IS. LncRNAs are found in the human bodily fluids, such as blood, urine, cerebrospinal fluid, and saliva. The expression profile of these circulating lncRNAs consists of a certain part of the cells, where they are modified and secreted in accordance with the physiological and pathological status of those cells. Due to their various ways of transport from cells into bodily fluids within exosomes or liposomes, lncRNAs are protected from the effect of RNases and remain in a stable form. Because of this, circulating lncRNAs are considered as novel biomarkers, which are of interest in many diseases, including IS. It likely appears that lncRNAs have the potential to be used in the diagnosis, management, and prevention of IS.

Introduction. Rapid progression of atherosclerosis and, consequently, an increase in the risk of stroke and myocardial infarction are associated with the presence of diabetes mellitus (DM). There is a search for new biomarkers of these pathological conditions, including their preclinical forms, primarily associated with insulin resistance (IR), which underlies these metabolic disorders. Development of the glucose and lipid toxicity is considered as one of the decisive factors in the development of IR and atherosclerotic cardiovascular disease in the presence of disturbances in carbohydrate and lipid metabolism. The negative consequences of isolated glucose- and/or lipid toxicity are less than the presence of both conditions simultaneously, known as glucolipotoxicity. The triglyceride glucose (TyG) index, initially developed to assess such combined changes, is of great interest to researchers as a marker or predictor of diseases associated with IR. Aim: to investigate the effect of glucolipotoxicity in patients with ischaemic stroke and to determine the diagnostic value of the TyG index. Materials and methods. The study included 251 people: group 1 (n = 145) patients with acute ischaemic stroke, and group 2 (n = 120) patients with carotid atherosclerosis and chronic cardiovascular disease but without stroke or acute coronary disease in the medical history. The control group (n = 86) consisted of people without atherosclerosis or cardiovascular disease. All patients underwent comprehensive clinical, laboratory and imaging tests, including biochemical tests measuring the TyG index. Results. Insulin resistance was found in all patient subgroups after acute stroke (irrespective of the ischaemic stroke subtype), and it was greater in patients with Type 2 DM (T2DM). The median TyG index value in patients with stroke and T2DM was 5 [4.8; 5.2], compared with 4.7 [4.6; 4.9] in patients with stroke but without T2DM. The TyG index was elevated in all patients with carotid atherosclerosis (median 4.9 [4.7; 5.2]), TyG index was statistically lower in people without atherosclerosis (median 4.6 [4.45; 4.7], p = 0.000). When the TyG index values were evaluated using ROC curves as a predictor of significant carotid artery stenosis (lumen narrowing of 60% or greater), the area under the curve was 0.821 and the TyG threshold value was 5.3 for patients with T2DM, while these values were 0.9153 and 4.71 for people without T2DM, respectively. Conclusion. The new method of glucolipotoxicity evaluation by calculating the TyG index has an important diagnostic and predictive role in identifying carotid atherosclerosis, IR, and metabolic syndrome in patients with cerebrovascular disease. This may allow us to stratify the patient categories that require vascular wall investigations, as well as to monitor treatment adequacy.

The article touches upon micro-RNA as new, potentially significant diagnostic, prognostic and therapeutic biomarkers in cerebrovascular pathology. Synthesis processes and effector mechanisms of micro-RNA are described. The micro-RNA that play an important role in the pathogenesis of major risk factors for cerebrovascular pathology (atherosclerosis, arterial hypertension, atrial fibrillation, diabetes mellitus) and the micro-RNA in acute cerebrovascular disorders are reviewed in detail. The need for thorough replication studies to justify the choice of micro-RNA and methods for micro-RNA detection is substantiated.

Introduction. Hemorheological abnormalities in patients with Ph-negative myeloproliferative disorders (MPD) may lead to the development and/or progression ofcerebrovascular pathology. Adequate preventive therapy in such cases lowers the risk of cerebral thrombotic complications. Objective. Evaluation of the effect of dipiridamole and acetylsalicylic acid (ASA) on platelet and erythrocyte aggregation, as well as morphofunctional properties of erythrocytes in patients with cerebrovascular disease (CVD) on the background of MPD. Materials and methods. The study comprised 40 patients with various forms of CVD and Рh-negative MPD: 20 patients received dipyridamole, 20 ASA for prevention of cerebral thrombotic complications. Mean study age was 44.6 years [35; 58.5]. A thorough clinical and neurological examination was performed, as well as neuroimaging studies, coagulation tests, analysis of platelet aggregation and rheological properties of erythrocytes. Results. Within the observation period (median 6.3 months) no acute cerebrovascular events in both groups were observed. Platelet aggregation (induced by ADP or adrenaline) was similar in both groups. Dipyridamole and ASA were also similar in their effect on functional properties of erythrocytes. Conclusion. Our findings suggest that the therapeutic effect of dipyridamole concerning CVD is similar to that of ASA. Dipyridamole can be recommended for use in patients with Рh-negative MPD if other antiplatelet agents are contraindicated.

Background: Disturbances of microcirculation play a significant role in the development and progression of both acute and chronic cerebrovascular diseases (CVD) and may be associated with different hemogram abnormalities. One of the reasons of the prothrombogenic state of the endothelium is the increase in the number of blood corpuscles leading to (non-Ph) myeloproliferative disorders (MPD) including essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PM). Materials and Methods: The study included 167 patients: 102 patients with Ph-MPD and the control group comprising 65 patients with CVD. According to MPD subtype, the patients were divided into three groups: patients with ET (37%, n = 38, male/female 7/31, age 52 ± 7 years), those with PV (40%, n = 41, male/female 20/21, age 50 ± 6 years) and those with PM (23%, n = 23, male/female 5/18, age 54 ± 4 years). Results: In 79% (n = 81) of cases in the study group (with Ph-MPD), patients had chronic CVD, with the most frequently identified symptoms being asthenia (92%) and headache (72%). Headache in Ph-MPD patients was more frequently (86%) associated with PM, while in patients with PV and ET it was equally distributed (70%). Neurological symptoms in 53% of cases were associated with focal changes of the brain on MRI localized in the subcortical area of the frontal and parietal lobes. Twenty-one (21%) patients suffered an acute cerebrovascular accident, 8 of them had thrombotic occlusion of one of the internal carotid arteries leading to hemispheric infarcts. Endothelial function (as measured by flow-dependent dilation of the brachial artery) was severely impaired in all study groups (median 5% with normal cut-off at 10%), the lowest degree of vasodilator activity being specific for patients with a history of stroke (p = 0.011). Conclusion: Patients suffering from MPD had asymptomatic focal changes in the brain in the absence of concomitant vascular disease (hypertension, atherosclerotic vascular disease, heart rhythm disorders) in 50% of cases. MPD, while remaining un- or underdiagnosed, presents a major concern in the cerebrovascular setting. A large number of thrombotic strokes occurring in patients with ET underline the necessity of early diagnostics and preventive therapy in these patients.