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Intracranial hemorrhage (ICH) is characterized by a high level of disability and mortality. One of the most important reasons that lead to an increased risk and an increase in the ICH prevalence are antithrombotic drugs: anticoagulant, antiplatelet and thrombolytic. The main risk factors for ICH are advanced age, arterial hypertension, and the use of antithrombotic drugs of different groups. Treatment of ICH while taking drugs affecting hemostasis, is an extremely difficult task and there is not enough sufficiently convincing recommendations and evidence. The decision to resume therapy with the drug, that led to the development of ICH, and the timing of this resumption, is also not a completely clear problem that requires a balance between ischemic and hemorrhagic complications. The most important aspect of prevention is strict adherence to current recommendations regarding combinations of antithrombotic drugs and protocols for thrombolytic therapy, which will minimize the risks of ICH.

Atrial fibrillation (AF) is the main cause of cardioembolic ischemic stroke (IS), it occurs in 25–35% of patients with IS, and its presence increases the risk of recurrent stroke compared with patients with sinus rhythm. The main method of preventing recurrent IS in AF is the administration of oral anticoagulants (OACs); in non-valvular AF, direct OACs (DOACs) have an advantage. Meta-analysis of randomized clinical trials showed a 19% greater reduction of stroke and systemic embolism risk in the DOACs group compared to warfarin (p

Drug-induced tremor (DIT) is a term used to describe tremors that develop or increase in severity due to various medications administration. As multiple drugs are associated with DIT it is quite common in clinical practice and medication dose is frequently associated with tremor severity. DIT is associated with commonly prescribed drugs such as amiodarone, antidepressants, β-agonists, cyclosporine, lithium, tacrolimus and valproic acid. DIT mechanisms include dopamine receptors block, gamma-aminobutyric acid depletion, cholinergic deficiency. DIT risk factors include older age, female sex, longer administration of drugs associated with tremor or/and their administration in higher doses, history of tremor in the patient and/or relatives, excessive caffeine intake. It is necessary to establish a causal relationship between the use of a potential inducer drug and the development/intensification of tremor to diagnose DIT. If DIT is detected, the inducer drug should be discontinued or its dose reduced. To decrease DIT risk, it is recommended to avoid prescribing drugs which are most commonly associated with DIT.

Among drug-induced liver injuries (DILI), the cholestatic type is second in frequency (from 20 to 40%), the most common is the hepatocellular variant (up to 78%). For this reason, practitioners of various specialties, including neurologists and psychiatrists, do not monitor cholestasis parameters, and drug-induced liver injury with cholestasis (DILIС) remains unrecognized. The urgency of this problem is great, because the frequency of deaths in DILIС is only slightly lower than t in the hepatocellular type; in addition, it DILIС is much more likely to become persistent increasing the risk of chronic liver injury.Among the drugs used in neurology and psychiatry, the “leaders” in terms of the number of DILIС are antidepressants, both tricyclic (amitriptyline, imipramine) and selective serotonin reuptake inhibitors (SSRIs: paroxetine, sertraline, fluoxetine, citalopram, escitalopram), antidepressants), antipsychotics (chlorpromazine, fluphenazine), anticonvulsants (mainly carbamazepine).If the patient has a history of DILI caused by any of the forementioned medications, the agent should be switched to another drug from the same group with a minimal risk of DILI. If there is a history of DILI associated with antidepressants, it is recommended to choose SSRIs. It is necessary to monitor not only the activity of transaminases and bilirubin, but also the cholestasis parameters (alkaline phosphatase, γ-glutamyl transpeptidase) during treatment.

The article presents the chronology of the symposium «How to Deal with Pain in the 21st Century? Experts' opinions», which took place on November 8 during the XII interdisciplinary international congress «Manage Pain». The lectures discussed issues of non-steroidal anti-inflammatory drugs (NSAIDs), including etoricoxib (Atorika tabs), administration on the example of a clinical case, problems of terminology associated with the concepts of «lumbago» and «sciatica», rare clinical syndromes (for example, heavy-purse syndrome) that we need to differentiate nonspecific back pain with, strategies for choosing NSAIDs in patients with osteoarthritis, the importance of timely administration of NSAIDs in the prevention of chronic pain syndromes, the influence of emotional and cognitive factors on the back pain chronization. The benefits of etoricoxib (Atorika) in the treatment of chronic back pain were reviewed, as well as the evidence for its safety.

Drug-induced parkinsonism (DIP) is the most common drug-induced movement disorder and is most commonly associated with antipsychotic drugs, monoamine reuptake inhibitors, and calcium channel blockers. DIP manifests as a typical movement disorder, which makes it practically indistinguishable from idiopathic Parkinson's disease (PD) and requires differential diagnosis. DIP symptoms develop fairly quickly (hours to weeks) after the antipsychotic is started or after the dose is increased. Therefore, DIP is predominantly a clinical diagnosis that must be kept in mind when a patient develops typical symptoms during treatment onset or increasing the dose of drugs that most often lead to such an adverse reaction (ADR). DIP evaluation includes using the Naranjo algorithm, which helps assess a causal relationship between drug intake and the development of parkinsonism symptoms. The primary DIP treatment is the reduction of the dose of the inducer drug, or its cancellation, or replacement with another drug. In patients with schizophrenia and antipsychotic-induced DIP, dose reduction, replacement with another medication, or prescription of a drug with anticholinergic activity may be possible. The awareness of the doctor and the patient about the possibility of developing this ADR is crucial in the prevention of DIP. Therefore, choosing a drug with the lowest risk of developing DIP is necessary for pharmacotherapy.

The disease caused by the SARS-CoV-2 virus is multi-organ and involves almost all organs and systems. Myalgias and arthralgias and, in particular, back pain are common symptoms of COVID-19 and can be observed both at the onset of the disease and in the postcovid period. The causes of muscle and joint damage include both systemic inflammation and direct viral injury. Traditionally, musculoskeletal pain is treated with non-steroidal anti-inflammatory drugs. However, using this drug class in patients with COVID-19 requires caution due to the presence of comorbid diseases and possible complications of viral infection. The review discusses clinical variants and pathophysiological mechanisms of joints and muscles damage in patients with COVID-19 and treatment tactics for patients with musculoskeletal pain.

The worldwide prevalence of prediabetes is steadily increasing, with up to a third of patients already showing signs of diabetic neuropathy (DN). Prediabetes includes impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or a combination of both.Recent diagnostic criteria of prediabetes according to Russian, European, and American clinical guidelines are presented. The review covers the most common forms of DN in patients with prediabetes (distal symmetric sensory polyneuropathy, painful DN, cardiovascular autonomic neuropathy) and their prevalence. Recommended methods of DN screening are discussed: diagnostic scales, sensory testing, nerve conduction study, autonomic testing, corneal confocal microscopy. The results of studies evaluating instrumental methods for diagnosing peripheral nervous system (PNS) dysfunction in prediabetes are discussed. Management tactics in patients with prediabetes and PNS dysfunction should include non-pharmacological and pharmacological interventions. Combining a low-calorie diet and regular physical activity can delay the development of diabetes mellitus and reduce the severity of neuropathic pain. In patients with painful DN, the first-line therapy includes pregabalin, gabapentin, and duloxetine. Since there is no current data on the effect of hypoglycemic therapy on the risks of development and/or progression of DN in patients with prediabetes, antioxidants are considered pathogenetic therapy. Alpha-lipoic acid (Berlition®) in the management of patients with prediabetes is discussed.

Recently, maximum attention has been drawn to the earliest forms of cognitive deficit - pre-mild cognitive decline (PMCD), which includes subjective (SjCD) and subtle cognitive decline (SCD), being the most promising in cognitive decline prevention.Objective: to assess the influence of genetic and comorbid emotional-affective factors on PMCD in middle-aged patients.Patients and methods. The study included 50 middle-aged people (60.76±9.5 years) with cognitive complaints. All patients underwent a cardiovascular assessment, including: biochemistry blood test (lipid profile, urea, glucose, vitamin В12, folic acid, homocysteine, thyroid hormones), duplex scan of the extracranial arteries, blood assay for АРОЕ4 determination, neuropsychological assessment with quantitative neuropsychological methods, emotional-affective background evaluation. In addition, magnetic resonance imaging (MRI) with morphometry of the hippocampus was performed in 20 patients.Results and discussion. Arterial hypertension, diabetes mellitus, and changes in laboratory parameters are significantly were more frequent in patients with SCD than patients with SjCD. The neuropsychological assessment showed maximum differences between SjCD and SCD groups in tests that evaluated reaction time (verbal fluency test, trail making test, part A, digit symbol substitution test, and Munsterberg test). Analysis of neuroimaging parameters revealed a smaller volume of the right hippocampus in APOE4 carriers. patients without depression performed significantly better on memory tasks, when depression was included in the analysis. In addition, patients with depression showed a significantly more pronounced degree of cortical atrophy on MRI.Conclusion. Patients with SCD have lower scores in neuropsychological tests than patients with SjCD. In addition, we observed a high significance of cardiovascular and emotional-affective risk factors in the PMCD development, emphasizing the importance of their evaluation and treatment in the management of patients with PMCD.

Daytime somnolence may be a symptom of different somatic, neurological and psychiatric diseases and develop due to abuse and/or discontinuation of various medications. Drug- induced hypersomnia (DIH) is defined as hypersomnolence caused by the intake of multiple drugs. DIH is one of the most frequently reported effects and/or side effects of drugs. DIH prevalence varies widely and can be as high as 75% in patients receiving specific medications. DIH risk factors include elderly and senile age, impaired drug metabolism, serum drug concentration, method and frequency of drug administration, single and daily doses of drugs, etc., as in many other drug- induced diseases and syndromes. DIH can occur both due to sedative agents administration and withdrawal of psychostimulants and other activating psychotropic medications. Most often, the development of DIH is associated with the use of levodopa-carbidopa, antipsychotics, antidepressants. The pathogenesis of DIH is complex and multifactorial and is associated with the mechanism of action of individual drugs and the presence of concomitant diseases. The article discusses the risk assessment of DIH development due to various medications, diagnosis and management tactics of patients with DIH.

One of the depression causes is the use of certain drugs, and in this case, the term drug-induced depression (DID), medication-induced or iatrogenic depression is used. Symptoms of DID are similar to those observed in patients with other types of depression. DID is also associated with morbidity and mortality. Its development leads to a decrease in treatment adherence, and in some cases, to discontinuation of drugs that have predictive value. The main point in the management of patients with DID is the rapid detection and correction of symptoms and the application of prompt measures to prevent their development when prescribing certain drugs. The features of the course of DID, pathogenetic mechanisms and risk factors for its development, possible approaches to the treatment and prevention are discussed.

The neurological manifestations of the novel coronavirus COVID-19 infection caused by SARS-CoV-2 are extremely diverse. At the same time, there is currently very little data on the neurological complications of COVID-19. There are more and more publications on the presence of a complication, such as cognitive impairment (CI). The latter is analyzed in patients with COVID-19 during their hospital stay and later on. The paper discusses possible mechanisms, including a hyperinflammatory state (cytokine storm), coagulopathy, and the neurotropic effect of the virus, which may play a role in the development of CI in patients with COVID-19. It considers management tactics for patients with CI in the presence of coronavirus infection and the possibility of their correction with citicoline (Noocil®).

Drug-induced dystonia (DID) is a rarely diagnosed adverse reaction to a sufficiently large number of drugs. Acute DID (ADID) occurs soon after starting to take a drug or raising its dose, and switching from one antipsychotic medication to another, especially to its injectable dosage form. Tardive DID (TDID) develops a few months or years after starting drug intake or 3 months after stopping therapy. The diagnosis of TDID is based on the persistence of dystonic hyperkinesis for more than 1 month, the use of a dopamine receptor blocking agent, and the absence of other causes of its development. The risk factors for DID are male sex; young age (less than 30 years of age); a history of dystonic reactions; hypocalcemia, alcohol use while taking the drug. DID is most commonly related to therapy with antipsychotics, metoclopramide, antidepressants, and antiepileptic drugs. The short-term use of anticholinergic drugs (benzotropin, diphenhydramine) is effective in treating ADID. Anticholinergic drugs and atypical antipsychotics (clozapine, quetiapine), benzodiazepines, muscle relaxants (baclofen), and dopamine reuptake inhibitors (tetrabenazine) are used to treat TDID. To prevent DID, it is very important that a physician should be aware of that this unwanted adverse reaction may occur and that a drug with the lowest risk for DID should be chosen.

Atrial fibrillation (AF) and cognitive impairment (CI) are among the most important problems of the modern health care system, which are characterized by an extremely high prevalence with the increasing trend of the latter; they lead to lower quality of life, shorter duration, and a larger number of disabled people. The specific feature of AF and CI is the presence of common risk factors. To date, the data of an increasing number of studies allow cerebral microbleeds (CMBs) to be considered as a new risk factor for CI, inter alia in patients with AF. In recent years, special attention has been paid to the role of oral anticoagulants (OACs) in the prevention of CI in AF, which is reflected in a number of studies and meta-analyses. In terms of the effect of OACs on the risk of CMBs, there is reason to believe that the latter increases with the use of warfarin, the effects of direct OACs (DOAC) in this regard require further investigation. At the same time, among the DOACs, apixaban is the only drug that has been proven to have no negative effect on the risk of CMBs in a randomized controlled clinical trial. In general, the available data indicate the positive effect of OACs in reducing the risk of CI and dementia in AF; moreover, DOACs have an advantage in this respect. Among the DOACs, apixaban is promising due to its optimal efficacy and safety profile.

Atrial fibrillation (AF) is a common rhythm disorder, especially in the elderly and senile people, and its incidence is expected to be only increasing. Another urgent problem of modern health care is cognitive impairment (CI) and dementia, which are also highly prevalent. Studies show that AF and CI are closely interrelated: patients with this heart rhythm disturbance are at increased risk for both CI in general and dementia in particular, their cognitive decline progresses faster regardless of whether AF is paroxysmal or permanent. The association between CI and AF is largely due to the commonality of risk factors, the main of which are considered to be elevated blood pressure, atherosclerotic vascular damage, diabetes mellitus, and age. To date, the specific pathogenetic mechanisms of CI development in AF have been described, indicating that both vascular and neurodegenerative changes are implicated in cognitive decline in the presence of cardiac arrhythmias in question. These changes include a history of stroke, the well-known risk factor for the cardioembolic type of which is AF; microembolism and microhemorrhage; predisposition to prothrombotic states; cerebral hypoperfusion and a proinflammatory shift associated with this arrhythmia. In addition, a potential adverse effect on CI can be produced by the use of antagonists of vitamin K, since the latter is an important trophic factor necessary for normal cognitive functioning.

Many classes of medications, such as antipsychotics, anticonvulsants, anticholinergics, and other commonly prescribed drugs, can cause cognitive impairment (CI). The negative effect of drugs on cognitive functions is due to the following pathophysiological mechanisms: a reduction in neuronal excitability, an increase in gamma-aminobutyric acid activity, and decreases in enzyme activity, the number of receptors, cerebral perfusion, as well as brain atrophy; moreover, a number of mechanisms have not been fully studied. An important role in the development of drug-induced CI is played by predisposing (senility or childhood, brain damage, chronic diseases, functional disorders, genetic causes, initial cognitive decline, polypragmasia), and precipitating (acute diseases, infections, metabolic disorders, dehydration, acute urinary retention, malnutrition, environmental influences, etc.) factors. The dose of a drug, the duration of its use is of absolute value. There is a need for the differential diagnosis of CI induced by drugs and CI directly related to the diseases, for which these drugs are prescribed. Drug-induced CI should be suspected if an association is established between a decline of cognitive functions and the start of drug intake. The treatment of this CI involves primarily dose withdrawal or reduction and the use of sustained-release dosage forms, if available. In some cases, cognitive training and/or special drug therapy may be required to correct the CI that has occurred. The measures to prevent drug-induced KI include the choice of the lowest-risk drugs, the use of current side-effect rating scales, in particular an anticholinergic burden scale.

Management of patients with cognitive impairment is one of the most relevant and important problems of neurology. It is especially important to identify cognitive impairment at the early (pre-dementia) stages, when appropriate medical measures are implemented, the progression of cognitive decline can be slowed down or stopped. Near-moderate cognitive decline (NMCD) at elderly and senile ages may be a predictor for the development of clinically significant cognitive impairment up to dementia. In most Western works, NMCD is associated with subjective cognitive decline, but it would be more legitimate to distinguish a form (a stage) of mild cognitive decline among NMCDs. It is assumed that NMCD is not necessarily a precursor to more severe cognitive impairment – the former can be a manifestation of age-related changes, emotional-affective disorders, and neurological and somatic diseases, although their presence substantially increases the risk of moderate and severe cognitive impairment. The review provides current ideas about the initial forms of cognitive decline, as well as neuroimaging data in these patients. It considers the influence of emotional-affective and cardiovascular factors on the development of cognitive deficit.

Tardive dyskinesia (TD) is a type caused by the use of different medications. The pathogenesis of TD is associated with dopamine receptor blockade, gamma-aminobutyric acid depletion, cholinergic deficiency, oxidative stress, impaired synaptic plasticity, and neurotoxicity. TD most often occurs after taking metoclopramide, antipsychotics, antidepressants, calcium channel blockers, and other drugs.The review considers an adequate assessment of the potential risk of TD when the patient uses prescribed drugs, as well as the monitoring and correction of risk factors for TD, discontinuation or replacement of drugs that potentially cause TD, as well as its treatment.

The paper reviews the data available in the literature on and the results of the authors' own investigations of the signs of brain damage in hypertension in its early stages. The signs of early brain damage in hypertension can be considered as deteriorated control functions, white matter hyperintensities (WMH), as evidenced by the standard modes of magnetic resonance imaging (MRI), decreased fractional anisotropy in the frontal lobes, as shown by diffusion tensor MRI, and reduced cerebral perfusion. The latter two signs are detected even in hypertensive patients without WMH. Cognitive function testing and brain MRI using special regimens make it possible to identify a group of hypertensive patients at higher risk for cerebrovascular complications just in the early stages of the disease.

The disease caused by COVID-19 is multi-organ and involves almost all organs and systems. Myalgias and arthralgias and back pain are common symptoms of COVID-19 and can be observed both at the onset of the disease and in the postcoid period. The cause of muscle and joint damage is both systemic inflammation and direct damage by the virus. Musculoskeletal pain can be observed both at the onset of the disease and in the post-COVID period. Traditionally, musculoskeletal pain is treated with NSAIDs, however, the use of this group of drugs in patients with COVID-19 requires caution as to comorbidity and possible complications of viral infection. The article discusses clinical variants and pathogenetic mechanisms of damage of joints and muscles against the background of COVID-19 infection as well as treatment tactics for patients with skeletal muscle syndrome.

Objective: to investigate the effect of indapamide/perindopril fixed-dose combination (FC) on 24-hour blood pressure (BP) and cognitive functions in antihypertensive treatment-naive middle-aged patients with uncomplicated grade 1–2 essential arterial hypertension (EAH) . Patients and methods. The open prospective study enrolled 25 patients (9 men and 16 women) aged 40–59 years with a diastolic BP of 90–109 mm Hg and/or a systolic BP of 140–179 mm Hg, as evidenced by routine measurements. As starting antihypertensive therapy, the patients received indapamide 1.25/perindopril 5 mg FC once daily in the morning; if necessary, after 2 weeks (if the routine blood pressure was ≥140/90 mm Hg) they took indapamide 2.5/perindopril 10 mg once daily in the morning. The follow-up period was 14–16 weeks. Before and at the end of the follow-up, the patients underwent 24-hour ambulatory BP monitoring (ABPM) and evaluation of cognitive functions using the Montreal Cognitive Assessment (MoCA), ten-words test (immediate and delayed word recall), verbal association test (literal and categorical associations), number connecting test (Trail making test (TMT), part A and numbers and letters connecting test (TMT) part B), and Stroop test. Results. At the end of the follow-up period, treatment with indapamide/perindopril fixed-dose combination showed a statistically significant reduction in BPs, as evidenced by routine measurements and ABPM (during 24-hour, and awake and sleep periods); a statistically significant cognitive improvement: an increase in the number of the so-called words in the ten-words test during both immediate (from 5.5±1.6 6.5±1.5 words; p=0.02 vs baseline) and delayed (from 6.2±1.7 to 7.4±1.4 words; p=vs baseline) recalls, a decrease in the performance time of TMTB (from 112.6±42.5 to 90.4±28.4 sec; p=0.02) and Stroop test Part 3 (from 135.5±50.1 to 112.6±19.6 sec; p=0.02), and a larger number of called words in the categorical associations test (from 6.5±2.4 to 8.1±2.9 words; p=0.02). Conclusion. The results obtained indicate that in treatment-naive middle-aged patients with EAH, indapamide/perindopril fixed-dose combination assures an effective reduction in BPs, as evidenced by routine measurements and ABPM, also improves cognitive functions, particularly attention, information processing speed, semantic memory, cognitive flexibility, and short-term and long-term memory.

Diffusion tensor magnetic resonance imaging (DT-MRI) is the only noninvasive technique that makes it possible to study white matter microstructure in vivo and to quantify the images obtained. Objective: to study white matter in middle-aged treatment-naХve patients with uncomplicated grade 1–2 essential hypertension (EH), by using DT-MRI. Patients and methods. The investigation enrolled 82 people aged 40–59 years (41 patients with EH and 41 healthy individuals (a control group)). Twenty-four blood pressure monitoring and brain MRI were performed in different modes (T1 MPRAGE, T2 TSE, T2 FLAIR, and DTI). Results. White matter hyperintensities (WMHs) were found in 7.3% of the healthy individuals and in 53.7% of the hypertensive patients (p=0.0002). The latter had significantly lower fractional anisotropy (FA) values in the white matter of the left inferior frontal gyrus than the healthy individuals (0.39±0.06 and 0.45±0.09, respectively; p

Arterial spin labeling (ASL) is a promising non-invasive method to assess cerebral perfusion, which identifies a decrease in cerebral blood flow (CBF).Objective: to assess cerebral perfusion in middle-aged untreated patients with uncomplicated grade 1–2 hypertension compared to same-age healthy controls.Patients and methods. 33 patients with essential hypertension and 40 healthy individuals (a control group) at the age of 40–59 years were examined. 24-hour blood pressure (BP) monitoring and brain magnetic resonance imaging were performed in different modes (T1 MPRAGE, T2 TSE, T2 FLAIR, DTI, and ASL).Results. White matter hyperintensive changes were found in 7.5% of the healthy individuals and in 51.5% of the hypertensive patients (p = 0.0002). In hypertensive patients, CBF in the cortical plate of anterior frontal regions was significantly (p < 0.001) lower than that in the controls: right CBF, 39.1±5.6 and 45.8±3.2 ml/100 g/min, respectively; left CBF, 39.2±6.2 and 45.2±3.6 ml/100 g/min, respectively. In hypertensive patients with white matter hyperintensive changes, CBF was significantly lower than that in the controls: right CBF, 38.5±5.9 ml/100 g/min (p = 0.0001); left CBF, 39.2±6.7 ml/100 g/min (p = 0.002), and in those without these changes, right CBF was 39.5±5.1 ml/100 g/min (p = 0.0002); left CBF was 38.9±4.3 ml/100 g/min (p = 0.00002). Correlation analysis revealed significant inverse correlations of CBF with BP and systolic BP variability.Conclusion. Lower cerebral perfusion occurs in middle-aged untreated patients with uncomplicated grade 1–2 hypertension even in the absence of white matter hyperintensity foci.

Hypertension is one of the main modifiable risk factors for cognitive impairment (CI) and dementia in middle-aged and elderly patients. CI occurs in patients with hypertension even with its short duration and is manifested by controlling dysfunctiona and cognitive speed decline. The paper presents the results of a neuropsychological examination in 50 patients of middle age (47.54±5.2 years) with short-term (2.6±5.5 years) and uncomplicated hypertension. Stable blood pressure normalization during antihypertensive therapy improves cognitive function and prevents the progression of CI and the development of dementia. The use of nicergoline in patients with hypertension and CI is discussed.