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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.

Stroke is an acute disturbance of the blood supply to the brain, characterized by the sudden onset of focal neurological symptoms, which persists for more than 24 hours or leads to the death of the patient in a shorter period of time due to cerebrovascular pathology. In the world and in Russia, stroke remains one of the leading causes of death and disability. At the same time, ischemic stroke (IS) is more common – about 80% of cases. Many classes of drugs, such as oral contraceptives, nonsteroidal anti-inflammatory drugs, and various psychoactive substances, can contribute to the development of drug-induced IS (DI IS). Data upon the frequency of DI IS is limited. In part, this reflects the problem of identifying and confirming the causal relationship between drug prescription and the development of IS. DI IS risk factors include: abuse of caffeine and alcohol, older age, smoking, drug addiction, high doses of drugs containing provoking agents, the simultaneous use of several drugs, the presence of comorbid diseases. Adverse drug reactions develop due to the following pathophysiological mechanisms: cerebral embolism, vasoconstriction of cerebral arteries, vasculitis of the central nervous system, orthostatic hypotension. The management of a patient with a DI IS does not differ significantly from the management of a patient with IS of a different etiology and includes thrombolysis or mechanical thromboextraction (in the absence of contraindications), as well as rational methods of secondary prevention. It is necessary to completely cancel or reduce the dose of the drug, the use of which led to the development of a stroke. DI IS prevention measures include the choice of drugs with the lowest risk of its occurrence and the use of modern scales for assessing the risk of this phenomenon.

Gender is an important factor affecting the risk of drug-induced adverse reactions in patients. According to scientific literature, the risk of drug-induced symptoms, syndromes, and diseases is 1.5–1.7 times higher in women than in men. The aim of the study was to analyse and systematise data on the factors responsible for increased risk of drug-induced diseases in women. It was demonstrated that the increased risk of complications in women following the use of certain pharmacological classes of drugs is associated with a combination of factors that affect pharmacokinetics and pharmacodynamics. These factors include anatomical and physiological characteristics, specificity of enzyme and transport protein activity/expression. Women, compared to men, have higher percentage of adipose tissue and lower percentage of water in the body, which affects the volume of distribution of lipophilic agents, such as opioids and benzodiazepines, resulting in their accumulation in the body. Women have a lower rate of renal excretion and elimination, as compared to men, which may lead to adverse reactions following the use of medicines with predominantly urinary excretion. Changes in the endocrine profile in women taking sex steroids as replacement therapy or a contraceptive measure, as well as fluctuations in endogenous sex steroids during the menstrual cycle, pregnancy, perimenopause, influence the volume of distribution, the activity of cytochrome P450 enzymes, and the glomerular filtration rate, and, thus, may affect the pharmacokinetics and pharmacodynamics of other medicinal products, which, in turn, affect the safety of pharmacotherapy. In order to increase the safety of pharmacotherapy in women, it is necessary to consider the revealed specific pharmacokinetic and pharmacodynamic parameters of the medicine in a given group of patients when selecting the treatment regimen, including the dosage regimen and routes of administration.

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 ® ).

In real clinical practice, the problem of polymorbidity and, in particular, its cardiometabolic phenotype, is now widespread. One of the its variants is a combination of arterial hypertension with diabetes mellitus, overweight, cognitive impairment, and peripheral atherosclerotic arterial disease. The clinical significance of such polymorbidity portrait, on the one hand, lies in its frequent occurrence, and, on the other hand, in the cardiovascular risk amplification in the settings of simultaneous coexistence of diseases initially characterized by an extremely unfavorable prognosis for the patient. The article presents a clinical case of a patient with a such polymorbidity variant and considers the nicergoline potential in the complex correction of mutually associated comorbidities. The nicergoline ability to improve cognitive functioning, to have a beneficial effect on peripheral circulation, which is reflected in an increase in the distance of painless walking, and also to realize some antihypertensive effect has been demonstrated. No less important is the fact that the high therapeutic efficacy of nicergoline was combined with an optimal safety profile, which consists in good tolerability of therapy and the absence of adverse drug reactions.

The relationship between blood pressure (BP) and cerebral blood flow (CBF) is not fully understood. This study evaluated the impact of a perindopril arginine/indapamide (Pa/I) single-pill combination (SPC) on CBF in middle-aged patients. A total of 22 treatment-naive patients with essential hypertension and at least one hypertension-mediated organ damage and 41 healthy controls were enrolled. At baseline, all participants underwent brain magnetic resonance imaging (MRI); patients with hypertension underwent an additional MRI at end of follow-up. Arterial spin labeling (ASL) was used to calculate CBF in the frontal lobe cortical plate. Patients with hypertension received once-daily Pa/I 5 mg/1.25 mg SPC, which could be increased to Pa/I 10 mg/2.5 mg at 2 weeks if necessary. Patients with hypertension underwent 24-h ambulatory BP monitoring (ABPM) at baseline and end of follow-up. Mean baseline BP values were 146.2/93.1 and 119.1/76.1 mmHg in the hypertension and control groups, respectively. Patients with hypertension had significantly (p

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.

Arterial hypertension is one of the main modifiable risk factor for cognitive impairement (CI). Most frequently executive dysfunction is seen independent of age. Pathophysiological mechanisms linking hypertension and CI include the impact of increased blood pressure on large and small cerebral arteries. Large arteries dysfunction leads to occlusion, remodeling and arterial stiffness. Hypertension also causes small arteries dysfunction: lipohyalinosis and fibrinoid necrosis and due to insufficient amount of anastomosis and collaterals can lead to white matter damage. Treatment approach for patients with hypertension and CI should be multimodal and include treatment of the main cause of CI (antihypertensive therapy, statins and antithrombotics if necessary), symptomatic therapy (e.g. anti-dementia medications) and pathogenic treatment drugs that influence microcirculation, neuromethabolic therapy. Antihypertensive therapy is known to decrease dementia incidence, but the interclass differences remain unclear. Nicergoline (the ergot alkaloid derivative) is used in 30 countries to treat CI. Nicergoline improves CI due to its multidoi modal action, which includes increasing glucose metabolism in the brain, stimulation of cholinergic neurotransmission, increasing cerebral blood flow, influencing microcirculation due to decreasing arterial stiffness, blocking α1-adrenergic receptors. Nicergoline is effective in treating hypertensive patients with CI according to the data of a number of studies and meta-analysis. Evidencebased data also shows good tolerance profile of nicergoline.

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.

Atrial fibrillation (AF) is one of the most common cardiac arrhythmias in clinical practice and important additional risk factor for the development of cognitive impairment (CI) and dementia as it has been shown in recent studies. According to the Diagnostic and statistical manual of mental disorders latest revision CI refers to a decrease of one or more higher cortical functions that provide the processes of perception, storage, transformation and transmission of information compared to the premorbid level. The main hypothesis that explains the relationship between AF and dementia is the assumption that in the presence of this arrhythmia a brain substance is damaged due to microembolism and cerebral microbleeding. The high clinical significance of AF as well as CI served as a background for the development by European experts several consensus documents concerning the problem of the relationships between these conditions. In addition, they emphasize the role of anticoagulant therapy as a preventing tool for the development of stroke, which can be a factor in the CI progression in patients with AF, with particular priority to direct oral anticoagulants (DOACs). In randomized clinical trials, meta-analyses and systematic reviews have been shown that the use of DOACs, as compared to vitamin K antagonists, is a more rational strategy for preventing stroke associated with AF. Among the DOAC class, rivaroxaban is worth noticing as a drug that has a favorable efficacy profile for primary and secondary stroke prevention. Rivaroxaban distinguishing characteristics are a once daily administration as well as a calendar package which is practically important for patients with CI.

Headache is considered to be one of the main symptoms of arterial hypertension (HT). Complaints of headache are presented by many patients with HT: from 44% to 87%. It is obvious that the majority of complaints of headache in patients with HT is not due to headaches due to increased blood pressure (BP), but multimorbidity (polymorbidity) – the presence of coexisting primary headaches, most often, as in the population as a whole, chronic tension headache (57-85%) and migraine (15-30%). On the other hand, the frequency of HT in patients with migraine ranges from 32% to 44%. The relationship between migraine and HT may be due to common exogenous (external) and endogenous (genetic) factors, as well as common pathophysiological mechanisms. External risk factors, which can be associated with both migraine and HT, include the nature of the diet (excessive consumption of table salt with food), low physical activity, chronic stress; both diseases are also associated with the presence of a connection with the metabolic syndrome. The role of hyperactivation of the renin-angiotensin-aldosterone and adrenergic system and endothelial dysfunction are actively discussed. Angiotensin-converting enzyme takes an active part in the BP control and vascular tone; it is known that some angiotensin converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) have demonstrated efficacy in preventing migraine attacks. The presence of HT can contribute to the chronic course of primary headache, and effective treatment of HT with antihypertensive drugs, on the contrary, can have a positive effect on the course of primary headaches. Antihypertensive drugs reduce the frequency of headaches compared to placebo, but heterogeneity between different classes was revealed. There was a statistically significant decrease in the frequency of headaches compared to placebo during treatment with beta-blockers, ACEI, ARB, diuretics, while calcium antagonists did not reduce the frequency of headaches. According to a number of studies, the frequency of headaches during the treatment with ARB (candesartan) is comparable to that in the placebo group. Some antihypertensive drugs are used to prevent migraine attacks.

Vascular cognitive impairment (VCI) and vascular dementia are the most common forms of cognitive disorder associated with cerebrovascular disease and related to increased morbidity and mortality among the older population. Growing evidence suggests the contribution of blood-pressure variability, cardiac arrhythmia, hyperactivation of the renin-angiotensin-aldosterone system, endothelial dysfunction, vascular remodeling and stiffness, different angiopathies, neural tissue homeostasis, and systemic metabolic disorders to the pathophysiology of VCI. In this review, we focus on factors contributing to cerebrovascular disease, neurovascular unit alterations, and novel approaches to cognitive improvement in patients with cognitive decline. One of the important factors associated with the neuronal causes of VCI is the S100B protein, which can affect the expression of cytokines in the brain, support homeostasis, and regulate processes of differentiation, repair, and apoptosis of the nervous tissue. Since the pathological basis of VCI is complex and diverse, treatment affecting the mechanisms of cognitive disorders should be developed. The prospective role of a novel complex drug consisting of released-active antibodies to S100 and to endothelial NO synthase in VCI treatment is highlighted.

Arterial hypertension (HT) is one of the main recognized risk factors for the development of cognitive impairment and dementia. The results of most studies indicate that the presence of HT in elderly and senile people is associated with a decrease in cognitive functions and an increased risk of dementia in people of this age group, although some studies have identified the so-called "U-shaped curve”. The state of cognitive functions in middle-aged patients with HT has been studied to a much lesser extent, but it has been established that the presence of HT in middle age is associated with deterioration of cognitive functions and an increased risk of dementia in the elderly. In middle-aged hypertensive patients, cognitive impairment affected all cognitive domens, but to a greater extent - neurodynamic indicators of cognitive functions (speech activity, ability to concentrate, speed of cognitive processes). There are few data that levels of systolic blood pressure (BP) during the day, during wakefulness and sleep periods, insufficient night BP decrease, increased daily BP variability, and increased magnitude of the morning BP rise are interrelated with deterioration of the control functions/speed of cognitive processes. Pathogenetic aspects of the relationship of cognitive impairment and HT are diverse and include the hyperactivation of neuro-humoral systems (renin-angiotensin-aldosterone and sympathoadrenal, hypothalamic-pituitary-adrenal system dysfunction, reduction of cerebral perfusion, endothelial dysfunction. Anxiety-depressive disorders are of great importance in the occurrence of cognitive impairment in patients with HT, their interrelation is complex, dualistic, possibly due to a decrease in brain perfusion.

One of the most frequent complaints of patients with hypertension (HT) is dizziness. Dizziness is understood as a variety of subjective sensations that patients define as “dizziness” – a sense of instability when walking, the illusion of rotation of surrounding objects, the feeling of approaching fainting, the inability to concentrate, and “fog” in the head. Experts share the systemic dizziness (vertigo) and non-systemic. The causes of vertigo in most cases are diseases of the inner ear (Meniere's disease, benign paroxysmal positional vertigo [BPPV], vestibular neuronitis. The most common form of dizziness is psychogenic dizziness. In the vast majority of cases, HT is not the cause of dizziness. The most common cause of vestibular (systemic) dizziness in patients with HT, as in the general population, is BPPV, and the most common cause of non-systemic dizziness is psychogenic dizziness. Among other causes of dizziness in patients with HT should be kept in mind too fast and/or intensive lowering of blood pressure, rhythm and conduction disorders, orthostatic hypotension (especially in elderly and senile patients in the presence of concomitant diabetes).

Restless legs syndrome (RLS) is a sensorimotor disorder characterized by complaints of a strong desire to move legs during periods of rest or inactivity, which is relieved by movement (most pronounced in the evening or at night). Multiple studies have reported drug-induced RLS caused by antipsychotics, antidepressants and antiepileptic medications. Risk factors for drug-induced RLS include older age, gastrointestinal diseases, high medication dose, simultaneous use of ≥2 drugs. The mechanism of drug-induced RLS is most often associated with the effect of medications on various receptors and neurotransmitter systems, in particular, the dopamine system. Drug-induced RLS treatment includes identification and withdrawal of a drug that caused RLS or a decrease in its dosage. Prevention of drug-induced RLS is based on compliance with the principles of rational pharmacotherapy.Синдром беспокойных ног (СБН) — сенсомоторное расстройство, которое характеризуется движением ног во время периодов отдыха или бездействия, облегчается при движении и наиболее ярко проявляется вечером или ночью. Имеется много сообщений о лекарственно-индуцированном СБН (ЛИСБН), который наиболее часто вызывают антипсихотические средства, антидепрессанты и противоэпилептические препараты. К факторам риска развития ЛИСБН относят пожилой возраст, курение, злоупотребление кофеином и алкоголем, заболевания желудочно-кишечного тракта, высокие дозы препаратов, одновременное применение двух препаратов и более. Механизм развития ЛИСБН связывается с действием лекарственных средств на различные рецепторы и нейромедиаторные системы, особенно дофаминергические. Лечение ЛИСБН предполагает прежде всего отмену лекарственного средства или, если она невозможна, снижение его дозы. Профилактика ЛИСБН основывается на соблюдении принципов рациональной фармакотерапии.

The article is devoted to the role of antihypertensive drugs in cerebroprotection, importance of such drugs in reducing the risk of stroke and cognitive disorders in patients with arterial hypertension (AH). The article provides the definition, classification and pathogenetic mechanisms of cognitive impairment in elevated blood pressure (BP). It also presents epidemiological characteristics of the incidence of stroke and cognitive disorders in hypertension. The influence of elevated blood pressure as a factor increasing the risk of cerebrovascular complications is considered. Particular attention is paid to the issue of a sharp rise in BP in the early morning hours, which is typical for patients with AH. The clinical significance of excessive early morning hypertension is discussed. The authors emphasize the difficulties and importance of correcting the morning rises in blood pressure as one of the objectives of antihypertensive therapy. The article presents data on the distinctive features of the pharmacokinetics and pharmacodynamics of candesartan, an angiotensin II receptor blocker with an extremely long-term action. The clinical efficacy of candesartan in the treatment of AH and the risk of cerebrovascular complications, especially stroke and cognitive impairment, has been demonstrated from the point of view of evidence-based medicine.

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-naХ ve 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.

Elevated pulse pressure (PP) is the one of simplest and most accessible markers of vascular damage and increased arterial stiffness in hypertension (HTN). To date, an extensive body of evidence has been accumulated in terms of the PP effect on central nervous system (CNS), leading to neuronal damage and death, which contribute to the development and progression of cognitive impairment (CI). Elevated PP violate the blood-brain barrier, can intensify the production of reactive oxygen species in the CNS, lead to endothelial dysfunction, microbleeds and directly stimulate the amyloid beta creation, which is a substrate of Alzheimer’s disease. Due to the important role of increased PP in CI, an important aspect of antihypertensives’ effects is their impact on PP and the ability to reduce it. Among antihypertensives, a single-pill combination of amlodipine/indapamide sustained release deserves special attention, since it has a body of evidence for reducing PP and thereby improving cognitive functioning in patients with HTN, which in turn will improve their quality of life.

There is a growing interest to the problem of drug-induced epileptic seizures (ES) due to their relatively high prevalence, poor prognosis, a large number of different drugs associated with the development of drug-induced ES, and low awareness among general practitioners. Drug-induced ES are most often associated with the use of antidepressants, antipsychotics, antiepileptic drugs (overdose or as a result of discontinuation), antibiotics, immunosuppressants and immunomodulators, antitumor agents, analgesics, central nervous system stimulators, anesthetics etc. The prevalence of drug-induced ES varies with different drugs. It is estimated that about 6.1% of the first occurring ES are drug-induced. Risk factors for drug-induced ES include a history of epilepsy or ES, cancer, blood-brain barrier dysfunction, several concomitant neurological diseases, mental disorders, childhood, old and very old age, fever, impaired liver metabolism in patients with liver diseases, impaired drug excretion in patients with kidney diseases, polypharmacy, pharmacokinetic properties of the drugs themselves, allowing them to penetrate the blood-brain barrier in the central nervous system (lipophilicity, transport and communication with blood plasma proteins), drug concentration in blood serum, method and frequency of drug administration, single and daily doses of drugs. No clinical guidelines for the management of patients with drug-induced ES are available. It is recommended to identify patients at risk: elderly patients, patients with impaired liver and kidney function and patients receiving drugs that can cause ES and/or lower the seizure threshold. Benzodiazepines are the first-line treatment in drug-induced status epilepticus, barbiturates and propofol are the second-line treatment. The general principles for the prevention of drug-induced ES include careful selection of the optimal dose of drugs that can cause ES, especially in patients with impaired liver and/or kidney function, monitoring of several parameters in blood serum (for example, liver enzymes, electrolytes, glucose etc.), monitoring of the blood plasma concentration of certain drugs, avoiding the simultaneous administration of several drugs that stimulate the central nervous system, and a rapid discontinuation of such drugs.В последние годы возрос интерес к проблеме лекарственно-индуцированных эпилептических приступов (ЭП) в связи с их достаточно высокой распространенностью, неблагоприятным прогнозом, большим количеством различных лекарственных средств (ЛС), прием которых ассоциирован с развитием лекарственно-индуцированных ЭП, и низкой осведомленностью практикующих врачей об этом вопросе. Лекарственно-индуцированные ЭП наиболее часто ассоциированы с приемом антидепрессантов, антипсихотических ЛС, противоэпилептических препаратов (передозировка или как результат прекращения их приема), антибиотиков, иммуносупрессоров (иммунодепрессантов) и иммуномодуляторов, противоопухолевых ЛС, анальгетиков, анестетиков, ЛС, стимулирующих центральную нервную систему (ЦНС), и др. Распространенность лекарственно-индуцированных ЭП варьирует при использовании разных ЛС. Считается, что около 6,1% впервые возникших ЭП являются лекарственно-индуцированными. К факторам риска развития лекарственно-индуцированных ЭП относят наличие эпилепсии или ЭП в анамнезе, онкологические заболевания, нарушение функции гематоэнцефалического барьера, наличие ряда сопутствующих неврологических заболеваний, психические расстройства, детский возраст, пожилой и старческий возраст, лихорадку, нарушение метаболизма ЛС в печени у пациентов с заболеваниями печени, нарушенное выведение ЛС у пациентов с болезнями почек, полипрагмазию, фармакокинетические свойства самих препаратов, позволяющие проникать через гематоэнцефалический барьер в ЦНС (липофильность, транспорт и связь с белками плазмы крови), концентрация ЛС в сыворотке крови, способ и кратность введения препаратов, разовые и суточные дозы ЛС. Единых клинических рекомендаций по ведению пациентов с лекарственно-индуцированными ЭП не существует. Рекомендуется четко идентифицировать пациентов, входящих в группу риска развития лекарственно-индуцированных ЭП, т.е. пожилых пациентов, пациентов с нарушением функции печени и почек и больных, получающих ЛС, которые способны вызвать ЭП и/или снизить порог судорожной готовности. Препаратами для стартовой терапии при лекарственно-индуцированном эпилептическом статусе являются бензодиазепины, препаратами второй линии - барбитураты и пропофол. К общим принципам профилактики лекарственно-индуцированных ЭП относят тщательный подбор оптимальной дозы ЛС, способного вызвать ЭП, особенно у пациентов с нарушением функции печени и/или почек; мониторинг уровня некоторых показателей в сыворотке крови (например, печеночные ферменты, электролиты, глюкоза и т.д.), мониторинг концентрации некоторых ЛС в плазме крови, избегание одновременного назначения нескольких ЛС, стимулирующих ЦНС, и резкого прекращения приема подобных ЛС.

Objective:Hypertension is a risk factor for mild cognitive deterioration and vascular dementia. In recent years, neuropsychology has recognized the impact of vascular pathology on cognitive function, as well as the importance of early detection and prevention. The purpose of the present study was to