Insomnia is a serious and widespread public health problem, but is often undetected and patients do not receive needed treatment. Insomnia is often comorbid with other diseases and conditions, such as arterial hypertension, type 2 diabetes mellitus, pain syndromes, anxiety and depressive disorders, etc. A separate problem is drug-induced insomnia, when patients develop symptoms due to other diseases treatments. Insomnia has a negative effect on the prognosis of comorbid diseases, including an increased risk of death, more severe disease, and decreased quality of life. The presence of sleep disorders makes it difficult to effectively treat the underlying disease, so clinical guidelines draft for the evaluation and treatment of insomnia in multimorbid patients is proposed. Diagnostic methods are reviewed and recommendations are given for the treatment of acute and chronic insomnia and features of the treatment of insomnia in multimorbid patients. A clinical algorithm has been proposed to determine treatment tactics in multimorbid patients.

Статин-индуцированная миастения может иметь различные клинические проявления вплоть до крайне тяжелых и угрожающих жизни пациента. Особое значение данная проблема приобрела в последнее время, когда ключевая роль в представлениях о патогенезе большого числа распространенных заболеваний отведена дислипидемии, а статины стали использоваться в клинической практике как терапия выбора. Необходима систематизация данных, касающихся факторов риска, патогенеза, разнообразных клинических проявлений лекарственно-индуцированной миастении, рекомендаций по диагностике и тактике ведения пациентов, а также по профилактике лекарственно-индуцированных осложнений у пациентов с ранее диагностированной миастенией. Миастения – заболевание с неуточненной этиологией, при котором зачастую трудно установить ведущий фактор. В частности, известно большое число лекарственных препаратов, вызывающих миастению, однако данные об их потенциальном риске малочисленны, спорны или отсутствуют. В случае полиморбидности пациента вероятно одновременное применение множества лекарственных средств, что дополнительно усложняет выявление искомого препарата. Механизмы развития миастении также до конца не изучены и включают генетическую предрасположенность, нарушения внутриклеточных метаболических процессов, дисфункцию иммунной системы. Кроме того, вариативность клинических проявлений затрудняет диагностику. Отсутствуют практические рекомендации по рутинному скринингу субклинических форм миастении перед началом терапии статинами, что представляет вызов для клинициста. Не выработаны алгоритмы ранней диагностики лекарственно-индуцированной миастении, что должно приводить к особой настороженности в реальной лечебной практике. При выявлении симптомов миастении клиницисту необходимо особенно тщательно собирать фармакологический анамнез. В усилении безопасности статинотерапии ведущее значение имеет осведомленность врачей о факторах риска, патогенетических механизмах, клинических проявлениях, возможностях лабораторно-инструментальной диагностики статин-индуцированной миастении, а также понимание важности динамического наблюдения за состоянием пациентов после инициации терапии статинами. Statin-induced myasthenia can have various clinical manifestations up to extremely severe and life-threatening for the patient. This problem has gained particular importance recently, when dyslipidemia has gained a key role in the understanding of the pathogenesis of a large number of common diseases, and statins have been used in clinical practice as a therapy of choice. Systematization of data on risk factors, pathogenesis, various clinical manifestations of drug-induced myasthenia, recommendations for the diagnosis and management of patients, and also for the prevention of drug-induced complications in patients with previously diagnosed myasthenia. Myasthenia is a disease with an unspecified etiology, in which it is often problematic to establish a leading factor. In particular, a large number of drugs that cause myasthenia are known, but data on their potential risk are few, controversial or absent. In the case of polymorbidity of the patient, simultaneous use of multiple drugs is likely, which further complicates the identification of the desired drug. The mechanisms of myasthenia development are also not fully understood and include genetic predisposition, disorders of intracellular metabolic processes, and dysfunction of the immune system. In addition, the variability of clinical manifestations makes diagnosis difficult. There are no practical recommendations for routine screening of subclinical forms of myasthenia before starting statin therapy, which poses a challenge for the clinician. Algorithms for the early diagnosis of druginduced myasthenia have not been developed, which should lead to special caution in real medical practice. When detecting symptoms of myasthenia gravis, the clinician must carefully collect a pharmacological history. In enhancing the safety of statin therapy, doctors’ awareness of risk factors, pathogenetic mechanisms, clinical manifestations, possibilities of laboratory and instrumental diagnosis of statin-induced myasthenia, as well as understanding the importance of dynamic monitoring of patients’ condition after initiation of statin therapy, is of leading importance.

The aim of the study was to evaluate the effect of anticholinergic load (AHN) on cognitive functions (CF) in elderly and senile multimorbid patients with arterial hypertension (AH).Materials and methods. 330 patients aged 60 years and older with essential AH were included in the study (median age 79 [72; 84] years, 158 (51 %) of women). All the patients were underwent the assesment of CF using the Montreal Cognitive Assessment Scale (MoCA), Mini-Mental Status Scale (MMS), Alzheimer’s Disease Assessment Scale-Cognitive (ADAS-cog), Trial Making Test (TMT), Digit Symbol Substitution Test (DSST), Verbal Association Test (literal (letter) and categorical (animal) associations), Boston Naming Test (BNT), Word-Color Interference Test, Stroop colorword conflict test. The anticholinergic load was determined using the anticholinergic load scale (Anticholinergic Cognitive Burden Scale, ACB).Results. Compared with patients who do not take anticholinergic drugs, multimorbid elderly and senile hypertensive patients with 2 or more points on the ACB scale had significantly lower final scores on the MoCA test (23 [21; 24.3] versus 24 [22; 25] points, respectively, p=0.042) and on MMSE (26 [24; 29] vs. 27.5 [25; 29] points, respectively, p=0.015), they spent statistically more time completing part B of the TMT test (217.5 [187.3; 246.3] vs. 204 [166.8; 247.3] seconds, respectively, p=0.038). The difference between the execution time of part B and part A of the TMT test in patients with 2 or more points on the ACB scale was statistically significantly greater than in patients with 0 points on this scale (141 [103.8; 168.5] versus 124 [83.8; 162] sec, respectively, p=0.034). Age, gender, education, and the structure of concomitant diseases did not differ between the groups.Conclusion. The results obtained indicate the adverse effect of аnticholinergic вurden on CF of multimorbid elderly and senile hypertensive patients and dictate the need to optimize pharmacotherapy in this category of patients.

Артериальная гипертензия (АГ) – одно из самых распространенных сердечно-сосудистых заболеваний в мире и основной модифицируемый фактор риска развития когнитивных нарушений (КН), причем как сосудистой деменции, так и деменции при болезни Альцгеймера. В обзоре представлено актуальное состояние проблемы поражения головного мозга у пациентов с АГ, включая взаимосвязь между возрастом, уровнями и вариабельностью артериального давления и КН, а также современные данные о механизмах развития КН при АГ. Описывается влияние АГ на крупные экстра- и интракраниальные сосуды, а также подробно рассматриваются нарушения микроциркуляции и дисфункция нейроваскулярных единиц, приводящие к КН при АГ. Приведены клинические признаки и особенности диагностики поражения головного мозга как органа-мишени АГ. Обсуждается тактика ведения пациентов с АГ и КН, включая модификацию образа жизни, антигипертензивную терапию и применение нейропротективных препаратов с твердой доказательной базой, среди которых преимущество имеет этилметилгидроксипиридина сукцинат (Мексидол). Arterial hypertension (AH) is one of the most common cardiovascular diseases in the world and the main modifiable risk factor for cognitive impairment (CI), both vascular dementia and Alzheimer’s disease dementia. The review presents current data upon hypertension-mediated brain damage, including the relationship between age, levels and variability of blood pressure and AH, as well as mechanisms of CI development in AH. The effect of AH on large extra- and intracranial vessels is described, as well as microcirculation disorders and dysfunction of neurovascular units leading to CI in AH are considered in detail. The clinical signs and features of the diagnosis of hypertension-mediated brain damage are presented. The tactics of managing patients with AH and CI, including lifestyle modification, antihypertensive therapy and the use of neuroprotective therapy with a robust evidence base, among which ethylmethylhydroxypyridine succinate (Mexidol) has an advantage, are discussed.

One of the reasons for the development or worsening of cognitive impairment (CI) may be the use of a number of drugs: non-steroidal anti-inflammatory drugs, antiarrhythmics, antidepressants, glucocorticosteroids, antitumor drugs and a number of others. The negative effect of drugs on cognitive functions is realized due to many pathophysiological mechanisms: disruption of hormonal regulation, decreased neuronal excitability, increased activity of gamma-aminobutyric acid receptors, decreased cerebral circulation, atrophic changes in the brain; many mechanisms have not been fully established. Risk factors for the development of drug-induced CIs are: old age or childhood, brain damage, chronic diseases, genetic factors, the patient's initial CI, polypharmacy, dose and duration of drug use, acute infectious diseases, metabolic disorders, dehydration, acute urinary retention, etc. To diagnose and differentially diagnose drug-induced CI, it is necessary to establish a connection between the start of taking a suspected drug-inducer and a decrease in cognitive functions. The first step in the treatment of drug-induced CI is the abolition of an inducer drug or a reduction in its dose, in cases where it is impossible to discontinue the drug and there is no replacement, special slow-release dosage forms can be considered. The main measures to prevent drug-induced CI include the use of drugs with the lowest risk of their development, assessment of drug interactions, and the use of modern scales to assess the risk of developing this side-effect (anticholinergic burden scale, etc.).

Scientific relevance. Being the main class of medicinal products for dyslipidaemia treatment, statins are widely used in clinical practice in various patient populations. However, statins can cause statin-associated muscle symptoms (SAMS), which are the most frequent and, in some cases, even life-threatening adverse reactions associated with these medicinal products.Aim. The study aimed to perform a systematic review of the epidemiology, classification, and physiological pathogenesis of SAMS, risk factors for this complication, and clinical guidelines for primary care physicians regarding the identification and treatment of patients with SAMS.Discussion. SAMS is an umbrella term that covers various forms of myopathies associated with satin therapy. According to the published literature, the prevalence of SAMS varies considerably and may depend on the study design, inclusion criteria, and the medicinal product used. SAMS has multiple putative pathogenic pathways that include genetically determined processes, abnormalities in mitochondrial function, defects in intracellular signalling and metabolic pathways, and immune-mediated reactions. The main known risk factors for developing SAMS include high-dose statins, drug–drug interactions, genetic polymorphisms, female sex, older age, Asian race, history of kidney, liver, and muscle disease, and strenuous physical activity. Given the lack of universally recognised algorithms for diagnosing SAMS, clinicians should consider the clinical presentation and the temporal relationship between statin therapy and symptoms. Other factors to consider include changes in muscle-specific enzyme levels and, in some cases, the results of blood tests for antibodies to 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase.Conclusions. To ensure the safety of statin therapy, it is essential to raise clinicians’ awareness of the risk factors for SAMS, indicative clinical and laboratory findings, and the need for dynamic patient monitoring, including the involvement of clinical pharmacologists.

OBJECTIVE:To analyze mental disorders in blepharospasm (BS) before and after botulinum therapy (BT).MATERIAL AND METHODS:We examined 25 patients with BS (9 men and 16 women), aged 50 to 85 years (mean 64.1±18.5), with BS (main study group). The control group consisted of 20 healthy individuals (7 men and 13 women, mean age 63.5±8.5). Patients were examined before and after BT (after 3 weeks) using a diagnostic structured interview Mini International Neuropsychiatric Interview, GAD-7, PHQ-9, fear of negative assessment (short version) and The Liebowitz Social Anxiety Scale (LSAS).RESULTS:Fifty-six percent of patients with BS, as assessed by the GAD-7, showed a high level of anxiety, while depression, measured by the PHQ-9 and found in 52% of patients, was mainly manifested by mild disorders. In the group of patients with BS, the mean scores were higher on the GAD-7, PHQ-9, fear of negative assessment (p<0.001) and LSAS (p<0.05) than in the control group. After treatment with BT, the levels of anxiety and depression in patients with BS decreased slightly and remained higher compared with the control group. Psychiatric examination in the majority (64%) of patients revealed mental disorders that could not be explained by the occurrence of BS. The remaining 36% of patients had adaptation disorders (nosogenic reactions) caused by BS. Affective mental pathology (recurrent depressive disorder and dysthymia) and anxiety disorders (social phobia and adjustment disorders) were more often observed in the main study group compared with the control group (24% versus 5% and 68% versus 10%, respectively).CONCLUSION:A significant proportion of patients with BS have anxiety and depressive disorders, the severity of which does not depend only on the severity of motor symptoms and does not significantly decrease after successful BT, but is caused by mental disorders that preceded the manifestation of BS. Identification of mental disorders to varying degrees associated with BS, not only on the basis of psychometric scales, but also consultation with a psychiatrist, will allow, in addition to the correction of motor symptoms of BS, to differentiate the therapeutic approach through psychotherapy and psychopharmacotherapy.

Sleep disorders are becoming increasingly important due to the high comorbidity with other diseases and a significant impact on the patient's quality of life. Insomnia is the most common sleep disorder both in the general population and in patients with multimorbid pathology. Its prevalence in the general population is 6-15%, while in patients with somatic diseases it increases up to 20-40% and can reach 90% in patients with comorbid mental disorders. Another problem is the development of drug-induced insomnia. Insomnia has negative impact on the prognosis of comorbid diseases, including an increased risk of death, more severe disease, and a worse quality of life. The presence of sleep disorders makes it difficult to effectively treat the underlying disease, so it is extremely important to identify and correct these disorders in the early stages, therefore recommendations for the diagnosis of insomnia in polymorbid patients are proposed. Modern methods of treating acute and chronic insomnia and features of insomnia treatment in polymorbid patients are also discussed.

The anticoagulant therapy with a priority of direct oral anticoagulants is an approach to the prevention of recurrent stroke in patients with atrial fibrillation (AF) that has presently proved its efficacy and is stated in international clinical guidelines. An extensive evidence-based database demonstrates advantages of rivaroxaban over other drugs of this class in secondary prevention of stroke in AF. Furthermore, these advantages are combined with the optimal safety profile. The rivaroxaban treatment may provide the most favorable prognosis due to the prevention of recurrent stroke in AF, reducing the rate of kidney disease progression, and slowing vascular atherosclerosis. An important beneficial feature of rivaroxaban is once-a-day intake, which is important in the context of a high incidence of cognitive disorders in this patient category, and may improve their compliance and, thus, help achieving the expected profile of treatment efficacy. Thus, rivaroxaban can be regarded as a drug of choice for secondary prevention of stroke in AF.

Arterial hypertension is one of the most common comorbidities in patients with cancer. Moreover, the treatment with anticancer agents can lead to the development of drug-induced arterial hypertension. The aim of this work is to systematize and analyze data about anticancer agents, the use of which can cause the development of drug-induced hypertension, about epidemiology, pathophysiological mechanisms, risk factors, clinical signs, diagnosis and differential diagnosis, treatment and prevention of hypertension associated with the use of anticancer drugs. It was found that anti-cancer drugs often contribute to the development of drug-induced hypertension. The mechanisms that determine the development of hypertension are diverse and may include the development of endothelial dysfunction, an increased arterial stiffness, capillary rarefaction, fluid and electrolyte imbalance, and genetic factors. It is important to remember about drugs that can cause drug-induced hypertension to reduce the risk of developing adverse reactions, and prevent cardiovascular disease. Treatment of drug-induced hypertension, caused by anticancer drugs, often requires immediate discontinuation of drugs, due to adverse reactions that are often life-threatening. In some situations, it is possible to reduce the dose of the drugs and / or prescribe antihypertensive drugs. Arterial hypertension is an important risk factor in the development of cardiovascular events, including stroke, coronary heart disease, heart failure.

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.

Intracerebral hemorrhage (ICH), which is a form of hemorrhagic stroke, is an extremely serious disease. This pathology is characterized by very high levels of disability and mortality. Despite the improvement in the treatment of those diseases that can lead to ICH, its frequency is currently increasing, which is largely due to the use of drugs, in which case the term «drug-induced intracerebral hemorrhage» (DI ICH) is used. One of the main reasons for drug-induced ICH is an increase in the frequency of prescribing anticoagulant therapy for the prevention of ischemic stroke in atrial fibrillation, as well as dual antithrombotic therapy. In addition to anticoagulants, thrombolytic drugs can lead to the development of this pathology. According to the literature, an increase in the risk of developing ICH is also associated with therapy with antidepressants from the group of selective serotonin reuptake inhibitors, as well as high doses of statins. Risk factors for this adverse reaction are age, smoking, hypertension, and thrombocytopenia. Treatment of DI ICH is an extremely difficult task and includes the withdrawal of the culprit medication, antihypertensive therapy, correction of intracranial hypertension, and, in some cases, the administration of antidotes. The main method of prevention is the use of antiplatelet drugs and other drugs, the use of which is associated with an increased risk of developing DI ICH, in strict accordance with modern protocols and recommendations.

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.

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.

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<0.0001), including a 51% greater hemorrhagic stroke (HS) risk reduction (p<0.0001). In an additional sub-analysis of the ARISTOTLE trial, patients with AF and a history of stroke/transient ischemic attack showed a significant reduction in the risk of all types of strokes and HS. Although no randomized trial explored the direct comparisons of drugs from the DOACs group, data from observational studies indicate the potential advantage of apixaban in terms of reducing the risk of IS. Russian 2020 clinical guidelines for AF treatment suggest that the resumption/initiation (1–3–12 days) of anticoagulant therapy after an IS should be determined by the decision of a multidis ciplinary team (neurologist, cardiologist, neuroimaging specialist) based on recurrent IS and bleeding risk assessment. According to the 2020 guidelines of the Ministry of Health, the resumption of OACs therapy after an intracranial hemorrhage in patients with AF may be recommended 4–8 weeks after the event, and the decision to reinitiate therapy, as well as after IS, should be made by a multidisciplinary team.

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.

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.

Arterial hypertension (AH) is the major modifiable risk factor for cognitive impairment (CI), including dementia, CI in cerebrovascular and neurodegenerative diseases, including Alzheimers disease. By 2050, the number of people with dementia will approximately 3 times increase due to the aging population and limited opportunities for drug prevention and treatment of severe CI. In connection with the above, it seems necessary to create an expert consensus, which would summarize the evidence-based medicine data available to date on the effect of antihypertensive therapy (AHT) on cognitive function (CF). In the expert consensus, the data of prospective randomized clinical trials, observational and population studies, meta-analyzes on the effect of AHT on the risk of dementia and CI progression, including certain CF, were summarized and analyzed. The consensus considers the effect of antihypertensive drugs (AHD) on various cognitive domains. Literature data give evidence that AHT reduces the risk for dementia, including vascular dementia, reduces the risk of for dementia in Alzheimers disease, as well as reduces the risk and can prevent the progression of non-dementia CI. The effect of AHT on various CF has been little studied. Most meta-analyzes did not reveal the benefits of any class of AHD; however, one study demonstrated the advantage of angiotensin receptor blockers, while another study diuretics. The consensus emphasizes that, given the high incidence of AH in the general population, AHT may be one of the most effective ways to prevent CI or delay CI progression. The effect of different classes of AHD on CF requires further study. It is necessary to conduct a larger number of well-designed randomized clinical trials that would assess the state of executive functions in patients with AH.