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Drug-induced parkinsonism (DIP) is one of the most frequent extrapyramidal disorders that develops against the background of prescribing a large number of medications. Initially, DIP was described as an adverse drug reactions (ADRs) against the background of the use of antipsychotic drugs, but later recognized as ADRs of a number of other drugs, including prokinetics, antidepressants, calcium channel blockers and antiepileptic drugs. The relative risk of developing LIP on the background of taking typical antipsychotics increased by 2.92 times compared to patients who do not take these drugs. The risk of developing DIP in patients receiving flunarizine is increased by 2.75-4.07 times. The risk of DIP with the use of antidepressants is increased by 2.14 times, among the drugs of this group with an increased risk of DIP, the use of selective serotonin reuptake inhibitors is most often associated with DIP (relative risk 1.24). Among other antidepressants, there is evidence of the development of DIP against the background of the use of duloxetine, mirtazapine, amitriptyll clomipramine, venlafaxine, trazodone. Among anticonvulsants, DIP can rarely develop against the background of the appointment of valproic acid, gabapentin, pregabalin, carbamazepine, oxcarbazepine. The risk of DIP in patients receiving metoclopramide is extremely low (0.06%), but it is 2.16 times higher compared to people who do not take this drug. Among drugs from other groups, DIP can occur against the background of the use of lithium carbonate, tacrolimus, cyclosporine, amiodarone, captopril, amphotericin B. If DIP develops, it is necessary, if possible, to reduce the dose or cancel the inducer drug, or replace it with another drug with minimal risk of DIP. Symptoms of DIP most often regress within a few weeks or months after dose reduction or withdrawal of the drug inducer. If the symptoms persist longer, it is necessary to exclude the presence of Parkinson’s disease or dementia with with Lewy bodies.

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.

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.

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.