The paper discusses the issues associated with the definition of the concept «transient ischemic attack» (TIA) and with the prognosis of cerebrovascular disease after prior TIA. It is stated that following TIA, there is a high risk for ischemic stroke and a risk for evolving and progressive cognitive impairments. Approaches to organizing a therapeutic and diagnostic process in patients with TIA are covered.

Moderate and mild cognitive impairment (CI) is often detected at the early stages of cerebral stroke, in some cases later transforming into severe impairments to cognitive processes [1][2][3][4]. At three years after stroke, the frequency of vascular dementia in patients with mild and moderate CI increases to 50%, and then at six years to 80% [4-9], resulting in not only medical, but also social-economic problems. This increasingly complex situation defines the search for diagnostic and therapeutic measures to prevent the formation and progression of CI in cerebral stroke. An answer to the question of CI in vascular pathology can only be obtained on the basis of an integral approach [10][11][12][13]. In particular, there is great interest in identifying clinical-biochemical correlates of developing CI.Apart from already known hormones regulating cognitive functions (adrenocorticotrophic hormone, the thyroid hormones, and vasopressin) [1, 14-16], many reports in the last decade have also established and supported relationships between CI and other hormones -prolactin, dehydroepiandrosterone (DHEA), and leptin [6,[16][17][18][19][20]. Thus, prolactin has a polymorphous action on virtually all organs and systems in both men and women [16,18]. As a hypophyseal peptide hormone, prolactin has activatory influences on neurotransmitter processes associated with successful learning; it has a role in forming new interneuronal connections, and it regulates the mechanism of formation of longterm memory. It may also have a role in the development of Alzheimer's disease [16,18].The reproductive hormones affecting the state of cognitive activity also include DHEA and its sulfated form -dehydroepiandrosterone sulfate (DHEAS) [17]. Recent views are that age-related changes in DHEAS levels are much more important for cognitive activity then decreases in testosterone content [ 8,17]. Experimental studies have identified the following biological effects of DHEAS: improvements in memory; antidepressant activity; avoidance of fear and panic; and reductions in aggression in animals [8,17]. Decreases in the circulating DHEAS level are seen in Alzheimer's disease and other forms of dementia [12,17]. Low DHEA levels have been shown to be associated with impairments to the functioning of the synaptic contacts of neurons and their differentiation [8,13,18].Serum hormone levels -thyroid-stimulating hormone, thyroxine, dehydroepiandrosterone (DHEA), DHEA sulfate, and prolactin -were studied in patients during the acute period of cerebral ischemic stroke with cognitive impairments of different severities on days 1, 7, and 21 of illness. An association was found between the concentrations of these hormones and the severity of cognitive impairments and this supports the view that they have roles in supporting cognitive functions and impairments to cognitive functions during the acute period of stroke. Deficiencies in the study hormones were most marked in the group with severe cognitive impairment. Analysis of the hormonal component of the regul...

¹Бюро судебно-медицинской экспертизы Московской области (нач.-д. м.н., проф. В. А. Клевно) ²Кафедра судебной медицины (зав.-д.м.н., проф. В.А. Клевно) ФУВ ГБУЗ МО МОНИКИ им. М.Ф. Владимирского Аннотация: Приведен случай смерти от анафилактического шока как реакции немедленного типа, развившегося после введения лидокаина во время медицинской манипуляции.

The article, which is a review-lecture, reflects the historical milestones in the description and study of cerebral edema (CE) from ancient times to the present. Great attention is paid to the Monroe–Kellie doctrine, without which it is impossible to understand the mechanism of development of a vitally significant complication of CE – intracranial hypertension. The importance of the Monroe–Kellie doctrine in substantiating the symptomatic treatment of increased intracranial pressure is emphasized. The possible involvement of the glymphatic system in both the decrease and the increase in increased intracranial pressure is discussed. The modern ideas about the blood-brain barrier (BBB), its role in the development of CE and an increase in intracranial volume are analyzed. With the study of the molecular mechanisms of BBB damage and the development of targeted therapy, the researchers associate future advances in the treatment of CE. The great interest of modern authors in the state of the BBB in various diseases, as well as in the violation of its integrity in COVID-19 is reflected. It is noted that the main and only, today, method for diagnosing CE is neuroimaging. Development has begun on the isolation of potential biochemical markers of CE from blood.