Measurements were made of plasma levels of free (f) thyroxine (fT4), triiodothyronine (fT3), thyrotropic hormone (TSH), adrenocorticotrophic hormone (ACTH), aldosterone, and renin in patients with dyscirculatory encephalopathy (DE). Their influences on the development of chronic circulatory insufficiency were assessed. A total of 39 patients were studied (aged 45-73 years) with DE stages I and II, without acute or chronic (in the exacerbation phase) somatic illness. These observations showed that diffuse lesions of brain tissues of different severities were accompanied by the following changes in thyroid homeostasis: 1) significant combined increases in TSH without alteration to the "fT3-TSH" negative feedback regulatory mechanism in patients with stage I DE; 2) significant combined decreases in TSH levels with marked suppression of the conversion of thyroxine into triiodothyronine and an interaction with impairments in the "fT3-hypophysis" system in patients with stage II DE. In addition, there were changes (increases) in cortisol levels with simultaneous decreases in renin levels in patients with stage II DE as compared with patients with stage I DE. Correlation analysis demonstrated the absence of any relationship between the age of the patients, the state of hormonal homeostasis, and the extent of vascular stenosis. These results suggest a role for hormones of the hypothalamo-hypophyseal-adrenal, thyroid, and renin-angiotensin systems in the mechanism by which DE develops as well as the possibility of using tests for these hormones as additional criteria for assessing the severity of diffuse brain lesions.

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...