INDICATORS OF NEUROLOGICAL STATUS IN CHRONIC CEREBRAL ISCHEMIA

Abstract

The main pathogenetic factors in the development of chronic cerebral ischemia are atherosclerotic vascular changes and arterial hypertension, which are observed in the overwhelming majority of cases (95–97%). Recent studies confirm the key role of endothelial dysfunction in initiating the atherosclerotic process, wherein the damaged endothelium loses its ability to regulate vascular tone, becomes permeable to atherogenic lipoproteins, and begins to produce pro-inflammatory and procoagulant substances [1,2,3]. In recent years, special attention has been paid to hyperhomocysteinemia as a significant factor of vascular damage. This sulfur-containing amino acid, formed during methionine metabolism, exerts multifaceted pathogenic effects: it induces oxidative stress through the generation of free radicals, reduces the bioavailability of nitric oxide, promotes the accumulation of modified lipoproteins, and decreases the elasticity of the vascular wall [1,2]. Additionally, homocysteine enhances thrombogenesis by increasing platelet aggregation, suppressing fibrinolytic activity, and disrupting the natural anticoagulant mechanisms [1,3,5]. The complex negative impact of homocysteine on the vascular system explains its role as an independent risk factor for cerebrovascular pathology.