NEUROLOGICAL ASPECTS OF CHRONIC CEREBRAL ISCHEMIA

Abstract

Chronic cerebral ischemia is a progressively developing impairment of cerebral blood circulation that leads to diffuse or small focal damage to brain tissue. This condition is accompanied by characteristic neurological and cognitive disorders [2]. The pathological process is based on an imbalance between intensified oxidative processes and insufficient activity of the brain’s antioxidant systems, which leads to the development of sustained oxidative stress [4,6]. Cerebral blood flow disorders provoke disruptions in energy metabolism, manifested in mitochondrial dysfunction and impaired endothelial function of blood vessels [5,6]. These pathological changes contribute to damage to both small and large vessels, with clinical manifestations depending on the stage of the disease and including increased fatigue, impaired thinking processes, various psychoneurological symptoms, and focal neurological deficits. The earliest and most significant diagnostic sign is cognitive impairment, which is often accompanied by emotional disturbances and tends to progressively worsen. Thus, chronic cerebral ischemia is a complex pathological process based on impaired cerebral perfusion, metabolic disturbances, and structural changes in the blood vessels, all of which together determine the typical clinical picture of this disease [2,3,5]. One of the contributing factors in the development of endothelial dysfunction in chronic cerebral ischemia (CCI) is an increased level of homocysteine in blood plasma. Hyperhomocysteinemia is associated with an increased risk of vascular catastrophes and is an independent risk factor for cognitive impairment in patients with CCI [1,2,5,6].