Causes of ischemic stroke

Causes of ischemic stroke

The cause of ischemic stroke is a decrease in cerebral blood flow as a result of damage to the main vessels of the neck and the cerebral artery in the form of stenosis and occlusive lesions.

The main etiological factors that lead to decreased blood flow:

• atherosclerotic and atherothrombotic stenosis and occlusion of extracranial arteries of the neck and large arteries of the base of the brain;
• arterio-arterial embolism from thrombotic deposits on the surface of an atherosclerotic plaque or arising as a result of its disintegration, which leads to occlusion of intracranial arteries by atheromatous emboli;
• cardiogenic embolism (in the presence of artificial heart valves, atrial fibrillation, dilated cardiac disease, myocardial infarction, etc.);
• hyalinosis of small arteries, which leads to the development of microangiopathy and the formation of lacunar cerebral infarction;
• dissection of the walls of the main arteries of the neck;
• hemorheological changes in the blood (in vasculitis, coagulopathy).

Much less frequently, the cause of obstruction of the carotid arteries is cicatricial traumatic and external inflammatory lesions of the vessels, fibromuscular dysplasia, as well as pathological bends and looping of the vessels.

Occlusion of the vertebral arteries in most cases is observed at the site of their origin from the subclavian arteries.

In addition to the sclerotic process, vertebral artery stenosis is often caused by osteophytes that form with osteochondrosis of the cervical spine.

Stenosis and thrombosis of the anterior and middle cerebral arteries usually occur at the branching site of the internal carotid artery.

When the vessels of the carotid artery system are affected, cerebral infarction often develops, and in the vertebrobasilar basin, mainly transient cerebral circulatory disorders occur.

Since ischemic stroke is not considered a separate disease, it is impossible to determine a single etiological factor for it.

Risk factors associated with an increased incidence of ischemic stroke are identified. They can be divided into non-modifiable (age, gender, hereditary predisposition) and modifiable (arterial hypertension of any origin, heart disease, atrial fibrillation, history of myocardial infarction, dyslipoproteinemia, diabetes mellitus, asymptomatic carotid artery disease).

Risk factors associated with lifestyle are also identified: smoking, excess body weight, low levels of physical activity, poor nutrition (in particular, insufficient consumption of fruits and vegetables, alcohol abuse), prolonged psycho-emotional stress or acute stress.

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Pathogenesis of ischemic stroke

Acute focal cerebral ischemia causes a certain sequence of molecular-biochemical changes in the brain substance, which can lead to tissue disorders ending in cell death (cerebral infarction). The nature of the changes depends on the magnitude of the decrease in cerebral blood flow, the duration of this decrease, and also on the sensitivity of the brain substance to ischemia.

Normally, cerebral blood flow is 50-55 ml of blood per 100 g of brain matter per minute. Moderate reduction in blood flow is accompanied by selective gene expression and a decrease in protein synthesis processes. A more pronounced reduction in blood flow (up to 30 ml per 100 g/min) is accompanied by activation of anaerobic glycolysis and the development of lactic acidosis.

When cerebral blood flow decreases to 20 ml per 100 g/min, glutamate excitotoxicity develops and the content of intracellular calcium increases, which triggers mechanisms of structural damage to membranes and other intracellular formations.

With significant ischemia (up to 10 ml per 100 g/min), anoxic depolarization of membranes occurs, and cell death usually occurs within 6-8 minutes.

In addition to cell necrosis, cell death occurs in the ischemic lesion site by the apoptotic type, for the implementation of which there are certain cellular mechanisms that include several levels of intracellular regulation (they are currently being actively studied).

With a moderate decrease in cerebral blood flow, an increase in the degree of oxygen extraction from arterial blood is noted, due to which the normal level of oxygen consumption in the brain substance may be maintained, despite the existing decrease in cerebral perfusion revealed by neuroimaging methods. It should also be noted that a decrease in cerebral blood flow may be secondary in nature and reflect a reduced need for energy by brain cells during a primary decrease in their activity, in particular, with some pharmacological and toxic effects on the brain.

The degree of reduction of cerebral blood flow and its duration in combination with factors affecting the sensitivity of the brain to hypoxic damage determine the degree of reversibility of tissue changes at each stage of the pathological process. The zone of irreversible damage is called the infarction core, the zone of ischemic damage of a reversible nature is designated by the term "penumbra" (ischemic penumbra). An important point is the time of existence of the penumbra, since over time reversible changes become irreversible, that is, the corresponding areas of the penumbra pass into the infarction core.

There may also be an oligemia zone, where the balance between tissue needs and the processes that provide these needs is maintained, despite the reduction in cerebral blood flow. This zone is not considered penumbra, as it can exist indefinitely without becoming the core of the infarction.