Dyscirculatory encephalopathy: causes and pathogenesis

Causes of discirculatory encephalopathy

The causes of both acute and chronic disorders of cerebral circulation are one. Among the main etiological factors, atherosclerosis and arterial hypertension are considered, a combination of these two conditions is often revealed. Other cardiovascular diseases can lead to chronic cerebral circulatory insufficiency, especially accompanied by signs of chronic heart failure, cardiac rhythm disturbances (both permanent and paroxysmal forms of arrhythmia), often leading to a drop in systemic hemodynamics. The anomaly of the vessels of the brain, neck, shoulder girdle, aorta, especially its arches, which may not manifest before the development of atherosclerotic vessels, is also important. Hypertensive or other acquired process. A major role in the development of discirculatory encephalopathy has recently been attributed to venous pathology, not only intra-, but also extracranial. A certain role in the formation of chronic cerebral ischemia can be played by compression of blood vessels, both arterial and venous. Consider not only the spondylogenic influence, but also the compression by altered neighboring structures (muscles, fasciae, tumors, aneurysms). Adverse effects on cerebral blood flow are affected by low blood pressure, especially in the elderly. This group of patients can develop a lesion of the small arteries of the head associated with senile arteriosclerosis. Another cause of chronic cerebral circulatory failure in elderly patients is cerebral amyloidosis - the deposition of amyloid in the vessels of the brain, leading to degenerative changes in the walls of blood vessels with a possible rupture.

Quite often discirculatory encephalopathy is detected in patients with diabetes mellitus, they develop not only micro-, but macroangiopathies of different localization. Other pathological processes may lead to chronic cerebrovascular insufficiency: rheumatism and other diseases from the group of collagens, specific and nonspecific vasculitis, blood diseases, etc. However, in ICD-10, these conditions are quite rightly classified in the headings of these nosological forms, which determines the correct treatment tactics.

As a rule, clinically detected encephalopathy can be a mixed etiology. In the presence of the main factors of the development of chronic insufficiency of the cerebral circulation, the rest of the diversity of the causes of this pathology can be treated as additional causes. The isolation of additional factors that significantly aggravate the course of chronic cerebral ischemia is necessary for the development of the correct concept of etiopathogenetic and symptomatic treatment.

Causes of discirculatory encephalopathy

Basic:

• atherosclerosis;
• arterial hypertension.

Additional:

• heart disease with signs of chronic circulatory failure;
• heart rhythm disturbances;
• vascular anomalies, hereditary angiopathies;
• venous pathology;
• compression of blood vessels;
• arterial hypotension;
• cerebral amyloidosis;
• diabetes;
• vasculitis;
• blood diseases.

Pathogenesis of discirculatory encephalopathy

The above-mentioned diseases and pathological conditions lead to the development of chronic brain hypoperfusion, that is, to prolonged failure of the brain to receive the main metabolic substrates (oxygen and glucose) delivered by the bloodstream. With the slow progression of brain dysfunction developing in patients with chronic cerebral circulatory insufficiency, pathological processes unfold primarily at the level of small cerebral arteries (cerebral microangiopathy). The widespread defeat of small arteries causes diffuse bilateral ischemic lesions, mostly white matter, and multiple lacunar infarctions in the deep regions of the brain. This leads to disruption of normal brain functioning and development of nonspecific clinical manifestations - encephalopathy.

To adequately work the brain requires a high level of blood supply. The brain, whose mass is 2.0-2.5% of body weight, consumes 20% of the circulating blood in the body. The cerebral blood flow in the hemispheres averages 50 ml per 100 g / min, but in gray matter it is 3-4 times higher than in white, and there is also relative physiological hyperperfusion in the anterior parts of the brain. With age, the magnitude of cerebral blood flow decreases, and frontal hyperperfusion disappears, which plays a role in the development and growth of chronic cerebral circulatory insufficiency. At rest, brain oxygen consumption is 4 ml per L00 g / min, which corresponds to 20% of all oxygen entering the body. The glucose consumption is 30 μmol per 100 g / min.

In the cerebral vascular system, three structural-functional levels are distinguished:

• the main arteries of the head are carotid and vertebral, carrying blood to the brain and regulating the volume of cerebral blood flow;
• superficial and perforating cerebral arteries that distribute blood across different regions of the brain;
• vessels of microcirculatory bed, providing metabolic processes.

In atherosclerosis, changes initially develop primarily in the main arteries of the head and arteries of the brain surface. With arterial hypertension, first of all, perforating intracerebral arteries, feeding the deep parts of the brain, suffer. Over time, with both diseases, the process extends to the distal parts of the arterial system and secondary reorganization of the vessels of the microcirculatory bed occurs. Clinical manifestations of chronic cerebral circulatory failure reflecting angioencephalopathy develop when the process is localized primarily at the microcirculatory level and in small perforating arteries. In this regard, a measure to prevent the development of chronic cerebral circulatory failure and its progression is an adequate treatment of the underlying background disease or diseases.

The cerebral blood flow depends on the perfusion pressure (the difference between systemic arterial pressure and venous pressure at the level of the subarachnoid space) and the resistance of the cerebral vessels. Normally due to the mechanism of autoregulation, cerebral blood flow remains stable, despite fluctuations in blood pressure from 60 to 160 mm Hg. When cerebral vessels are affected (lipogialinosis with the development of the inactive vascular wall), the cerebral blood flow becomes more dependent on systemic hemodynamics.

With long-term arterial hypertension, displacement of the upper boundary of the systolic pressure is noted, at which the cerebral blood flow remains stable and for quite a long time there is no disturbance of autoregulation. Adequate perfusion of the brain is maintained while increasing the vascular resistance, which in turn leads to an increase in the load on the heart. It is assumed that an adequate level of cerebral blood flow is possible until pronounced changes of small intracerebral vessels occur with the formation of a lacunar state peculiar to arterial hypertension. Consequently, there is a certain amount of time when timely treatment of hypertension can prevent the formation of irreversible changes in the vessels and brain or reduce their severity. If the basis of chronic failure of cerebral circulation is only arterial hypertension, then the use of the term "hypertensive encephalopathy" is legitimate. Severe hypertensive crises are always a disruption of autoregulation with the development of acute hypertensive encephalopathy, which always aggravates the phenomenon of chronic cerebral circulatory insufficiency.

A certain sequence of atherosclerotic vascular lesions is known: first the process is localized in the aorta, then in the coronary vessels of the heart, then in the vessels of the brain and later in the limbs. Atherosclerotic lesions of the brain vessels are, as a rule, multiple, localized in the extra- and intracranial parts of the carotid and vertebral arteries, as well as in the arteries forming the Willis circle and its branches.

Numerous studies have shown that hemodynamically significant stenoses develop with a narrowing of the lumen of the main arteries of the head by 70-75%. But cerebral blood flow depends not only on the severity of stenosis, but also on the state of collateral circulation, the ability of the cerebral vessels to change its diameter. These hemodynamic reserves of the brain allow to exist asymptomatic stenoses without clinical manifestations. However, even with hemodynamically insignificant stenosis, chronic cerebral circulatory insufficiency will practically inevitably develop. For the atherosclerotic process in the vessels of the brain, not only local changes in the form of plaques, but also hemodynamic restructuring of the arteries in a site localized distal to stenosis or occlusion are characteristic.

Of great importance is the structure of the plaques. So-called unstable plaques lead to the development of arterio-arterial embolism and acute disorders of cerebral circulation, more often as a type of transient ischemic attacks. Hemorrhage into such a plaque is accompanied by a rapid increase in its volume with an increase in the degree of stenosis and aggravation of signs of chronic insufficiency of cerebral circulation.

With the defeat of the main arteries of the head, cerebral blood flow becomes very dependent on systemic hemodynamic processes. Such patients are especially sensitive to arterial hypotension, which can lead to a drop in perfusion pressure and an increase in ischemic disorders in the brain.

In recent years, two main pathogenetic variants of chronic cerebrovascular insufficiency are considered. They are based on morphological signs - the nature of the damage and the primary localization. In the case of diffuse bilateral lesions of white matter, a leukoencephalopathic, or subcortical biswanger, variant of discirculatory encephalopathy is isolated. The second is a lacunar version with the presence of multiple lacunar foci. However, in practice, mixed variants are often encountered. Against the background of a diffuse white matter lesion, multiple small infarctions and cysts are found, in the development of which, in addition to ischemia, an important role can play repeated episodes of cerebral hypertensive crises. In hypertensive angioencephalopathy, lacunas are located in the white matter of the frontal and parietal lobes, the shell, the bridge, the thalamus, and the caudate nucleus.

The lacunar variant is most often caused by the direct occlusion of small vessels. In the pathogenesis of the diffuse lesion of white matter, the leading role is played by repeated episodes of the fall of systemic hemodynamics - arterial hypotension. The cause of the fall in blood pressure may be inadequate antihypertensive therapy, a reduction in cardiac output, for example, in paroxysmal heart rhythm disorders. There is also the importance of persistent cough, surgical interventions, orthostatic arterial hypotension due to vegetative-vascular insufficiency. In this case, even a slight decrease in blood pressure can lead to ischemia in the end zones of the adjacent blood supply. These zones are often clinically "mute" even with the development of infarcts, which leads to the formation of a multi-infarction state.

In conditions of chronic hypoperfusion, the main pathogenetic link of chronic cerebral circulatory insufficiency, the compensation mechanisms can be depleted, the energy supply of the brain becomes insufficient, as a result, first develop functional disorders, and then irreversible morphological damage. Chronic hypoperfusion of the brain reveals a slowdown in cerebral blood flow, a decrease in oxygen and glucose in the blood (energy hunger), oxidative stress, a shift in glucose metabolism towards anaerobic glycolysis, lactate acidosis, hyperosmolarity, capillary stasis, a tendency to thrombogenesis, depolarization of cell membranes, activation microglia, which begins to synthesize neurotoxins, which along with other pathophysiological processes leads to cell death. In patients with cerebral microangiopathy, granular atrophy of cortical areas is also often detected.

The multifocal pathological state of the brain with the predominant lesion of the deep divisions leads to disruption of the links between the cortical and subcortical structures and the formation of so-called separation syndromes.

Reduction of cerebral blood flow is obligatory combined with hypoxia and leads to the development of energy deficiency and oxidative stress, a universal pathological process, one of the main mechanisms of cell damage in brain ischemia. The development of oxidative stress is possible in conditions of both insufficiency and excess oxygen. Ischemia has a damaging effect on the antioxidant system, leading to a pathological way of utilizing oxygen - the formation of its active forms as a result of the development of cytotoxic (bioenergetic) hypoxia. The released free radicals mediate damage to cell membranes and mitochondrial dysfunction.

Acute and chronic forms of ischemic impairment of cerebral circulation can pass into each other. Ischemic stroke, as a rule, develops on an already changed background. Morphofunctional, histochemical, and immunological changes are revealed in patients, caused by the previous discirculatory process (mainly atherosclerotic or hypertonic angioencephalopathy), the signs of which significantly increase in the postinsult period. Acute ischemic process, in turn, triggers a cascade of reactions, some of which terminate in an acute period, while some remain for an indefinite period and contribute to the emergence of new pathological conditions leading to an increase in signs of chronic cerebral circulatory insufficiency.

Pathophysiological processes in the postinsult period are manifested by further damage to the blood-brain barrier, microcirculatory disturbances, changes in immunoreactivity, depletion of the antioxidant defense system, progression of endothelial dysfunction, depletion of anticoagulant reserves of the vascular wall, secondary metabolic disorders, violation of compensatory mechanisms. There is a cystic and cystic-gliotic transformation of the damaged parts of the brain, delimiting them from morphologically undamaged tissues. However, at the ultrastructural level around the necrotic cells, cells with apoptosis-like reactions that are triggered in the acute period of a stroke may persist. All this leads to aggravation of chronic cerebral ischemia, which occurs before the stroke. Progression of cerebrovascular insufficiency becomes a risk factor for recurrent stroke and vascular cognitive disorders up to dementia.

The post-stroke period is characterized by an increase in the pathology of the cardiovascular system and disorders of not only cerebral, but also general hemodynamics.

In the residual period of ischemic stroke, depletion of the antiaggregational potential of the vascular wall is noted, leading to thrombosis, an increase in the severity of atherosclerosis, and the progression of cerebral blood supply insufficiency. This process has a special significance in elderly patients. In this age group, irrespective of the preceding stroke, activation of the blood coagulation system, functional deficiency of anticoagulant mechanisms, deterioration of rheological properties of blood, disorders of systemic and local hemodynamics are noted. The aging process of the nervous, respiratory, cardiovascular system leads to disruption of autoregulation of cerebral circulation, as well as to the development or increase of brain hypoxia, which in turn contributes to further damage to autoregulation mechanisms.

However, improvement of cerebral blood flow, elimination of hypoxia, optimization of metabolism can reduce the severity of impaired functions and contribute to the preservation of brain tissue. In this regard, timely diagnosis of chronic cerebral circulatory insufficiency and adequate treatment are very relevant.

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