Ischemic atherothrombotic stroke in the left cm basin. Cerebral infarction in the left cm basin. What is vertebrobasilar insufficiency

Relevance. Ischemic strokes in the posterior cerebral arteries (PCA) account, according to various sources, from 5 - 10 to 25% of cases of all ischemic strokes. They can cause a number of clinical symptoms, which are not always timely and adequately recognized by the patients themselves, their relatives and doctors, because an acute gross motor deficit, which is usually associated with a stroke, in this case may be unexpressed or completely absent. At the same time, a delay in timely diagnosis or an incorrect diagnosis casts doubt on the possibility of providing the patient with adequate therapy (primarily), which in turn cannot but affect the outcome of the disease.

Etiology. The most common cause of isolated infarctions in the PCA territory is embolic occlusion of the PCA and its branches, which occurs in 80% of cases (cardiogenic > arterio-arterial embolism from the vertebral and basilar [syn.: main] arteries > cryptogenic embolism). In 10% of cases, thrombosis in situ is detected in the PCA. Vasoconstriction associated with migraine and coagulopathy are the causes of cerebral infarction in 10% of cases. If isolated infarctions in the PCA territory in most cases are of a cardioembolic nature, then involvement of the brainstem and/or cerebellum in combination with an infarction in the PCA territory is most often associated with atherosclerotic lesions of the vessels of the vertebrobasilar region (VBB). A very rare cause of infarction in this region can also be arterial dissection affecting the PCA. Regardless of the cause of the infarction, it usually only partially involves the PCA area.

Anatomy. Paired PCAs, which are formed by the bifurcation of the basilar artery (BA) and are its terminal branches, serve as the main sources of blood supply to the upper part of the midbrain, thalami and posteroinferior parts of the cerebral hemispheres, including the occipital lobes, mediobasal parts of the temporal lobes and inferomedial parts of the parietal.

In the early stages of development of the human body, the posterior cerebral artery is a branch of the internal carotid artery (ICA) and is supplied with blood from the carotid system, while the posterior communicating artery (PCA) plays the role of its proximal segment. Subsequently, blood begins to flow into the posterior cerebral arteries from the OA, and the PCA, being a branch of the internal carotid artery, becomes the most significant anastomosis between the carotid and vertebrobasilar regions (the PCA flows into the PCA approximately 10 mm distal to the bifurcation of the basilar artery). According to various sources, from 17 to 30% of adults have a fetal (embryonic) type of PCA structure, in which the ICA remains the main source of blood supply to the PCA throughout life. The fetal type of PCA structure is in most cases observed unilaterally, while the opposite PCA usually begins from an asymmetrically located, curved OA. In cases where both posterior cerebral arteries are branches of the internal carotid arteries, as a rule, well-developed large posterior communicating arteries are observed, and the upper segment of the OA is shorter than usual (the OA ends with two superior cerebellar arteries arising from it). In approximately 8% of cases, both PCAs originate from the same ICA.

Each PMA can be divided into 3 parts:

■ precommunicative part (P1-segment [according to Fisher]) - the area of ​​the PCA proximal to the place where the PCA flows into it; from this segment depart the paramedian mesencephalic, posterior thalamoperforating and medial posterior choroidal arteries, which are involved primarily in the blood supply to the ventrolateral nuclei of the thalamus and the medial geniculate body (the left and right posterior thalamoperforating arteries can arise from a common trunk called the artery of Percheron; a similar variant of the structure is usually found in combination with unilateral hypoplasia of the P1 segment and fetal structure of the PCA);

■ postcommunication part (P2-segment) – a section of the PCA located distal to the place where the PCA flows into the PCA; from this segment depart the peduncular perforator, thalamogeniculate and lateral posterior choroidal arteries, supplying the lateral geniculate body, the dorsomedial nuclei and thalamic cushion, part of the midbrain and the lateral wall of the lateral ventricle;

■ the final (cortical) part (P3 and P4 segments), giving off branches to the corresponding areas of the cerebral cortex; the main cortical branches of the PCA are the anterior and posterior temporal, parietotemporal and calcarine arteries (the boundaries of the watershed of the basins of the middle and posterior cerebral arteries fluctuate significantly; usually the boundary of the PCA basin is the Sylvian fissure, but sometimes the middle cerebral artery supplies blood to the outer parts of the occipital lobe up to the occipital poles; in this case, the PCA always supplies blood to the areas of the cerebral cortex in the area of ​​the calcarine sulcus, and the optic radiation in some cases receives blood from the middle cerebral artery, respectively, homonymous hemianopsia does not always imply infarction in the PCA territory).

Symptoms of the lesion . With ischemic strokes in the PCA region, depending on the location of the vessel occlusion, as well as on the state of collateral blood supply, the clinical picture may reveal symptoms of damage to the midbrain, thalamus and cerebral hemispheres. In general, up to 2/3 of all infarctions in the PCA region are cortical, the thalamus is involved only in 20 - 30% of cases, and the midbrain in less than 10% of cases. Accordingly, the most common option ischemic stroke in the PCA basin there is an isolated infarction of the cerebral hemispheres, primarily the occipital lobes; combined damage to the thalamus and cerebral hemispheres is less common, in a small percentage of cases - an isolated infarction of the thalamus and, finally, a combination of damage to the midbrain, thalamus and/or hemispheres is the rarest option.

OA apex syndrome. Sometimes there is bilateral damage to areas of the brain supplied by blood from the PCA. This occurs primarily in top of the basilar syndrome, which is an embolic occlusion of the distal basilar artery and is characterized by depression of consciousness, visual disturbances, oculomotor and behavioral disturbances, often without motor dysfunction.

According to a number of authors, the most characteristic signs of infarctions in the PCA area are: visual disturbances > homonymous hemianopsia > central paresis of the facial nerve > headache, mainly in the occipital region > sensory disturbances > aphasic disorders > hemiparesis > neglect (ignoring [unilateral spatial neglect, in mainly with damage to the right hemisphere]). Patients usually have a combination of symptoms.

Visual impairment . Homonymous hemianopia occurs on the contralateral side with infarctions in the areas of blood supply to the hemispheric branches of the PCA due to damage to the striate cortex, optic radiation or lateral geniculate body. In the absence of occipital pole involvement, macular vision remains intact. The visual field defect may be limited to only one quadrant. Superior quadrant hemianopsia occurs when the striate cortex is infarcted below the calcarine sulcus or inferior portion of the optic radiate in the temporo-occipital region. Inferoquadrant hemianopsia is a consequence of damage to the striate cortex above the calcarine sulcus or the upper part of the optic radiance in the parieto-occipital region. Occlusion of the calcarine sulcus may also be associated with pain in the ipsilateral eye. Visual disturbances may also be more complex, especially with bilateral occipital lobe lesions, including visual hallucinations, visual and color agnosia, prosopagnosia (agnosia for familiar faces), blindness denial syndrome (Anton syndrome), visual attention deficits, and optomotor agnosia ( Balint's syndrome). Often, visual impairment is accompanied by afferent disorders in the form of paresthesia, disorders of deep, pain and temperature sensitivity. The latter indicate involvement of the thalamus, parietal lobe, or brainstem (due to occlusion of the proximal VSB).

Neuropsychological disorders, associated with infarctions in the PCA, vary significantly and are present in more than 30% of cases. A stroke in the basin of the callosal branches of the left PCA in right-handed people, affecting the occipital lobe and splenium of the corpus callosum, is manifested by alexia without agraphia, sometimes color, object or photographic anomia. Right hemisphere infarctions in the PCA territory often cause contralateral hemiglect. With extensive infarctions involving the medial parts of the left temporal lobe or bilateral mesotemporal infarctions, amnesia develops. Also, with mono- or bilateral mesotemporal infarction, agitated delirium may develop. Extensive infarcts in the territory of the left posterior temporal artery may clinically manifest as anomia and/or sensory aphasia. Thalamic infarctions in the areas of blood supply to the penetrating branches of the PCA can cause aphasia (if the left pillow is involved), akinetic mutism, global amnesia and Dejerine-Roussy syndrome (disorders of all types of sensitivity, severe dysesthesia and/or thalamic pain and vasomotor disturbances in the contralateral half of the body, combined with usually transient hemiparesis, choreoathetosis and/or ballism). Also, infarctions in the PCA region may be associated with dyscalculia, spatial and temporal disorientation.

Bilateral thalamic infarcts are often associated with deep coma. Thus, occlusion of the Percheron artery causes the development of bilateral infarcts in the intralaminar nuclei of the thalamus, which leads to severe impairment of consciousness.

Hemiparesis in case of infarctions in the PCA region, it occurs in only 1/5 of patients, is more often mild and transient, and is usually associated with involvement of the cerebral peduncles in the pathological process. Cases of infarctions in the PCA region have been described, when patients exhibited hemiparesis without involvement of the cerebral peduncles. These patients had damage to the distal parts of the PCA, primarily involving the thalamogeniculate, lateral and medial posterior choroidal arteries. It is assumed that hemiparesis during infarctions in the posterior choroidal arteries may be associated with damage to the corticobulbar and corticospinal tracts, even in the absence of visible damage to the internal capsule or midbrain according to neuroimaging. There are opinions that the development of hemiparesis is associated with compression of the internal capsule by edematous tissue of the thalamus.

In approximately 1/5 of patients, infarctions in the PCA territory mimic infarctions in the carotid area, especially with combined damage to the superficial and deep branches of the PCA, which is observed in approximately 1/3 of cases. Differential diagnosis can be difficult due to the presence of aphasic disorders, neglect, sensory deficits, and usually mild and transient hemiparesis resulting from the involvement of the pyramidal tracts. In addition, memory impairment and other acute neuropsychological disorders can significantly complicate the evaluation of such patients. Among other conditions that often clinically mimic infarctions in the PCA region, we should highlight some infectious diseases (primarily toxoplasmosis), neoplastic lesions, both primary and metastatic, and thalamic infarctions caused by deep cerebral vein thrombosis. Neuroimaging methods often play a decisive role in making a diagnosis..

Neuroimaging . Computed tomography (CT) usually does not detect ischemic changes in the brain parenchyma during the first few hours after the onset of stroke, the time most important for initiating therapy, and sometimes even later. late dates diseases. Visualization of the posterior regions of the brain is especially difficult due to artifacts caused by the bones of the skull. However, with strokes in the territory of the PCA, as well as with strokes in the territory of the middle cerebral artery, in some cases, CT may show a hyperintense signal from the PCA itself, which is the most early sign stroke in its basin and is detected in 70% of cases within the first 90 minutes from the onset of the disease and in 15% of cases within 12 to 24 hours. This sign appears due to visualization of a calcified embolus or atherothrombosis in situ.

Magnetic resonance imaging (MRI) makes it possible to more accurately determine the presence and nature of ischemic changes in the brain during stroke. Diffusion-weighted imaging (DWI) can detect early ischemic changes, often within an hour of symptom onset, and localize and extend lesions more accurately than CT. The combined use of DWI, ADC and FLAIR modes makes it possible to differentiate acute, subacute and chronic ischemic changes in the brain parenchyma, as well as to distinguish cytotoxic brain edema observed in ischemic stroke from vasogenic edema in the syndrome of posterior reversible leukoencephalopathy and hypertensive encephalopathy.

CT angiography (CTA) plays a significant role in the non-invasive diagnosis of steno-occlusive lesions of large extra- and intracranial arteries. This technique makes it possible to identify the degree of stenosis, the morphology of the plaque, as well as the presence of arterial dissection both in cases of lesions of the vessels of the SBB and carotid basins. In addition, the anatomical features of the collaterals and circulation options of the PCA are assessed. Additional information about vascular anatomy can be obtained using contrast-enhanced MR angiography, which in combination with CTA allows for data that previously could only be obtained using classical angiography. In addition, these methods are important in assessing the effectiveness of thrombolytic therapy in cases of arterial recanalization (currently

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Etiology of ischemic stroke

Less commonly, the main disease complicated by a heart attack is hypertension, and even more rarely, rheumatism. In rheumatism, the main cause of ischemic stroke is cardiogenic embolism of cerebral vessels, much less often thrombovaeculitis. Among other diseases that can be complicated by ischemic stroke, mention should be made of arteritis of an infectious and infectious-allergic nature, blood diseases (erythremia, leukemia). Aneurysms of the cerebral arteries after their rupture can be complicated by spasm and cause the development of cerebral infarction.

Pathogenesis of ischemic stroke

It can be considered proven that there is no direct correlation between the frequency of verified stenosis and occlusion of extra- and intracranial arteries and the incidence of ischemic stroke. This is evidenced by angiographic and clinical-morphological data on the relatively frequent detection of asymptomatic stenoses and occlusion.

Thus, it is obvious that atherosclerotic changes in extra- and intracranial vessels do not necessarily entail the development of cerebral infarction, and even when the latter occurs, a direct cause-and-effect and temporal connection (with the development of atherosclerosis) is not always established.
A significant role in compensating for circulatory deficiency during stenosis and occlusion of extra- and intracranial arteries belongs to collateral circulation, the degree of development of which varies from person to person. Vessel occlusion can be caused by thrombus, embolus, or due to its obliteration. In the presence of complete blockage of the vessel (extracranial, intracranial or intracerebral), cerebral infarction may not develop if the collateral circulation is well developed and, what is especially important, if the collateral network quickly turned on from the moment of vessel occlusion. In other words, the development of cerebral infarction in the presence of complete vascular occlusion depends on the degree of development and rate of inclusion of collateral circulation.

With the development of stenosis of extracranial or intracerebral vessels, conditions are also created for local ischemia of the brain substance if blood pressure suddenly drops. A drop in pressure can be caused by myocardial infarction, bleeding, etc. In addition, with vascular stenosis, conditions are created for turbulent blood movement, which promotes the gluing of blood cells - red blood cells and platelets and the formation of cellular aggregates - microemboli, which can close the lumen of small vessels and be cause cessation of blood flow to the corresponding part of the brain. In addition, high blood pressure (200//100 mm Hg and above) is regarded as an unfavorable factor that contributes to constant microtrauma of the arterial intima and separation of embolic fragments from stenotic areas.

In addition to thrombosis, embolism, hemodynamic factors, as well as arterio-arterial embolism, the reaction plays a certain role in the development of cerebral infarction vascular system brain and blood cells on cerebral circulation deficiency, as well as energy demands of brain tissue.
The response of the cerebral vascular system to a decrease in local cerebral blood flow varies. Thus, in some cases, ischemia is replaced by excess blood flow, leading to filtration perifocal edema, in others, the ischemic zone is surrounded by dilated vessels, but not filled with blood (the phenomenon of “unrestored” blood flow). The mechanism of such different reactions of cerebral vessels in response to ischemia is not completely clear. Perhaps this depends on different degrees of hypoxia and the hydrodynamic properties of the blood changing in connection with this. If, in the case of maximum vasodilation with developing regional edema that occurs after ischemia, one can think of a disruption of the normal autoregulatory mechanisms of the cerebral vessels themselves in the zone of local ischemia, then the phenomenon of “unrestored” blood flow cannot be explained by the reaction of the cerebral vessels alone. In the mechanism of the appearance of empty capillaries and arterioles in the area of ​​local circulatory deficiency, a certain role appears to be played by changes in the functional properties of blood cellular elements, which lose the ability to move normally through the microcirculatory bed in the ischemic zone.

It is known that capillary blood flow depends on the aggregation properties of erythrocytes and platelets, on the ability of erythrocytes to change their shape when moving through narrow capillaries, as well as on blood viscosity. Red blood cells, having a diameter greater than the diameter of narrow capillaries, under normal blood circulation conditions easily change their shape (deform) and, like an amoeba, move along the capillary bed. In patients with vascular diseases, the ability of red blood cells to change shape decreases and they become more rigid. An even greater decrease in the deformability of red blood cells develops in hypoxic foci of any location where the osmotic pressure changes. A significant decrease in the elasticity of the red blood cell will not allow it to pass through a capillary whose diameter is smaller than the red blood cell. Consequently, an increase in the rigidity of erythrocytes, as well as an increase in the aggregation of platelets and erythrocytes in the area of ​​local cerebral ischemia may be one of the main factors preventing the flow of blood through dilated vessels during the phenomenon of “unrestored” blood flow. Thus, if the cause that caused local cerebral ischemia disappears , then regional edema or the pathological phenomenon of “unrestored” blood flow developing after ischemia can lead to disruption of the normal functioning of neurons and the development of cerebral infarction.
From what has been said, it is clear that as in the development of occlusion of blood vessels supplying the brain (thrombosis, embolus, microembolus). and in ischemia that develops as a result of hemodynamic disorders (a drop in blood pressure due to various reasons), an important role belongs not only to changes in blood vessels, but also to the physicochemical properties of the blood, changes in which determine the outcome of cerebrovascular accident, i.e., the development of cerebral infarction .

In the pathogenesis of cerebral ischemia, the dominant role among the factors causing occlusion is played by thrombosis and embolism of cerebral vessels, the differentiation of which presents significant difficulties not only in the clinic, but also at autopsy. A thrombus is often a substrate that embolizes cerebral arteries, which is reflected in the widespread use of the term “thromboembolism.”
The formation of a blood clot in the affected vessel is facilitated (according to currently existing ideas) by additional, or “thrombosis-producing” factors. The main ones should be considered changes in the functional properties of platelets and (the activity of biologically active monoamines, imbalance of blood coagulation and anticoagulation factors, as well as changes in hemodynamic parameters. Changes in the functional state of platelets (increased their aggregation and adhesive ability, inhibition of disaggregation) are clearly observed already in the initial stages of atherosclerosis. Aggregation significantly increases as atherosclerosis progresses with the appearance of transient cerebrovascular accidents and stenotic processes in the main arteries of the head. The local tendency to aggregation, gluing, and then disintegration (viscose metamorphosis) of platelets in the area where the intima is damaged is explained by the fact that that it is in this place that a chain reaction develops, depending on a number of humoral and hemodynamic factors.

Violation of the integrity of the intima and exposure of collagen fibers reduce the negative electrical charge of the vascular wall and, accordingly, reduce the adsorption of plasma fibrinogen in this area. The accumulation of fibrinogen, in turn, reduces the electrical potential of platelets and creates conditions for their adhesion to the damaged intima and rapid destruction. This releases a number of procoagulant factors of the plates, which help accelerate the conversion of prothrombin to thrombin, fibrinogen to fibrin and fibrin retraction. At the same time, there is inhibition of local fibrinolytic activity of plasma and local accumulation of thrombin. For massive thrombus formation, which sharply limits the lumen of the vessel and turns out to be the cause of ischemic stroke, only the thrombogenic activity of disintegrated platelet aggregates is not enough. Of decisive importance is the disruption of the normal ratio of plasma thrombogenic and antithrombogenic factors formed in the affected area of ​​the vessel.

Immediately on the first day of development of ischemic stroke there is an increase in blood clotting in the cerebral bloodstream, which indicates difficulty in microcirculation and the formation of reversible microthrombi in the arterioles and precapillaries of the brain. Subsequently, a protective anticoagulation reaction occurs, which, however, is insufficient to overcome the rapidly developing generalized hypercoagulation throughout the vascular bed.
In the simultaneous processes of thrombus formation and thrombolysis, a complex multi-stage complex of coagulant and anticoagulant factors is involved, and depending on the final prevalence of one of them in the affected segment of the vessel, different degrees and thrombotic outcomes. Sometimes the process is limited by stenosis, partial deposition of platelets and fibrin, and sometimes dense conglomerates are formed, completely obstructing the lumen of the vessel and gradually increasing in length.

In addition to blood hypercoagulability, the increase in “thrombus growth” is facilitated by a slowdown in blood flow and turbulent, vortex, movements (of blood plates. Relative hypocoagulation makes the structure of blood clots looser, which can be a prerequisite for the formation of cellular embolisms and, apparently, turns out to be a factor playing a significant role in spontaneous recanalization of blood clots. Thrombotic lesions of the extracranial and large intracranial arteries are one of the sources of arterio-arterial embolism of cerebral vessels.
The source of cerebral embolism can also be damage to various organs and systems. The most common are cardiogenic embolisms that develop as a result of detachment of parietal thrombi and warty layers in valvular heart defects, recurrent endocarditis, congenital heart defects and during operations for congenital or acquired heart defects. Cardiogenic embolism of cerebral vessels can develop during myocardial infarction, during acute post-infarction cardiac aneurysms with the formation of parietal thrombi and thromboemboli.

The source of embolism can be parietal thrombi formed at a disintegrating atheroclerotic plaque during atherosclerosis of the aorta and great vessels of the head. The cause of cardiogenic embolism is various lesions that cause atrial fibrillation and decreased contractility of the heart (rheumatism, atheroaclerotic or post-infarction cardiosclerosis, post-infarction aneurysms), as well as fresh myocardial infarctions accompanied by thromboendocarditis.

The frequency of detection of emboli in the arterial system of the brain varies according to different authors from 15 to 74% [Sheffer D. G. et al., 1975; Zilch, 1973]. The presented data once again demonstrates the great difficulty of differential diagnosis of thrombosis and embolism not only intravitally, but also at autopsy.

Definite psychoemotional stress factors are important in the pathogenesis of ischemic strokes, leading to an increased secretion of catecholamines, which under normal conditions are peculiar catalysts of the sympathetic-adrenal system that maintains homeostatic balance. In relation to the problem under consideration, it should be noted that catecholamines are powerful activators of platelet aggregation. If healthy individuals catecholamines only stimulate platelet aggregation, then in patients with atherosclerosis (with their rapid release into the vascular bed) they cause sharply increased aggregation and destruction of platelets, which leads to a significant release of serotonin, the main carrier of which are platelets, and intravascular thrombus formation. Many researchers consider the overproduction of catecholamines as a link between psychogenic factors - chronic or acute emotional stress and atherosclerotic changes in the vascular wall.

In compensating for cerebral circulation deficiency, not only the individually developed network of collateral circulation plays a role, but also the age-related characteristics of the energy demands of brain tissue. As the body ages and biochemical and clinical signs of atherosclerosis appear, brain mass and the intensity of cerebral circulation decrease. By the age of 60, the intensity of cerebral blood flow and the brain's consumption of oxygen and glucose decreases by 20-60% compared to those in healthy young people, and no noticeable dysfunction may occur. Relative compensation of cerebral hemodynamics without the appearance of neurological symptoms can be observed in patients with atherosclerosis with a very significant deficit (Blood circulation, in conditions of chronic ischemia, characterized by a decrease in total blood flow to 36.4 ml (s/100 g of the brain) with a norm of 58 ml (s/100 g ) and oxygen consumption up to 2.7 ml (instead of 3.7 ml).In some observations, neurological symptoms are reversible even in conditions of a decrease in the level of metabolism of nerve cells by 75-80%.

A lively discussion takes place when discussing the role of cerebral vasospasm in the genesis of ischemic stroke and PMI. The possibility of vasospasm of cerebral arteries and arterioles is currently beyond doubt. Under normal conditions, vasospasm is a common compensatory reaction in response to decreased cerebral blood flow, increased oxygen content and decreased concentration of carbon dioxide in the blood. According to modern concepts, central vasospasm is caused by many humoral mechanisms. Of the humoral factors, catecholamines, adrenocorticotropic hormone, and platelet breakdown products have spasmogenic properties. Prostaglandins, mainly fraction E, released mainly from destroyed platelets, have a spasmogenic effect.

Angiospasm of cerebral vessels- an important link in the system of autoregulation of cerebral circulation. Most researchers express doubts because until recently there has been no direct evidence of the role of neurogenic spasm in the development of cerebral infarction. An exception may be a spasm that complicates the course of subarachnoid hemorrhage, which develops in response to a rupture of the vascular wall and leads to the development of cerebral infarction. However, the development of arterial spasm during subarachnoid hemorrhage is associated with the direct effect of the spilled blood on the sympathetic plexuses of the arteries.

Pathological anatomy of ischemic stroke

Ischemic Stroke Clinic

Infarctions in the internal carotid artery.

Stenosis and even complete blockage of the internal carotid artery may not be accompanied by the development of cerebral infarction if the occlusion is localized extracranially, in the neck. In this case, a full-fledged arterial circle of the cerebrum carries out replacement blood circulation from the internal carotid artery of the other side or from the vertebral arteries. When the collateral circulation is defective, a stenosing lesion of the extracranial part of the internal carotid artery in the initial period often occurs in the form of PNMK, clinically expressed by short-term weakness in the limbs, numbness in them, aphatic disorders, and decreased vision in one eye.

With intracranial occlusion (thrombosis) The internal carotid artery, which flows with the separation of the arterial circle of the cerebrum, develops hemiplegia and grossly expressed cerebral symptoms - disturbance of consciousness, headache, vomiting, with subsequent disruption of vital functions caused by compression and displacement of the trunk by rapidly developing cerebral edema. Intracranial occlusion of the internal carotid artery often ends in death.
In the area of ​​vascularization of the anterior cerebral artery, extensive infarctions rarely develop. They can be observed when the main trunk of the anterior cerebral artery is blocked after the anterior communicating artery departs from it.

Clinical picture of infarctions in the anterior cerebral artery basin characterized by spastic hemiparesis of the opposite limbs with a predominant development of paresis in the proximal arm and distal leg. Urinary retention may occur. Of the pathological foot reflexes, reflexes of the flexion type - Rossolimo, Bekhterev - are evoked with great constancy, and the grasping reflex and reflexes of oral automatism are also observed. Sometimes mild sensory disturbances are found on the paralyzed leg. Due to ischemia of the additional speech zone on the medial surface of the hemisphere, the development of dysarthria, aphonia and motor aphasia is possible.
With foci of infarction in the anterior cerebral artery basin, mental disorders, decreased criticism, memory, and elements of unmotivated behavior are noted. The above-mentioned mental disorders are more severely expressed with bilateral foci of infarction in the anterior cerebral artery basin.
More often, small infarctions develop in the anterior cerebral artery basin due to damage to the branches of the anterior cerebral artery. Thus, with occlusion of the paracentral branch, monoparesis of the foot develops, reminiscent of peripheral paresis, and with damage to the pericallosal branch, left-sided apraxia occurs. Damage to the premotor area with the pathways in this area causes a gross increase in muscle tone, significantly exceeding the degree of paresis, and a sharp increase in tendon reflexes with pathological flexion-type foot reflexes.

Most often, infarctions develop in the territory of the middle cerebral artery, which can be affected in the area of ​​the main trunk before the emergence of deep branches, after their branching and in the area of ​​individual branches, which determines clinical picture heart attack in each specific case.
When the main trunk of the middle cerebral artery is occluded, an extensive infarction is observed, leading to the development of hemiplegia, hemihypesthesia in the limbs opposite to the source of the infarction and hemianopsia. When the left middle cerebral artery is damaged, i.e. when the infarction is located in the left hemisphere, aphasia develops, often total; with right hemisphere infarctions, anosognosia is observed in the area of ​​vascularization of the right middle cerebral artery (unawareness of the defect, ignoring paralysis, etc.).

Infarction in the basin of the deep branches of the middle cerebral artery causes spastic hemiplegia, sometimes with impaired sensitivity and motor aphasia with foci in the left hemisphere.
Damage to the cortical-subcortical branches leads to the development of hemiparesis with a predominant disturbance of movements in the hand, a disorder of all types of sensitivity, hemianopsia, as well as sensory-motor aphasia, impairment of writing, counting, reading, praxis (with left hemisphere localization of the infarction) and anosognosia and disorder of the body diagram when the infarction is localized in the right hemisphere.

In the basin of the posterior branches of the middle cerebral artery, the infarction manifests itself syndrome of damage to the parietal-temporo-occipital region - hemihypesthesia, impaired deep sensitivity, astereognosis, afferent paresis of the limbs, hemianopsia, and in the case of left hemisphere localization of the process - sensory aphasia, agraphia, acalculia and apraxia.

Infarctions in the basin of individual branches of the middle cerebral artery are expressed by less severe symptoms: with damage to the Rolandic artery, hemiparesis is observed with a predominance of weakness in the hand, with a heart attack in the bed of the posterior parietal artery, hemihypesthesia of all types of sensitivity is observed with the development of afferent paresis, and in the basin of the precentral artery - paresis of the lower facial muscles, tongue and weakness in the hand, motor aphasia (with damage to the dominant hemisphere).

In case of circulatory disorders in the vessels of the vertebrobasilar region systemic dizziness, hearing and vision impairment, attacks of sudden falling, vegetative disorders are observed, and sometimes coma, tetraplegia, respiratory and cardiac dysfunction, diffuse hypotension or hormetonia occur.

Infarction due to vertebral artery occlusion leads to the development of symptoms from the medulla oblongata, cerebellum and partly the cervical spinal cord. Foci of infarction due to blockage of the vertebral artery can develop not only in the region of the cerebellum and medulla oblongata, but also at a distance, in the region of the midbrain, in the area of ​​adjacent blood circulation, two vascular systems - the vertebral and carotid basins. Infarctions in the area of ​​adjacent circulation are more typical for occlusion of the extracranial segment of the vertebral artery. It is possible to develop the above-mentioned attacks of sudden falling with loss of muscle tone (drop attace), as well as vestibular disorders (dizziness, ataxia, nystagmus), cerebellar coordination and static disorders, oculomotor disorders, and rarely, visual disturbances.

Occlusion of the intracranial vertebral artery is characterized by: Wallenberg-Zakharchenko, Babinsky-Nageotte syndromes and other syndromes of damage to the lower parts of the trunk. Infarctions in the basin of the branches of the vertebral artery supplying the medulla oblongata and cerebellum are most often accompanied by the development of Wallenberg-Zakharchenko syndrome, caused by damage to the inferior posterior cerebellar artery, the largest branch of the vertebral artery.
Clinically, on the side of the infarction there is paralysis of the muscles of the pharynx, soft palate, larynx (as a result of which dysphagia and dysphonia develop), cerebellar ataxia (dynamic and static with decreased muscle tone), Gorier's syndrome (due to damage to the hypothalamospinal sympathetic pathway), hypoesthesia of pain and temperature sensitivity on half of the face corresponding to the side of the lesion, and on the opposite half of the body, caused by damage to the spinal descending root of the trigeminal nerve and the spinothalamic tract.

Symptoms of damage to the pyramidal tract are usually absent or mild. Frequent symptoms of occlusion of the inferior cerebellar artery are dizziness, vomiting, and nystagmus associated with damage to the vestibular nuclei. There are several variants of Wallenberg-Zakharchenko syndrome, caused by different numbers of branches of the posterior inferior cerebellar artery, as well as individual characteristics collateral circulation.

With occlusive processes in the vertebral arteries Babinsky-Nageotte syndrome, close to Wallenberg-Zakharchenko syndrome, develops (paralysis of the velum palatine with preservation of vocal cord function, cross hemiparesis with dissociated hemihypesthesia and cerebellar ataxia on the side of the lesion).

Infarcts in the pons can be caused by occlusion of both the branches of the basilar artery and its main trunk. Infarcts in the region of the branches of the basilar artery are characterized by a large polymorphism of clinical manifestations; hemiplegia of the contralateral limbs is combined with central paralysis of the facial and hypoglossal nerves and with pontine gaze palsy or abducens nerve palsy on the affected side. Peripheral paresis of the facial nerve (alternating Foville syndrome) can also be observed on the side of the lesion. Alternating hemihypesthesia is possible - impaired pain and temperature sensitivity on the face on the side of the infarction and on the opposite half of the body.

Bilateral pontine infarcts cause the development of tetraparesis, pseudobulbar syndrome and cerebellar symptoms.
Occlusion of the basilar artery leads to the development of an extensive infarction with symptoms of damage to the pons, cerebellum, midbrain and hypothalamus, and sometimes cortical symptoms from the occipital lobes of the brain.

Acute basilar artery blockage leads to the development of symptoms primarily from the midbrain and pons - a disorder of consciousness, oculomotor disorders caused by damage to the III, IV, VI pairs of cranial nerves, tetraplegia, impaired muscle tone, bilateral pathological reflexes, trismus of the lower jaw, hyperthermia and disturbance of vital signs develop. functions. In the majority of cases, occlusion of the basilar artery is fatal.

The midbrain is supplied with blood by arteries arising from the posterior cerebral and basilar arteries. With a heart attack in the basin of these arteries, inferior red nucleus syndrome is observed - paralysis of the oculomotor nerve on the side of the lesion, ataxia and intention tremors in the contralateral limbs due to damage to the superior cerebellar peduncle near the red nucleus (in the area from Wernecking's decussation to the red nucleus) or the red nucleus itself. When the anterior parts of the red nucleus are affected, there may be no symptoms from the oculomotor nerve, but choreoform hyperkinesis may be observed.
With a heart attack in the basin of the quadrigeminal artery, upward gaze paralysis and convergence paresis develop (Parinaud's syndrome), sometimes combined with nystagmus. An infarction in the region of the cerebral peduncle causes the development of Weber syndrome.

Infarction in the posterior cerebral artery territory occurs both due to occlusion of the artery itself or its branches, and when the main or vertebral arteries are damaged. Ischemia in the basin of the cortical and subcortical branches of the posterior cerebral artery can affect the occipital lobe, III and partly II temporal gyri, basal and medial-basal gyri of the temporal lobe (in particular, the hippocampal gyrus). Clinically, homonymous hemianopsia develops with preservation of macular (central) vision; damage to the occipital cortex (fields 18, 19) can lead to visual agnosia and metamorphopsia. With left hemisphere infarctions of the ib region of the posterior cerebral artery, alexia and mild sensory aphasia can be observed. When ischemia spreads to the hippocampal gyrus and mamillary bodies, memory disorders such as Korsakov's syndrome occur with a predominant impairment of short-term memory for current events, while memory for distant past events is preserved.

Damage to the posterior inferior parts of the parietal cortex on the border with the occipital leads to disruption of optical-spatial gnosis, disorientation in place and time. It is also possible to develop emotional and affective disorders in the form of anxiety-depressive syndrome, a state of psychomotor agitation with attacks of fear, anger, and rage.

With the formation of post-ischemic foci of convulsive activity, temporal lobe epilepsy develops, characterized by polymorphism of epileptic paroxysms; large epileptic seizures, absence seizures, mental equivalents, etc.

With a heart attack in the basin of the deep branches of the posterior cerebral artery(a. thalamogeniculata) thalamic Dejerine-Rusey syndrome develops - hemianesthesia, hyperpathia, transient hemiparesis, hemiavopea, hemiataxia, and a heart attack in the a. thalamoperforata is clinically characterized by the development of severe ataxia, choreoathetosis, thalamic hand, and intention tremor in the contralateral limbs. When the dorsomdial nucleus of the optic thalamus is damaged, akinetic mutism sometimes develops. In the first days of ischemic stroke, temperature reactions and significant changes in peripheral blood, as a rule, are not observed. However, with extensive infarctions with severe cerebral edema involving the brain stem, the development of hyperthermia and leukocytosis, as well as an increase in the content of sugar and urea in the peripheral blood, is possible.

On the part of the blood coagulation and anticoagulation system, most patients with ischemic stroke show a shift towards blood hypercoagulation. An increase in fibrinogen, prothrombin, plasma tolerance to heparin, the appearance of fibrinogen B with reduced or normal fibrinolytic activity is usually expressed in the first 2 weeks of the disease. In some cases, it is possible to replace blood hypercoagulation with hypocoagulation. In this case, there is a sudden drop in the level of fibrinogen in the blood, a decrease in the prothrombin index and a decrease in the number of platelets. The listed plasma (fibrinogen, prothrombin) and cellular blood coagulation factors are consumed for intraocular coagulation, and blood deprived of coagulation factors penetrates the vascular wall, causing hemorrhagic complications: Common hemorrhagic complications develop as a result of intravascular coagulation (consumption syndrome, thrombohemorrhagic syndrome, disseminated intravascular coagulation syndrome).

In patients with ischemic stroke in the acute period, significantly high platelet aggregation and adhesiveness are observed. It remains at its highest levels for 10-14 days, returning to subnormal levels on the 30th day of the stroke. Cerebrospinal fluid is usually clear with normal protein and cellular content. There may be a slight increase in protein and lymphocytic cytosis in areas of infarction that border the cerebrospinal fluid space and cause reactive changes in the ventricular ependyma and meninges.

Echoencephalography in ischemic stroke usually does not show a shift in the median M-echo signal. However, with extensive infarctions, due to the development of edema and displacement of the brain stem, displacements of the M-echo can be observed already by the end of the first day after the development of the infarction. Ultrasound fluorometry (Doppler method) allows you to detect occlusion and severe stenoses of the main arteries of the head. Important information is provided by angiography, which reveals in patients with cerebral infarction the presence or absence of occlusive and stenotic processes in the extra- and intracranial vessels of the brain, as well as the functioning pathways of collateral circulation. The EEG reveals interhemispheric asymmetry and sometimes a focus of pathological activity. Characteristic changes during a cerebral infarction are detected by computed tomography, which reveals a focus of reduced density of the brain parenchyma in the infarction zone and peri-infarct area, in contrast to the changes detected during a cerebral hemorrhage, when tomography reveals the opposite changes - a focus of increased density.

Diagnosis of ischemic stroke

These include:

1. traumatic brain injury in the acute period (cerebral contusion, traumatic intrathecal hemorrhage);
2. myocardial infarction accompanied by impaired consciousness;
3. brain tumors with apoplectiform development caused by hemorrhage into the tumor;
4. epilepsy, in which post-ictal paralysis develops;
5. hyper- or hypoglycemic coma;
6. uremia.

It should also be borne in mind that in acute cardiac weakness, sometimes there is a disturbance of consciousness caused by a sharp decrease in volumetric cerebral blood flow and secondary hypoxia of brain tissue. In addition to confusion, respiratory failure, vomiting, and a drop in blood pressure are noted. Focal symptoms of damage to the hemispheres and brain stem are not detected, except in cases where myocardial infarction is combined with the development of cerebral infarction.

Often (especially in older people) difficulties arise in differentiating a brain tumor complicated by hemorrhage and a vascular process. Spovgioblastoma multiforme can be latent for some time, and their first manifestations occur as a result of hemorrhage into the tumor. Only the subsequent course with increasing symptoms of brain damage makes it possible to recognize the tumor. The diagnosis of epilepsy, hyper- or hypoglycemic coma, as well as uremia is confirmed or rejected on the basis of updated anamnestic information, the amount of sugar and urea in the blood, urine analysis and EEG indicators.
Thus, data from anamnesis, clinical features, examination of cerebrospinal fluid, fundus of the eye, echo and electroencephalography, ECG, blood sugar and urea levels, as well as radiographic studies - craniography, angiography allow one to correctly differentiate stroke from other apoplectiform but ongoing diseases.

Distinguish cerebral infarction from hemorrhagic stroke in a number of observations presents great difficulties. Nevertheless, determining the nature of the stroke is necessary for differentiated treatment. It should be recognized that there are no individual (Symptoms that are strictly pathognomonic for hemorrhage or cerebral infarction. The sudden development of a stroke, characteristic of hemorrhage, is often observed with occlusion of a large vessel, leading to the development of acute cerebral infarction. And at the same time with hemorrhages, especially diapedetic in nature, symptoms of damage to the brain substance can increase over several hours, gradually, which is considered most characteristic of the development of cerebral infarction.

It is well known that during sleep, as a rule, a cerebral infarction develops, however, although much less frequently, cerebral hemorrhages can also occur at night. Severe cerebral symptoms, so characteristic of cerebral hemorrhage, are often observed with extensive cerebral infarctions, accompanied by edema. Arterial hypertension is often complicated by hemorrhage, but atherosclerosis accompanying hypertension is often the cause of the development of a heart attack, which is often observed in patients suffering from atherosclerosis with arterial hypertension. High blood pressure values ​​at the time of a stroke should not always be considered as its cause; An increase in blood pressure may also be a reaction of the brainstem vasomotor center to a stroke.
From the results it is clear that individual symptoms have relative diagnostic value for determining the nature of the stroke. However, certain combinations of symptoms with additional research data make it possible to correctly recognize the nature of a stroke in the vast majority of cases. Thus, the development of a stroke during sleep or immediately after sleep against the background of cardiac pathology, especially accompanied by cardiac arrhythmias, a history of myocardial infarction, and moderate arterial hypertension are characteristic of ischemic stroke. And the onset of a stroke with an acute headache, repeated vomiting during the day, especially at the moment of emotional stress in a patient suffering from hypertension, and impaired consciousness are most characteristic of cerebral hemorrhage. It is necessary to take into account that leukocytosis with a shift to the left, which appeared on the first day of the stroke, an increase in body temperature and the presence of blood or xanthochromia in the cerebrospinal fluid, a shift in the M-echo and the presence of a focus of increased density on computed tomography indicate the hemorrhagic nature of the stroke.

In approximately 20% of cases, macroscopically, cerebrospinal fluid during hemorrhage is transparent and colorless. However, a microscopic examination in this category of patients allows one to detect red blood cells, and a spectrophotometer detects blood pigments (bilirubin, oxy- and methemoglobin). During a heart attack, the liquid is colorless, transparent, and the protein content may increase. Coagulogram data, as well as EEG and REG do not reliably confirm the nature of the stroke. Angiography should be recognized as an informative method, however, due to the risk of complications, arteriographic studies are recommended to be carried out in cases where surgical treatment is advisable. Currently, computed tomography data are of greatest importance in determining the nature of a stroke, allowing one to detect foci of different densities during cerebral infarction and cerebral hemorrhage.

Hemorrhagic infarction is one of the most difficult conditions to diagnose. There is still no consensus among pathomorphologists and pathophysiologists regarding the mechanism of development of hemorrhagic infarctions. With a hemorrhagic infarction, ischemic damage initially develops, and then (or simultaneously) hemorrhage appears in the infarct zone. Hemorrhagic infarctions differ from another form of cerebrovascular accident - hemorrhagic diapedetic impregnation both in the mechanism of development and in morphological changes [Koltover A. N., 1975]. Most often, hemorrhagic infarctions are localized in the gray matter, cerebral cortex, subcortical ganglia and thalamus optica. Most researchers associate the development of hemorrhages in the ischemic area with a sudden increase in blood flow in the ischemic zone due to the rapid flow of blood into this area through collaterals.
Hemorrhagic changes more often occur with extensive, rapidly forming cerebral infarctions.

In terms of the development of the disease and clinical manifestations, a hemorrhagic infarction resembles a hemorrhagic stroke - hemorrhage in the brain as a hematoma or as a hemorrhagic diapedetic impregnation, therefore a hemorrhagic infarction is diagnosed during life much less often than at autopsy.

Treatment of ischemic stroke

Any acute cerebrovascular accident requires immediate medical attention, since the outcome of the disease depends on correct and targeted therapeutic intervention in the early stages of the disease. Emergency therapy provided by a specialized care team, early hospitalization and intensive complex therapy in a hospital are the main factors determining the effectiveness of treatment.
The treatment system is based on those ideas about the pathogenesis of cerebral stroke that have developed in recent years. It includes a complex of therapeutic measures emergency care patients with cerebral stroke, regardless of its nature (undifferentiated care) and differentiated treatment of cerebral infarction.

Undifferentiated therapy aimed at normalizing vital functions - breathing and cardiac
activities. This includes the fight against cerebral edema, hyperthermia, as well as the prevention of stroke complications. First of all, it is necessary to ensure free passage of the airways with the help of special suctions, oral and nasal air ducts, wiping the patient’s oral cavity, and holding the lower jaw. If measures aimed at eliminating blockage of the respiratory tract are ineffective, intubation and tracheostomy are performed.
Intubation or tracheostomy is used for sudden cessation of breathing, progressive respiratory distress, with bulbar and pseudobulbar symptoms, when there is a danger of aspiration. If breathing suddenly stops and there is no apparatus, it is necessary to perform artificial respiration from mouth to mouth, from mouth to nose.

With concomitant pulmonary edema, cardiotonics are indicated: 1 ml of 0.06% solution of corglycon or 0.5 ml of 0.05% solution of strophanthin is administered intravenously. In addition to the above remedies, it is recommended to inhale oxygen with alcohol vapor through an oxygen inhaler or Bobrov apparatus in order to reduce foaming in the alveoli. Inhalation of alcohol vapor continues for 20-30 minutes, then repeated after a 20-minute break.

Raise the head end of the bed to give the patient an elevated position. Prescribe furosemide (Lasix) intramuscularly, diphenhydramine, atropine. In case of a sharp drop in blood pressure, 1 ml of 1% mesaton solution, 1 ml of 0.06% korglykon solution, 1 ml of 0.1% norepinephrine solution, 0.05 g of hydrocortisone with 5% glucose solution or sodium bicarbonate solution are prescribed intravenously at a rate of 20-40 drops per minute. Infusion therapy should be carried out under the control of acid-base balance and plasma electrolyte composition. Compensation of water-electrolyte balance and correction of acid-base balance are carried out in patients who are unconscious. It is necessary to administer parenteral fluids in a volume of 2000-2500 ml per day in 2-3 doses.
An isotonic sodium chloride solution, Ringer-Locke solution, and 5% glucose solution are administered. Since acid-base imbalance is often accompanied by potassium deficiency, it is necessary to use potassium nitrate salt or potassium chloride in amounts up to 3-5 g per day. To eliminate acidosis, along with increasing pulmonary ventilation and oxygen therapy, as well as measures that increase cardiac output, a 4-5% solution of sodium bicarbonate (200-250 ml) is administered intravenously.
Measures aimed at combating cerebral edema are carried out in cases of extensive cerebral infarctions. In these cases, furosemide (Lasix), 1-2 ml ib/m or orally in tablets of 0.04 g once a day, 5-10 ml of a 5% ascorbic acid solution is prescribed to reduce the permeability of the vascular wall. Hydrocortisone and prednisolone have an anti-edema effect, which should be prescribed during the first 2-3 days, depending on the severity of cerebral edema. A good anti-edematous effect can be obtained by using mannitol, which is an osmotic diuretic. The use of urea is less desirable, since the vicarious dilation of cerebral vessels that follows a powerful anti-edematous effect can lead to repeated, even more severe edema and possible bleeding into the brain parenchyma. Glycerin has a dehydrating effect, increasing the osmotic pressure of the blood without disturbing the electrolyte balance.

It is necessary to use means aimed at preventing and eliminating hyperthermia. At a body temperature of 39 °C and above, 10 ml of a 4% amidopyrine solution or 2-3 ml of a 50% analgin solution IM are prescribed. Reduce the temperature of mixtures consisting of diphenhydramine, novocaine, amidopyrine. Regional hypothermia of large vessels is also recommended (ice packs on the carotid arteries in the neck, axillary and groin areas).
In order to prevent pneumonia, it is necessary, from the first day of a heart attack, to turn the patient in bed every 2 hours, circular cups should be placed on the chest, alternating them every other day with mustard plasters. If the development of pneumonia is suspected, sulfa drugs and antibiotics are prescribed. Monitoring of activities is necessary bladder and intestines. In case of urinary retention, catheterization is indicated 2 times a day with rinsing the bladder with antiseptic agents. To avoid bedsores, it is necessary to monitor the cleanliness of the linen, the condition of the bed - eliminate folds in the sheets, unevenness of the mattress, wipe the body with camphor alcohol.

When treating cerebral infarction, it is necessary to direct all efforts to improve impaired cerebral circulation and try to eliminate the developed ischemia. This can be done to a certain extent by increasing cardiac activity and improving venous outflow of blood, therefore it is advisable to use cardiotonic drugs that increase the stroke and minute volume of the heart, as well as improve the outflow of venous blood from the cranial cavity (strophanthin or corglycon intravenously).

It is advisable to prescribe vasodilators in the form of subcutaneous or intramuscular injections in cases where it is necessary to achieve a hypotensive effect, reduce very high blood pressure, and avoid the risk of developing hemorrhagic complications in the area of ​​cerebral infarction. The idea that vasodilator drugs can improve cerebral circulation and increase local cerebral blood flow has been revised in recent years. Some researchers express the view that the use of vasodilators in cerebral infarction is inappropriate and even harmful. These statements are based on the fact that in experiments, as well as in angiographic studies of the state of the vascular system of the brain and in studies of local cerebral blood flow using radioactive xenon in patients, data were obtained that vessels in the area of ​​ischemia either do not respond to stimuli at all, or react weakly, and sometimes even paradoxically. Therefore, conventional cerebral vasodilators (papaverine, etc.) lead to the expansion of only unaffected vessels that draw blood from the area of ​​the infarction. This phenomenon is called the intracerebral steal phenomenon.
The vessels of the peri-infarction zone, as a rule, are maximally dilated (in particular, due to local acidosis), and dilation of the vessels of the unaffected area under the influence of vasodilators can reduce the pressure in the dilated collaterals and thereby reduce the blood supply to the ischemic area.

It is difficult to agree with the recommendations of some clinicians to use vasodilators in cases where vasospasm is assumed to be the main cause of the infarction, since the causal dependence of cerebral infarction on vasospasm has not yet been proven, and papaverine and other vasoactive drugs can be used to induce cerebral infarction after rupture of the aneurysm. do not work [Kandel E" 1975; Flamm, 1972].

To improve collateral circulation and microcirculation in the area of ​​cerebral infarction, it is advisable to prescribe medications that reduce blood viscosity and reduce the aggregation properties of its formed elements. For this purpose, 400 ml of low molecular weight dextran - rheopolyglucin - is injected intravenously. The drug is administered drip-wise at a frequency of 30 drops per minute, daily, for 3-7 days.

The administration of rheopolyglucin improves local cerebral blood flow and leads to an antithrombogenic effect. The effect of rheopolyglucin is most pronounced in arterioles, precapillaries, and capillaries.

As a result of a sharp decrease in the aggregation of erythrocytes and platelets, the intensity of the microcirculatory sedimentation syndrome, expressed by low perfusion pressure, slowing of blood flow, increased blood viscosity, aggregation and stasis of blood elements, and the formation of blood clots, decreases. Due to the known hypervolemic and hypertensive effects of rheopolyglucin, blood pressure control is necessary, and the tendency to arterial hypertension can be adjusted by reducing the frequency of drops of the administered solution. The antiaggregation effect of rheopolyglucin is observed within 4-6 hours, therefore it is advisable to recommend oral aspirin, camphor monobromide, trental, etc. in the intervals between the administration of rheopolyglucin and after stopping its injections.

The antiaggregation effect can be achieved by intravenous administration of 10 ml of a 24% solution of aminophylline, as well as 2 ml of a 2% solution of papaverine. Aminophylline derivatives, as well as papaverine, have an inhibitory effect on phosphodiesterase, due to which cyclic adenosine monophosphoric acid accumulates in blood cells, which is a powerful inhibitor of aggregation. Regular intake of blood cell aggregation inhibitors orally after five-day or weekly use in the form of injections makes it possible to achieve reliable prevention of thrombus formation in the entire vascular system as a whole throughout the entire acute period of a heart attack. It is advisable to continue taking aggregation inhibitors for two years, which is a dangerous period for the development of recurrent infarctions. The use of antiplatelet agents of blood cells has made it possible in recent years to significantly reduce the use of anticoagulants, which require regular monitoring of blood clotting and prothrombin index for their use. In cases of thromboembolic syndrome, against the background of which a cerebral infarction has developed, the use of fibrinolytic drugs with anticoagulants is indicated.

Anticoagulant therapy begins with the use of a direct anticoagulant - heparin. Heparin is prescribed intravenously or intramuscularly at a dose of 5000-10,000 units 4-6 times a day for 3-5 days. With intravenous administration, the effect of heparin occurs immediately, with intramuscular administration - after 45-60 minutes. Initially, 10,000 units of heparin are administered intravenously, then every 4 hours, heparin is administered intramuscularly at 5,000 units.
Treatment with heparin should be carried out under the control of blood clotting time. The optimal lengthening of coagulation is considered to be 2.5 times. 3 days before discontinuation of heparin, indirect anticoagulants are prescribed - phenylin orally (or syncumar, omefin, etc.) at a dose of 0.03 g 2-3 times a day, while simultaneously reducing the daily dose of heparin by 5000 units. Treatment with indirect-acting anticoagulants is carried out under the control of the prothrombin index, which should not be reduced to more than 40%.

Fibrinolysin is used for a thrombolytic effect. The administration of fibrinolysin is indicated in the first day and even hours from the onset of a heart attack. Fibrinolysine must be administered simultaneously with heparin.

In recent years, in the complex treatment of cerebral infarction, agents have been used that increase the resistance of brain structures to hypoxia. The feasibility of using antihypoxants is determined by the fact that metabolic disorders in the cells of the brain parenchyma usually precede in time severe brain damage in the form of edema and, in addition, are one of the leading causes of edema.

It has been suggested that it is not cerebral edema, but metabolic changes and energy deficiency, if they occur over a large area of ​​the brain or during rapidly developing ischemia, that are the factor determining impaired consciousness and other cerebral symptoms in ischemic stroke. In this regard, antihypoxic therapy can be considered more promising than the treatment of developed cerebral edema. The advisability of prescribing antihypocoic therapy is also determined by the fact that in conditions of acute deficiency of cerebral blood supply and metabolic disorganization, it is more profitable to temporarily reduce the energy needs of the brain and thereby, to some extent, increase its resistance to hypoxia.
Accordingly, it is considered justified to prescribe drugs that have an inhibitory effect on energy balance. For this purpose, antipyretic drugs and regional hypothermia, new synthetic agents that have an inhibitory effect on enzymatic processes and metabolism in the brain, as well as substances that increase energy production under hypoxic conditions are used. These substances include methylphenazine derivatives, urea derivatives - gutimin and piracetam (nootropil), which are prescribed 5 ml IV or 1 ml 3 times a day IM. This group of antihypoxants has a positive effect on the processes of tissue respiration, phosphorylation and glycolysis. WITH positive side Phenobarbital has proven itself to clearly reduce oxygen consumption in the brain and increase brain experience by reducing metabolic processes and slowing down the accumulation of intracellular fluid.

Course and prognosis of ischemic stroke

Mortality in ischemic stroke is 20-25% of cases. Patients who have suffered an ischemic stroke remain at risk of developing recurrent cerebrovascular accidents. Repeated heart attacks develop more often in the first 3 years after the first. The 1st year is considered the most dangerous and very rarely repeated heart attacks develop 5-10 years after the first heart attack.

Prevention of cerebral infarction includes a set of measures aimed at systematically monitoring the health of patients with cardiovascular diseases, organizing the patient’s work and rest regime, nutrition, improving working and living conditions, and timely treatment of cardiovascular diseases. Transient ischemic attacks pose a certain risk of developing a heart attack. These patients are prescribed long-term therapy with antiplatelet agents to prevent heart attack.

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One of the most serious pathologies of the vascular system are acute (ACVE) and chronic processes characterized by cerebral circulatory failure. According to statistics, more than 80% of patients who have suffered an ischemic stroke in the vertebrobasilar system lose their ability to work or remain disabled, unable to self-care, and only about 20% of patients, after treatment and recovery, return to their professional activity. Among surviving patients, there is a high risk of recurrent stroke in the next 5-7 years.

Ischemic stroke or cerebral infarction occurs in more than 80% of all cases of stroke. It develops against the background of narrowing or blockage of the arteries supplying the brain. As a result, the supply of sufficient blood flow decreases and oxygen starvation occurs, after which symptoms of ischemic brain damage appear within a few minutes.

It has been established that about 70% of all transient ischemic attacks occur as a result of stroke in the vertebrobasilar region.

Development of vertebro-basilar insufficiency

The vertebrobasilar basin is formed by the right and left vertebral arteries, which supply the occipital lobe of the brain, the cerebellum and the trunk. They provide more than 25% of the blood flow to the brain.

VBB insufficiency is one of the types of cerebrovascular pathology, characterized by circulatory disorders in the vertebral and basilar arteries. Manifested by episodes of ischemic damage to brain tissue with subsequent development of functional disorders of the central nervous system. Episodes of transient ischemic attacks (TIAs) may recur. Vascular disorders occur in patients of various age categories, in particular in children.

Pathological processes of circulatory disorders in the vertebrobasilar region are reversible, subject to timely diagnosis and treatment. Without rendering medical care the likelihood of a cerebral infarction increases.

What leads to stroke?

Circulatory disorders in the vessels that form the VBB have many different causes. The most common ones include:

• genetic factors;
• congenital anomalies of the vascular system (Kimmerly's anomaly, underdevelopment of the vertebral arteries);
• damage to the cervical spine (due to sports injuries, car accidents, etc.);
• vasculitis (inflammatory processes of vascular walls);
• atherosclerosis (damage to the arteries of the VBB occurs, during which cholesterol deposits form on the vascular walls);
• diabetes;
• persistent increase in blood pressure (hypertension);
• antiphospholipid antibody syndrome (APS): promotes the formation of blood clots;
• dissection (dissection) of arteries: tearing of the vascular wall and penetration of blood between its membranes is the cause of acute cerebral infarction;
• compression of vertebral vessels during intervertebral hernia of the cervical spine, displacement of the vertebrae, degenerative processes of the spinal column.

Symptoms of vertebro-basilar insufficiency

In case of circulatory failure in the vertebral-basilar basin, temporary and permanent symptoms are distinguished. Temporary symptoms are characteristic of TIA, with the duration of manifestations ranging from several hours to two to three days.

Signs of VBI of a temporary nature manifest themselves in the form of pressing sensations of pain in the occipital region, uncomfortable and painful manifestations in the cervical spine, as well as severe dizziness.

Symptoms of a constant nature bother a person all the time; with the progression of the pathology, their severity increases. Quite often, an exacerbation occurs, against the background of which transient ischemic attacks occur and the risk of heart attack increases.

Persistent symptoms of circulatory failure VBB:

• constant pain in the back of the head, pulsating in nature or manifested by pressing pain;
• hearing loss and tinnitus, which in advanced cases is constantly present, at any time of the day;
• decreased memory and attention;
• visual dysfunction: blurred contours of objects, diplopia, spots or blurred vision, narrowing (loss) of visual fields;
• impaired balance and coordination of movements;
• fatigue, constant feeling of weakness and weakness, in the evening patients feel a complete loss of strength;
• dizziness, which occurs mainly during an uncomfortable position of the neck, nausea, short-term loss of consciousness;
• increased irritability, sudden mood swings, in childhood - crying for no apparent reason;
• increased sweating, feeling hot;
• increased heart rate;
• Hoarseness appears in the voice, a feeling of soreness and a lump in the throat.

As the disease progresses, symptoms manifest themselves in the form of speech disorders, swallowing dysfunction, and sudden falls. In the later stages of the disease, cerebral infarction develops.

Diagnostic tests for VBI

Modern diagnosis of VBB blood flow disorders consists of collecting anamnestic data and conducting a physical and instrumental examination. The diagnosis of VBI is made provided that the patient simultaneously exhibits at least three symptoms characteristic of impaired blood flow, as well as in the presence of the results of studies confirming the presence of pathological processes in the vessels of the vertebrobasilar system.

Making an accurate diagnosis presents some difficulties, since the symptoms described above can also occur with other cerebral circulatory disorders.

For cerebrovascular accidents, the following are used:

• Ultrasound Dopplerography (Doppler ultrasound) - during the study, the patency of the great vessels of the neck and head, hemodynamic parameters (volumetric and linear blood flow velocity), and the condition of the arterial walls are determined;
• TCD (transcranial Dopplerography) is one of the ultrasound diagnostic methods for assessing blood flow through intracerebral vessels;
• MR angiography and CT angiography mode - the introduction of a contrast agent followed by visualization of the vessels of the vertebral-basilar basin and the brain, allows to identify various pathologies, atherosclerotic changes, wall dissection, malformation of blood vessels, their diameter;
• MRI and CT - these methods are not very informative for pathologies of the VSD vessels, but they allow one to identify possible etiological factors: structural changes in the spinal cord and spinal column, the presence of herniated intervertebral discs;
• general and biochemical blood test - allows you to determine possible changes in the properties of biological fluid that appear with diabetes mellitus, atherosclerosis, inflammatory processes and other pathologies.

Doppler ultrasound

Scheme of treatment measures for VBI

The main actions for disorders of blood flow in the vertebrobasilar system are aimed at identifying and eliminating the main causes of the pathological condition, restoring normal blood circulation and blood supply to blood vessels, and preventing ischemic attacks of the brain. Treatment consists of the use of drug therapy, massage, gymnastics, physiotherapy and surgery.

Drug treatment

If there is insufficient blood supply to the brain, the following groups of medications are prescribed:

• medications to lower blood lipid levels - niacin (nicotinic acid, vitamin B3 or PP), fibrates, bile acid sequestrants;
• drugs that prevent blood clots (antiplatelet agents) - acetylsalicylic acid;
• vasodilator drugs;
• neurometabolic stimulants (nootropics) – improve brain performance;
• antihypertensive drugs that regulate blood pressure (prescribed if necessary, on a strictly individual basis);
• symptomatic treatment - analgesic, antiemetic and hypnotic drugs, antidepressants and sedatives.

Treatment with physical methods

The use of therapeutic exercises is of great importance in case of disturbances in the blood flow of the VBB. Exercises should not bring discomfort or cause pain; movements should be performed smoothly and easily. Daily gymnastic exercises eliminate muscle spasms, strengthen the muscles of the back and neck, and contribute to the formation of posture.

An equally important method of treating cerebral circulatory disorders is massage. Massage movements have a positive effect on the vascular system, promoting their expansion, thereby improving blood circulation.

Physiotherapeutic methods are also aimed at improving blood supply to the main vessels of the neck and head and eliminating the symptomatic complex. Physiotherapy consists of the use of laser radiation, magnetic therapy and ultraphonophoresis.

To reduce pain, dizziness and visual disturbances, reflexology is prescribed. The kinesiological taping method is a new direction in the treatment of VBI, aimed at eliminating muscle spasms and vascular constrictions.

Surgical intervention

Surgical treatment is prescribed exclusively for severe VBI and an increased risk of development. During surgical intervention, actions are aimed at restoring normal blood circulation in the vertebral arteries by eliminating causes such as narrowing of the lumen of blood vessels due to spasm, compression or stenosis.

Forecast

Timely diagnosis of pathological changes and implementation of correct therapeutic measures makes it possible to completely eliminate vascular insufficiency in the vertebrobasilar system.

In the absence of therapy or incorrectly selected drugs and physiotherapeutic methods in a particular case, the development of a chronic process is possible, accompanied by a constant deterioration of the condition and an increase in the intensity of symptoms, which leads to frequent TIAs and increases the risk of acute and dyscirculatory encephalopathy.

Treatment of VBI is a rather long and labor-intensive process, taking from two months to several years. But only by following all medical recommendations is it possible to protect yourself from serious consequences, often leading to disability or even death.

Catad_tema Stroke - articles

Ischemic stroke: malignant infarction in the middle cerebral artery. Clinical recommendations.

Ischemic stroke: malignant infarction in the middle cerebral artery territory

ICD 10: I63.0, I63.1, I63.2, I63.3, I63.4, I63.5, I63.8

Year of approval (revision frequency): 2016 (revised every 10 years)

ID: KR573

Professional associations:

• Association of Neurosurgeons of Russia

Approved

Agreed

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14. Krieger D. Cooling for acute ischemic brain damage (COOL AID): an open pilot study of induced hypothermia in acute ischemic stroke. Stroke 2001; 32:1847-1854.

15. Quizilbash N, Lewington SL, Lopez-arietta J. Corticosteroids for acute ischemic stroke. Cochrane library. Oxford (United Kingdom): Update software.- 2001 (1).

16. Qureshi A.I., Suarez J., Yahia A.M. et al. Timing of neurological deterioration in massive middle cerebral artery infarction: a multicenter review. Crit. Care Med 2003; 31: 272-277.

17. Schwab S., Schwarz S., Spranger M. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998; 29(12): 2461-2466.

18. Simard D., Paulson O. Artificial hyperventilation in stroke. Trans. Am. Neurol. Assoc. 1973; 98: 309-310.

19. Steiner T., Pilz J., Schellinger P. Multimodal online monitoring in middle cerebral artery territory stroke. Stroke 2001; 32 (11): 2500-2506.

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22. Woodcock J., Ropper A., ​​Kennedy S. High dose barbiturates in non-traumatic brain swelling: ICP reduction and effect on outcome. Stroke 1982;.13: 785-787.

Appendix A1. Composition of the working group

1. Neurosurgery
2. Neurology
3. Anesthesiology and resuscitation

Table P1. Levels of evidence, indicating the classification of levels of evidence used

Table P2. Levels of strength of evidence indicating the classification of levels of strength of evidence used

Appendix B. Patient management algorithms

Algorithm 1. Stroke duration less than 24 hours

no Yes

Appendix B: Patient Information

Patients with a malignant infarction in the middle cerebral artery in the acute period of the disease are deeply disabled. After discharge from the hospital, where the patient was treated for stroke, comprehensive rehabilitation in a specialized center is indicated, aimed at partial regression of the neurological deficit. The nature of rehabilitation and the number of courses is determined by a rehabilitation specialist. Outside the rehabilitation center on an outpatient basis, the patient is under the supervision of a neurologist at the place of residence, who determines treatment. Activities aimed at regressing neurological deficits (physical therapy, massage, classes with a speech therapist), prevention and treatment of extracranial complications continue. All patients require care in the first 3-6 months after a stroke. During rehabilitation, 3-6 months after a stroke, 50% of patients are restored to the level of moderate disability with the ability to walk independently and self-care.

Vertebro-basilar insufficiency(synonyms Vertebrobasilar insufficiency and VBI) - a reversible disorder of brain function caused by a decrease in blood supply to the area supplied by the vertebral and basilar arteries.

Synonymous with "Vertebrobasilar Arterial System Syndrome" is official name vertebrobasilar insufficiency.

Due to the variability of manifestations of vertebrobasilar insufficiency, the abundance of subjective symptoms, the difficulty of instrumental and laboratory diagnosis of vertebrobasilar insufficiency and the fact that the clinical picture resembles a number of other pathological conditions - in clinical practice, overdiagnosis of VBI often occurs when the diagnosis is established without compelling evidence. then the reasons.

Causes of VBI

The causes of vertebrobasilar insufficiency or VBI are currently considered:

1. Stenosing lesion of the great vessels, primarily:

Extracranial region of vertebrates

Subclavian arteries

Innominate arteries

In most cases, obstruction of the patency of these arteries is caused by atherosclerotic lesions, and the most vulnerable are:

The first segment is from the beginning of the artery to its entrance into the bone canal of the transverse processes of the C5 and C6 vertebrae

The fourth segment is a fragment of an artery from the site of perforation of the dura mater to the confluence with another vertebral artery at the border between the pons and the medulla oblongata, at the area where the main artery is formed

Frequent damage to these areas is due to local features of the geometry of the vessels, which predispose to the emergence of areas of turbulent blood flow and damage to the endothelium.

2. Congenital features of the structure of the vascular bed:

Anomalous origin of the vertebral arteries

Hypoplasia/aplasia of one of the vertebral arteries

Pathological tortuosity of the vertebral or basilar arteries

Insufficient development of anastomoses at the base of the brain, primarily the arteries of the circle of Willis, limiting the possibilities of collateral blood supply in conditions of damage to the main artery

3. Microangiopathy due to arterial hypertension, diabetes mellitus may be the cause of VBI (damage to small cerebral arteries).

4. Compression of the vertebral arteries by pathologically altered cervical vertebrae: with spondylosis, spondylolisthesis, significant osteophytes (in recent years, the role of compression on the vertebral arteries has been reconsidered as an important cause of VBI, although in some cases there is quite pronounced compression of the artery when turning the head, which, in addition to reducing blood flow through the vessel may be accompanied by arterio-arterial embolism)

5. Extravasal compression of the subclavian artery by the hypertrophied scalene muscle, hyperplastic transverse processes of the cervical vertebrae.

6. Acute injury to the cervical spine:

Transport (whiplash)

Iatrogenic due to inadequate manual therapy manipulations

Improper performance of gymnastic exercises

7. Inflammatory lesions of the vascular wall: Takayasu’s disease and other arteritis. Women of childbearing age are the most vulnerable. Against the background of an existing defective vessel wall with thinning of the media and thickened, compacted intima, its dissection is possible even in conditions of minor trauma.

8. Antiphospholipid syndrome: may be the cause of a combination of impaired patency of extra- and intracranial arteries and increased thrombus formation in young people.

Additional factors contributing to cerebral ischmia in vertebrobasilar insufficiency (VBI):

Changes in the rheological properties of blood and microcirculation disorders with increased thrombus formation

Cardiogenic embolism (the frequency of which reaches 25% according to T.Glass et al., (2002)

Small arterio-arterial embolisms, the source of which is a loose parietal thrombus

Complete occlusion of the lumen of the vessel as a consequence of atherosclerotic stenosis of the vertebral artery with the formation of a parietal thrombus

Increasing thrombosis of the vertebral and/or basilar artery at a certain stage of its development can manifest itself as a clinical picture of transient ischemic attacks in the vertebrobasilar system. The likelihood of thrombosis increases in areas of arterial trauma, for example, when the transverse processes CVI-CII pass through the bone canal. Probably, the provoking moment for the development of vertebral artery thrombosis in some cases can be a long stay in an uncomfortable position with a forced position of the head.

Data from sectional and neuroimaging research methods (primarily MRI) reveal the following changes in brain tissue (brain stem, pons, cerebellum, occipital lobe cortex) in patients with VBI:

Lacunar infarctions of various ages

Signs of neuronal death and proliferation of glial elements

Atrophic changes in the cerebral cortex

These data, confirming the existence of an organic substrate of the disease in patients with VBN, indicate the need for a thorough search for the cause of the disease in each specific case.

Symptoms of vertebrobasilar insufficiency

The diagnosis of circulatory failure in the Air Force is based on a characteristic symptom complex that combines several groups of clinical symptoms:

Visual disorders

Oculomotor disorders (and symptoms of other cranial nerve dysfunction)

Violations of statics and coordination of movements

Vestibular (cochleovestibular) disorders

Pharyngeal and laryngeal symptoms

Headache

Asthenic syndrome

Vegetative-vascular dystonia

Conduction symptoms (pyramidal, sensitive)

It is this symptom complex that occurs in most patients with circulatory insufficiency in the vertebrobasilar region. In this case, a presumptive diagnosis is determined by the presence of at least two of these symptoms. They are usually short-term and often go away on their own, although they are a sign of trouble in this system and require clinical and instrumental examination. A thorough medical history is especially necessary to clarify the circumstances of the occurrence of certain symptoms.

The core of the clinical picture of vertebrobasilar insufficiency is the development of neurological symptoms, reflecting transient acute cerebral ischemia in the areas of vascularization of the peripheral branches of the vertebral and basilar arteries. At the same time, some pathological changes can be detected in patients even after the completion of an ischemic attack. The same patient with VBI usually combines several clinical symptoms and syndromes, among which it is not always easy to identify the leading one.

Conventionally, all symptoms of VBI can be divided into:

Paroxysmal (symptoms and syndromes that are observed during an ischemic attack)

Permanent (observed for a long time and can be detected in the patient in the interictal period).

In the basin of the arteries of the vertebrobasilar system, the development of:

Transient ischemic attacks

Ischemic strokes of varying severity, including lacunar strokes.

The unevenness of arterial damage leads to the fact that brain stem ischemia is characterized by mosaic, “spotting”.

The combination of signs and the degree of their severity are determined:

Localization of the lesion

Size of the lesion

Possibilities of collateral circulation

The neurological syndromes described in the classical literature are relatively rarely encountered in their pure form in practice due to the variability of the blood supply to the brain stem and cerebellum. It is noted that during attacks the side of predominant motor disorders (paresis, ataxia), as well as sensory disorders, may change.

1. Movement disorders in patients with VBI are characterized by a combination of:

Central paresis

Coordination disorders due to damage to the cerebellum and its connections

As a rule, there is a combination of dynamic ataxia in the limbs and intention tremor, gait disturbances, and unilateral decrease in muscle tone.

It should be noted that clinically it is not always possible to identify the involvement of the blood supply zones of the carotid or vertebral arteries in the pathological process, which makes the use of neuroimaging methods desirable.

2. Sensory disorders manifest themselves:

Symptoms of prolapse with the appearance of hypo- or anesthesia in one limb, half of the body.

Paresthesia may occur, usually involving the skin of the extremities and face.

Disorders of superficial and deep sensitivity (occur in a quarter of patients with VBI and, as a rule, are caused by damage to the ventrolateral thalamus in the areas of blood supply to the a. thalamogeniculata or posterior external villous artery)

3. Visual impairment can be expressed as:

Loss of visual fields (scotomas, homonymous hemianopsia, cortical blindness, less often - visual agnosia)

The appearance of photopsia

Blurred vision, blurred vision of objects

The appearance of visual images - “flies”, “lights”, “stars”, etc.

4. Cranial nerve dysfunction

Oculomotor disorders (diplopia, convergent or divergent strabismus, vertical separation of the eyeballs),

Peripheral facial nerve paresis

Bulbar syndrome (less commonly pseudobulbar syndrome)

These symptoms appear in various combinations; their isolated occurrence due to reversible ischemia in the vertebrobasilar system is much less common. The possibility of combined damage to brain structures supplied by the carotid and vertebral artery systems should be taken into account.

5. Pharyngeal and laryngeal symptoms:

Feeling of a lump in the throat, pain, sore throat, difficulty swallowing food, spasms of the pharynx and esophagus

6. Attacks of dizziness (lasting from several minutes to hours), which may be due to the morphofunctional characteristics of the blood supply to the vestibular apparatus, its high sensitivity to ischemia.

Dizziness:

As a rule, it is systemic in nature (in some cases, dizziness is non-systemic in nature and the patient experiences a feeling of sinking, motion sickness, unsteadiness of the surrounding space)

It manifests itself as a sensation of rotation or linear movement of surrounding objects or one’s own body.

Associated autonomic disorders are characteristic: nausea, vomiting, profuse hyperhidrosis, changes in heart rate and blood pressure.

Over time, the intensity of the sensation of dizziness may weaken, while the emerging focal symptoms (nystagmus, ataxia) become more pronounced and become persistent.

However, it must be taken into account that the feeling of dizziness is one of the most common symptoms, the frequency of which increases with age.

Dizziness in patients with VBI, as well as in patients with other forms of vascular lesions of the brain, can be caused by suffering of the vestibular analyzer at various levels, and its nature is determined not so much by the features of the main pathological process (atherosclerosis, microangiopathy, arterial hypertension), but localization of the ischemic focus:

Lesions of the peripheral vestibular apparatus

Damage to the central part of the vestibular apparatus

Psychiatric disorders

Sudden onset of systemic dizziness, especially in combination with acutely developed unilateral deafness and a sensation of noise in the ear, may be a characteristic manifestation of labyrinthine infarction (although isolated dizziness is rarely the only manifestation of VBI).

Differential diagnosis of vertebrobasilar insufficiency

In addition to vertebrobasilar insufficiency, a similar clinical picture may have:

Benign paroxysmal positional vertigo (caused by damage to the vestibular apparatus and not associated with disorders of its blood supply; Hallpike tests are a reliable test for its diagnosis)

Vestibular neuronitis

Acute labyrinthitis

Meniere's disease, hydropos labyrinth (due to chronic otitis media)

Perilymphatic fistula (resulting from trauma or surgery)

Acoustic neuroma

Demyelinating diseases

Normal pressure hydrocephalus (combination of persistent dizziness, balance problems, unsteadiness when walking, cognitive impairment)

Emotional and mental disorders (anxiety, depressive disorders)

Pathology of the degenerative and traumatic nature of the cervical spine (cervical vertigo), as well as craniocervical transition syndrome

Hearing impairment (decreased hearing acuity, tinnitus) are also common manifestations of VBI. It should, however, be taken into account that about a third of the older population systematically report a sensation of noise, while more than half of them regard their sensations as intense, causing them significant inconvenience. In this regard, all audiological disorders should not be regarded as manifestations of cerebrovascular pathology, given the high frequency of degenerative processes developing in the middle ear.

At the same time, there is evidence that short-term episodes (up to several minutes) of unilateral reversible hearing loss in combination with tinnitus and systemic vertigo are prodromes of thrombosis of the anterior inferior cerebellar artery, which requires close attention to such patients. As a rule, the source of hearing impairment in this situation is the cochlea itself, which is extremely sensitive to ischemia; the retrocochlear segment of the auditory nerve, which has rich collateral vascularization, is relatively less likely to suffer.

Diagnosis of vertebrobasilar insufficiency

In the diagnosis of VBI, ultrasound methods for studying the vascular system of the brain have now become the most accessible and safe:

Doppler ultrasound allows you to obtain data on the patency of the vertebral arteries, linear speed and direction of blood flow in them. Compression-functional tests make it possible to assess the condition and resources of collateral circulation, blood flow in the carotid, temporal, supratrochlear and other arteries.

Duplex scanning demonstrates the condition of the arterial wall, the nature and structure of stenotic formations.

Transcranial Doppler ultrasound (TCDG) with pharmacological tests is important for determining cerebral hemodynamic reserve.

Doppler ultrasound (USDG) - detection of signals in the arteries gives an idea of ​​the intensity of microembolic flow in them, cardiogenic or vascular embologenic potential.

Data on the condition of the main arteries of the head obtained by MRI angiography are extremely valuable.

When deciding on thrombolytic therapy or surgical intervention on the vertebral arteries, contrast X-ray panangography becomes of decisive importance.

Indirect data on the vertebrogenic effect on the vertebral arteries can also be obtained from conventional radiography performed with functional tests.

The best method for neuroimaging brain stem structures remains MRI, which allows you to see even small lesions.

Otoneurological research occupies a special place, especially if it is supported by computer electronystagmographic and electrophysiological data on auditory evoked potentials characterizing the state of brain stem structures.

Studies of the coagulating properties of blood and its biochemical composition (glucose, lipids) are of particular importance.

The sequence of application of the listed instrumental research methods is determined by the peculiarities of determining the clinical diagnosis.

Treatment of vertebrobasilar insufficiency

The vast majority of patients with VBI receive conservative treatment on an outpatient basis. It must be borne in mind that patients with acute focal neurological deficit should be hospitalized in a neurological hospital, since the possibility of increasing thrombosis of a large arterial trunk with the development of stroke with persistent neurological deficit should be taken into account.

1. Modern understanding of the mechanisms of development of VBI, in particular the recognition of the leading role of stenotic lesions of the extracranial sections of the great arteries, as well as the introduction of new medical technologies into clinical practice, allows us to consider as an alternative drug treatment In such patients, angioplasty and stenting of the corresponding vessels, endarterectomy, extra-intracranial anastomoses, and in some cases the possibility of thrombolysis may be considered.

Information has been accumulated on the use of transluminal angioplasty of the main arteries, including the proximal segment, in patients with VBI.

2. Therapeutic tactics in patients with VBI are determined by the nature of the underlying pathological process, and it is advisable to correct the main modifiable risk factors for cerebrovascular diseases.

The presence of arterial hypertension requires an examination to exclude its secondary nature (renal hypertension, thyrotoxicosis, adrenal hyperfunction, etc.). Systematic monitoring of blood pressure levels and provision of rational diet therapy are necessary:

Restriction in the diet of table salt

Elimination of alcohol consumption and smoking

Dosed physical activity

If there is no positive effect, drug therapy should be started in accordance with generally accepted principles. Achieving the target pressure level is necessary primarily in patients with existing target organ damage (kidneys, retina, etc.) and suffering from diabetes mellitus. Treatment can be started with ACE inhibitors and angiotensin receptor blockers. It is important that these antihypertensive drugs provide not only reliable control of blood pressure levels, but also have nephro- and cardioprotective properties. A valuable consequence of their use is remodeling of the vascular bed, the possibility of which is also assumed in relation to the vascular system of the brain. If the effect is insufficient, it is possible to use antihypertensive drugs from other groups (calcium channel blockers, b-blockers, diuretics).

In elderly people in the presence of stenotic lesions of the main arteries of the head, a careful reduction in blood pressure is necessary, since there is evidence of progression of vascular damage to the brain with excessively low blood pressure.

3. In the presence of stenotic lesions of the main arteries of the head, a high probability of thrombosis or arterio-arterial embolism effective way prevention of episodes of acute cerebral ischemia is to restore the rheological properties of the blood and prevent the formation of cellular aggregates. Antiplatelet agents are widely used for this purpose. The most affordable drug that combines sufficient effectiveness and satisfactory pharmacoeconomic characteristics is acetylsalicylic acid. The optimal therapeutic dose is considered to be 0.5–1.0 mg per 1 kg of body weight per day (the patient should receive 50–100 mg of acetylsalicylic acid daily). When prescribing it, the risk of developing gastrointestinal complications and allergic reactions should be taken into account. The risk of damage to the mucous membrane of the stomach and duodenum is reduced with the use of enteric-soluble forms of acetylsalicylic acid, as well as with the simultaneous administration of gastroprotective agents (for example, omeprazole). In addition, 15–20% of the population has low sensitivity to the drug. The inability to continue monotherapy with acetylsalicylic acid, as well as the low effect of its use, require the addition of another antiplatelet agent or a complete replacement with another drug. For this purpose, dipyridamole, GPI-1b/111b complex inhibitor clopidogrel, and ticlopidine can be used.

4. Along with antihypertensive drugs and antiplatelet agents, drugs from the group of vasodilators are used to treat patients with VBI. The main effect of this group of drugs is considered to increase cerebral perfusion by reducing vascular resistance. At the same time, research in recent years suggests that some of the effects of these drugs may be due not only to a vasodilatory effect, but also to a direct effect on brain metabolism, which must be taken into account when prescribing them. The appropriateness of their vasoactive agents, the doses used and the duration of treatment courses are determined by the patient’s condition, his adherence to treatment, the nature of the neurological deficit, the level of blood pressure, the rate of achievement positive result. It is advisable to time the course of treatment to coincide with a meteorologically unfavorable period (autumn or spring season), a period of heightened emotional and physical activity. Treatment should begin with minimal dosages, gradually increasing the dose to the therapeutic dose. If there is no effect from monotherapy with a vasoactive drug, it is advisable to use another drug with a similar pharmacological action. The use of a combination of two drugs with similar effects makes sense only in selected patients.

5. For the treatment of patients with various forms of cerebrovascular pathology, drugs that have a positive effect on brain metabolism and have a neurotrophic and neuroprotective effect are widely used. Piracetam, Cerebrolysin, Actovegin, Semax, glycine, and a large number of other drugs are used. There is evidence of normalization of cognitive functions when used in patients with chronic cerebrovascular disorders.

6. In the complex treatment of patients with BVN, symptomatic medications should be used:

Drugs that reduce the severity of dizziness

Drugs that help normalize mood (antidepressants, anxiolytics, sleeping pills)

Painkillers (if indicated)

7. It is rational to include non-drug methods of treatment - physiotherapy, reflexology, therapeutic exercises.

The need to individualize the tactics of managing a patient with VBI should be emphasized. It is taking into account the basic mechanisms of the development of the disease and an adequately selected set of medicinal and non-medicinal treatment methods that can improve the quality of life of patients and prevent the development of stroke.

Symptoms of ischemic stroke

Symptoms of ischemic stroke are varied and depend on the location and volume of the brain lesion. The most common localization of the focus of cerebral infarction is the carotid (80-85%), less often - the vertebral-basilar region (15-20%).

Infarctions in the blood supply of the middle cerebral artery

A feature of the blood supply of the middle cerebral artery is the presence of a pronounced collateral circulatory system. When the proximal middle cerebral artery (segment Ml) is occluded, a subcortical infarction may occur, while the cortical area of ​​the blood supply remains unaffected with sufficient blood flow through the meningeal anastomoses. In the absence of these collaterals, an extensive infarction may develop in the area of ​​the blood supply to the middle cerebral artery.

With a heart attack in the area of ​​blood supply to the superficial branches of the middle cerebral artery, deviation of the head and eyeballs towards the affected hemisphere may acutely occur; if the dominant hemisphere is damaged, total aphasia and ipsilateral ideomotor apraxia may develop. When the subdominant hemisphere is damaged, contralateral neglect of space, anosognosia, aprosody, and dysarthria develop.

Cerebral infarctions in the area of ​​the superior branches of the middle cerebral artery are clinically manifested by contralateral hemiparesis (mainly of the upper limbs and face) and contralateral hemianesthesia with the same preferential localization in the absence of visual field defects. With extensive lesions, concomitant abduction of the eyeballs and fixation of gaze towards the affected hemisphere may appear. With lesions of the dominant hemisphere, Broca's motor aphasia develops. Oral apraxia and ideomotor apraxia of the ipsilateral limb are also common. Infarctions of the subdominant hemisphere lead to the development of spatial unilateral neglect and emotional disturbances. With occlusion of the lower branches of the middle cerebral artery, motor disorders, sensory agraphia and astereognosis can develop. Visual field defects are often found: contralateral homonymous hemianopsia or (more often) superior quadrant hemianopia. Lesions of the dominant hemisphere lead to the development of Wernicke's aphasia with impaired understanding of speech and retelling, and paraphasic semantic errors. An infarction in the subdominant hemisphere leads to the development of contralateral neglect with sensory predominance, anosognosia.

An infarction in the blood supply of the striatocapsular arteries is characterized by severe hemiparesis (or hemiparesis and hemihypesthesia) or hemiplegia with or without dysarthria. Depending on the size and location of the lesion, paresis mainly extends to the face and upper limb or to the entire contralateral half of the body. With extensive striatocapsular infarction, typical manifestations of occlusion of the middle cerebral artery or its pial branches (for example, aphasia, neglect, and homonymous lateral hemianopia) may develop.

Lacunar infarction is characterized by the development in the area of ​​blood supply of one of the single perforating arteries (single striatocapsular arteries). The development of lacunar syndromes is possible, in particular isolated hemiparesis, hemihypesthesia, ataxic hemiparesis or hemiparesis in combination with hemihypesthesia. The presence of any, even transient, signs of deficiency of higher cortical functions (aphasia, agnosia, hemianopsia, etc.) allows us to reliably differentiate striatocapsular and lacunar infarctions.

Infarctions in the blood supply of the anterior cerebral artery

Infarctions in the blood supply of the anterior cerebral artery are 20 times less common than infarctions in the blood supply of the middle cerebral artery. The most common clinical manifestation is motor disorders; with occlusion of the cortical branches, in most cases, motor deficits develop in the foot and the entire lower limb and less pronounced paresis of the upper limb with extensive damage to the face and tongue. Sensory disorders are usually mild and sometimes completely absent. Urinary incontinence may also occur.

Infarctions in the blood supply of the posterior cerebral artery

With occlusion of the posterior cerebral artery, infarctions of the occipital and mediobasal parts of the temporal lobe develop. The most common symptoms are visual field defects (contralateral homonymous hemianopsia). Photopsia and visual hallucinations may also be present, especially if the subdominant hemisphere is affected. Occlusion of the proximal segment of the posterior cerebral artery (P1) can lead to the development of brainstem and thalamic infarcts, due to the fact that these areas are supplied by some of the branches of the posterior cerebral artery (thalamo-subthalamic, thalamogeniculate and posterior choroidal arteries).

Infarctions in the vertebrobasilar blood supply

Occlusion of the single perforating branch of the basilar artery results in limited brainstem infarction, especially in the pons and midbrain. Brainstem infarctions are accompanied by symptoms of cranial nerve damage on the ipsilateral side and motor or sensory disturbances on the opposite side of the body (so-called alternating brainstem syndromes). Occlusion of the vertebral artery or its main penetrating branches arising from the distal parts can lead to the development of lateral medullary syndrome (Wallenberg syndrome). The blood supply to the lateral medullary region is also variable and can be provided by small branches of the posterior inferior cerebellar, anterior inferior cerebellar and basilar arteries.

Classification of ischemic stroke

Ischemic stroke is a clinical syndrome of acute vascular damage to the brain; it can be an outcome various diseases of cardio-vascular system. Depending on the pathogenetic mechanism of development of acute focal cerebral ischemia, several pathogenetic variants of ischemic stroke are distinguished. The most widely used classification is TOAST (Trial of Org 10172 in Acute Stroke Treatment), which distinguishes the following types of ischemic stroke:

atherothrombotic - due to atherosclerosis of large arteries, which leads to their stenosis or occlusion; when an atherosclerotic plaque or thrombus fragments, arterio-arterial embolism develops, also included in this option stroke; cardioembolic - most common reasons embolic infarction includes arrhythmia (atrial flutter and fibrillation), valvular heart disease (mitral), myocardial infarction, especially less than 3 months old; lacunar - due to occlusion of small-caliber arteries, their damage is usually associated with the presence of arterial hypertension or diabetes mellitus; ischemic, associated with other, more rare causes: non-atherosclerotic vasculopathies, blood hypercoagulation, hematological diseases, hemodynamic mechanism of development of focal cerebral ischemia, dissection of the arterial wall; ischemic of unknown origin. It includes strokes with an unknown cause or with the presence of two or more possible reasons when it is impossible to make a definitive diagnosis.

Based on the severity of the lesion, a minor stroke is distinguished as a special variant; the neurological symptoms associated with it regress during the first 21 days of the disease.

In the acute period of stroke, according to clinical criteria, mild, moderate and severe ischemic stroke are distinguished.

Depending on the dynamics of neurological disorders, stroke in development is distinguished (“stroke in progress” - with an increase in the severity of neurological symptoms) and completed stroke (with stabilization or reverse development of neurological disorders).

There are different approaches to the periodization of ischemic stroke. Taking into account epidemiological indicators and modern ideas about the applicability of thrombolytic drugs for ischemic stroke, we can distinguish following periods ischemic stroke:

the most acute period is the first 3 days, of which the first 3 hours are defined as the therapeutic window (the possibility of using thrombolytic drugs for systemic administration); if symptoms regress in the first 24 hours, a transient ischemic attack is diagnosed; acute period - up to 28 days. Previously, this period was determined to be up to 21 days; Accordingly, regression of symptoms until the 21st day of the disease remains as a criterion for diagnosing a minor stroke; early recovery period - up to 6 months; late recovery period - up to 2 years; period of residual effects - after 2 years.