The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension, atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. In the complex treatment of patients with CNM, drugs are used that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. One of these drugs is Vasobral (dihydroergocriptine + caffeine) - an effective and safe treatment for CNM.

Key words: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular disease (CCVD) is a progressive form of cerebrovascular pathology with gradual development of neurological and neuropsychological disorders. The main causes leading to chronic hypoperfusion of the brain are hypertension, atherosclerosis, and heart disease accompanied by chronic heart failure. In the complex treatment of patients with CCVD, drugs with comprehensive antioxidant, angioprotective, neuroprotective and neurotrophic action are usually used. One these drugs is Vazobral (dihydroergocryptine + coffein), effective and safe preparation for treatment of CCVD.

Key words: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular accidents (CVA) are a progressive form of cerebrovascular pathology, characterized by multifocal or diffuse ischemic brain damage with the gradual development of a complex of neurological and neuropsychological disorders. This is one of the most common forms of cerebrovascular pathology, usually occurring against the background of general cardiovascular diseases.

There are many extracerebral causes leading to pathology of cerebral circulation. First of all, these are diseases accompanied by a disorder of systemic hemodynamics, leading to a chronic decrease in adequate blood supply - chronic cerebral hypoperfusion. The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension (AH), atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. Other causes include diabetes mellitus, vasculitis in systemic connective tissue diseases, other diseases accompanied by vascular damage, blood diseases leading to changes in its rheology (erythremia, macroglobulinemia, cryoglobulinemia, etc.).

Pathomorphological changes in CNM

A high level of perfusion is required for adequate brain function. The brain, whose mass is 2.0-2.5% of body weight, consumes 15-20% of the blood circulating in the body. The main indicator of brain perfusion is the level of blood flow per 100 g of brain matter per minute. The average value of hemispheric cerebral blood flow (CBF) is approximately 50 ml/100 g/min, but there are significant differences in the blood supply to individual brain structures. The magnitude of MK in gray matter is 3-4 times higher than in white matter. At the same time, in the anterior parts of the hemispheres, blood flow is higher than in other areas of the brain. With age, the value of MB decreases, and frontal hyperperfusion also disappears, which is explained by diffuse atherosclerotic changes in cerebral vessels. It is known that with CNM, the subcortical white matter and frontal structures are more affected, which may be explained by the indicated characteristics of the blood supply to the brain. Initial manifestations of insufficiency of cerebral blood supply to the brain occur if the blood flow to the brain is less than 30-45 ml/100 g/min. The advanced stage is observed when the blood supply to the brain decreases to a level of 20-35 ml/100 g/min. The threshold of regional blood flow within 19 ml/100 g/min (functional threshold of blood supply to the brain), at which the functions of the corresponding areas of the brain are impaired, is considered critical. The process of death of nerve cells occurs when regional arterial cerebral blood flow is reduced to 8-10 ml/100 g/min (infarction threshold of cerebral blood supply).

In conditions of chronic brain hypoperfusion, which is the main pathogenetic link of CNM, compensation mechanisms are depleted, the energy supply of the brain becomes insufficient, as a result, first functional disorders develop, and then irreversible morphological damage. In chronic cerebral hypoperfusion, a slowdown in cerebral blood flow, a decrease in oxygen and glucose levels in the blood, a shift in glucose metabolism towards anaerobic glycolysis, lactic acidosis, hyper-osmolarity, capillary stasis, a tendency to thrombus formation, depolarization of cells and cell membranes, activation of microglia, which begins to produce neurotoxins, which, along with other pathophysiological processes, leads to cell death.

Damage to small penetrating cerebral arteries (cerebral microangiopathy), on which the blood supply to the deep parts of the brain depends, in patients with CNM is accompanied by various morphological changes in the brain, such as:

diffuse damage to the white matter of the brain (leukoencephalopathy);

multiple lacunar infarctions in the deep parts of the brain;

microinfarctions;

microhemorrhages;

atrophy of the cerebral cortex and hippocampus.

To implement autoregulation of cerebral circulation, it is necessary to maintain certain values ​​of blood pressure (BP) in the main arteries of the head. On average, systolic blood pressure (SBP) in the main arteries of the head should range from 60 to 150 mm Hg. Art. With long-term hypertension, these limits shift slightly upward, so autoregulation does not become impaired for a long time and MB remains at a normal level. Adequate brain perfusion is maintained by increasing vascular resistance, which in turn leads to an increase in the load on the heart. Chronic uncontrolled hypertension leads to secondary changes in the vascular wall - lipohyalinosis, which is observed mainly in the vessels of the microvasculature. The resulting arteriolosclerosis leads to changes in the physiological reactivity of blood vessels. Under these conditions, a decrease in blood pressure as a result of the addition of heart failure with a decrease in cardiac output or as a result of excessive antihypertensive therapy, or as a result of physiological circadian changes in blood pressure leads to the occurrence of hypoperfusion in the areas of the terminal circulation. Acute ischemic episodes in the basin of deep penetrating arteries lead to the occurrence of small-diameter lacunar infarcts in the deep parts of the brain. If the course of hypertension is unfavorable, repeated acute episodes lead to the emergence of the so-called. lacunar state, which is one of the variants of multi-infarct vascular dementia.

In addition to repeated acute disorders, the presence of chronic ischemia in the areas of terminal circulation is also assumed. A marker of the latter is a rarefaction of the periventricular or subcortical white matter (leukoaraiosis), which pathomorphologically represents a zone of demyelination, gliosis and expansion of the perivascular spaces. In some cases of an unfavorable course of hypertension, subacute development of diffuse damage to the white matter of the brain with a clinical picture of rapidly progressing dementia and other manifestations of disconnection is possible, which is sometimes referred to in the literature as “Binswanger’s disease.”

Another significant factor in the development of CNM is atherosclerotic damage to cerebral vessels, which is usually multiple, localized in the extra- and intracranial parts of the carotid and vertebral arteries, as well as in the arteries of the circle of Willis and their branches, forming stenoses. Stenoses are divided into hemodynamically significant and insignificant. If a decrease in perfusion pressure occurs distal to the atherosclerotic process, this indicates a critical or hemodynamically significant narrowing of the vessel.

It has been shown that hemodynamically significant stenoses develop when the vessel lumen narrows by %. But cerebral blood flow depends not only on the severity of stenosis, but also on the mechanisms that prevent the development of ischemia: the state of collateral circulation, the ability of cerebral vessels to dilate. These hemodynamic reserves of the brain allow “asymptomatic” stenoses to exist without complaints or clinical manifestations. However, the obligatory development of chronic cerebral hypoperfusion during stenosis leads to CNM, which is detected by magnetic resonance imaging (MRI). MRI visualizes periventricular leukoaraiosis (reflecting ischemia of the white matter of the brain), internal and external hydrocephalus (caused by atrophy of brain tissue); Cysts may be detected (as a consequence of previous cerebral infarctions, including clinically “silent” ones). It is believed that CNMC is present in 80% of patients with stenotic lesions of the main arteries of the head. Atherosclerotic changes in the vessels of the brain are characterized not only by local changes in the form of plaques, but also by hemodynamic restructuring of the arteries in the area distal to atherosclerotic stenoses and occlusions. All this leads to the fact that “asymptomatic” stenoses become clinically significant.

The structure of the plaques is also of great importance: the so-called. unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents - often of a transient type. When hemorrhaging into such a plaque, its volume quickly increases with an increase in the degree of stenosis and worsening of the signs of CNM. In the presence of such plaques, blocking the lumen of the vessel up to 70% will be hemodynamically significant.

In the presence of damage to the main arteries of the head, cerebral blood flow becomes very dependent on systemic hemodynamic processes. Such patients are especially sensitive to arterial hypotension, which can occur when moving to a vertical position (orthostatic hypotension), with cardiac arrhythmias leading to a short-term decrease in cardiac output.

Clinical manifestations of CNM

The main clinical manifestations of CNM are disturbances in the emotional sphere, balance and gait disorders, pseudobulbar disorders, impairment of memory and learning ability, neurogenic urination disorders, which gradually lead to maladjustment of patients.

During CNM, three stages can be distinguished:

At stage I, the clinic is dominated by subjective disorders in the form of general weakness and fatigue, emotional lability, sleep disturbances, decreased memory and attention, and headaches. Neurological symptoms do not form distinct neurological syndromes, but are represented by anisoreflexia, discoordination, and symptoms of oral automatism. Violations of memory, praxis and gnosis can be identified, as a rule, only when special tests are carried out.

At stage II, there are more subjective complaints, and neurological symptoms can already be divided into distinct syndromes (pyramidal, discoordination, amyostatic, dysmnestic), with one neurological syndrome usually dominating. Professional and social adaptation of patients decreases.

At stage III, neurological symptoms increase, a distinct pseudobulbar syndrome appears, and sometimes paroxysmal conditions (including epileptic seizures); Severe cognitive impairment leads to disruption of social and everyday adaptation and complete loss of working capacity. Ultimately, CNMK contributes to the formation of vascular dementia.

Cognitive impairment is a key manifestation of CNM, which largely determines the severity of the patient’s condition. They often serve as the most important diagnostic criterion for CNM and are a sensitive marker for assessing the dynamics of the disease. It is worth noting that the location and extent of vascular changes detected by MRI or computed tomography are only partially correlated with the presence, type and severity of neuropsychological findings. In case of CNMC, there is a more pronounced correlation between the severity of cognitive impairment and the degree of brain atrophy. Correcting cognitive impairment is often critical to improving the quality of life of the patient and his relatives.

Methods for diagnosing cognitive impairment

To assess the overall severity of cognitive defect, the Mini-Mental State Examination scale is most widely used. However, this method is not an ideal screening tool, since its results are significantly influenced by the patient's premorbid level and type of dementia (the scale is less sensitive to frontal cortex dysfunction and therefore better detects the early stages of Alzheimer's disease than the early stages of vascular dementia). In addition, its implementation requires more than 10-12 minutes, which the doctor does not always have at an outpatient appointment.

Clock drawing test: subjects are asked to draw a clock with its hands pointing to a specific time. Normally, the subject draws a circle, places the numbers from 1 to 12 inside it in the correct order at equal intervals, draws 2 hands (the hour hand is shorter, the minute hand is longer), starting in the center and showing the specified time. Any deviation from correct test performance is a sign of fairly severe cognitive dysfunction.

Speech activity test: subjects are asked to name as many names of plants or animals as possible in a minute (semantically mediated associations) and words starting with a certain letter, for example “l” (phonetically mediated associations). Normally, most elderly people with secondary and higher education name from 15 to 22 plants and from 12 to 16 words starting with “l” per minute. Naming fewer than 12 semantically mediated associations and fewer than 10 phonetically mediated associations usually indicates significant cognitive dysfunction.

Visual memory test: patients are asked to remember 10-12 images of simple, easily recognizable objects presented on one sheet; Subsequently, the following are assessed: 1) immediate reproduction, 2) delayed reproduction after interference (a verbal association test can be used as an interfering effect), 3) recognition (the patient is asked to recognize previously presented objects among other images). Failure to remember more than half of previously presented images may be considered a sign of severe cognitive dysfunction.

Main directions in the treatment of CNM

The main directions in the treatment of CNM stem from the etiopathogenetic mechanisms that led to this process. The main goal is to restore or improve brain perfusion, which is directly related to the treatment of the underlying disease: hypertension, atherosclerosis, heart disease with the elimination of heart failure.

Taking into account the diversity of pathogenetic mechanisms underlying CNM, preference should be given to agents that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. In this regard, the use of drugs that combine several mechanisms of action is justified. Among such drugs, I would like to mention Vasobral, a combined drug that has both nootropic and vasoactive effects. It contains an ergot derivative (dihydroergocryptine) and caffeine. Dihydroergocriptine blocks α1 and α2 adrenergic receptors of vascular smooth muscle cells, platelets, and erythrocytes, and has a stimulating effect on dopaminergic and serotonergic receptors of the central nervous system.

When using the drug, the aggregation of platelets and erythrocytes decreases, the permeability of the vascular wall decreases, blood supply and metabolic processes in the brain improve, and the resistance of brain tissue to hypoxia increases. The presence of caffeine in Vasobral determines the stimulating effect on the central nervous system, mainly on the cerebral cortex, respiratory and vasomotor centers, and increases mental and physical performance. Studies have shown that Vasobral has a vegetative stabilizing effect, which manifests itself in increased pulse blood filling, normalization of vascular tone and venous outflow, which is due to the positive effect of the drug on the sympathetic nervous system while reducing the activity of the parasympathetic system. A course of treatment with Vasobral leads to a decrease or disappearance of symptoms such as dizziness, headache, palpitations, and numbness of the extremities. Positive dynamics of the neuropsychological status of the patient with CNM are noted: increased attention span; improving orientation in time and space, memory for current events, intelligence; increased mood, decreased emotional lability. The use of Vasobral helps reduce fatigue, lethargy, and weakness; there is a feeling of cheerfulness.

The drug is prescribed in a dose of 2-4 ml (1-2 pipettes) or 1/2-1 tablet 2 times a day for 2-3 months. The drug is taken with a small amount of water. Side effects occur rarely and are mild. It should be noted that due to the presence of liquid and tablet forms, double dosing and good tolerability, Vasobral is convenient for long-term use, which is extremely important in the treatment of chronic diseases.

Non-drug ways to correct the manifestations of CNM should include:

proper organization of work and rest, avoidance of night shifts and long business trips;

moderate physical activity, therapeutic exercises, measured walking;

diet therapy: limiting the total calorie content of food and salt consumption (up to 2-4 g per day), animal fats, smoked meats; introduction of fresh vegetables and fruits, fermented milk and fish products into the diet;

climatic treatment at local resorts, in low altitudes and at sea resorts; balneotherapy, which has a positive effect on central hemodynamics, contractile function of the heart, and the state of the autonomic nervous system; the means of choice are radon, carbon dioxide, sulfide, iodine-bromine baths.

In general, an integrated approach to the treatment of CNM and repeated pathogenetically based course treatment can contribute to better adaptation of the patient in society and prolong the period of his active life.

Kotova Olga Vladimirovna - researcher at the Department of Pathology of the Autonomic Nervous System of the Research Center of the First Moscow State Medical University named after. THEM. Sechenov.

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Hyperperfusion and hypoperfusion of the brain

Cerebral hyperperfusion

A rare but dangerous complication is cerebral hyperperfusion. It occurs when, as a result of anatomical variations in the origin or accidental cannulation of the common carotid artery, a significant portion of the blood coming from the arterial cannula is sent directly to the brain.

The most serious consequence of this complication is a sharp increase in cerebral blood flow with the development of intracranial hypertension, edema and rupture of brain capillaries. In this case, the development of unilateral otorrhea, rhinorrhea, facial edema, petechiae, and conjunctival edema is possible.

If cerebral hyperperfusion is not detected in time and active therapy for intracranial hypertension is not started, then this complication can lead to death of the patient (Orkin F.K., 1985).

Cerebral hypoperfusion

A decrease in perfusion pressure to a level below the autoregulation threshold (about 50 mmHg) is associated with low cerebral blood flow. Hypoperfusion plays an important role not only in the development of fatal diffuse encephalopathy, which is based predominantly on necrotic processes in the brain, but also in the formation of various reduced forms of encephalopathy.

Clinically, it manifests itself from the development of mild postoperative disorders in the central and peripheral nervous systems in the form of behavioral changes, intellectual dysfunction, epileptic seizures, ophthalmological and other disorders, to global cerebral damage with a persistent vegetative state, neocortical brain death, total cerebral and brainstem death (Show P.J., 1993).

The definition of "acute ischemia" has been revised.

Previously, acute ischemia was considered only as a deterioration in the delivery of arterial blood to an organ while maintaining venous outflow from the organ.

Currently (Bilenko M.V., 1989), acute ischemia is understood as a sharp deterioration (incomplete ischemia) or complete cessation (complete, total ischemia) of all three main functions of local circulation:

1. delivery of oxygen to tissue,
2. delivery of oxidation substrates to tissue,
3. removal of tissue metabolic products from tissue.

Only a violation of all processes causes a severe symptom complex, leading to severe damage to the morphofunctional elements of the organ, the extreme degree of which is their death.

The state of cerebral hypoperfusion may also be associated with embolic processes.

Example. Patient U., 40 years old, was operated on for rheumatic disease (restenosis) of the mitral valve and a parietal thrombus in the left atrium. With technical difficulties, mitral valve replacement with a disc prosthesis and removal of a thrombus from the left atrium were performed. The operation lasted 6 hours (duration of ECC - 313 minutes, aortic cross-clamping - 122 minutes). After the operation, the patient is on mechanical ventilation. In the postoperative period, in addition to pronounced signs of total heart failure (BP - 70 - 90/40 - 60 mm Hg, tachycardia up to 140 per minute, ventricular extrasystoles), signs of post-ischemic encephalopathy developed (coma, periodic tonic-clonic convulsions) and oliguria. 4 hours after the operation, acute myocardial infarction of the posterolateral wall of the left ventricle of the heart was detected. 25 hours after the end of the operation, despite vasopressor and pacemaker therapy, hypotension occurred - up to 30/0 mmHg. Art. followed by cardiac arrest. Resuscitation measures with 5-fold defibrillation were not successful.

At autopsy: the brain weighs 1400 g, the gyri are flattened, the grooves are smoothed, at the base of the cerebellum there is a groove from a herniation into the foramen magnum. The cut brain tissue is moist. In the right hemisphere, in the area of ​​the subcortical nuclei, there is a cyst measuring 1 x 0.5 x 0.2 cm with serous contents. Bilateral hydrothorax (on the left - 450 ml, on the right - 400 ml) and ascites (400 ml), severe hypertrophy of all parts of the heart (heart weight 480 g, thickness of the myocardium of the wall of the left ventricle - 1.8 cm, right - 0.5 cm, ventricular index - 0.32), dilatation of the heart cavities and signs of diffuse myocardial cardiosclerosis. In the posterolateral wall of the left ventricle there is an acute extensive (4 x 2 x 2 cm) myocardial infarction with a hemorrhagic rim (about 1 day old). Histologically confirmed the presence of severe edema of the brain stem, venous and capillary congestion, ischemic (even necrotic) damage to neurons in the cerebral cortex. Physicochemically - pronounced hyperhydration of the myocardium of all parts of the heart, skeletal muscles, lungs, liver, thalamus and medulla oblongata. In the genesis of myocardial infarction in this patient, in addition to atherosclerotic lesions of the coronary arteries, long periods of surgical intervention as a whole and its individual stages were important.

Recommendations and opinions published on the site are for reference or popular information and are provided to a wide range of readers for discussion. The information provided does not replace qualified medical care based on medical history and diagnostic results. Be sure to consult your doctor.

Cerebral hypoperfusion treatment

Phytoestrogens in early manifestations of menopausal syndrome in women with chronic cerebral ischemia

V. Shishkova, Candidate of Medical Sciences

Center for Speech Pathology and Neurorehabilitation, Moscow

In women with menopausal syndrome that has developed against the background of manifestations of chronic cerebral ischemia, the use of phytoestrogens appears to be a safe alternative to traditional hormone replacement therapy. The use of Inoclim in women with cerebrovascular disease was evaluated in an open, prospective, placebo-controlled study.

Key words: menopausal syndrome, phytoestrogens, Inoclim, chronic cerebral ischemia.

PHYTOESTROGENS IN EARLY MANIFESTATIONS OF MENOPAUSAL SYNDROME IN WOMEN WITH CHRONIC BRAIN ISCHEMIA

V. Shishkova, Candidate of Medical Sciences

Center for Speech Pathology and Neurorehabilitation, Moscow

The use of phytoestrogens in women with menopausal syndrome developing in the presence of manifestations of chronic brain ischemia is a safe alternative to traditional hormone replacement therapy. The administration of Inoclim in women with cerebrovascular disease was assessed in an open-label placebo-controlled study.

Key words: menopausal syndrome, phytoestrogens, Inoclim, chronic brain ischemia.

According to the World Health Organization (WHO), the trend towards an increase in the number of people in the older age group will continue in the 21st century. It is expected that by 2015, about 46% of all women will be over 45 years of age. This explains the great interest in studying the changes occurring in a woman’s body during this period.

The duration of the active period of a woman’s life, regardless of her age and menopausal status, largely depends on lifestyle, nutrition, the presence and severity of concomitant somatic diseases, psychological well-being, as well as socio-economic living conditions. The highest average active life expectancy is observed among women in Japan (74.5 years) and the lowest in African countries (about 30 years); in Russia this figure currently exceeds 60 years.

Menopause is a natural transition to the non-reproductive period in a woman’s life, however, the somatic and psychological problems accumulated by this time, expressed in hormonal and metabolic changes, lead to the development of menopausal syndrome of varying severity in 48% of women.

Thus, by the time of menopause, most women, unfortunately, have concomitant somatic diseases that affect the psychological and intellectual spheres of health, as well as worsen the course of the menopause. The most common pathology is type 2 diabetes mellitus (T2DM), obesity, arterial hypertension (AH), coronary heart disease, atherosclerosis, atrial fibrillation and chronic cerebral ischemia (CHI), which also serve as a springboard for the development of ischemic stroke of the brain.

One of the first places among the causes of morbidity, mortality and disability throughout the world is occupied by vascular diseases of the brain, and, according to the results of epidemiological studies, their frequency is constantly increasing. The annual mortality rate from strokes in Russia is one of the highest in the world.

Morbidity and mortality rates from stroke among people of working age in Russia have increased over the past 10 years by more than 30%. Early 30-day mortality after stroke is 34.6%, and about 50% of patients die within 1 year. Stroke is the leading cause of disability in the population; 1/3 of patients who have suffered it require outside assistance, another 20% cannot walk independently, and only every 5th person can return to work. A stroke imposes special obligations on the patient’s family members, significantly reducing their work potential, and places a heavy socio-economic burden on society as a whole.

Menopausal syndrome acts as a risk factor for the development of cerebrovascular pathology, while the presence of long-term CCI, a precursor of stroke, significantly worsens the course of the menopausal period. For a practicing obstetrician-gynecologist, the meaning of many neurological terms is hidden under a layer of years that have passed since studying at the department of neurology during the institute years. However, the high prevalence of pathology of the central nervous system (CNS) in women in the peri- and postmenopausal periods and the obvious comorbidity of pathologies dictate, on the one hand, the need to fill the knowledge gap in this area of ​​medicine, and on the other hand, to learn how to effectively and safely correct menopausal disorders against the background diseases of the central nervous system, in particular such as CCI.

CHEM AND ITS CAUSES

CCI is a slowly progressive state of gradual decrease or change in normal brain activity, resulting from diffuse and (or) small-focal damage to brain tissue in conditions of long-term insufficiency of cerebral blood supply, regardless of age.

Doctors of different specialties who encounter such patients in their practice and deal with this problem often use different terms (not always CCI), implying this particular pathology. The term most often used is “dyscirculatory encephalopathy” or simply “encephalopathy” (despite the absence of such a term in the International Classification of Diseases, 10th revision - ICD-10), less often “chronic cerebrovascular insufficiency”, “slowly progressive cerebral circulatory failure”, “ ischemic brain disease”, “cerebrovascular insufficiency”, “cerebrovascular disease”, etc. .

As a rule, CCI does not reflect an isolated lesion of only the cerebral vessels. There are many other causes and diseases that lead to pathology of cerebral circulation. The development of CCI is promoted by a number of conditions that are commonly called risk factors. The latter are divided into correctable (they can be influenced by medication or other treatment) and non-correctable, i.e. unchangeable.

Uncorrectable risk factors include: old age, gender and hereditary predisposition. It is known, for example, that a stroke or CCI in parents increases the likelihood of developing vascular diseases in children. These factors cannot be influenced, but they help to identify in advance those at increased risk of developing cerebrovascular pathology and help prevent them from developing the disease early.

The main and main correctable factors in the development of CCI, and subsequently stroke, are atherosclerosis and hypertension. Diabetes, obesity, smoking, alcohol, insufficient physical activity, irrational and unbalanced nutrition are the reasons leading to additional progression of atherosclerosis in the vessels of the brain and deterioration of the patient’s condition. Identification of additional factors that significantly aggravate the course of CCI is necessary to develop the correct treatment tactics, taking into account all the causes and manifestations of the disease.

Currently, as a rule, clinically detected CCI is of mixed etiology, i.e. 1 patient has many factors – both correctable and non-correctable.

So, for the main reasons, atherosclerotic, hypertensive and mixed CCI are distinguished, although other, rarer causes are also possible (rheumatism, vasculitis of other etiologies, blood diseases, etc.).

MECHANISM OF CHEMICAL DEVELOPMENT

The universal mechanism for the development of CCI at any age is acute or chronic brain hypoperfusion, i.e. prolonged lack of supply by the brain of basic vital substances - oxygen and glucose, delivered by the bloodstream.

HOW DOES BRAIN HYPOPERFUSION DEVELOP?

A high level of blood flow is required for adequate brain function. The brain, which weighs only 2–2.5% of the total body weight, consumes up to 15–20% of the blood circulating in the body. The main indicator of the completeness of the blood supply to the brain is the level of blood flow per 100 g of brain matter per minute. The average cerebral blood flow (CBF) is approximately 50 ml/100 g/min, but there are significant differences in the blood supply to individual brain structures. For example, in gray matter, MK is 3–4 times higher than in white matter; There is also a relative physiological acceleration of blood flow in the frontal regions of the brain (the so-called frontal lobes). With age, the value of blood flow MK decreases, and the acceleration of blood flow in the anterior parts of the brain also disappears, which plays a certain triggering role in the development and increase of CCI.

Under resting conditions, the brain's oxygen consumption is 4 ml per 100 g/min, which corresponds to approximately 20% of the total oxygen entering the body. Glucose consumption is 30 µmol per 100 g/min - this is also the maximum requirement for the body as a whole.

Under conditions of intense work or stress (for example, while reading this article), the brain's needs for oxygen and glucose increase significantly compared to those at rest. Critical values ​​of cerebral blood flow have been established: when it decreases to 50%, reversible disorders of brain function are observed; with a persistent decrease in blood flow, 90% of them will suffer from T2DM. According to data presented at the congress of the International Diabetes Federation, in Russia in 2011 the number of patients with diabetes reached 12.5 million, which is almost 10% of the country's population.

The high prevalence of diabetes is associated with high morbidity, disability and mortality. The main cause of mortality in patients with T2DM is vascular complications, including the prevailing cerebrovascular ones - acute cerebrovascular accidents (stroke) and CCI. Diabetes is the most important risk factor for the development of ischemic strokes and transient ischemic disorders in the brain, even at a young age in men and women. The relative risk of stroke increases with the development of diabetes by 1.8–6 times. The MRFIT study showed that the risk of death from stroke among patients with diabetes was 2.8 times higher than in patients without diabetes, death from ischemic stroke was 3.8 times higher, from subarachnoid hemorrhage was 1.1 times higher, and from intracerebral hemorrhage – 1.5 times.

Diabetes is a risk factor for the development of cerebrovascular accidents, regardless of the presence of other risk factors (increased blood pressure and cholesterol levels). The majority of patients with diabetes (72–75%) have an ischemic stroke, which is higher than among the general population). It has also been noted that patients with diabetes have a worse recovery process after a stroke. CCI plays a major role in the development of stroke in diabetes. A significant role in the development of CCI in diabetes is played by the pathology of the MAG: the carotid and vertebral arteries, which in diabetes are quickly affected by atherosclerosis. It has been proven that diabetes and hyperglycemia without diabetes (prediabetes - impaired fasting glycemia and glucose tolerance) are independent risk factors for the development of systemic atherosclerosis with damage to vessels of various locations, including the brain.

In addition, DM is characterized by systemic damage to the microvasculature (microangiopathy), which is accompanied by the development of microcirculation disorders in the target organ, including the brain. Microangiopathy of cerebral vessels aggravates the metabolic disorders that develop with CCI and increases the risk of developing dementia, while there is a significant increase in the risk of Alzheimer's disease.

An additional problem in diabetes is compensation of blood sugar levels, which is associated with the risk of severe hypoglycemia (a decrease in blood glucose to a level below normal). It is known that the hypoglycemia index increases with a duration of diabetes >6 years, while in patients severe hypoglycemia is associated with a high risk of dementia, and its additional risk in the group of those examined without hypoglycemic episodes and with the presence of them was 2.39% per year. Numerous publications indicate that in diabetes, much earlier than in isolated hypertension or atherosclerosis, there is a decrease in the speed of psychomotor reactions, dysfunction of the frontal lobe, memory impairment, complex motor disorders, decreased attention and other clinical manifestations of CCI.

Thus, the severity of brain damage in diabetes is determined by the degree and duration of the decrease in sUA (due to atherosclerosis and (or) hypertension) and metabolic disorders in the brain.

Clinical manifestations of cerebrovascular pathology in diabetes are very diverse. Leukoaraiosis, which characterizes hypertensive and post-hypoglycemic brain lesions, can be asymptomatic or manifest as a combination of cognitive disorders progressing to dementia syndrome and various neurological disorders.

MANIFESTATIONS OF CHEMO IN PATIENTS

Clinical manifestations of CCI are not always detected by computed tomography (CT) and magnetic resonance imaging (MRI). Therefore, the diagnostic significance of neuroimaging methods cannot be overestimated. To make a correct diagnosis for a patient, the doctor needs an objective analysis of the clinical picture and instrumental examination data.

As the severity of the clinical picture increases, pathological changes in the vascular system of the brain intensify. The clinical picture of CCI in its progressive development is divided into 3 stages according to the severity of symptoms: initial manifestations, subcompensation and decompensation.

In stage I of the disease, patients may complain of headache and a feeling of heaviness in the head, general weakness, dizziness, noise and (or) ringing in the head or ears, deterioration of memory and attention, decreased mental performance, and sleep disturbances. As a rule, these symptoms occur during a period of significant emotional and mental stress, requiring a significant increase in MC. If 2 or more of these symptoms are often repeated or exist for a long time (at least the last 3 months) and there are no signs of another serious disease of the nervous system, a presumptive diagnosis of CCI is made.

At this stage, as a rule, the formation of distinct neurological syndromes has not yet occurred, and with adequate therapy, it is possible to reduce the severity or eliminate both individual symptoms and the disease as a whole. The advantage of identifying the disease at this stage is the patient’s almost complete recovery, since the processes in the brain tissue are still completely reversible.

At stage II of CCI, patients more often complain of more severe memory impairment, loss of ability to work, severe dizziness, instability when walking, and less often of manifestations of an asthenic symptom complex (general weakness, fatigue). At the same time, focal neurological symptoms become more distinct: revival of reflexes of oral automatism, central insufficiency of the facial and hypoglossal nerves, oculomotor disorders, pyramidal insufficiency. At this stage, a diagnosis of mild cognitive impairment is possible. Treatment is determined by the severity of existing symptoms of CCI progression.

In stage III of CCI, objective neurological disorders associated with serious brain damage, up to the development of psychoorganic syndrome and dementia, are more clearly identified. Paroxysmal conditions are more often observed: falls, fainting. In the stage of decompensation, cerebral circulation disorders are possible in the form of “small strokes” or transient MB disturbances (with reversible ischemic manifestations), the duration of focal disorders in which ranges from 24 hours to 2 weeks. Another manifestation of decompensation may be a progressive “complete stroke” and residual effects after it.

In CCI, there is a clear correlation between the severity of neurological symptoms and the age of the patients. Along with the progression of neurological symptoms, as the pathological process develops in the neurons of the brain, cognitive disorders increase. This applies not only to memory and intelligence, which are impaired in stage III to the level of dementia, but also to such functions as praxis and gnosis. Initial, essentially subclinical disorders of these functions are observed already in stage I, even in the middle age of the patient, then they intensify, change, and become distinct; Stages II and especially III of the disease are characterized by pronounced impairments of higher brain functions, which sharply reduces the quality of life and social adaptation of patients.

SELECTION OF OPTIMAL THERAPY FOR PATIENTS WITH CHEMISTRY

Treatment of a patient with CCI should be aimed at preventing further progression of the disease and include mandatory correction of hypertension, hyperlipidemia, control of blood sugar levels, treatment of all concomitant somatic diseases, and cerebroprotective therapy. Non-medicinal means also play a certain role: increasing physical activity, limiting the intake of table salt and alcohol, quitting smoking, and increasing the content of vegetables in the diet.

The frequency of detection of stages I and II of CCI in women in the peri- and postmenopausal period determines the need to use in gynecological practice drugs that are safe from the point of view of the risk of strokes and deterioration of cerebral circulation to relieve early vasomotor symptoms of menopausal syndrome, which worsen the course of CCI itself.

CLIMACTERIC PERIOD IN PATIENTS WITH CNS DISEASES AND THE PROBLEM OF CHOOSING THERAPY

It has been established that in menopausal women, the prevalence of cerebral vascular diseases - CCI of an atherosclerotic, hypertensive or mixed nature is about 43%. The severe course of the climacteric syndrome itself additionally leads to the early formation of late and severe forms of cerebrovascular pathology. Treatment of menopausal symptoms in the presence of cerebrovascular pathology - slowly and imperceptibly progressing CCI - is a complex problem.

An effective method for correcting the vegetative manifestations of menopausal syndrome is the prescription of hormone replacement therapy, however, in conditions of a woman already having cardiovascular disease or subclinical vascular atherosclerosis or CCI, this will be an absolute contraindication.

We conducted a comparative analysis of the course of premenopause and early postmenopause in women with CCI and without signs of cerebral vascular damage, and also assessed the effectiveness and safety of using the drug Inoclim (Laboratory Innotec International, France) in patients with CCI.

The prospective study included 2 groups of pre- and postmenopausal women: 1st (main) group (n=88) women aged 44 to 58 years (average age 51.39±3.50 years) with established CCI (in accordance with ICD-10); The 2nd (control) group (n=85) consisted of women without clinical signs of CCI (average age 52.4±3.30 years).

Exclusion criteria for this study were: duration of postmenopause >5 years; a history of surgical interventions on the pelvic organs with removal of the ovaries; oncological diseases at the time of the study and in the anamnesis; use of hormone replacement therapy (HRT) and other methods of treating menopausal syndrome at the time of the study and in history; use of combined oral contraception during the period of inclusion in the study and during the 10 years preceding this period, previous stroke, lack of independent movement.

All women were surveyed using a specially designed card, which included blocks of medical and social history, the presence of somatic and gynecological diseases, and a contraceptive history; The climacteric syndrome was assessed using the Kupperman menopausal index scale modified by E.V. Uvarova (1982), which is based on the definition of neurovegetative, metabolic-endocrine and psycho-emotional symptom complexes. Clinical and laboratory examination included assessment of somatic and neurological status; standard gynecological examination with a cytogram of the endo-exocervix and determination of the degree of purity of the vaginal secretion; transvaginal sonography of the pelvic organs. All women had their body mass index (BMI) assessed (WHO criteria, 1999); performed a breast examination and mammography; electrocardiography; according to indications - ultrasound of the thyroid gland; laboratory tests (blood glucose, coagulogram, lipid profile - total cholesterol, triglycerides, low and high density lipoproteins); neuroimaging methods (MRI and CT of the brain, ultrasound of cerebral vessels).

The average age at the onset of natural menopause was almost the same: in group 1 – 49.55±1.90 years, in group 2 – 49.13±1.48 (p>0.05). It was found that in women with CCI, the first manifestations of climacteric syndrome (neurovegetative) more often occurred in premenopause - in 52 (59%) and with the onset of menopause - in 31 (35%), and 1-2 years after menopause - only in 5 (6%), while in the 2nd group - in the premenopausal period - in 25 (29%), with the onset of menopause - in 8 (9%) and during early postmenopause - in 52 (61 %) (R

Modern therapy of chronic cerebrovascular accident

Chronic cerebrovascular accident (CVA) is a syndrome of chronic progressive brain damage of vascular etiology, which develops as a result of repeated acute cerebrovascular accidents (clinically obvious or asymptomatic) and/or chronic cerebral hypoperfusion.

In Russia, most specialists consider CNMC as a holistic condition without distinguishing individual clinical syndromes. This idea also forms a holistic approach to the selection of therapy. To designate CNM, various diagnoses are used: “slowly progressive cerebral circulatory failure”, “dyscirculatory encephalopathy”, “cerebrovascular insufficiency”, “chronic cerebral dysfunction of vascular etiology”, “chronic cerebral ischemia”, etc.

In Europe and North America, it is customary to associate certain symptoms with risk factors and highlight the characteristics of the damaging effect of a vascular factor on brain functions. This is how the terms “moderate vascular cognitive impairment” (vascular mild cognitive impairment), “post stroke depression”, “cognitive impairment in patient with carotid stenosis”, etc. appeared.

From a clinical point of view, both approaches are correct. Generalization of world experience and domestic traditions will increase the effectiveness of therapy. All patients with brain damage due to vascular risk factors should be included in the CNMK group.

This is a group of patients with heterogeneous causes of CNMK: patients with arterial hypertension (AH), atrial fibrillation, chronic heart failure (CHF), stenosis of the brachiocephalic arteries, patients with ischemic stroke (IS) or transient ischemic attack (TIA) or hemorrhage, patients with metabolic disorders and multiple “silent” strokes.

Modern ideas about the pathogenesis of cerebrovascular diseases reveal a number of features of the metabolism of nervous tissue against the background of risk factors and in conditions of altered perfusion. This determines patient management tactics and influences the choice of drug therapy.

Firstly, the triggering factors for CNM are increased blood pressure (BP), cardiogenic or arterial embolism, hypoperfusion associated with damage to small (microangiopathy, hyalinosis) or large (atherosclerosis, fibromuscular dysplasia, pathological tortuosity) vessels. Also, the cause of progression of cerebrovascular accident can be a sharp decrease in blood pressure, for example, with aggressive antihypertensive therapy.

Secondly, the processes of brain damage have two vectors of development. On the one hand, damage can be caused by acute or chronic impairment of brain perfusion; on the other hand, vascular damage leads to the activation of degenerative processes in the brain. Degeneration is based on the processes of programmed cell death - apoptosis, and such apoptosis is pathological: not only neurons suffering from insufficient perfusion are damaged, but also healthy nerve cells.

Degeneration is often the cause of CI. Degenerative processes do not always develop at the time of cerebrovascular accident or immediately after it. In some cases, degeneration can be delayed and manifests itself a month after exposure to the triggering factor. The reason for such phenomena remains unclear.

The involvement of cerebral ischemia in the activation of degenerative processes plays an important role in patients with a predisposition to such common diseases as Alzheimer's disease and Parkinson's disease. Very often, the progression of vascular disorders and impaired cerebral perfusion become a trigger for the manifestation of these diseases.

Thirdly, cerebrovascular accident is accompanied by macroscopic changes in brain tissue. The manifestation of such a lesion can be a clinically obvious stroke or TIA or a “silent” stroke. Magnetic resonance imaging (MRI) can detect changes in the brain in such patients, but the main method is a clinical assessment of existing disorders.

MRI in patients with CNM can identify the following syndromes, knowledge of which allows us to objectify some of the neurological disorders:

• multifocal brain damage - consequences of multiple lacunar infarctions in the deep parts of the brain;
• diffuse damage to the white matter of the brain (leukoencephalopathy, leukoaraiosis);
• replacement hydrocephalus - expansion of the Virchow-Robin space, increase in the size of the ventricles of the brain, subarachnoid space;
• hippocampal atrophy;
• stroke in strategic areas;
• multiple microhemorrhages.

Fourth, modern data from fundamental research reveal previously unknown features of the pathogenesis of brain damage in CNM. The brain has a high potential for regeneration and compensation.

Factors that determine the likelihood of brain damage:

• duration of ischemia – short-term ischemia with early spontaneous restoration of blood flow contributes to the development of TIA or “silent” stroke, and not the stroke itself;
• activity of compensation mechanisms - many neurological disorders are easily compensated due to preserved functions;
• the activity of the mechanisms of autoregulation of cerebral blood flow allows you to quickly restore perfusion due to the opening of collateral blood flow;
• neuroprotective phenotype - many pathological conditions can promote the activation of endogenous protective mechanisms (for example, diabetes mellitus - diabetes - is an example of metabolic preconditioning), which can increase the resistance of brain tissue to ischemia.

Thus, the metabolic features of brain tissue make it possible to compensate for many, including severe, disorders of brain perfusion in patients with a long history of vascular risk factors. CI and focal symptoms do not always correlate with the severity of morphological brain damage.

The presence of multiple risk factors does not necessarily lead to significant brain damage. The mechanisms of endogenous protection of nervous tissue play a great role in the development of damage, some of which are congenital, and some are acquired.

Clinical manifestations of CNM

As noted, CNM is a syndrome of brain damage in patients with a variety of cardiovascular disorders, united by common features of blood flow and degenerative processes. This allows us to distinguish three groups of symptoms in such patients: CI syndrome; affective (emotional) disorders; focal neurological disorders (consequences of clinically obvious or “silent” strokes). This separation is of great importance for patient management.

Affective (emotional) disorders

The development of emotional disorders is associated with the death of monoaminergic neurons of the brain, in which serotonin, norepinephrine and dopamine act as the main neurotransmitters. It is believed that their deficiency or imbalance in the central nervous system leads to the appearance of emotional disorders.

Clinical manifestations of affective disorders associated with deficiency of serotonin, dopamine and norepinephrine:

• symptoms associated with serotonin deficiency: anxiety, panic attacks, tachycardia, sweating, tachypnea, dry mucous membranes, indigestion, pain;
• symptoms associated with dopamine deficiency: anhedonia, indigestion, impaired smoothness and meaningfulness of thinking;
• symptoms associated with norepinephrine deficiency: fatigue, impaired attention, difficulty concentrating, slowed thought processes, motor retardation, pain.

The doctor can group the patient’s complaints depending on whether they belong to the group of monoamine deficiency symptoms and, based on this, select drug therapy. Thus, many drugs belonging to the group of neuroprotectors affect monoamine systems and in some situations can affect the emotional sphere. However, there is little research on this topic.

Thus, behind all complaints, emotional disorders and diagnoses are hidden: a syndrome of decreased activity in the central nervous system of GABA neurons, serotonin neurons, dopamine neurons; syndrome of increased activity in the central nervous system and autonomic nervous system: histamine neurons, glutamate neurons, norepinephrine neurons, substance P.

Damage to monoaminergic neurons leads to the formation of various groups of syndromes: depression, anxiety, asthenia, apathy, “reduced threshold of perception from intero- and exteroceptors”, etc. “Reduced threshold of perception from intero- and exteroceptors” in combination with somatic diseases and age-related characteristics of the patient contributes to the formation of the following syndromes and complaints: polymyalgic syndrome, numbness in the extremities, feeling of heartbeat, lack of air, noise in the head, “floaters before the eyes,” irritable bowel syndrome, etc.

Affective disorders in patients with cerebrovascular disorders differ from those in patients with normal cerebral blood flow:

• the severity of depression, as a rule, does not reach the level of a major depressive episode according to DSM-IV criteria;
• depression is often combined with anxiety;
• in the early stages of the disease, emotional disorders are hidden under the “mask” of hypochondria and somatic symptoms (sleep disturbance, appetite, headache, etc.);
• the leading symptoms are anhedonia and psychomotor retardation;
• there is a large number of cognitive complaints (decreased concentration, slowness of thinking);
• the severity of depressive symptoms in CNMC depends on the stage of the disease and the severity of neurological disorders;
• Neuroimaging reveals damage primarily to the subcortical parts of the frontal lobes. The presence and severity of depressive symptoms depend on the severity of focal white matter changes in the frontal lobes of the brain and neuroimaging signs of ischemic damage to the basal ganglia;
• there is a paradoxical response to drugs;
• there is a high response to placebo;
• characterized by a high frequency of undesirable effects of antidepressants (it is recommended to use small doses and selective drugs with a favorable tolerability profile);
• mimicry of somatic diseases is observed.

Depression requires mandatory treatment, as it not only affects the quality of life of patients with CNM, but is also a risk factor for stroke. Depression can lead to decreased cognitive function and makes it difficult to communicate with the patient. Long-term depression causes degenerative processes in the form of deterioration of metabolism and structural changes in the brain.

Against the background of long-term depression and cognitive deficits, there may be a violation of the ability to recognize one’s sensations and formulate complaints: co-anesthesia (a feeling of vague total physical ill-being) and alexithymia (the patient’s inability to formulate one’s complaints), which is an unfavorable prognostic sign.

Depression in CNMC is closely related to CI. Patients are aware of increasing intellectual and motor impairments. This makes a significant contribution to the formation of depressive disorders (provided there is no pronounced decrease in criticism in the early stages of the disease).

Affective disorders and CI may result from dysfunction of the frontal regions of the brain. Thus, normally, connections between the dorsolateral frontal cortex and the striatal complex are involved in the formation of positive emotional reinforcement when achieving the goal of an activity. As a result of the phenomenon of disconnection in chronic cerebral ischemia, a lack of positive reinforcement occurs, which is a prerequisite for the development of depression.

The emotional state of patients can also worsen as a result of therapy with somatotropic drugs. There are known cases of drug-induced anxiety and depression. Some somatotropic drugs contribute to the development of anxiety and depressive disorders in patients with CNM: anticholinergics, beta-blockers, cardiac glycosides, bronchodilators (salbutamol, theophylline), non-steroidal anti-inflammatory drugs, etc.

Features of cognitive impairment

The most common syndrome in CNM is a violation of cognitive (cognitive) functions. In the group of vascular CIs there are:

• moderate CI;
• vascular dementia;
• mixed (vascular-degenerative) type - a combination of Alzheimer's type CI with cerebrovascular disease.

The relevance of the problem of diagnosing and treating CI is beyond doubt; it is of particular importance for doctors who, in everyday clinical practice, have to encounter a heterogeneous group of patients with cardiovascular pathology and impaired cognitive functions.

Higher rates of hospitalization, disability and mortality have been proven in patients with CI compared to patients without these disorders. This is largely due to decreased cooperation in this group of patients and impaired ability to adequately assess the symptoms of the underlying disease.

CIs often precede the development of other neurological disorders, such as gait disturbances, pyramidal and extrapyramidal movement disorders, and cerebellar disorders. It is believed that vascular CI is a predictor of the development of stroke and vascular dementia. Thus, early diagnosis, prevention and effective therapy of CI are an important aspect of the management of patients with CIMC.

A variety of diseases of the cardiovascular system, which lead to acute cerebrovascular accidents or chronic cerebral ischemia, are the causes of vascular CI. The most important of them are hypertension, cerebral artery atherosclerosis, heart disease, and diabetes. Rarer causes may be vasculitis, hereditary pathology (for example, CADASIL syndrome), senile amyloid angiopathy.

Ideas about the pathogenesis of CI in CNMC are constantly being improved, but the opinion that has remained unchanged for decades is that their development is based on a long-term pathological process, leading to a significant disruption of the blood supply to the brain.

Clinical and pathogenetic variants of vascular CI described by V.V. Zakharov and N.N. Yakhno, allow us to clearly understand the mechanism of their development and choose the direction of diagnosis and treatment necessary in each clinical case.

The following CN options are distinguished:

• CI due to a single cerebral infarction that developed as a result of damage to the so-called strategic zones (thalamus, striatum, hippocampus, prefrontal frontal cortex, parieto-temporo-occipital junction area). CIs arise acutely and then completely or partially regress, as happens with focal neurological symptoms in stroke;
• CN due to repeated large-focal cerebral infarctions of thrombotic or thromboembolic nature. There is an alternation of stepwise intensification of disorders associated with repeated cerebral infarctions and episodes of stability;
• subcortical vascular CI due to chronic uncontrolled hypertension, when high blood pressure leads to changes in small-caliber vessels, primarily affecting the deep structures of the cerebral hemispheres and basal ganglia with the formation of multiple lacunar infarctions and zones of leukoaraiosis in this group of patients. There is a steady progression of symptoms with episodes of their intensification;
• CI due to hemorrhagic stroke. A picture is revealed that resembles that of repeated cerebral infarctions.

The clinical picture of vascular CI is heterogeneous. However, their subcortical variant has characteristic clinical manifestations. Damage to the deep parts of the brain leads to separation of the frontal lobes and subcortical structures and the formation of secondary frontal dysfunction. This is primarily manifested by neurodynamic disorders (decreased speed of information processing, deterioration in switching attention, decrease in working memory), and impaired executive functions.

The decrease in short-term memory is secondary in nature and is due to the neurodynamic disorders present in such patients. Often these patients experience emotional and affective disorders in the form of depression and emotional lability.

The clinical features of other variants of vascular CI are determined by both their pathogenesis and the localization of the pathological focus. Deterioration of short-term memory with signs of primary insufficiency of memorizing information is rare in CNM. The development of the “hippocampal” type of mnestic disorders (there is a significant difference between immediate and delayed reproduction of information) in this group of patients is prognostically unfavorable with respect to the development of dementia. In this case, further dementia is mixed (vascular-degenerative in nature).

A thorough study of cognitive functions and their impairments in various groups of patients with CNM makes it possible to identify the features of these disorders depending on the leading etiological factor. Thus, it has been established that patients with systolic CHF are characterized by the frontal-subcortical type of cognitive dysfunction (CI of a dysregulatory nature) and signs of deterioration of short-term memory.

Disorders of the frontal-subcortical type include disorders of executive functions and neurodynamic changes: slowing down the speed of information processing, deterioration in switching attention and working memory. At the same time, an increase in the severity of CHF to functional class III is accompanied by an increase in the degree of dysfunction of the parietotemporal-occipital region of the brain and visuospatial disorders.

Knowledge of the characteristics of CI in patients with CNM will allow not only to determine the causes of their development, but also to formulate recommendations when conducting schools for such patients. For example, patients with the frontal-subcortical type of CI should be taught algorithms of behavior when their health status changes, and for patients with dysfunction of the parieto-temporo-occipital region, it is advisable to repeat the necessary information multiple times, while visually perceived information should be as simple as possible for memorization.

In the case of the development of vascular type dementia, the clinical picture, in addition to signs of professional, everyday, social maladjustment, contains gross behavioral disorders - irritability, decreased criticism, pathological eating and sexual behavior (hypersexuality, bulimia).

Features of focal symptoms

Focal symptoms are an integral part of CNM; they appear in the advanced stage of the disease. Focal symptoms also cause poor quality of life and may lead to frequent falls.

The most typical focal symptoms include gait disturbance (slowness, stiffness, shuffling, staggering and difficulties in spatial organization of movements). Many patients also have mild bilateral pyramidal insufficiency and frontal symptoms. Thus, early markers of movement disorders in CNMC are impaired initiation of walking, “freezing,” and pathological step asymmetry.

The leading cause of impaired walking and posture may be amyostatic syndrome. With the development of parkinsonism syndrome, it is advisable to prescribe drugs from the group of dopamine receptor agonists (piribedil) and amantadines. The use of these antiparkinsonian drugs can have a positive effect on the patient's walking and also improve cognitive function.

Modern therapy for CNM

It is impossible to create a universal drug that could act on vascular damaging factors of the brain, CI, affective disorders and at the same time be a neuroprotector. Therefore, all qualitative studies were carried out for individual clinical situations: vascular CI, depression during stroke, prevention of stroke and CI, etc. Therefore, we cannot talk about universal drugs for the treatment of CIMC.

The main principle of treatment for CIMC is an integrated approach, since it is necessary not only to influence symptoms and complaints, but also to prevent the progression of CI and emotional disorders by reducing cardiovascular risk.

The second principle of treatment for CNM is patient adherence to treatment and feedback. Each patient should have a dialogue with his doctor and regularly follow his instructions, and the doctor should listen to the patient's complaints and explain the need for taking medications.

Comprehensive effective therapy for CNM should include:

• secondary prevention of stroke and CI;
• treatment of CI;
• treatment of depression and other mood disorders;
• neuroprotective therapy.

Secondary prevention of ischemic stroke

In case of chronic stroke, the principles of secondary stroke prevention are applicable. The goal of secondary prevention is to reduce the risk of stroke, brain damage and progression of CI. Prevention should be aimed at preventing not only stroke, but also myocardial infarction, TIA and sudden cardiac death. In such patients, the problem of comorbidity and the need to combine several drugs comes to the fore.

Secondary prevention is a key element in the treatment of CNM. Firstly, it allows you to stop or slow down the progression of the disease. Second, the lack of secondary prevention impedes effective treatment for CI, mood disorders, and neuroprotection.

Thus, it has been shown that the effectiveness of neuroprotection is significantly reduced in patients with stenosis and occlusion of the cerebral arteries. This means that without ensuring adequate cerebral blood flow and metabolism, the effectiveness of drugs will be low.

Basic therapy for CNMC includes modification of risk factors, antihypertensive, lipid-lowering and antithrombotic therapy.

To successfully select basic therapy, it is necessary to determine the underlying disease that caused the cerebrovascular accident. This is especially important in the initial stages of the disease, when one factor causes the development of brain damage. However, in the advanced stage of the disease, one of the factors may also prevail and cause the progression of all relevant syndromes.

The patient needs to be explained what medications are prescribed to him and what their mechanism of action is. It should be pointed out that the effect of some drugs cannot be felt immediately, since it manifests itself in inhibiting the progression of depression and CI.

When prescribing antithrombotic therapy, it is necessary to specifically draw patients' attention to the importance of regularly taking medications. Skipping medications can lead to treatment failure and the development of a new stroke. “Medicine holidays” and skipping medications are an independent risk factor for stroke.

Treatment of cognitive impairment

At the stage of vascular and mixed dementia, central acetylcholinesterase inhibitors (galantamine, rivastigmine, donepizil) and the reversible NMDA receptor blocker memantine are successfully used for symptomatic purposes.

There are no clear recommendations for the treatment of vascular non-dementia (mild and moderate) CI. Various therapeutic approaches have been proposed. From our point of view, the use of drugs based on the neurochemical mechanisms underlying the development of vascular CI is justified.

It is known that one of the most important mediators for cognitive processes is acetylcholine. Acetylcholinergic deficiency has been shown to significantly correlate with the overall severity of CI. The role of acetylcholine is to ensure sustained attention, which is necessary to remember new information. Thus, acetylcholine deficiency, the main source of which is the mediobasal parts of the frontal lobes (their structures are projected into the hippocampus and parietotemporal areas of the brain), leads to increased distractibility and poor memorization of new information.

The transmitter dopamine (produced in the ventral part of the tegmentum of the brain stem, the structures of which are projected into the limbic system and prefrontal cortex of the frontal lobes) plays an important role in ensuring the speed of cognitive processes, switching attention, and the implementation of executive functions. Its deficiency leads primarily to neurodynamic disorders and disorders of executive functions. Both mechanisms for the development of cognitive impairment are realized in vascular CI.

Treatment of depression and other mood disorders

Treatment of depression in CNM is a serious problem that cannot be described in detail within the scope of this article. However, it should be noted that when selecting psychotropic drugs, the causes and clinical manifestations of neurotransmitter deficiency must be taken into account. The selection of drugs should be based on an assessment of the neurochemical pathogenesis of brain damage and the characteristics of the drugs’ action.

Antidepressants are used as the main means. For syndromes with a complex structure, for example, when depression is combined with severe anxiety, antipsychotics and tranquilizers are additionally used.

In patients with CNMC, it is important to remember the safety of therapy. Therefore, it is undesirable to use drugs that increase the level of systemic blood pressure, affect urination and reduce the threshold of epileptic activity. When carrying out complex therapy, it is necessary to take into account the problem of interaction of various drugs.

Neuroprotective therapy

Despite the large number of studies devoted to this problem, there are currently very few drugs with proven neuroprotective effects that have demonstrated effectiveness in large studies. In Russia, a special situation has arisen in which drugs belonging to the group of neuroprotectors are widely used for various clinical syndromes.

Most of these drugs have not been studied according to Good Clinical Practice rules. Many doctors prescribe multiple neuroprotectants, although there are no studies demonstrating the use of multiple drugs. Very often these drugs are prescribed to the detriment of secondary prevention. Unreasonable and incorrect use of drugs can lead to polypharmacy and is dangerous for elderly patients. With a balanced and rational approach, the prescription of neuroprotectors can be effective both in acute cerebrovascular accidents and in chronic cerebrovascular accidents.

A peculiarity of the action of neuroprotectors is the dependence of their effect on brain perfusion. If brain perfusion is reduced, the drug may not reach the ischemic zone and have no effect. Therefore, the primary task of treating CNM is to identify the causes of perfusion disturbances and eliminate them.

The second feature of the action of neuroprotectors is the dependence of the effect on the damaging factor. These drugs are most effective during the action of a damaging factor, i.e., in clinical practice, risk situations should be identified and neuroprotectors should be prescribed to reduce damage.

One of the most studied drugs in the group of neuroprotectors is citicoline (ceraxon), which is involved in the synthesis of structural phospholipids of cellular, including neuronal, membranes, ensuring the repair of the latter. In addition, citicoline, as a precursor of acetylcholine, ensures its synthesis, increasing the activity of the cholinergic system, and also modulates dopamine and glutamatergic neurotransmission. The drug does not interfere with the mechanisms of endogenous neuroprotection.

Many clinical trials of citicoline have been carried out in patients with CNMC, including trials according to the rules of good clinical practice, assessing its effect on vascular CI of varying severity - from mild to severe. Citicoline is the only drug that is assessed as a promising agent in the European guidelines for the treatment of acute ischemic stroke.

For the treatment of CNMC and the prevention of CI, it is advisable to use Ceraxon in the form of an oral solution of 2 ml (200 mg) 3 times a day. To form a stable neuroprotective response, the course of therapy should be at least 1 month. The drug can be used for a long time, for several months.

Citicoline has a stimulating effect, so it is preferable to administer it no later than 18 hours. In acute conditions, therapy should be started as early as possible, 0.5–1 g 2 times a day intravenously, for 14 days, and then 0.5–1 g 2 times a day intramuscularly. After this, a transition to oral administration of the drug is possible. The maximum daily dose should not exceed 2 g.

The effectiveness of neuroprotection will be higher if its goals are clearly defined. Firstly, it is advisable to use neuroprotectors in CI to slow down their progression. In this case, the cause of CI, as mentioned above, can be various somatic factors, for example, changes in blood pressure, decompensation of renal failure or CHF, infection, etc. These factors can disrupt brain perfusion. This ischemic process can continue for a long time and subsequently lead to degeneration.

Therefore, as CI progresses, long-term courses of neuroprotective therapy are necessary. It is preferable to use oral medications for several weeks or months. It is also justified to prescribe at the beginning of therapy an infusion course of a neuroprotective drug for 10–20 days, followed by long-term oral administration.

Secondly, the use of neuroprotectors is advisable for the prevention of brain damage in patients with CNMC. As our experimental studies show, neuroprotectors prescribed as a preventative regimen are more effective. Since cerebral circulation can be impaired in a number of clinical situations (atrial fibrillation, pneumonia, hypertensive crisis, myocardial infarction, decompensation of diabetes, etc.), it is advisable to use neuroprotectors prophylactically before the onset of symptoms.

Third, neuroprotectors should be used to prevent stroke in patients undergoing surgery. Surgery is a significant risk factor for stroke and postoperative CI. This is especially true for patients with CNMC, in whom the likelihood of developing CI is higher than in healthy people.

The high risk of perioperative stroke is caused by hypoperfusion associated with the surgical stages. One of the stages of surgery for carotid atherosclerosis is occlusion of the carotid artery for several minutes, and with stenting and angioplasty of cerebral vessels, a large number of arterioarterial athero- and thromboembolisms can occur.

During heart surgery using artificial blood circulation machines, the average systemic blood pressure decreases to 60–90 mm Hg. Art., with stenosis of cerebral vessels or impaired autoregulation of cerebral blood flow, one of the forms of brain damage can develop.

Thus, patients scheduled for surgery are at risk for ischemic brain injury and may be candidates for neuroprotective prophylaxis. The use of neuroprotectors can reduce the number of complications after surgery.

Fourth, neuroprotectors can be used to prevent stroke in patients at high vascular risk, either in the presence of TIA or in the presence of cerebral arterial stenosis. As long as Russia has a quota system, patients with carotid artery stenosis will wait several weeks for surgery. During this period, the patient should be prescribed neuroprotectors. Patients with TIA and atherosclerosis may be advised to carry neuroprotectors, for example, Ceraxon.

Fifthly, neuroprotectors can be prescribed during rehabilitation to stimulate reparative processes and speedy functional recovery.

Thus, CNM is a syndrome of brain damage caused by vascular risk factors, in which both ischemic damage and degenerative processes act as damage. Among the manifestations of CNM are CI, affective disorders and focal syndromes, which require an integrated approach in the selection of preventive, psychotropic and neuroprotective therapy.

Thus, CNM syndrome is a collective concept and cannot be considered as a separate nosological unit. Further studies of CNMC and identification of certain syndromes associated with risk factors and clinical manifestations are needed (for example, CI in patients with hypertension, depressive syndrome in patients with atrial fibrillation, etc.).

In each such clinical situation, the pathogenesis should be studied and effective therapy and methods of prevention should be selected based on the mechanisms underlying the detected disorders. The first steps in this direction have already been taken, both abroad and in Russia.

Shmonin A.A., Krasnov V.S., Shmonina I.A., Melnikova E.V.

• Manifestations of cerebral vascular disease
• Conservative treatment
• Drugs for vasodilation
• Drugs to strengthen the walls of blood vessels
• Herbal preparations
• Medicines for migraine therapy

Dysfunction of cerebral vessels is associated with spasm or decreased tone, increased permeability of the wall, a tendency to form blood clots and defects due to exposure to unfavorable factors of the external and internal environment. A fast pace of life, poor nutrition, low physical activity, bad habits and constant stress are at risk for developing cerebral vascular pathology. As a result, the supply of nutrients and oxygen to neurons is disrupted, and under-oxidized products and substances accumulate. This causes hypoxia and death of nerve cells, which adversely affects the functioning of the entire organism. To prevent the development of the disease and severe complications, complex drug treatment is prescribed, depending on the cause and severity of the pathological process.

Manifestations of cerebral vascular disease

The human brain is the control center for the functioning of all organs and systems, but at the same time it is most vulnerable to the development of hypoxia and lack of glucose. As a result of the lack of sufficient nutrients and oxygen, irreversible changes occur in neurons - highly specialized cells that have lost the ability to divide. Therefore, it is extremely important to prevent the death of brain tissue at an early stage of the disease.

The most common pathology of cerebral vessels:

• atherosclerosis – develops when fat metabolism is impaired, characterized by the formation of an atherosclerotic plaque that blocks the lumen of the cerebral artery;
• discirculatory encephalopathy – a transient disruption of the blood supply to the brain tissue, causing chronic hypoxia;
• vegetative-vascular dystonia (VSD) – a violation of the regulatory mechanism of the autonomic system on the tone of cerebral vessels;
• aneurysm - a sac-like protrusion of a thinned artery wall as a result of exposure to increased intravascular pressure;
• Migraine is angiospasm of the arteries of a neurotic nature.

Each disease has its own distinctive clinical signs and features of treatment tactics.

Symptoms of atherosclerosis:

• fast fatiguability;
• drowsiness;
• decreased mental activity (attention, memory, thinking);
• irritability;
• dizziness.

Symptoms of dyscirculatory encephalopathy:

• impairment of intellectual abilities;
• memory loss;
• recurrent headaches;
• emotional lability;
• exacerbation of character traits.

Symptoms of VSD:

• nervousness followed by apathy;
• sleep disturbance;
• trembling in the body, nausea, sometimes vomiting;
• chronic headaches;
• discomfort in the heart area;
• increase or decrease in blood pressure.

Symptoms of cerebral aneurysm:

• intense headaches;
• change in facial expressions;
• disturbance of smell, touch, vision;
• decreased sensitivity.

Migraine symptoms:

• regular pain in one half of the head of high intensity;
• the appearance of warning signs of an attack (numbness of the limbs, loss of visual fields, fear of light);
• redness of the face, nasal congestion, swelling of the eyes;
• lacrimation;
• nausea and vomiting that does not bring relief.

At the first clinical manifestations of cerebral vascular pathology, it is necessary to consult a doctor for a comprehensive examination and timely treatment. Otherwise, severe consequences of hypoxia of brain tissue (ischemic stroke), violation of the integrity of the artery (hemorrhagic stroke), development of neurological symptoms (paresis, paralysis, speech impairment), and decreased mental abilities develop. This significantly worsens the quality of life, reduces social adaptation in society, and leads to loss of ability to work.

Conservative treatment of cerebral vascular pathology

Modern medicine has a rich arsenal of medicines containing natural and synthetic components that can stop the pathological process in the blood vessels of the brain and significantly improve the general condition. It should be remembered: the earlier complex therapy is started, the more favorable the outcome of the disease for recovery and a full life.

Drugs for vasodilation

Arterial spasm causes a decrease in the flow of oxygenated blood to the brain tissue during migraine, atherosclerosis, hypertensive VSD (with increased blood pressure), discirculatory encephalopathy. To prevent the processes of brain hypoxia, medications from the group of calcium antagonists are prescribed, which have been produced and improved for many years.

First generation calcium antagonists include:

• verapamil (isoptin, finoptin);
• diltiazem (diazem);
• nifedipine (Corinfar, phenigidine, cordafen).

Second generation calcium antagonists include:

• falipamil, gallopamil;
• lomir;
• Clentiazem;
• nicardipine, riodipine, amlodipine.

The second generation of drugs has a longer effect and high selectivity on the pathologically changed area of ​​the artery, and has fewer side effects. The latest generation of calcium antagonists can act directly on the vessels of the brain without affecting arteries of other locations. These include effective tablets such as cinnarizine and nimodipine. It should be remembered that drug therapy must be prescribed by a doctor; self-medication can lead to undesirable consequences and significantly worsen the prognosis of the disease.

Drugs to strengthen the walls of blood vessels

For normal tone and blood circulation, the vessel wall must be strong, elastic, without defects in the inner layer (endothelium). Otherwise, an aneurysm develops, permeability increases with the leakage of plasma into the surrounding tissue and the development of edema of areas of the brain. A change in the integrity of the endothelium favors the deposition of fat, cholesterol, and platelet accumulation, which leads to the formation of atherosclerotic plaque and blood clots. They disrupt the normal flow of blood through the vascular bed and cause the development of hypoxia.

The preparations contain vitamins and microelements:

• nicotinic acid (nicoshpan, enduratin) – dilates capillaries, strengthens the vascular wall, reduces the synthesis of low-density cholesterol and its deposition in the endothelium;
• vitamin P and ascorbic acid (ascorutin) – the combined effect of vitamins normalizes metabolic processes in the walls of arteries and veins, reduces their permeability, increases resistance to pressure and traumatic factors;
• dihydroquerticin – is an extract of biologically active substances of Dahurian larch, has a beneficial effect on the elasticity of blood vessels;
• selenium, potassium, silicon are important microelements for normalizing metabolism in the arterial wall and maintaining the tone of cerebral vessels.

Medicines in this group are prescribed in courses in the form of tablets and injection forms under the supervision of a doctor for therapeutic and preventive purposes. For the treatment of atherosclerosis, agents are additionally prescribed that improve fat metabolism, stabilize and dissolve atherosclerotic plaque, and prevent the formation of blood clots. These include fibrates (gemfibrozil, fenofibrate), statins (lovastatin, fluvastatin), antiplatelet agents (cardiomagnyl, thromboass).

Herbal preparations

Medicines based on plant alkaloids include:

• periwinkle preparations (Cavinton, Vinpocetine, Bravinton, Telektol) – have an antispasmodic effect, normalize vascular tone, improve metabolic processes in brain tissue, prevent pathological thrombus formation, optimize brain microcirculation;
• Gingko biloba preparations (gingium, tanakan, ginkor fort, bilobil) are made from a relict plant containing biologically active substances that dilate blood vessels, improve the metabolism of brain tissue, prevent the formation of blood clots, neutralize free radicals, and have an anti-edematous effect.

As a result of regular medication use, mental activity improves, sleep and emotional state normalize, headaches stop, and neurological symptoms disappear (impaired sensitivity, facial expressions, motor activity).

Medicines for migraine therapy

The development of migraine attacks is associated with spasm and then weakening of the tone of cerebral vessels, which leads to their expansion and stagnation of blood. As a result of a violation of the permeability of the walls of arteries and veins, plasma leaks into the surrounding tissues and causes swelling of the brain in the area of ​​the pathological process. This condition can last from half an hour to several days, after which vascular tone is restored. With frequent attacks, the microcirculation of parts of the brain is aggravated, and irreversible changes in neurons may appear.

Medicines to treat migraines include:

• analgesics and antispasmodics (spasmolgon, amigrenin) - prescribed at the beginning of an attack, which is accompanied by vasospasm;
• vasoconstrictors (caffeine, ergotamine) - narrow the arteries during the period of paralytic state of vascular tone;
• serotonin antagonists (imigran, zomig, maxalt) – prevent dilation of the arteries of the head and neck;
• non-steroidal anti-inflammatory drugs (indomethacin, diclofenac) - have a decongestant, analgesic effect, reduce the inflammatory process.

Vasoconstrictors are also prescribed for hypotonic VSD in order to improve cerebral blood flow. To improve the functional productivity of the brain, it is recommended to take nootropics (piracetam, aminolon), neuropeptides (Semax), and metabolic agents (glycine).

Prevention and treatment of cerebral vessels should be carried out in a timely manner under the close supervision of a physician. This approach will be the key to health and prevention of the development of ischemic brain damage. Equally important for maintaining the normal functioning of neurons is a balanced diet, an active lifestyle, overcoming alcohol and nicotine addiction, and a proper daily routine.

Disorders of the venous circulation of the head: causes, signs, manifestations, elimination

Modern man is not immune from such a phenomenon as cerebral venous discirculation. Experts note that short-term disturbances occur during normal physiological processes: coughing, singing, defecation, turning the head, physical activity. Therefore, we have all encountered, albeit for a short time, this phenomenon, without even knowing what happened.

Experts have been studying this disease for a long time and have identified three main stages:

1. Latent stage. At this stage, clinical symptoms do not appear, and the person lives a normal life, without any special complaints;
2. Cerebral venous dystonia, in which a typical picture of paraclinical changes is observed. The person exhibits some symptoms but can continue to lead a normal life.
3. Venous encephalopathy with the development of stable organic microsymptoms. Here you will need the help of a specialist, otherwise the person’s normal life will be at risk.

This classification by stages has been recognized by many experts. In 1989, M. Ya. Berdichevsky introduced a classification of venous discirculation based on the forms of manifestation.

Classification of venous discirculation according to Berdichevsky

The scientist identified two main forms of disturbance of venous outflow.

Primary form

It is expressed in disruption of circulatory processes in the brain due to changes in the tone of the veins.

This may be a consequence of TBI (traumatic brain injury), hyperinsolation, alcohol or nicotine intoxication, hypertension and hypotension, diseases of the endocrine system, venous hypertension, etc.

Stagnant form

It develops when there are mechanical difficulties in the outflow of venous blood. That is, in the cranium, venous outflow is so difficult that this leads to the extinction of the mechanics of the process. In this case, it is impossible to do without outside intervention.

Causes of pathology

The causes of disturbances in venous outflow can be serious traumatic brain injuries with bone fractures, as well as the formation of internal hematomas; previous strokes with subsequent cerebral edema; tumors leading to compression of the brain and blood vessels; reduction or underdevelopment of the network of veins, etc.

If we talk about external causes that lead to difficulty in the venous outflow of the brain, then there may be the following disorders: blockage of the veins, the occurrence of tumors in the cervical region, strangulation lesions, injuries to the abdomen and chest, osteochondrosis of the cervical spine, prolapse of spinal discs, etc. d..

In other words, the causes of cerebral venous discirculation can be both in the skull and outside it - in the spine, abdomen, neck. It is important to note here that with any problems with the spine, the consequences are global and disturbances in the functioning of organs appear in the most unexpected ways. After all, when an intervertebral disc protrudes or prolapses, blood flow is disrupted, and this leads to serious consequences.

Symptoms of cerebral venous circulation

Any disease manifests itself with certain symptoms. If we talk about venous discirculation, it manifests itself as a dull headache, which is most pronounced in the morning. A person suffering from this disease has difficulty getting out of bed. It seems to him that his body is not listening, he feels lethargic, as if he had not slept at all. Painful sensations increase while moving the head in different directions. When changing atmospheric pressure, as well as temperature, pain can also intensify. Excitement, stress, and alcohol consumption also often cause pain. The pain is accompanied by noise or buzzing in the head, cyanosis of the cheeks, lips, nose, ears, mouth appears, the lower eyelids swell, and the veins in the fundus dilate. These symptoms are most pronounced in the morning immediately after waking up.

As for venous pressure, it is in the range of 55-80 mmH2O. Art., and the arterial value most often corresponds to the normal value.

Symptoms of impaired venous outflow may include dizziness, a feeling of dizziness, darkening of the eyes, numbness of the limbs and fainting. In some cases, seizures of epilepsy and mental disorders occur. If venous congestion is pronounced, then the patient will not be able to lower his head or take a horizontal position.

If the doctor decides that there is a possibility of a violation of the venous outflow, the pressure in the ulnar vein is measured, and an X-ray of the skull and venography are also performed.

Currently, most adults exhibit symptoms of this disease, even in a mild form. It manifests itself especially strongly in the spring-autumn period, when the season changes. Some endure the inconvenience, trying to live their previous lives, while others resort to injections of special drugs that help dilate the blood vessels on their own. We'll talk about some drugs a little later.

What to do if symptoms of venous outflow disturbance are detected?

If you have symptoms of the disease, do not panic. In the early stages, you can easily correct the functioning of the blood vessels in the brain. Moreover, sometimes it is enough to change the lifestyle that leads to a deterioration of the general condition in order to get rid of the disease. In any case, there is no need to delay, but if possible, turn to specialists. With their help, the necessary examinations will be carried out and a course of treatment will be prescribed.

It is hardly worth self-medicating and injecting medications every season, which, by the way, many doctors do to themselves. They believe that this is all due to bad weather or age (meaning non-specialized doctors who, by their specifications, do not come into contact with this disease in practice). This is partly true, but the “root of evil” is buried deeper and must be eradicated by taking a professional approach to the treatment process.

Treatment

To make an accurate diagnosis of whether the patient’s venous outflow from the brain is impaired or not, studies must be carried out. The most accurate data can be obtained after undergoing an MRI. This drug is located in every major city, it is served by a specialist trained in specialized courses. If abnormalities are found in the jugular veins, then this may be the reason why headaches and some associated symptoms occur. When diagnosing blood flow disorders, attention is paid to the fundus of the eye, where stagnation may occur.

If a violation of the venous blood flow in the brain is diagnosed, the neurologist will be able to prescribe the correct course of treatment. You can also contact a vascular surgeon. Don’t let the word “surgeon” scare you, because turning to him doesn’t mean you’ll have to go under the knife. The surgeon just has experience and knowledge. They will help in making an accurate diagnosis, on the basis of which a course of treatment will be prescribed.

It often happens that a patient with pathology also has varicose veins. Then, at the same time, you will be prescribed medications that help thin the blood.

Currently, Detralex is most often used in the treatment of poor venous outflow from the head. It is designed to improve blood flow. In addition, Detralex can improve the condition of veins, adding elasticity to them.

In some cases, massage performed in the neck area has a very beneficial effect. However, if you have been diagnosed with signs of the disease, do not rush to contact a massage therapist. You should resort to a massage procedure only if recommended by a doctor. Otherwise, there is the option of causing severe harm instead of benefit. The massage itself should be performed exclusively by a specialist.

Bad habits: drinking alcohol, tobacco, fast food should remain a thing of the past forever. Often they are the cause of the disease. To thin the blood, it is advisable to add more greens, fruits and vegetables to your diet. Excellent assistants that will help in recovery are nettle and grape juice.

Lifestyle most often leads to the appearance of a greater number of diseases, including those associated with blood vessels. An active lifestyle, proper food and clean water can protect a person from multiple diseases. According to many doctors, 70% of human diseases occur due to poor nutrition and bad habits. In order not to overwhelm your body and then bring yourself back to normal with emergency measures, it is better to worry about yourself in advance and start leading a healthy lifestyle.

But if various pathologies lead to the disease, then even a healthy lifestyle does not guarantee anything.

Drugs that improve venous outflow

Currently, there are drugs that improve venous outflow. They can help not only improve outflow, but also normalize the functioning of blood vessels. Venotonics are modern drugs that help improve blood flow. They are also good for prevention.

What effect do venotonics have on the human body:

1. Strengthening blood vessels. The permeability of blood vessels is normalized, their fragility decreases, swelling decreases, microcirculation improves;
2. Strengthening the general tone in the veins, giving them greater elasticity;
3. Fighting inflammatory processes with their further prevention;
4. Increased overall tone.

At the moment, the most common herbal venotonics are:

• Aescusan (gel or cream), venoplant, herbion-esculus (they are obtained from horse chestnut);
• “Doctor Theiss” (the preparation contains calendula extract and elements of horse chestnut), Venen-gel;
• Antistax – gel and capsules (contains red grape leaf extract);
• Ginkor-gel, ginkor-fort (contain gingobilob extract);
• Anavenol, Getralex, Ellon-gel, etc..

In any case, these drugs should be used after consultation with a doctor. Do not neglect to follow the instructions for use of the drugs.

Some “populists” and people who try to get rid of ailments on their own offer an integrated approach to improve blood flow in general:

1. Massage;
2. Phytotherapy;
3. Relaxation;
4. Full sleep;
5. Regular contrast shower;
6. Frequent and moderate exercise;
7. Long walks outdoors.

Exercises to help improve venous drainage

In some cases, when venous outflow is impaired, simple and accessible exercises can help. Sometimes it is enough to work on your neck to get rid of pain within a few weeks. In this case, exercises to improve venous outflow can be done several times a day, without particularly disturbing your rhythm of life. They will take about ten minutes to complete.

Exercise 1. Head tilt

The purpose of the exercise is to improve venous outflow from the head. You need to sit on a chair, resting your hands on the back. The muscles of the legs and arms are relaxed, the head is thrown back freely. Try sitting in this position for a minute. Breathing is free and deep. After you finish the exercise, walk a little and repeat it twice.

Exercise 2. Long neck

The exercise can be performed standing or sitting. The main thing is to relax and lower your head to your chest. As you inhale, begin to lift your head up, looking at the ceiling. Then stretch your neck, as if an invisible thread is pulling you up. When you lower your head, exhale. The exercise is repeated up to eight times depending on how you feel.

Exercise 3. Drawing eights

The exercise is performed in a relaxed state. Start drawing an imaginary figure eight using the top of your head. One circle to the left, the other circle to the right. Breathing is free, the body is relaxed. The exercise is repeated up to six times.

Exercise 4. Power Bend

Sit straight on a chair and clasp your fingers under your chin. While exhaling, tilt your head down, pressing on it with your palms and the back of them. As you inhale, tilt your head back, resisting the movement with your palms placed on the back of your head. The exercise is repeated up to twelve times. It is not recommended to hold your breath.

These exercises help a lot with asymmetry of venous outflow, as it often occurs when the neck is incorrectly positioned or pinched in the cervical spine. These four common exercises can bring a lot of benefits.

Additional physical activity

Yoga classes are good for improving venous outflow. In this practice there are many asanas aimed at strengthening blood vessels and improving blood flow. In addition, specific breathing through the larynx during exercise helps pump air, which in itself increases blood flow.

Running is great for improving overall blood flow. Considering that running is not accessible to everyone, you can start with regular long-distance walking. It’s good if walking and running are done in a place with clean air and beautiful views of nature. This will have a double effect.

Some argue that lifting weights can not only help prevent venous dyscirculation, but also cure it. Most likely, those who affirm this postulate mean the early stages of the disease, when everything is not yet advanced. In any case, before you start practicing physical activity, consult your doctor.

What about the bathhouse? In a bathhouse, a sharp change in maximum heat and cold has a strong effect on the blood vessels. Yes, blood flow increases, but if the vessels are weak, then harm can be done to the body. Still, the bathhouse is more suitable for prevention, as a means of pumping blood and strengthening the vascular system.

Video: exercises to improve blood supply to the head

Problems at an early age

Unfortunately, situations where venous outflow is significantly obstructed in a child occur frequently. The child suffers greatly from this, especially if he is not yet a year old. He often screams in response to pain. Parents do not always think of contacting a specialist who can conduct an examination. In the early stages, some diseases are treated easier and faster.

If the cause of the baby’s frequent cries is not recognized in time, he will subsequently be forced to limit himself in exercise. In modern schools you can often find healthy-looking children who study well, but often experience severe headaches, especially during sudden changes in weather. Often during physical education classes they are forced to recover for a long time after performing exercises, since venous outflow is difficult and they have to wait some time for the dizziness to pass.

Prospects

Since humanity discovers new diseases every year, it is difficult to imagine what will happen to our health and medicine in ten to twenty years. Cerebral venous dysfunction is already causing a lot of problems, as the number of patients with this disease is growing. As mentioned above, there are many reasons. One of the main reasons is difficult childbirth. Children who have suffered a difficult birth often have many deviations in health and further development. They have to try too hard to feel normal compared to others. Medicine can help here, but not completely. Still, impaired lymphatic drainage is not always completely restored. Treatment requires a bit of luck and the patient’s perseverance. Not everyone will be able to take charge of themselves, change their previous harmful lifestyle - give up alcohol, tobacco, eat huge amounts of junk food, start playing sports.

Venous dysgemia is observed even in athletes who perform in professional sports. The desire to achieve high results and perseverance help them achieve their goals. Only occasionally do you find information in newspapers and on the Internet that another young athlete lost consciousness during a competition or was out of action for an indefinite period of time.

We are all at risk, so it is extremely important to lead a healthy lifestyle, but without much fanaticism. Then the risk of cerebral venous discirculation disease will be reduced to zero.

Video: specialists about venous disorders of the blood supply to the head

CT brain perfusion is one of the new examination methods. Thanks to the presence of special functions in the tomograph, the images are clear and allow you to evaluate not only the structure of the brain itself, but also how dense its tissues are and what features the blood flow in the central nervous system has.

Perfusion is the process of fluid, including blood, passing through tissue. Perfusion computed tomography of the brain in this case makes it possible to study the characteristics of blood flow in the tissues of the organ. This is a type of CT angiography, but in a more accurate, expanded form. This type of examination allows you to study cerebral hemodynamics at the capillary level.

With the help of brain CT, perfusion is clearly visible, and numerous parameters of cerebral blood flow are measured, based on an assessment of the density of brain tissue. The study allows you to diagnose the presence of any damage, even small ones, in the early stages.

The main indicators are assessed:

1. The rate at which the volume of blood passes through brain tissue in a given time.
2. The volume of blood in one or another part of the organ (capillaries, veins, venules, arterioles, arteries).
3. The time it took for the contrast to reach the examined area of ​​the brain.
4. The period during which blood passes through the vessels in the part of the organ being studied.

This type of study allows not only to assess the degree of damage to tissues and areas, but also to make predictions regarding the further course of the disease and the possibility of full recovery.

Indications and contraindications for examination

CT perfusion is prescribed:

1. When there is a need to diagnose the consequences of strokes or traumatic brain injuries, brain pathologies.
2. For oncology. It is possible not only to diagnose the presence of a tumor, but also to determine its size and analyze the effectiveness of the treatment.
3. For frequent headaches, loss of consciousness.
4. Before plastic surgery.

Like most diagnostic procedures, CT has a number of contraindications that are identified during a preliminary examination of the patient. These include:

1. Pregnancy and breastfeeding. Irradiation can have a negative effect on the fetus, and the contrast, if it gets into the milk, can cause an allergic reaction in the baby. An exception is an emergency situation in which other research methods cannot be used.
2. Allergy to iodine, which is part of the substance administered before the procedure.
3. If you have diabetes, kidney disease, or thyroid disease, the administration of contrast may cause an exacerbation of the condition.
4. Various mental illnesses or claustrophobia. In emergency cases, medicated sleep or sedatives.
5. Tendency to cramps and spasms.
6. Children's age up to 5 years. Associated with the inability to remain completely still. But if the situation is urgent, the child is diagnosed under anesthesia or in a state of medicated sleep.
7. The patient’s weight is more than 150 kg (the volume of the patient’s body does not correspond to the diameter of the tomograph capsule).
8. Diseases of the cardiovascular system – heart failure, arrhythmia.

All these contraindications can be divided into 2 groups: absolute, when the examination is categorically impossible to carry out, and relative, when the procedure is not recommended, but is still possible with some preparatory manipulations.

What are the advantages of such a survey?

The advantages of such a study are obvious:

1. Availability.
2. High quality pictures from different angles.
3. Time 5-45 minutes (average 20-30 minutes).
4. Selectivity, i.e. Only the required part of the organ is examined.
5. Minimum contraindications.
6. It is carried out on an outpatient basis.
7. Possibility of creating a three-dimensional model of tissues and skull.
8. Saving information on storage media.

Possible risks

Risks are associated with complications if the patient has at least one of the following diseases:

• intolerance to the components that make up the contrast agent;
• hyperthyroidism;
• diabetes;
• renal or liver failure;
• bronchial asthma in an advanced stage;
• obesity;
• foreign bodies in the skull.

The resulting complications can be fatal.

How to prepare for a CT scan?

A couple of weeks before the procedure, you should donate blood (biochemistry). An important indicator is creatinine, which determines whether a contrast agent can be administered or not.

Several hours before the procedure, you should not take food or take any medications, and women should not use cosmetics.

Before the examination, you must remove jewelry, metal and other objects, as well as turn off and put away your mobile phone. Clothing should not restrict movement.

How is cerebral perfusion performed?

In appearance, the MRI machine is almost identical to the equipment used for traditional MRI. The subject is placed on a table that slides into the capsule. A contrast agent is supplied in a volume of 40-50 ml/4ml/sec. The dose depends on the patient's weight.

X-ray scanning occurs at intervals of 1 second, mode – 40 seconds. From the resulting images, a three-dimensional model of the examined area of ​​the brain will be formed, on which the state of the blood supply to the head will be clearly visible.

In order for the contrast agent to be eliminated from the body faster, it is recommended to drink at least 6 glasses of water. And those who have kidney problems may even be prescribed special medications.

When examination is absolutely necessary and the patient has metal objects in the body, RPI (radionuclide perfusion study) is allowed. Used to examine patients with suspected cancer. The operating principle of this method is the accumulation of special radiopharmaceuticals in the tumor. The concentration in the affected area should be higher than in healthy tissue.

Saturation occurs due to the fact that substances enter the inner surface of the lymph nodes and blood vessels of the unhealthy area. They move through the vascular wall into the intercellular space of the affected area.

The images obtained in this way give an idea of ​​whether or not there is a pathological neoplasm at both the cellular and molecular levels. The level of radiation in this case is comparable to the radiation background of the environment.

Features of the procedure with contrast

The use of a contrast agent containing iodine is a prerequisite for the examination. Non-ionic drugs are used.

Modern equipment and special computer programs make it possible to administer the drug in strictly dosage, this allows for a more clear separation of the phases of administration (venous, arterial). In addition, this method of administration reduces the risk of adverse reactions.

How long does a CT scan take?

Time is the main advantage of this method. The procedure can take from 5 to 45 minutes, no more. It all depends on the area of ​​the brain being examined and how still the patient lies.

What is the radiation dose?

Thanks to modern equipment, the radiation dose is minimal - 1-2 mSv. In addition, some of the radiation is absorbed by special protective shields (if they are used).

How often can I do it?

Even though modern equipment neutralizes some of the harmful radiation, it is not recommended to conduct examinations more than 1-2 times a year.

Prices

The average cost of a CT scan of the brain is 2800 rubles, and a CT scan of the brain vessels is 3500 rubles.

What does such a study diagnose?

This diagnostic method allows you to see:

1. The consequences of injuries are hematomas.
2. Measure bleeding parameters and predict consequences.
3. Aneurysms.
4. Locations of stenosis.
5. Tumors of various origins and tissues adjacent to the source of the lesion to take a biopsy.
6. The nature of damage to nerve fibers and differentiate them.

Interpretation of perfusion scanning

During the study, special attention is paid to 3 indicators:

1. Cerebral blood flow volume (CBV). This indicator allows you to estimate the amount of blood per mass of brain tissue. The norm is 2.5 ml of blood per 100 g of white and gray matter. Reduced perfusion indicates the presence of ischemic processes.
2. Blood flow velocity (CBF) - how much contrast material passes through 100 g of brain tissue in the required amount of time. A downward deviation indicates the presence of thrombosis or embolism.
3. Average contrast circulation time (MCT). Normally, it should not exceed 4-4.5 seconds. If the norm is exceeded, it means that the lumen of the vessels has closed.

After collecting this data, a special computer program calculates and analyzes everything.

Alternatives

If for some reason CT scanning is not possible, then MSCT brain perfusion is prescribed as an alternative to this method. It differs from CT in time, radiation exposure and examination accuracy.

Since the alternative technique appeared relatively recently, and in the 21st century. The devices have also been improved, and now it is the most accurate, reliable and productive method of examination. The images are of higher quality and more detailed, making it possible to study even the smallest organs and their individual elements.

These innovative methods make it possible not only to study the condition of the organ in detail, but also, based on the results, to adjust the treatment regimen, evaluate the results of the therapy, and even predict the further course of the disease.

Vertebral artery syndrome (VAS) is a complex of symptoms resulting from disruption of blood flow in the vertebral (or vertebral) arteries. In recent decades, this pathology has become quite widespread, which is probably due to the increase in the number of office workers and people leading a sedentary lifestyle who spend a lot of time at the computer. If previously the diagnosis of SPA was made mainly to elderly people, today the disease is diagnosed even in twenty-year-old patients. Since any disease is easier to prevent than to treat, it is important for everyone to know for what reasons vertebral artery syndrome occurs, what symptoms are manifested and how this pathology is diagnosed. We will talk about this, as well as the principles of SPA treatment, in our article.

Fundamentals of Anatomy and Physiology

Blood enters the brain through four large arteries: the left and right common carotid and the left and right vertebral. It is worth noting that 70-85% of the blood passes through the carotid arteries, so disruption of blood flow in them often leads to acute cerebrovascular accidents, that is, ischemic strokes.

The vertebral arteries supply the brain with only 15-30% of blood. Violation of blood flow in them, as a rule, does not cause acute, life-threatening problems - chronic disorders occur, which, however, significantly reduce the patient’s quality of life and even lead to disability.

The vertebral artery is a paired formation originating from the subclavian artery, which in turn arises on the left - from the aorta, and on the right - from the brachiocephalic trunk. The vertebral artery goes upward and slightly backward, passing behind the common carotid artery, enters the opening of the transverse process of the sixth cervical vertebra, rises vertically through similar openings of all overlying vertebrae, through the foramen magnum enters the cranial cavity and follows to the brain, supplying blood to the posterior parts of the brain : cerebellum, hypothalamus, corpus callosum, midbrain, partially temporal, parietal, occipital lobes, as well as the dura mater of the posterior cranial fossa. Before entering the cranial cavity, branches depart from the vertebral artery, carrying blood to the spinal cord and its membranes. Consequently, when blood flow in the vertebral artery is disrupted, symptoms arise that indicate hypoxia (oxygen starvation) of the areas of the brain that it supplies.

Causes and mechanisms of development of vertebral artery syndrome

Along its length, the vertebral artery comes into contact with both the hard structures of the spinal column and the soft tissues surrounding it. Pathological changes that occur in these tissues are the prerequisites for the development of SPA. In addition, the cause may be congenital characteristics and acquired diseases of the arteries themselves.

So, there are 3 groups of causative factors of vertebral artery syndrome:

1. Congenital structural features of the artery: pathological tortuosity, course anomalies, kinks.
2. Diseases that result in a decrease in the lumen of the artery: atherosclerosis, all kinds of arteritis (inflammation of the artery walls), thrombosis and embolism.
3. Compression of the artery from the outside: osteochondrosis of the cervical spine, abnormalities of bone structure, trauma, scoliosis (these are vertebrogenic, that is, associated with the spine, causes), as well as tumors of the neck tissue, their scar changes, spasm of the neck muscles (these are non-vertebrogenic causes).

Often, SPA occurs under the influence of several causative factors.

It is worth noting that RAS develops more often on the left, which is explained by the anatomical features of the left vertebral artery: it arises from the aortic arch, which often has atherosclerotic changes. The second leading cause, along with atherosclerosis, is degenerative diseases, that is, osteochondrosis. The bone canal in which the artery passes is quite narrow, and at the same time mobile. If there are osteophytes in the area of ​​the transverse vertebrae, they compress the vessel, disrupting blood flow to the brain.

In the presence of one or more of the above reasons, factors predisposing to the deterioration of the patient’s well-being and the appearance of complaints are sudden turns or tilts of the head.

Symptoms of vertebral artery syndrome

Patients with vertebral artery syndrome often experience dizziness and headaches.

The pathological process in SPA goes through 2 stages: functional disorders, or dystonic, and organic (ischemic).

Stage of functional impairment (dystonic)

The main symptom at this stage is headache: constant, aggravated by head movements or prolonged forced positions, burning, aching or throbbing in nature, covering the back of the head, temples and moving forward to the forehead.

Also at the dystonic stage, patients complain of dizziness of varying intensity: from a feeling of slight instability to a feeling of rapid rotation, tilting, and falling of one’s own body. In addition to dizziness, patients are often bothered by tinnitus and hearing impairment.

Various visual disturbances may also occur: sand, sparks, flashes, darkening of the eyes, and when examining the fundus, a decrease in the tone of its blood vessels.

If at the dystonic stage the causative factor is not eliminated for a long time, the disease progresses and the next, ischemic stage occurs.

Ischemic or organic stage

At this stage, the patient is diagnosed with transient disorders of cerebral circulation: transient ischemic attacks. They are sudden attacks of severe dizziness, impaired coordination of movements, nausea and vomiting, and speech disorders. As mentioned above, these symptoms are often provoked by a sharp turn or tilt of the head. If, with such symptoms, the patient takes a horizontal position, there is a high probability of their regression (disappearance). After an attack, the patient feels tired, weak, tinnitus, sparks or flashes before the eyes, and headache.

Clinical variants of vertebral artery syndrome

These are:

• drop attacks (the patient suddenly falls, his head is thrown back, he cannot move or stand up during the attack; consciousness is not impaired; within a few minutes, motor function is restored; this condition occurs due to insufficient blood supply to the cerebellum and caudal parts of the brain stem);


• syncopal vertebral syndrome, or Unterharnsteidt syndrome (with a sharp turn or tilt of the head, as well as in the case of a prolonged stay in a forced position, the patient loses consciousness for a short time; the cause of this condition is ischemia of the region of the reticular formation of the brain);
• posterior cervical sympathetic syndrome, or Bare-Lieu syndrome (its main symptom is constant intense headaches of the “removing the helmet” type - localized in the occipital region and spreading to the anterior parts of the head; pain intensifies after sleeping on an uncomfortable pillow, when turning or tilting head; the nature of the pain is pulsating or shooting; may be accompanied by other symptoms characteristic of SPA);
• vestibulo-atactic syndrome (the main symptoms in this case are dizziness, a feeling of instability, imbalance, darkening of the eyes, nausea, vomiting, as well as disorders of the cardiovascular system (shortness of breath, pain in the heart and others);
• basilar migraine (the attack is preceded by visual disturbances in both eyes, dizziness, unsteadiness of gait, tinnitus and blurred speech, after which intense headache occurs in the back of the head, vomiting, and then the patient loses consciousness);


• ophthalmic syndrome (complaints from the organ of vision come to the fore: pain, a feeling of sand in the eyes, lacrimation, redness of the conjunctiva; the patient sees flashes and sparks before the eyes; visual acuity decreases, which is especially noticeable when there is strain on the eyes; fields partially or completely fall out vision);
• cochleo-vestibular syndrome (the patient complains of decreased hearing acuity (perception of whispered speech is especially difficult), tinnitus, a feeling of swaying, body instability or rotation of objects around the patient; the nature of the complaints changes - they directly depend on the position of the patient’s body);
• syndrome of autonomic disorders (the patient is concerned about the following symptoms: chills or a feeling of heat, sweating, constantly wet cold palms and feet, stabbing pain in the heart, headaches, and so on; often this syndrome does not occur on its own, but is combined with one or more others );
• transient ischemic attacks, or TIA (the patient notes periodically occurring transient sensory or motor disturbances, disturbances in the organ of vision and/or speech, unsteadiness and dizziness, nausea, vomiting, double vision, difficulty swallowing).

Diagnosis of vertebral artery syndrome

Based on the patient’s complaints, the doctor will determine the presence of one or more of the above syndromes and, depending on this, will prescribe additional research methods:

• X-ray of the cervical spine;
• magnetic resonance or computed tomography of the cervical spine;
• duplex scanning of the vertebral arteries;
• vertebral Dopplerography with functional loads (flexion/extension/rotation of the head).

If the diagnosis of SPA is confirmed during further examination, the specialist will prescribe appropriate treatment.

Treatment of vertebral artery syndrome

The effectiveness of treatment for this condition directly depends on the timeliness of its diagnosis: the earlier the diagnosis is made, the less thorny the path to recovery will be. Complex spa treatment should be carried out simultaneously in three directions:

• therapy for pathology of the cervical spine;
• restoration of the lumen of the vertebral artery;
• additional treatment methods.

First of all, the patient will be prescribed anti-inflammatory and decongestant drugs, namely non-steroidal anti-inflammatory drugs (meloxicam, nimesulide, celecoxib), angioprotectors (diosmin) and venotonics (troxerutin).

In order to improve blood flow through the vertebral artery, agapurine, vinpocetine, cinnarizine, nicergoline, instenon and other similar drugs are used.

To improve the metabolism (metabolism) of neurons, use citicoline, gliatilin, cerebrolysin, actovegin, mexidol and piracetam.

To improve metabolism not only in nerves, but also in other organs and tissues (vessels, muscles), the patient takes mildronate, trimetazidine or thiotriazoline.

In order to relax the spasmodic striated muscles, mydocalm or toldel will be used, vascular smooth muscles - drotaverine, better known to patients as No-shpa.

For migraine attacks, antimigraine drugs, such as sumatriptan, are used.

To improve the nutrition of nerve cells - B vitamins (Milgamma, Neurobion, Neurovitan and others).

To eliminate mechanical factors compressing the vertebral artery, the patient may be prescribed physical treatment (manual therapy, post-isometric muscle relaxation) or surgical intervention.

During the recovery period, neck massage, physical therapy, acupuncture, and sanatorium-resort treatment are widely used.

Prevention of vertebral artery syndrome

The main preventive measures in this case are an active lifestyle and healthy sleep on comfortable bedding (it is highly desirable that they be classified as orthopedic). If your work involves keeping your head and neck in one position for a long time (for example, working at a computer or activities associated with continuous writing), it is strongly recommended to take breaks from it, during which you perform gymnastics for the cervical spine. If the complaints mentioned above appear, you should not wait for their progression: the right decision would be to consult a doctor as soon as possible. Do not be ill!

Source: doctor-neurologist.ru

There are several ways to alleviate the condition of a patient with hypoplasia of the right vertebral artery:

1. Traditional drug treatment. It involves the use of medications that have a positive effect on blood composition, improve blood circulation in the cerebral vessels and accelerate metabolism. Medicines will not lead to a complete cure, but will help prevent critical deterioration of the condition. As a rule, the drugs prescribed are acetylsalicylic acid, Thiocytes, Ceraxon, Trental, Cinnarizine, Actovegin, Cerebrolysin, Vinpocetine, etc.
2. Surgical intervention. It is resorted to only in extreme cases, after unsuccessful attempts to improve cerebral circulation using conservative therapy. The operation is quite complex - it is an endovascular intervention and is performed by neurosurgeons.

Treatment of the disease does not lead to positive dynamics in all cases. However, in the absence of therapy, the prognosis looks much worse.

Medicines

Drug name	Directions for use and doses	Side effects	special instructions
Cinnarizine	Prescribe 1 tablet three times a day.	Reactions such as drowsiness, dyspepsia, and allergies are possible.	Cinnarizine is best taken after meals to minimize irritation to the digestive tract.
Actovegin	Prescribe 1-2 tablets orally three times a day before meals.	Sweating, increased body temperature, and allergies may occur.	In severe cases, parenteral administration of the drug is used.
Cerebrolysin	Administered intramuscularly or intravenously, after dilution in sodium chloride solution or 5% glucose solution. Dosages are individual.	Rarely, with rapid administration, dizziness, headache, and tachycardia are observed.	The drug is not used to treat patients with allergic diathesis and renal failure.
	Prescribe 2-4 tablets up to three times a day, or intravenously in the form of a solution - according to indications.	Possible redness of the face, headache, irritability.	Trental is used with caution for stomach ulcers, heart failure, and also in the postoperative period.
Vinpocetine	Prescribe 1-2 tablets three times a day, for a long time.	Symptoms such as dizziness, nausea, redness of the upper body, tachycardia are possible.	In severe cases, Vinpocetine is administered intravenously.

Vitamins

To prevent complications, treatment must be supplemented with vitamins that are included in food products or in the form of pharmaceutical preparations. The following vitamins are considered the most suitable for hypoplasia:

• Retinol (A) – improves metabolism, prevents vascular damage by atherosclerosis. Contained in fish oil, dairy products, carrots, pumpkin, bell pepper.
• Ascorbic acid (C) – prevents the formation of cholesterol plaques, strengthens the heart and vascular walls. Contained in berries, fruits, citruses.
• Rutin (P) – makes the vascular wall strong. Contained in citrus fruits, berries, rose hips.
• Tocopherol (E) is an antioxidant, improves fat metabolism and prevents intoxication. Contained in vegetable oils, eggs, nuts.
• Pyridoxine (B 6) – removes excess cholesterol, stabilizes metabolic processes. Contained in fish, dairy products, brown rice, beans.

• Vitrum cardio;
• Doppel Hertz cardio system-3;
• Vitalarix Cardio;
• Cardio forte;
• Centrum cardio.

Physiotherapeutic treatment

For hypoplasia of the right vertebral artery, physiotherapy is not the primary therapeutic method. However, its use helps alleviate the patient’s condition and eliminate certain unpleasant signs of the disease.

The following physiotherapeutic effects are allowed:

• Exercise therapy – includes a set of exercises to restore blood circulation, walking.
• Mud therapy – normalizes the activity of the nervous and cardiovascular systems.
• Hydrotherapy, mineral waters, contrast shower.
• Fresh baths with warm water relax and calm the nervous system.
• Dry carbon dioxide bath – helps to dilate blood vessels and lower blood pressure.

Electric sleep, pine baths and other procedures improve well-being. The standard course of physiotherapy lasts 10 days.

Traditional treatment

Treatment with folk remedies, unfortunately, cannot completely cure the disease. But with the help of such recipes, you can improve the patient’s condition and prevent the development of exacerbations and complications. It is better if folk remedies are used against the background of traditional treatment prescribed by a doctor.

• Pour six full tablespoons of dried hawthorn berries and motherwort herbs into a thermos. Pour 1500 ml of boiling water and leave overnight. In the morning, filter the infusion and consume 100 ml up to 4 times a day.
• Squeeze the juice from ten lemons. We peel five heads of garlic and pass the cloves through a press. Mix all the ingredients with a liter of honey, place in a jar, cover with a lid and put in the refrigerator for one week. After seven days, the medicine can be consumed: 4 tsp. half an hour before dinner, gradually dissolving the mass in the mouth.
• We definitely include dried apricots in our diet: it is recommended to eat 100-150 g every day. This will improve the condition of the heart and blood vessels.
• Prepare a decoction of bean leaves in a ratio of 1:10. We drink it 100 ml three times a day 30 minutes before meals. The decoction improves heart function, relieves edema, prevents atherosclerosis, and normalizes blood pressure.
• We use natural honey 1 tbsp. l. three times a day. Honey can be diluted in warm water or poured over fruits.

Herbal treatment

• Such a well-known plant as dandelion perfectly stabilizes blood cholesterol levels. For example, dandelion rhizome powder is taken one-third of a teaspoon three times a day, about half an hour before meals.

Fresh leaves are added to salads and soups: in addition to the atherosclerotic effect, the leaves have antianemic and joint-protective activity.

• To prevent complications with hypoplasia, it is recommended to prepare tea from St. John's wort (20 g), fireweed (50 g), motherwort (15 g), and birch leaves (15 g). One tablespoon of the mixture is infused in 300 ml of boiling water for twenty minutes. Used instead of tea throughout the day.
• Elecampane tincture helps: 30 g of rhizome is poured with 300 ml of vodka and kept in the dark for 40 days. For treatment, take 35 drops of tincture in 100 ml of water 20 minutes before meals.

Homeopathy

Along with medications, homeopathic remedies, prescribed by a doctor in the appropriate field, are also successful. Homeopathy affects the body according to the principle of “treating like with like.” There are a number of drugs that have a positive effect on the vertebral arteries and blood vessels of the brain.

• Cholesterinum – lowers cholesterol levels, improves the condition of blood vessels in atherosclerosis.
• Gold iodine is effective against atherosclerosis of cerebral vessels.
• Conium - helps with stroke and post-stroke conditions.
• Crategus – improves cerebral circulation.

In case of circulatory insufficiency, complex homeopathic preparations can be used:

• Traumeel in the form of tablets and ointments;
• Goal T - in the form of tablets and ointments;
• Discus compositum in the form of intramuscular injections.

The dosage of drugs is selected individually. There are practically no side effects: only occasionally does an allergic reaction to a particular drug occur - in isolated cases.

Surgery

The essence of the operation for hypoplasia of the right vertebral artery is the restoration of normal blood flow in it, which at the same time serves as the prevention of severe and life-threatening consequences.

Previously, to improve the patient's condition, surgical extra-intracranial anastomosis was performed. But such an operation was subsequently recognized as ineffective and lost its relevance.

In order to qualitatively restore blood flow, the following surgical methods are currently used:

1. Stenting is the insertion of a special “insert” into a narrowed area of ​​a vessel to prevent further narrowing. Stents can be a mini-frame-like structure, which is often additionally impregnated with medicinal solutions to prevent thrombosis and the formation of scarring in the vessel.
2. Angioplasty is the restoration of the artery to its original shape. During the operation, a mechanical effect is applied to the narrowed area (usually balloon dilatation of the vessel), which allows the previous lumen diameter to be restored.
3. A reconstructive operation is the removal of a narrowed section of a vessel with its further prosthetics. A part of the patient’s own vein, which is taken from other areas, is usually used as a prosthesis. Such an operation is performed only in the most severe cases.

Often, stenting and angioplasty are performed in combination with each other.

After surgery, patients are prescribed blood-thinning therapy and special exercises to normalize general circulation. Moderate physical activity after surgery can prevent the formation of blood clots. However, the loads should be moderate: intense exercise and heavy lifting are contraindicated during this period.

Source: ilive.com.ua

What reasons need to be dealt with?

A feature of the anatomy of the vertebral arteries is their varying degrees of risk during the process of compression (narrowing). Before ascending to the cervical spine, the left artery arises directly from the aorta, and the right artery arises directly from the subclavian artery. Therefore, the left side is more susceptible to stenosis of atherosclerotic origin. In addition, an anomaly in the structure of the first rib (additional cervical rib) often develops here.

One of the main influencing factors is a change in the bone structure of the canal formed by the transverse processes of the thoracic and cervical vertebrae. The patency of the canal is impaired when:

• degenerative-dystrophic changes associated with cervical osteochondrosis;
• intervertebral hernia;
• proliferation of osteophytes in spondylosis;
• inflammation of facet (joints between vertebrae) joints;
• vertebral injuries.

These causes are classified as vertebrogenic, associated with the spine. But there are also non-vertebral factors that should be taken into account in treatment. These include:

• atherosclerosis of one or both vertebral arteries;
• abnormal narrowing or tortuosity (congenital hypoplasia);
• increased influence of sympathetic innervation, causing spastic contractions of the vessel walls with a temporary decrease in blood flow.

How does ICD-10 differentiate syndromes by cause?

In ICD-10, compression of the vertebral artery is taken into account along with the anterior spinal artery and is included in 2 classes of diseases:

• diseases of the musculoskeletal system with code M47.0;
• lesions of the nervous system with code G99.2.

Accurate diagnosis, taking into account the development of anastomoses and anastomoses with other cervical arteries, allows you to choose treatment that is as close as possible to the source of the disease.

Main directions of treatment

Before treating vertebral artery syndrome, the patient must undergo a comprehensive examination to diagnose the type of vascular compression. The doctor receives essential information after:

• Ultrasound of head and neck vessels;
• magnetic resonance imaging;
• angiography of vertebral and other cerebral vessels.

The methods allow you to accurately determine the degree of narrowing of the arteries. If normally the diameter should be from 3.6 to 3.9 mm, then with pathology its sharp decrease is detected. Localization of the narrow area is important for the likely surgical approach.

Main treatment options:

• long-term use of medications that improve blood flow;
• course physiotherapy;
• using the possibilities of physical therapy and a special set of exercises;
• surgical intervention according to indications.

Drug therapy

In the treatment of vertebral artery syndrome, a complex of drugs is used that affect the patency of the artery and extravasal pathology.

The most important drugs are non-steroidal anti-inflammatory drugs. They cause anti-inflammatory, analgesic effects by inhibiting the migration of neutrophils to the site of inflammation, in addition, they reduce the ability of platelets to stick together and form blood clots. From the entire group, drugs are selected that are least toxic to the patient’s stomach and intestines. These include:

• Nimesulide,
• Meloxicam,
• Celecoxib,
• Aceclofenac (Aertal).

Airtal is a new drug in this series, its toxicity is 2 times less than Diclofenac.

Muscle relaxants - centrally acting drugs are used, they relieve increased tone, muscle cramps, and reduce pain. Applicable:

• Tolperisone,
• Baclofen,
• Mydocalm.

Of these drugs, Mydocalm has the greatest analgesic effect. By reducing muscle spasm, it simultaneously activates blood circulation.

For acute symptoms, drugs are prescribed intramuscularly.

Vasodilators or vasoactive drugs such as Cavinton, Trental, Instenon can improve microcirculation in ischemic neurons of the brain. They act at the level of metabolic activation and provide energy to cells by accumulating ATP. At the same time, vascular tone and the ability of the brain to regulate its own blood circulation are restored.

Medicines to activate metabolism in brain cells:

• Glycine,
• Piracetam,
• Actovegin,
• Cerebrolysin,
• Semax.

They eliminate tissue hypoxia and have antioxidant properties. Treatment courses are carried out for 3 months twice a year. If necessary, synthetic antioxidants are prescribed: vitamins A, E, C, drugs Ionol, Phenosan.

Symptomatic remedies - according to indications, sedatives and antidepressants are used. For dizziness, Betaserc is prescribed. It is not recommended for long-term use.

Physiotherapeutic methods

In the acute phase of the disease, physiotherapy helps block pain impulses along sympathetic nerve fibers. For this we use:

• diadynamic current for 5 minutes;
• ultrasound in pulsed mode;
• phonophoresis with solutions of Analgin, Anestezin;
• electrophoresis with ganglion blockers;
• d'Arsonval's currents on the head.

In the subacute stage, you can use electrophoresis with iodine, Novocaine, Euphyllin, Papaverine.

Reliable physiotherapeutic methods include: acupuncture, galvanization of the collar area. An individual mode of pulsed currents and ultrasound is also selected.

Manual therapy and massage can only be entrusted to a trained specialist.

Surgery

Surgery is prescribed for patients with ineffective conservative treatment and identified narrowing of the lumen of the vertebral artery to 2 mm or more.

In specialized departments of vertebrology and neurosurgery, surgical interventions are currently performed using endoscopic techniques. In this case, the skin incision is up to 2 cm, eliminating the risk of damage to vital organs. The technique comes down to two options:

• excision of the site of narrowing and plasticity of the vessel;
• insertion of a balloon with a stent;
• in cases of detection of a tumor or hernia, the operation should eliminate the compressive effect on the arteries as much as possible.

The effectiveness of the surgical method is up to 90%. In patients, symptoms of insufficient blood supply to the brain completely disappear.

If the narrowing of the vertebral artery is associated with osteochondrosis, then neurologists recommend wearing a Shants collar for 2.5 hours a day.

Only a semi-rigid mattress or a shield is suitable for sleeping. You should purchase a pillow at an orthopedic supply store or make your own low, hard, flat cushion. It should prevent bending in the cervical spine.

To relieve pain, you can use wool scarves, rubbing with bee and snake venom.

A home remedy - a roller massager - is convenient to use while sitting in front of the TV.

As an antioxidant therapy, patients are recommended to include fresh berries, fruit juices, prunes, sea buckthorn, cranberries, currants, chokeberries, nuts, and beans in their diet.

Physiotherapy

The areas of the hands have a reflex effect on the vessels of the neck. Therefore, the following light exercises are recommended:

• clenching your fingers into a fist and sharply spreading them out;
• circular movements in both directions in the wrist joint;
• finger massage.

To relieve heaviness and “pinching” in the neck area, any flexion and rotation movements of the arms are suitable:

• lifting and lowering;
• "mill";
• training biceps with light weight;
• “shrug” of the shoulders with lifting and lowering up and down.

While lying in bed, you can try to tense your muscles and rest the back of your head and heels on the surface of the bed. Or do this exercise while standing against a wall. While sitting, you can slowly tilt your head to the sides, back and forth.

If any symptoms of vertebral artery syndrome appear, you should undergo an examination. If it is possible to obtain good results from the use of medications, then the person lives and forgets about previously suffered ischemic manifestations.

Source: icvtormet.ru

Definition. Cerebral hyperperfusion syndrome (CHS or hyperperfusion syndrome) is a complication of revascularization interventions on the carotid arteries, manifested in the carotid region on the ipsilateral side by a significant increase in cerebral cerebral blood flow (CMB) with the development of persistent clinical and morphological signs of cerebral damage associated with impaired vascular autoregulation.

A significant increase in CMB is defined as an increase of 2 times or more compared to the initial level (usually hyperperfusion is defined as an increase in CMB by 100% or more relative to the preoperative value). However, clinical signs of SCHP may also be present in patients with a moderate increase in CMB, that is, 30 - 50% higher than the initial one (in many patients with developed intracerebral hemorrhage, an intraoperative study with 133Xe and a magnetic resonance study with contrast revealed an increase in CMB only by 20 - 44%).

Revascularization interventions on the carotid arteries that can lead to the development of SCGP are: carotid endarterectomy (CAE), stenting of the carotid (CA) and subclavian arteries, endovascular embolectomy, blood vessel replacement (which involves the cerebral circulation), angioplasty of the carotid and vertebral arteries, extra -intracranial shunting.

Due to the lack of uniform, clearly formulated diagnostic criteria for SCGP and due to different understanding by researchers of the boundary between the presence of signs of hyperperfusion (reperfusion) and the formation of SCGP, data on the prevalence of SCGP varies significantly: according to different authors, from 0.4 to 14% of cases of surgical interventions on carotid arteries.

Pathogenesis. The most important pathophysiological factor of SCGP is considered to be a violation of the autoregulation of cerebral hemodynamics due to long-term ischemia against the background of severe stenosis of the carotid arteries. Under conditions of initially impaired autoregulation, a significant increase in arterial inflow, which occurred against the background of dilatation of the microvascular bed, is no longer accompanied by the adequate response necessary for the regulation of cerebral blood flow—spasm at the level of arterioles. As a result, a zone of hyperemia is formed, which is the pathophysiological basis of hyperperfusion syndrome (CHPS).

The first peak of the increase in CMB occurs during surgery, immediately after restoration of blood flow through the internal carotid artery. This phase is short-lived and, as a rule, by the end of the operation there is a slight decrease in the CMB. It should be noted that this stabilization occurs under conditions of anesthetic protection and accompanying hemodynamic monitoring. The second peak of the increase in CMB develops in the postoperative period from the first day and lasts up to two weeks. In patients with cerebral hyperperfusion, CMB usually reaches its maximum 3 to 4 days after surgery and decreases to its initial state on the 7th day. However, the period of stabilization of autoregulation may take 6 weeks.

Arterial hypertension (AH) plays an important role in the development of SCGP. It undoubtedly increases cerebral blood flow and disrupts the autoregulatory mechanism, leading to hyperperfusion. The role of hypertension as a trigger for the development of hemorrhage has not been proven, but is present in almost all “symptomatic” patients in the postoperative period. Preoperative hypertension is the single most important determinant of the development of postoperative hypertension (including due to baroreceptor dysfunction). The presence of hypertension in the postoperative period is considered by many authors as the main factor in the development of severe, including lethal, forms of SCGP. Blood pressure instability is observed in 2/3 of patients during the first 24 hours after CE surgery. Postoperative hypertension (defined as systolic blood pressure >200 mmHg or diastolic blood pressure >100 mmHg) is reported in approximately 19–35% of patients following CE surgery.

Urgent CEA, that is, a short period of time between ischemic symptoms and endarterectomy, has also been identified as a potential risk factor for SCGP. Some scientists believe that a significant risk factor for the development of SCGP is severe bilateral damage to the carotid arteries, both on its own and in combination with hypertension and a history of adverse vascular events (transient ischemic attacks). It has been suggested that age over 72 years is a predictor of SCGP. Of great interest are the data of Russian authors on the relationship between venous blood flow and the development of cerebral hyperperfusion. It is suggested that in patients with an initially existing difficulty in venous outflow, venous congestion, arteriovenous relationships are disrupted and their imbalance develops, which leads to impaired perfusion of the organ, including the brain.

Clinic. The time period for the development of clinical manifestations of SCGP (see below) in most cases ranges from 1 to 8 days (mostly within 5 days), but symptoms can develop as early as the 1st day after revascularization. Delayed development of SCGP is considered quite rare - more than 1 week after the intervention. There is evidence of the development of SCGP 3 weeks after SSA (and even a month later). Therefore, some researchers extend the period of postoperative observation of patients to 30 days. A rare clinical case of repeated occurrence of HPS in a patient after restentation is described, and the second episode of HPS was significantly more severe, ending in bleeding into the basal ganglia and death.

In the classical sense, from a clinical point of view, SCGP is understood as the development of a symptom complex, including a triad of clinical (neurological) manifestations: headache, often unilateral, with nausea and vomiting (signs of intracerebral hypertension and cerebral edema), convulsive syndrome, as well as focal neurological symptoms (in the absence of cerebral ischemia or the development of cerebral circulatory disorders of the hemorrhagic type). These manifestations in most patients are accompanied by the development of systemic hypertension.

Three subtypes of cephalgia have been described after both CEA and SSA. Most often, in the first days after surgery, diffuse minor limited pain of a benign nature is noted, which soon goes away on its own. The second subtype is unilateral cluster-like pain, occurring with a frequency of 1 - 2 times a day in the form of attacks lasting 2 - 3 hours; usually goes away within 2 weeks. The third subtype of headache (typical of SCGP and caused by pronounced congestion of the cerebral vessels on the side of the operation) is characterized by high intensity, pulsation, localization on the side ipsilateral to the intervention, a feeling of pressure and pain in the corresponding eyeball (these signs determine the migraine-like nature of the headache), and also the lack of effect from conventional analgesic therapy. Headache is often the first symptom of hyperperfusion and is regarded by many authors as the initial sign of SCGP. The occurrence of headache is associated with arterial congestion on the affected side, and in the presence of only this symptom, SCGP is quite easily relieved.

The occurrence of a convulsive syndrome, initially local, followed by generalization, is a more serious clinical manifestation of SCGP. Epileptiform seizures most often develop within 24 hours after the intervention. Some authors associate this fact with a possible pathogenetic mechanism for the formation of electrical activity in the brain as a result of disruption of the blood-brain barrier and extravasation of albumin. This mechanism is still being studied. Some authors consider the development of generalized seizures to be a predictor of severe forms of SCGP (i.e., the development of severe neurological complications) and recommend intensive therapy for such patients. Changes in the electroencephalogram in the form of focal symptoms have diagnostic value, but do not always appear and do not appear immediately. Moreover, after relief of the convulsive syndrome, there is a tendency to decrease the bioelectrical activity of the brain. Many authors insist on the importance of dynamic EEG in such patients.

Local neurological deficits (usually cortical) resulting from SCGP may manifest in a variety of ways. More often this is weakness, motor disturbances in the limbs - hemiplegia (but usually weakness develops in the upper limbs, depending on the side of the lesion). Aphasia and hemianopsia develop less frequently. A case of SCGP with clinical manifestations in the form of neurological deficit (hemianopia, confusion) as a result of hemorrhage in the vertebrobasilar region (against the background of hypertension) after stenting of the subclavian artery is also described. Such variants of GPS are extremely rare.

Another early clinical sign of hyperperfusion is cognitive impairment, which may be associated with reversible swelling of brain tissue and may be a sign of SCGP in the absence of morphological changes in the brain. The incidence of cognitive impairment is quite high and reaches 45% in patients with asymptomatic hyperperfusion. However, structural changes are not always detected on MRI. It follows that cognitive impairment may indicate the development of hyperperfusion in the early stages. In some cases, the manifestation of SCGP can be mental disorders - psychoses, usually occurring along with headaches and cognitive impairment.

A rarer and one of the most severe clinical manifestations of SCGP is subarachnoid hemorrhage. Even less common in the literature is a description of cases of isolated subarachnoid hemorrhage in patients after revascularization interventions. Clinically, it manifests itself as a neurological deficit in the form of hemiplegia or hemiparesis, depression of sensory functions. Despite the low incidence of this complication, neuroimaging after CEA or SSA is recommended for its timely diagnosis. The incidence of the most serious clinical manifestation of SCGP - intracerebral hemorrhage after CEAE is 0.3 - 1.2%. It is characterized by the occurrence of general cerebral symptoms (impaired consciousness, depression of vital functions, decerebrate rigidity, etc.), and the progression of focal symptoms. With the development of cerebral edema and hemorrhage in the stem structures, death occurs. In some cases, hemorrhagic stroke ends in recovery. A predictor of death as a result of intracerebral hemorrhage is old age (over 75 years).

It is interesting that initially a fairly high incidence of strokes after CEA and SSA was associated exclusively with ischemic disorders and embolism. It was only in the late 1990s and early 2000s that it was established that a significant proportion of postoperative strokes are hemorrhagic in nature and occur as a result of hyperperfusion. In this case, the clinical picture is not clearly defined, which determines the importance of instrumental monitoring of SCGP.

Diagnostics. To date, there are no uniform standards for diagnosing and determining the risks of hyperperfusion. Transcranial Doppler sonography (TCD), single-photon emission computed tomography (SPECT), as well as perfusion modes of computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET) are most often used to diagnose SCGP. The easiest way to diagnose hyperperfusion in terms of efficiency, ease of use and economic feasibility is TCD, which determines the linear velocity of blood flow in the cerebral vessels. In addition, the TCD method is also applicable for predicting hyperperfusion. However, the results of such studies are quite contradictory. In recent years, information has begun to appear in the literature on the use of angiography to assess changes in intracerebral blood flow in patients during and after revascularization interventions on the carotid arteries. It is likely that angiographic determination of changes in blood flow after CE and SSA may be appropriate to identify the risk of hemorrhagic complications. Some authors argue that the use of cerebral angiography allows for more accurate detection of local hyperperfusion after revascularization compared with SPECT.

When discussing issues of timely assessment of the risk of developing SCGP, most authors agree that preoperative determination of vascular disorders, regardless of the technique used, is the optimal and even the only proven way to predict and prevent its severe forms. And yet, despite numerous attempts by researchers to predict and prevent the development of SCGP based on the identified initial vascular disorders, a clear identification of a high-risk group is still not possible. We can speak with confidence only about factors that increase risk to one degree or another, and about methods of compensating them. In general, this issue requires further study.

Prevention. In order to prevent SCHP, many researchers emphasize the role of maintaining optimal blood pressure in the pre-, intra- and postoperative periods (according to a number of researchers, at a level of 140/90 mm Hg, and in patients with risk factors for SCHP at a level of less than 120/80 mmHg.). Other methods for preventing SCGP have been proposed. One such method is the use of an intraoperative small-diameter intraluminal shunt in patients with critical bilateral stenoses or contralateral occlusion of the internal carotid artery. Another way to prevent hyperperfusion in severe carotid artery stenosis is the so-called “stepped” angioplasty, which consists of gradually, in several stages, increasing the lumen of the stenotic artery.

Treatment. The treatment of SCGP is based on therapeutic measures (including the use of antihypertensive, decongestant and anticonvulsant drugs) aimed at relieving clinical symptoms and preventing their progression. To relieve cephalgic syndrome, only opioid analgesics are recommended. [!] If hyperperfusion is detected, it is necessary to strictly control blood pressure. Further reduction of blood pressure should be carried out even in normotensive patients with hyperperfusion, since in some cases hypertension may be delayed. The prognosis for SCGP depends on the timeliness of diagnosis and the initiation of adequate therapy. With early detection and full treatment, in most situations, complete recovery is observed; in advanced cases, there is a high risk of death and (or) permanent disability.

Read more about SCGP in the following sources:

article “Cerebral hyperperfusion syndrome in patients with stenotic and occlusive lesions of the internal carotid arteries after surgical treatment. Literature review” A.V. Kokshin, A.M. Nemirovsky, V.I. Danilov; Children's Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan, Kazan; Kazan State Medical University, Kazan; Interregional Clinical Diagnostic Center of the Ministry of Health of the Republic of Tatarstan, Kazan (magazine “Neurological Bulletin” No. 4, 2018) [read];

article “Cerebral hyperperfusion syndrome” by T.V. Strelkova, A.G. Hayroyan; FSBI Scientific Center for Cardiovascular Surgery named after. A.N. Bakulev" (director - academician of the Russian Academy of Sciences and Russian Academy of Medical Sciences L.A. Bockeria) Ministry of Health of Russia, Moscow (journal "Clinical Physiology of Circulation" No. 3, 2015) [read] or [read];

article “Surgical treatment of patients with bilateral lesions of the carotid arteries” Yu.V. Belov, R.N. Komarov, P.A. Karavaykin; First Moscow State Medical University named after. THEM. Sechenov, Moscow (magazine “Cardiology and Cardiovascular Surgery” No. 5, 2014) [read]

Attention! The article is addressed to medical specialists

Kozlovsky V.I.

Vitebsk State Medical University, Belarus

Cerebral hypoperfusion in arterial hypertension.

Some aspects of medical tactics

Summary. The issues of microcirculatory disorders as the main cause of hypoperfusion and brain damage were discussed, and the need to use, along with antihypertensive therapy, drugs that improve the deformability and aggregation of erythrocytes was noted. The effectiveness of this approach was confirmed in the treatment of 554 patients with stage II arterial hypertension. In the main group (n=268), patients received antihypertensive drugs and Cavinton forte (30 mg per day), in the control group (n=286) - only antihypertensive drugs. Cavinton was prescribed in courses of 3 months with a break of 1 month. After 5 years, those receiving Cavinton forte showed a significant decrease in the number of strokes and deaths.

Keywords: cerebral hypoperfusion, arterial hypertension, treatment.

Medical news. - 2017. - No. 11. - WITH . 24-28.

Summary. The problems of microcirculatory disorders as the main cause of hypoperfusion and brain lesions were discussed, along with antihypertensive therapy, drugs improving the deformability and aggregation of erythrocytes. The effectiveness of the approach was confirmed in the treatment of 554 patients with grade II arterial hypertension. In the main group, 268 patients received antihypertensive drugs and Cavinton forte 30 mg per day, in the control group 286 patients - only antihypertensive drugs. Cavinton forte was appointed courses for 3 months with a break of 1 month. After 5 years, the patients receiving Cavinton forte had a significant decrease in the number of strokes, lethal outcomes.

Keywords: cerebral hypoperfusion, arterial hypertension, treatment.

Meditsinskie news. - 2017. - N11. - P. 24-28.

Arterial hypertension is the most its frequent and significant cause of damage to vital organs. The development of strokes, myocardial infarction, and kidney damage is accompanied by significant social losses associated with temporary and permanent disability, as well as deaths.

It should be noted that brain lesions are most often associated with a chronic decrease in blood supply, microcirculation disorders, which is accompanied by the formation of lesions of subcortical structures in the form of lacunar infarctions, leukoaraiosis, and subsequently significant brain atrophy.

Chronic cerebral ischemia or cerebral hypoperfusion is a condition that occurs due to progressive insufficiency of blood supply to the brain, leading to structural cerebral changes and the development of focal neurological disorders. In the CIS countries, the term “dyscirculatory encephalopathy” is still used to describe pathological disorders.

The main causes of the development of chronic cerebrovascular insufficiency are arterial hypertension and atherosclerosis, small emboli from the surface of atherosclerotic vessels, fibrotic valves, from dilated chambers of the heart, external compression of blood vessels, cardiac arrhythmias, vascular abnormalities, hereditary angiopathy, venous pathology, cerebral amyloidosis, diabetes mellitus. diabetes, vasculitis, blood diseases and arterial hypotension.

With ultrasound methods of studying brachiocephalic vessels and angiography of cerebral vessels, hemodynamically significant stenoses are detected only in 20-30% of patients who have suffered an ischemic stroke. In other cases, cerebral blood flow disorders are associated with disorders of the rheological properties of blood, systemic hemodynamic disorders and microembolism. In this case, the most “vulnerable” are the areas of the brain fed by small perforating arteries, in particular the deep subcortical structures. N The immediate cause of disturbances in cerebral blood flow is an increase in the aggregation of erythrocytes and platelets, the formation of leukocyte-platelet aggregates, an increase in the adhesion of leukocytes to the vascular wall, and a decrease in the deformability of erythrocytes.

In arterial hypertension, impaired blood flow in small vessels is caused not only by a decrease in the number of functioning capillaries, but also by damage to the vascular wall with desquamation of endothelial cells and the formation of microaneurysms. Ruptures of microaneurysms are accompanied by varying severity of microhemorrhages, the appearance of free hemoglobin in the perivascular zones and lead to the formation of both a local inflammatory reaction and subsequent fibrosis.

It should be noted that the erythrocyte component of microcirculation is most significant in the formation of cerebral hypoperfusion, since the state of erythrocytes mainly determines increased blood viscosity both due to their large number and due to the possibility of blocking blood flow by aggregated erythrocytes (sludge phenomenon), blockade capillary blood flow with a decrease in their deformability (flexibility). Yes, dl In order to freely pass through the capillaries (average diameter 5 microns), a red blood cell with a diameter of 7 microns must change shape and appear in the form of a “bullet”. If the red blood cell is hard, which is quite common in arterial hypertension, then it blocks capillary blood flow.

Our preliminary studies determined that with microcirculation disorders, not only damage to the endothelium occurs, but also to erythrocytes. This is due not only to the formation of fibrin threads in the vascular bed and their “dissection” of red blood cells in the flow, but also due to the destruction of their red blood cell aggregates and damage to hard red blood cells in turbulent blood flow. Intravascular hemolysis and the release of erythrocyte contents into the vascular bed is associated with a significant increase in the aggregation of both platelets and erythrocytes, an increase in the activity of lipid peroxidation, a local decrease in the production of nitric oxide, and an acute increase in blood pressure. It turned out that such markers of erythrocyte damage as blood schizocytes and the level of free hemoglobin in patients with arterial hypertension significantly correlate with an increase in the number of strokes and myocardial infarctions.

These data indicate the need to develop new approaches to the correction of microcirculation disorders in patients with arterial hypertension, aimed primarily at the erythrocyte component, preventing and reducing aggregation, increasing the deformability of erythrocytes, as well as reducing their damage in the vascular bed.

Table 1. Drugs recommended for the primary choice of treatment ( JNC-8)

Group drugs	Drugs of choice
Diuretics	hydrochlorothiazide 12.5-50 mg chlorthalidone 12.5-25 mg indapamide 1.25-2.5 mg triamterene 100 mg spironolactone 25-50 mg amiloride 5-10 mg triamterene 100 mg furosemide 20-80 mg twice daily torasemide 10-40 mg
ACE inhibitors, angiotensin II receptor blockers	ACE inhibitors: lisinopril, benazepril, fosinopril, quinapril 10-40 mg, ramipril 5-10 mg trandolapril 2-8 mg Angiotensin II receptor blockers: losartan 50-100 mg candesartan 8-32 mg valsartan 80-320 mg olmesartan 20-40 mg telmisartan 20-80 mg
Beta blockers	Metoprolol succinate 50-100 mg and tartrate 50-100 mg twice daily nebivolol 5-10 mg propranolol 40-120 mg twice daily carvedilol 6.25-25 mg twice daily bisoprolol 5-10 mg labetalol 100-300 mg twice daily
Calcium channel blockers	Dihydropyridines: amlodipine 5-10 mg nifedipine ER 30-90 mg Non-dihydropyridines: diltiazem ER 180-360 mg verapamil 80-120 mg 3 times a day or verapamil ER 240-480 mg
Vasodilators	hydralazine 25-100 mg twice daily minoxidil 5-10 mg, terazosin 1-5 mg doxasosin 1-4 mg before bedtime
Centrally acting drugs	clonidine 0.1-0.2 mg twice daily methyldopa 250-500 mg twice daily guanfacine 1-3 mg

Antihypertensive therapy for patients with arterial hypertension is one of the convincingly proven factors in reducing strokes and heart attacks (Table. 1) . However, lowering blood pressure alone is not enough to reduce the risk of developing brain damage; an integrated approach is required with correction of existing risk factors, treatment of concomitant diseases, correction of dyslipoproteinemia, and, if necessary, taking anticoagulants. In case of severe lesions of the vascular system of the brain and brachiocephalic vessels, reconstructive surgical treatment methods are necessary (Table 2).

Table 2. Basic approaches to the prevention of cerebral blood flow lesions in patients with arterial hypertension

It should be noted that the core of the clinical picture of cerebral hypoperfusion and its distinctive feature are: motor, cognitive and mental disorders. However, drugs that actively lower blood pressure do not exclude the pathological symptoms of encephalopathy; they often reduce cerebral blood flow or cause stealing syndromesvaniya. All this significantly complicates the individual choice of drug therapy in patients with arterial hypertension. This fact was highlighted by a group of experts in national guidelines for the diagnosis and treatment of arterial hypertension in the United States ( J.N.C. 8). “...The recommendations discussed in this guideline provide clinicians with an analysis of evidence based on randomized clinical trials about what is known and what is not known about blood pressure thresholds and targets and about drug treatment strategies for hypertension. . However, they should not replace clinical assessment of the situation, and decisions about treatment tactics should be made individually for each patient, taking into account his clinical characteristics and associated circumstances" ( J.N.C. 8, Section "Document Limitations").

So what possibilities exist to prevent damage to the subcortical structures of the brain fed by small perforating vessels?The available data in the literature are presented in Table 3. First of all, if there are clear symptoms of cerebral hypoperfusion, you should not use drugs that reduce cerebral blood flow, provoke pronounced orthostatic reactions, especially orthostatic hypotension, and do not prescribe medicationsdrugs that cause steal syndrome.

Table 3. How to avoid damage to the subcortical structures of the brain?

In choosing an additional drug in combination with antihypertensive drugs for the treatment of patients with arterial hypertension and cerebral hypoperfusion, it is rational to take into account its effect both on the main clinical syndromes and on the effectiveness of the effect on the rheological properties of blood and reducing damage to the endothelium, as well as erythrocytes. These provisions are briefly formulated and presented in Table 4.

Table 4. Properties that a drug should have to prevent brain damage in arterial hypertension

·?Reliably reduce the manifestations of cerebral hypoperfusion - improve cognitive disorders, reduce motor disorders

·?Reduce endothelial damage, hypertrophy of vascular smooth muscles and inflammatory processes in them

·?Reduce the damaging effects of hypoxia

·?Improve blood flow in small cerebral vessels due to: Increasing the number of functioning capillaries; Improving the rheological properties of red blood cells: reducing their aggregation (sludge) and increasing deformability; Reducing the adhesion of leukocytes to the vascular wall (neutrophils and monocytes); Absence of both systemic and local steal syndrome; Reducing the inflammatory response in blood vessels

It has been convincingly proven that the deterioration of the rheological properties of blood is determined mainly by the erythrocyte component, primarily by the aggregation and deformability of erythrocytes. Therefore, a choice of drugs is necessary, most effective in relation to this component of microcirculation.

A clear decrease in erythrocyte aggregation and an increase in their deformability, an improvement in the rheological properties of blood is observed during treatment with phosphodiesterase inhibitors, such as pentoxifylline and vinpocetine (Cavinton). These drugs also provide a fairly significant reduction in platelet aggregation and leukocyte-platelet suspension, which is associated with the accumulation of cAMP in cellular elements.

In our opinion, for the correction of cerebral hypoperfusion, the most optimal choice is between pentoxifylline and vinpocetine (Cavinton), since other drugs have little effect on erythrocyte aggregation or their deformability (Table 5).

Table 5. Selecting a drug that actively affects certain microcirculation parameters

A drug	Deformability red blood cells	Aggregation platelets	Leukocyte adhesion	Small vessel tone	Cupping inflammatory reaction in microvessels
Cinnarizine
Pentoxifylline
Xanthinol nicotinate
Vinpocetine

The advantage of using Cavinton is the selectivity of the effect on cerebral hemodynamics, the absence of steal syndrome (including coronary), and the presence of a “regulating” effect on the venous component of cerebral blood flow (Table 6).

Table 6. Comparison of the effects of vinpocetine and pentoxifylline

Index	Vinpo- cetin	Pentoxifylline
Phosphodiesterase inhibitor
Increasing the deformability of red blood cells
Systemic effect
Coronary steal
Selective effect on brain microvessels
Improving venous blood flow of cerebral vessels
Blockade of NF factor -kB and decreased transcription pro-inflammatory genes

The anti-inflammatory effects of Cavinton are associated with the blockade of the universal transcription factor (NF-kB), which controls the expression of immune response genes, apoptosis and the cell cycle. The result is a decrease in production: tumor necrosis factor -??- TNF? , interleukin - IL,macrophage inflammatory protein-2 - MIP -2, monocytic chemoattractant protein-1 - M SR-1, With vascular adhesion molecules-1 - VCAM-1, factors determining the development of the inflammatory process in the vascular wall.

In an animal experiment, convincing morphological evidence of a decrease in eye remodeling was obtained muscle tissue with long-term use of vinpocetine, reduction of damage due to carotid vein ligation in mice.

A number of fairly large studies have been conducted in the Russian Federation to prove the effectiveness of Cavinton in people with arterial hypertension and dyscirculatory encephalopathy. Thus, the CALIPSO study included 4,865 patients; Cavinton was used at the initial stage intravenously drip up to 50 mg per day, then orally at 30 mg per day for 97 days. Significant changes in the clinical picture were obtained: reduction in headaches in 82% of patients, non-systemic dizziness in 75%, tinnitus in 46%, improvement in memory in 41%, gait in 52%, mood in 68%.

The SOKOL study assessed the effectiveness of Cavinton in patients with arterial hypertension who had suffered an ischemic stroke. The main group included 344 (52%) patients; Cavinton was prescribed on days 5-14 from the onset of stroke. There were 317 (48%) people in the comparison group. The duration of observation is 102-111 days. As a result, it was noted that in patients after ischemic stroke, Cavinton reduces motor and sensory disorders by 2.3 times, speech disorders by 2.6 times, reduces complaints of memory impairment by more than 2 times, and attention disorders by 3 times. provides significantly greater independence in everyday life.

The results of complex therapy of patients with arterial hypertension were previously published II degree with short-acting drugs (adelfan, captopril, nifedipine) and Cavinton, carried out in 1980-1990. Then, against the background of 5 years of therapy, a decrease in the number of acute disorders of cerebral blood flow and deaths was obtained. The emergence of long-acting new antihypertensive drugs once again required an answer to the question of whether Cavinton could be just as successful against the backdrop of modern antihypertensive therapy.

Table 7. Characteristics of the main and control groups

Index		Main group (n=268)	Control group (n=286)
Average age, years
Average blood pressure, mm Hg. Art.	at the beginning of observation
	at the end of observation
Medications taken
Lisinopril
Hypothiazide
Perindopril
Enalapril
Indapamide
Metoprolol
Bisoprolol
Lerkamen
Amlodipine

554 patients with arterial hypertension were examined II degrees, risk 2-3. All of them were divided into main and control groups (Table 7), comparable in gender composition, average age and antihypertensive therapy (p> 0,05) . In the main group, patients received antihypertensive drugs and Cavinton Forte at a dose of 30 mg per day, and in the control group - only antihypertensive drugs. Cavinton was prescribed in courses of 3 months with a break of 1 month. The duration of observation is 5 years. Treatment results were assessed by the number of strokes, myocardial infarctions, deaths, and the number of hospitalizations associated with cardiovascular pathology (Table 8).

Table 8. Results of 5-year follow-up

Index	Main group (n=268)	Control group (n=286)
Strokes
Fatalities
Myocardial infarction*
Hospitalizations due to with cardiovascular pathology

Note: * - unreliable difference in indicators.

As a result, it was determined that patients receiving Cavinton forte experienced a significant reduction in the number of strokes and deaths. There was a significantly lower number of people requiring hospitalization due to cardiovascular pathology. In addition, there was a fairly clear trend in a decrease in the number of myocardial infarctions. In the main group, there was a highly significant reduction in the total number of adverse events (stroke, myocardial infarction, death) by 38.2% (p< 0,001 ).

The data obtained confirm the effectiveness of using Cavinton forte in combination with modern antihypertensive therapy. Moreover, first of all, a reduction in the number of strokes and deaths is achieved. It cannot be excluded that improvement of rheological properties, primarily of red blood cells, cognitive and motor functions, normalization of cerebral blood flow are unique systemic effects of Cavinton, which is manifested by a decrease in damage to the cardiovascular system, the total number of adverse events, as well as the need for hospitalization.

It is possible that the results obtained are associated with more pronounced effects of antihypertensive drugs, but this is less likely, since the mean arterial pressure, both at the beginning and at the end of treatment, did not differ significantly.

Taking into account the identified new effects associated with a decrease in the inflammatory response and endothelial damage, as well as hypertrophy of the smooth muscles of the vascular wall, it is necessary to take a fresh look at the role of Cavinton in the complex treatment of a number of pathological conditions, primarily associated with vascular pathology of the brain.

Conclusion

In recent years, new data have appeared on the effects of Cavinton, which has allowed us to take a different look at the treatment and prevention of a number of pathological conditions accompanied by cerebral hypoperfusion and, above all, arterial hypertension.

The inclusion of Cavinton in courses of 3 months in a complex of standard antihypertensive therapy for 5 years provides a significant reduction in the incidence of strokes and deaths.

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