Hypertension and atherosclerosis are among the most common in the world vascular pathologies. As a consequence of the gradual involvement of cerebral vessels in their pathological processes, the initial manifestations of insufficiency are formed cerebral circulation. It has been proven that it manifests itself if the blood flow in the brain structures decreases by 15-20%. In medicine, such manifestations are referred to as chronic cerebrovascular insufficiency.

Causes

So, the primary pathologies leading to disturbances in the blood supply to the brain are:

1. Arterial hypertension, especially if it is not constant high pressure, and its jumps from high to low numbers and vice versa, which is typical for untreated hypertension.
2. cerebral vessels.
3. Vegetative-vascular dystonia with surges in blood pressure, pathological changes in vascular tone.

At the pathophysiological level, the following changes, which lead to primary pathologies, contribute to the formation of insufficiency of cerebral blood flow:

1. Pathological changes in the regulation of vascular wall tone.
2. Changes in the lumen of blood vessels for any reason (blockage by a thrombus, occlusion by an atherosclerotic plaque). This leads to both insufficient oxygen supply to the brain structures and to stagnation of blood in the veins of the brain, venous insufficiency of cerebral circulation.
3. Changes in the physical characteristics of the blood composition (its thickening, accumulation and formation of clots from cellular elements of the blood).
4. Disturbance of metabolic processes in brain structures.

The following factors provoke the formation of circulatory disorders:

• age from 40 years;
• alcohol, smoking;
• excess weight;
• diabetes;
• heredity, sedentary lifestyle life.

Symptoms of cerebrovascular insufficiency

Symptoms of cerebrovascular insufficiency are as follows:

1. . They can have different characteristics: from mild to intense. Patients, as a rule, do not identify a clear location for pain. In this case, there is no relationship with high blood pressure. However, their dependence on physical and mental stress, strong emotions, fatigue, and changes in body position can be traced.
2. Dizziness. This symptom is usually observed when changing body position or sudden movements.
3. Noise in the head. It manifests itself periodically or is present to varying degrees constantly. The sensation of noise in the head appears as a consequence of pathological blood flow through the disturbed lumens of the brain vessels, which are localized close to the auditory labyrinth.
4. Pathological changes in memory. Memory, which retains information about professional experience and skills, is practically not impaired. Memories of events from past life are also saved. Only the memorability of real, current phenomena and events suffers.
5. Decreased performance.

Important! There may be a decrease in the ability to concentrate. There are also some less pronounced pathological changes emotionally mental sphere, irritability, nervousness. But there are no mental changes difficult character. Relatively preserved high level functioning of central nervous activity.

Diagnostics

Primary manifestations of cerebrovascular insufficiency are diagnosed with the proven presence of a primary disease and one of five signs (headache, dizziness, memory impairment, fatigue). Provided that these symptoms are repeated weekly for three months.

In addition, it must be proven that there is no history of traumatic brain injury, brain tumors, acute brain failure in the form of strokes, or infectious pathologies of the brain that can give similar symptoms. Therefore, examination and conversation with the patient is very important.

Hardware and laboratory methods studies may show not very large deviations from the norm. Especially in the early stages of cerebral blood flow disorders. Used for diagnostics:

• rheoencephalography;
• Dopplerography of cerebral vessels;
• laboratory tests (biochemical blood test, blood coagulation parameters);
• examination of the fundus by an ophthalmologist;
• CT and MRI of the brain.

Treatment

The leading directions in the treatment of initial cerebrovascular accident are as follows:

1. Therapy and compensation of primary pathology (monitoring and correction of blood pressure, treatment of VSD, anti-atherosclerotic therapy).
2. Normalization of the daily routine, including time for work and rest.
3. Incorporating moderate physical activity into a sedentary life.
4. Cerebropreventive drugs.
5. Increasing stress resistance, psychotherapy.
6. Sanatorium holiday.

Complications

Complications of initial disturbances of cerebral blood flow are very serious: acute failure cerebral circulation from transistor ischemic attack to hemorrhagic or ischemic stroke.

It is customary to distinguish the initial manifestations of cerebrovascular accident as an early stage of CNM and DE (dyscirculatory encephalopathy) - multifocal brain damage caused by chronic circulatory failure.

In turn, the following forms of DE are distinguished:

• atherosclerotic;
• hypertensive;
• venous;
• mixed.

Causes and pathogenesis of CNM

As a rule, chronic cerebrovascular accident is a consequence of cardiovascular pathology. Typically, CNM develops against the background of:

• vegetative-vascular dystonia;
• atherosclerosis, hypertension;
• diabetes;
• heart diseases of various etiologies;
• vasculitis;
• blood diseases accompanied by a violation of its rheological properties.

These pathologies change general and cerebral hemodynamics and lead to a decrease in cerebral perfusion (less than 45-30 ml/100 g per minute). The most important factors involved in the pathogenesis of CNM include:

• changes in the extra- and intracranial sections of the vessels of the head;
• insufficiency of collateral circulation;
• violation of autoregulation of blood circulation;
• violation of rheology.

Obesity, physical inactivity, alcohol abuse and smoking play a significant role in the progression of CNM.

Symptoms of chronic cerebrovascular accident

In the early stages of CNM, the picture is characterized by patient complaints of a feeling of heaviness in the head, mild dizziness, instability when walking, noise in the head, fatigue, decreased attention and memory, and sleep disturbance. Initial manifestations of circulatory failure occur after psychoemotional and/or physical stress, against the background of alcohol consumption, and under unfavorable meteorological conditions. Patients show signs of vegetative-vascular and emotional lability, some slowness of thinking processes, and possible convergence insufficiency. The progression of the initial manifestations of circulatory failure leads to the formation of the next stage - DE.

Depending on the severity of manifestations, three stages of chronic cerebrovascular accident are distinguished. In stage I, symptoms are mild, patients usually remain able to work; in stage II the symptoms are moderate, and in stage III patients become disabled.

With atherosclerotic encephalopathy, i.e. with DE caused by atherosclerotic damage to the vessels supplying blood to the brain, in stage I there is a decrease in attention and memory, especially for current events, it is difficult to memorize new information, and it is difficult for the patient to switch from one activity to another. At the same time, mild cognitive impairment, as a rule, is compensated by preserved everyday and professional skills, as well as intellectual capabilities. Patients often complain of increased fatigue and decreased performance; emotional lability with a decrease in psycho-emotional background is often observed. Diffuse noise in the head is noted. Patient complaints of instability when walking are typical. The neurological status reveals minor scattered symptoms in the form of moderate signs pseudobulbar syndrome, tendon hyperreflexia and anisoreflexia, as well as postural instability.

In stage II, clinical manifestations progress, cognitive impairment increases, performance decreases, patients become touchy and irritable. A narrowing of interests is noted, and memory disorders increase. Dull headaches, dizziness, and unsteadiness when walking are often present. Neurological status reveals anisoreflexia, pseudobulbar symptoms, vestibulo-cerebellar disorders and subcortical symptoms.

In stage III, further worsening of neurological manifestations is noted. Patients exhibit significant diffuse neurological symptoms in the form of an increase in pyramidal insufficiency, pseudobulbar disorders, cerebellar and extrapyramidal symptoms, as well as impaired control of the pelvic organs. Epileptic seizures are possible. Stage III is characterized by pronounced disturbances of higher mental functions: significant cognitive impairment to dementia, the likely development of apatoabulic syndrome, pronounced emotional and personal changes. In later stages, patients lose self-care skills. Drowsiness after eating, Windscheid's triad, are typical for atherosclerotic encephalopathy. In stage III, Hackebusch's disease, or pseudo-Alzheimer's form of atherosclerosis, can be observed - a symptom complex, the main manifestation of which is dementia. At the same time, they note a decrease in memory, confabulation, a pronounced narrowing of the range of interests, uncriticality, speech disorders, gnosis and praxis. In addition, in the late stage of atherosclerotic encephalopathy, the formation of Demaget-Oppenheim syndrome, which is characterized by gradually developing central tetraparesis, is possible.

Chronic hypertensive encephalopathy is a form of DE caused by arterial hypertension. Arterial hypertension leads to diffuse damage to brain tissue; the disease progresses quite quickly with significant fluctuations in blood pressure and repeated hypertensive crises. The disease can manifest itself in quite at a young age, on average 30-50 years. In the initial stages, the clinical picture of hypertensive encephalopathy is characterized by sufficient dynamics and reversibility of symptoms. Characterized by a neurosis-like syndrome, frequent headaches, predominantly in the occipital region, and noise in the head. In the future, signs of bilateral pyramidal insufficiency, elements of akinetic-rigid syndrome, tremor, emotional-volitional disorders, decreased attention and memory, and slow mental reactions may appear. As it progresses, personality disorders arise, the range of interests narrows, speech intelligibility is impaired, anxiety increases, and weakness is noted. Patients are characterized by disinhibition.

In stage III hypertensive encephalopathy, patients, as a rule, develop severe atherosclerosis; the condition is characterized by features typical of atherosclerotic encephalopathy - developing dementia. At an advanced stage, patients lose the ability to self-care, control pelvic functions, and signs of apatho-abulic or paranoid syndromes may appear.

A variant of hypertensive encephalopathy in combination with atherosclerotic brain damage is Binswanger encephalopathy (progressive vascular leukoencephalopathy). It usually manifests itself at the age of 50 years and is characterized by memory loss, cognitive impairment, and motor impairment in chronic cerebrovascular accident of the subcortical type. Sometimes there are epileptic seizures. As a rule, encephalopathy in chronic cerebrovascular accident develops gradually, although stepwise progression associated with vascular crises, blood pressure fluctuations and cardiac disorders is also possible.

Venous DE is characterized by venous congestion in the skull, chronic hypoxia and intracranial hypertension. Venous DE more often develops in patients with cardiopulmonary diseases, as well as with arterial hypotension.

Diagnostic procedures for CNM include collecting anamnesis, taking into account information about somatic pathology (especially cardiovascular diseases), analysis of patient complaints, neurological, neuropsychological examination. Instrumental examination involves Doppler ultrasound (USDG), rheoencephalography, CT) or MRI, ophthalmoscopy and angiography. As a rule, an examination of the heart is necessary (electrocardiography - ECG, echocardiography), as well as a study of the rheological properties of blood.

Treatment of chronic cerebrovascular accident

Arterial hypertension is one of the the most important factors risk of CNM, however, episodes of hypotension are also unfavorable for patients with DE. During the correction process, it is advisable to maintain blood pressure at a stable level, slightly higher than the “optimal” indicators: 140-150 mm Hg. Medications for chronic cerebrovascular accidents should be selected taking into account the characteristics of the patient and his reaction to prescribed medications. For the treatment of arterial hypertension, angiotensin-converting enzyme inhibitors are used - ACE (captopril, perindopril, enalapril, enalaprilat), angiotensin II receptor antagonists (candesartan, eprosartan), β-blockers (in particular, atenolol, labetalol, metoprolol, propranolol, esmolol), agonists central α-adrenergic receptors (clonidine), slow blockers calcium channels(nifedipine). Diuretics as antihypertensive therapy used only when indicated (for example, heart failure, ineffectiveness of other antihypertensive drugs) due to a possible deterioration in blood rheology.

Forecast

Typically, chronic cerebrovascular accident is characterized by a slowly progressive course, although stepwise progression is possible (usually after vascular crises). In stage I, the ability to work and everyday adaptation of patients is preserved in most cases; in stage II, there is a slight or moderate decrease in working capacity; in stage III, patients are disabled and often incapable of self-care.

Transient cerebrovascular accident (TCI)- short-term acute cerebral ischemia, accompanied by transient cerebral and focal symptoms that completely disappear within no more than 24 hours from the onset of the attack. Clinical manifestations are varied, depending on the type and topic of PNMK. Diagnosis is carried out retrospectively and includes neurological, ophthalmological and cardiological examination, cerebral blood flow examination (USDG, duplex scanning, MRA), radiography and CT scan of the spine. Treatment of PNMK is aimed at normalizing cerebral blood supply and metabolism, preventing relapses and preventing the occurrence of stroke. When hemodynamically significant occlusion large arteries can undergo surgical treatment performed by angiosurgeons.

General information

Transient cerebrovascular accident has an etiology and development mechanisms similar to ischemic stroke. Distinctive feature is its short duration (lasting no more than a day) and the transient nature of all emerging symptoms. It is generally accepted in world and domestic neurology that cases where clinical manifestations of acute cerebrovascular accident (ACVA) persist for more than 24 hours are usually regarded as a stroke.

Transient disorders of cerebral circulation include transient ischemic attack (TIA) and cerebral variant of hypertensive crisis. PNMK is one of the most common forms of cerebral circulatory disorders. However, it is difficult to obtain reliable statistical data on the structure of the incidence of PNMC, since, on the one hand, many patients do not seek medical care in a timely manner, and on the other hand, it is difficult for doctors to diagnose the fact of PNMC based only on medical history.

Etiology and pathogenesis

PNMK is based on a decrease in blood flow through the arteries supplying blood to the brain. There are many factors leading to such dyscirculatory changes. In first place among them are atherosclerosis and hypertension. Etiofactors also include diabetes mellitus, infectious-allergic and systemic vasculitis (Kawasaki disease, periarteritis nodosa, Wegener's granulomatosis), and vascular lesions due to collagenosis. Congenital malformations of blood vessels - pathological tortuosity, hypoplasia - play a certain role.

The main pathogenetic mechanism for the occurrence of PNMC in this case is arterio-arterial embolism. Emboli are particles of a parietal thrombus formed in the lumen of a pathologically altered vessel, or a disintegrating atherosclerotic plaque. The source of emboli can be blood clots that form in the cavities of the heart due to acquired or congenital defects, myxoma, post-infarction aneurysm. An embolus formed in a large artery travels through the bloodstream to the terminal branches cerebral vessels, leading to their occlusion and a sharp decrease in blood supply to the corresponding part of the brain.

Transient cerebrovascular accident can occur repeatedly with carotid artery occlusion. The etiofactors of hypertensive cerebral crisis are spasm of the cerebral arteries and venous deposition of blood. PNMK in the vertebrobasilar region occurs when the vertebral artery is compressed due to instability of the cervical spine, osteochondrosis, cervical spondylosis, or spinal trauma. In some cases, the cause of PNMK is compensatory arterial spasm, which develops during severe arterial hypotension, for example, during acute blood loss, myocardial infarction, and severe arrhythmias. With occlusion of the subclavian artery, the development of PNMK is possible through the “stealing” mechanism, when the collateral blood supply to the arm comes from the vertebrobasilar basin to the detriment of cerebral blood flow.

The main pathogenetic point that ensures the short duration of cerebral ischemia in PNMC is a well-developed collateral circulation system. Thanks to it, during arterial occlusion, blood flow is quickly redistributed along alternative bypass paths in such a way that it ensures sufficient blood supply to the ischemic area and full recovery its functions within 1 day from the moment of occlusion. If this does not happen, irreversible changes occur in the ischemic cerebral cells, leading to more permanent neurological impairment and classified as ischemic stroke.

Symptoms of PNMK

Typically sudden and acute development. General cerebral symptoms of PNMK include headache, weakness, nausea (maybe vomiting), blurred vision, vegetative-vascular reactions (hot flashes, trembling, sweating, etc.), short-term disturbances of consciousness. Focal symptoms depend entirely on the topic of the ischemic process. On average, PNMK lasts from several minutes to several hours. Pathognomonic is the complete restoration of impaired neurological functions within 24 hours.

PNMK in the ICA system (internal carotid artery) is characterized by variable zones of hypoesthesia and/or paresthesia, covering individual areas of the skin of the extremities or face on the side opposite (heterolateral) to the ischemic focus. May be observed central paresis, spreading to local muscle groups or one limb. Less common are hemihypesthesia and hemiparesis. Muscle strength is usually moderately reduced. Anisoreflexia is typical, sometimes pathological Rossolimo and Babinsky reflexes are present. Aphasia or dysarthria is often noted. There may be a decrease in visual acuity in one eye, the appearance of paroxysm of Jacksonian epilepsy, in in some cases turning into a generalized epileptic attack.

PNMK in the vertebrobasilar basin manifests itself as systemic dizziness with tinnitus, autonomic disorders, vestibular ataxia (discoordination of movements, unsteadiness of gait, instability in the Romberg position, etc.), visual disturbances in the form of metamorphopsia, photopsia, loss of visual fields. Horizontal nystagmus is noted. Dysarthria, dysphonia, diplopia, dysphagia, and the occurrence of alternating syndromes are possible. PNMK in the vertebrobasilar area is usually accompanied by a headache in the back of the head, the intensity of which is associated with head movements.

A transient disorder of cerebral circulation in the brain stem area is manifested by systemic dizziness, paresis of the extraocular muscles, hearing loss, and double vision. Transient disturbances in swallowing and articulation, hemianopsia, and local hypoesthesia of the facial skin may appear. With PNMK in the region of the medulla oblongata ( reticular formation, lower olives) are marked by the so-called. drop attacks - transient paroxysms of immobility as a result of a sharp muscle weakness. With PNMK in the medial parts of the temporal lobe, short-term Korsakov's syndrome is observed - loss of orientation in the environment and time, combined with a memory disorder about current events.

It should be noted that simultaneous stenosis of several arteries of the head is possible, leading to transient ischemia in several vascular territories. In such cases, the clinical picture of PNMK combines symptoms of damage to all cerebral areas involved in the ischemic process.

Diagnostics of PNMK

IN in rare cases patients are examined by a neurologist directly during PNMK. More often, patients who have undergone PNMK at home come for a consultation with a neurologist, and the ischemic episode can be recorded by a local therapist or emergency physician. Some patients do not even know about the stroke they suffered, but with detailed questioning it is possible to identify the presence of similar attacks in the past. A history of PNMK has important in choosing further tactics for patient management.

The neurological status after undergoing PNMJ usually does not reveal significant deviations. Appointment required additional examinations- consultation with an ophthalmologist with perimetry and ophthalmoscopy; coagulograms, determination of blood sugar, cholesterol and lipids; REG, duplex scanning or ultrasound of head and neck vessels, MRI of the brain, MR angiography. As a rule, examinations record signs of chronic cerebral ischemia and dyscirculatory encephalopathy; it is possible to identify occlusion of the carotid or vertebral arteries.

The study of the vertebral arteries is carried out using REG and USDG with functional tests (for example, with turns and tilts of the head), supplemented by radiography of the spine in the cervical region or CT of the spine. When diagnosing thrombosis of the great vessels supplying the brain, consultation with a vascular surgeon is recommended to decide on the advisability of surgical treatment. In the presence of cardiovascular diseases, a consultation with a cardiologist, ECG, 24-hour blood pressure monitoring, and ultrasound of the heart are carried out.

Treatment of PNMK

In mild cases, when PNMK lasts no more than an hour, therapy is carried out in an outpatient setting. For more severe manifestations or repeated PNMK, treatment in a neurological hospital is indicated. The main goals in the treatment of PNMK are to improve cerebral circulation and restore adequate metabolism of cerebral tissues.

Medications that improve blood rheological parameters (pentoxifylline, dextran) are prescribed. For the course of treatment, 3-5 daily intravenous drips are recommended. Then long-term use of acetylsalicylic acid is prescribed. Bromcamphor is recommended for patients with PNMK who have contraindications to taking salicylates (for example, in the presence of gastric ulcer). Among neurometabolites, piracetam, porcine cerebral hydralysate, gamma-aminobutyric acid, and vitamins are widely used. IN.

Normalization of blood pressure numbers is important. For this purpose, intravenous or intramuscular administration of dibazole, papaverine, intramuscular administration of magnesium sulfate, drotaverine is carried out. For systemic dizziness and severe vegetative symptoms, belladonna alkaloids, phenobarbital, belladonna extract, diazepam are prescribed, and, if indicated, chlorpromazine. Sedative therapy with valerian, trioxazine, tazepam or elenium is recommended for 1-2 weeks after PNMK.

Diagnosed stenosis of the carotid artery exceeding 70% of its lumen is an indication for surgical treatment. The most suitable choice is made individually surgical tactics- eversion or classic carotid endarterectomy, stenting, prosthetics, carotid-subclavian bypass. Also, according to indications, stenting or prosthetics of the vertebral artery is performed.

Forecast and prevention of PNMK

In terms of complete elimination of the resulting neurological deficit, PNMK has a favorable prognosis. The repeatability typical for PNMK is unfavorable. The frequency of relapses can reach several times a year. Each subsequent episode of PNM increases the likelihood of developing an ischemic stroke. The most favorable prognosis is for PNMK in the area of ​​the internal auditory artery. When disorders are localized in the carotid region, the prognosis is worse than with PMNK of the vertebrobasilar region. Typically, such patients have a stroke within 1 year.

The basis for the prevention of PNMK is healthy image life, excluding factors that adversely affect the condition of blood vessels - smoking, drinking large doses of alcohol, excessive consumption of animal fats. TO preventive measures includes control of blood pressure, blood sugar levels, lipid spectrum; adequate treatment of arterial hypertension, diabetes, vascular diseases. Secondary prevention PNMK consists of regular observation by a neurologist with repeated courses of vascular therapy.

Catad_tema Chronic cerebral ischemia - articles

Chronic cerebrovascular insufficiency

NEUROLOGY

NATIONAL GUIDELINES

This brochure contains a section on chnonic cerebrovascular insufficiency (authors V.I. Skvortsova, L.V. Stakhovskaya, V.V. Gudkova, A.V. Alekhin) from the book “Neurology. National leadership" ed. E.I. Guseva, A.N. Konovalova, V.I. Skvortsova, A.B. Gekht (M.: GEOTAR-Media, 2010)

Chronic cerebral circulatory insufficiency is a slowly progressive brain dysfunction resulting from diffuse and/or small-focal damage to brain tissue in conditions of long-term insufficiency of cerebral blood supply.

Synonyms: discirculatory encephalopathy, chronic cerebral ischemia, slowly progressive cerebrovascular accident, chronic ischemic brain disease, cerebrovascular insufficiency, vascular encephalopathy, atherosclerotic encephalopathy, hypertensive encephalopathy, atherosclerotic angioencephalopathy, vascular (atherosclerotic) parkin sonism, vascular (late) epilepsy , vascular dementia.

The most widely used of the above synonyms in domestic neurological practice The term “dyscirculatory encephalopathy” was introduced, which retains its meaning to this day.

Codes according to ICD-10. Cerebrovascular diseases are coded according to ICD-10 in categories I60-I69. The concept of “chronic cerebrovascular insufficiency” is absent in ICD-10. Discirculatory encephalopathy (chronic cerebral circulatory failure) can be coded in rubric I67. Other cerebrovascular diseases: I67.3. Progressive vascular leukoencephalopathy (Binswanger's disease) and I67.8. Other specified cerebrovascular diseases, subsection “Cerebral ischemia (chronic)”. The remaining codes from this section reflect either only the presence of vascular pathology without clinical manifestations(vessel aneurysm without rupture, cerebral atherosclerosis, Moyamoya disease, etc.), or the development acute pathology(hypertensive encephalopathy).

An additional code (F01*) can also be used to indicate the presence of vascular dementia.

Rubrics I65-I66 (according to ICD-10) “Occlusions or stenosis of precerebral (cerebral) arteries that do not lead to cerebral infarction” are used to code patients with asymptomatic this pathology.

EPIDEMIOLOGY

Due to the noted difficulties and discrepancies in the definition of chronic cerebral ischemia, the ambiguity in the interpretation of complaints, the nonspecificity of both clinical manifestations and changes detected by MRI, there are no adequate data on the prevalence chronic failure cerebral circulation.

To some extent, it is possible to judge the frequency of chronic forms of cerebrovascular diseases based on epidemiological indicators of the prevalence of stroke, since acute cerebrovascular accident, as a rule, develops against a background prepared by chronic ischemia, and this process continues to increase in the post-stroke period. In Russia, 400,000-450,000 strokes are recorded annually, in Moscow - more than 40,000 (Boiko A.N. et al., 2004). At the same time, O.S. Levin (2006), emphasizing the special significance of cognitive disorders in the diagnosis of dyscirculatory encephalopathy, suggests focusing on the prevalence of cognitive dysfunctions, assessing the frequency of chronic cerebrovascular insufficiency. However, these data do not reveal the true picture, since only vascular dementia is recorded (5-22% among the elderly population), without taking into account pre-dementia conditions.

PREVENTION

Due to common risk factors for the development of acute and chronic cerebral ischemia, preventive recommendations and measures do not differ from those reflected in the section “Ischemic stroke” (see above).

SCREENING

To identify chronic cerebrovascular insufficiency, it is advisable to carry out, if not a mass screening examination, then at least an examination of individuals with major risk factors (arterial hypertension, atherosclerosis, diabetes mellitus, heart and peripheral vascular diseases). Screening examination should include auscultation of the carotid arteries, ultrasound examinations main arteries of the head, neuroimaging (MRI) and neuropsychological testing. It is believed that chronic cerebral circulatory failure is present in 80% of patients with stenotic lesions of the main arteries of the head, and stenoses are often asymptomatic up to a certain point, but they are capable of causing hemodynamic restructuring of the arteries in the area located distal to the atherosclerotic stenoses (echeloned atherosclerotic brain damage), leading to the progression of cerebrovascular pathology.

ETIOLOGY

The causes of both acute and chronic cerebrovascular accidents are the same. Among the main etiological factors atherosclerosis and arterial hypertension are considered, and a combination of these 2 conditions is often identified. Other diseases can also lead to chronic cerebrovascular insufficiency of cardio-vascular system, especially accompanied by signs of chronic heart failure, heart rhythm disturbances (both permanent and paroxysmal forms of arrhythmia), often leading to a drop in systemic hemodynamics. Anomalies in the vessels of the brain, neck, shoulder girdle, and aorta, especially its arch, are also important, which may not appear until an atherosclerotic, hypertensive, or other acquired process develops in these vessels. A major role in the development of chronic cerebrovascular insufficiency in Lately attributed to venous pathology, not only intra-, but also extracranial. Compression of blood vessels, both arterial and venous, can play a certain role in the formation of chronic cerebral ischemia. One should take into account not only the spondylogenic effect, but also compression by altered neighboring structures (muscles, fascia, tumors, aneurysms). Low blood pressure has an adverse effect on cerebral blood flow, especially in older people. This group of patients may develop damage to the small arteries of the head associated with senile arteriosclerosis.

Another cause of chronic cerebral circulatory failure in elderly patients is cerebral amyloidosis - deposition of amyloid in the blood vessels of the brain, leading to degenerative changes the walls of blood vessels with possible rupture.

Very often, chronic cerebral circulatory insufficiency is detected in patients with diabetes mellitus; they develop not only micro-, but macroangiopathies of various localizations. Other pathological processes can also lead to chronic cerebral vascular insufficiency: rheumatism and other diseases from the group of collagenoses, specific and nonspecific vasculitis, blood diseases, etc. However, in ICD-10 these conditions are quite rightly classified under the headings of the specified nosological forms, which determines the correct treatment tactics.

As a rule, clinically detectable encephalopathy is of mixed etiology. In the presence of the main factors for the development of chronic cerebrovascular insufficiency, the rest of the variety of causes of this pathology can be interpreted as additional reasons. Identification of additional factors that significantly aggravate the course of chronic cerebral ischemia is necessary to develop the correct concept of etiopathogenetic and symptomatic treatment.

Causes of chronic cerebrovascular insufficiency

Basic:

Atherosclerosis;

Arterial hypertension. Additional:

Heart disease with signs of chronic circulatory failure;

Heart rhythm disturbances;

Vascular anomalies, hereditary angiopathy;

Venous pathology;

Vascular compression;

Arterial hypotension;

Cerebral amyloidosis;

Diabetes;

Vasculitis;

Blood diseases.

PATHOGENESIS

The above diseases and pathological conditions lead to the development of chronic brain hypoperfusion, that is, to a long-term lack of supply by the brain of the main metabolic substrates (oxygen and glucose) delivered by the blood flow. With the slow progression of brain dysfunction developing in patients with chronic cerebrovascular insufficiency, pathological processes unfold primarily at the level of small cerebral arteries(cerebral microangiopathy). Extensive small artery disease causes diffuse bilateral ischemic damage, mainly white matter, and multiple lacunar infarctions in the deep parts of the brain. This leads to disruption of normal brain function and the development of nonspecific clinical manifestations - encephalopathy.

For adequate brain function, a high level of blood supply is required. The brain, whose mass is 2.0-2.5% of body weight, consumes 20% of the blood circulating in the body. The amount of cerebral blood flow in the hemispheres averages 50 ml per 100 g/min, but in the gray matter it is 3-4 times higher than in the white matter, and there is also relative physiological hyperperfusion in the anterior parts of the brain. With age, the amount of cerebral blood flow decreases, and frontal hyperperfusion also disappears, which plays a role in the development and increase of chronic cerebral circulatory failure. Under resting conditions, the brain's oxygen consumption is 4 ml per 100 g/min, which corresponds to 20% of the total oxygen entering the body. Glucose consumption is 30 µmol per 100 g/min.

In the vascular system of the brain there are 3 structural and functional levels:

The main arteries of the head are carotid and vertebral, carrying blood to the brain and regulating the volume of cerebral blood flow;

Superficial and perforating arteries of the brain, which distribute blood to various regions of the brain;

Vessels of the microcirculatory bed, providing metabolic processes.

In atherosclerosis, changes initially develop mainly in the main arteries of the head and arteries of the surface of the brain. In arterial hypertension, the perforating intracerebral arteries that supply the deep parts of the brain are primarily affected. Over time, in both diseases, the process spreads to the distal parts of the arterial system and secondary restructuring of the microvasculature occurs. Clinical manifestations of chronic cerebral circulatory failure, reflecting angioencephalopathy, develop when the process is localized mainly at the level of the microvasculature and in small perforating arteries. In this regard, a measure to prevent the development of chronic cerebrovascular insufficiency and its progression is adequate treatment of the underlying underlying disease or diseases.

Cerebral blood flow depends on perfusion pressure (the difference between systemic blood pressure and venous pressure at the level of the subarachnoid space) and cerebral vascular resistance. Normally, thanks to the autoregulation mechanism, cerebral blood flow remains stable, despite blood pressure fluctuations from 60 to 160 mmHg. When cerebral vessels are damaged (lipohyalinosis with the development of unresponsiveness of the vascular wall), cerebral blood flow becomes more dependent on systemic hemodynamics.

With long-term arterial hypertension, a shift in the upper limit of systolic pressure is noted, at which cerebral blood flow still remains stable and autoregulation disorders do not occur for quite a long time. Adequate brain perfusion is maintained by an increase in vascular resistance, which in turn leads to an increase in the load on the heart. It is assumed that an adequate level of cerebral blood flow is possible until pronounced changes in small intracerebral vessels occur with the formation of a lacunar state characteristic of arterial hypertension. Therefore, there is a certain margin of time when timely treatment arterial hypertension can prevent the formation irreversible changes in the vessels and brain or reduce their severity. If the basis of chronic cerebrovascular insufficiency is only arterial hypertension, then the use of the term “hypertensive encephalopathy” is legitimate. Severe hypertensive crises are always a breakdown of autoregulation with the development of acute hypertensive encephalopathy, which each time aggravates the phenomena of chronic cerebral circulatory failure.

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

Numerous studies have shown that hemodynamically significant stenoses develop when the lumen of the main arteries of the head narrows by 70-75%. But cerebral blood flow depends not only on the severity of stenosis, but also on the state of collateral circulation and the ability of cerebral vessels to change their diameter. These hemodynamic reserves of the brain allow asymptomatic stenoses to exist without clinical manifestations. However, even with hemodynamically insignificant stenosis, chronic cerebral circulatory failure will almost certainly develop. The atherosclerotic process in the vessels of the brain is characterized not only by local changes in the form of plaques, but also by hemodynamic restructuring of the arteries in an area localized distal to the stenosis or occlusion.

Great importance also has a plaque structure. So-called unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents, most often in the form of transient ischemic attacks. Hemorrhage into such a plaque is accompanied by a rapid increase in its volume with an increase in the degree of stenosis and worsening signs of chronic cerebral circulatory failure.

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

In recent years, 2 main pathogenetic variants of chronic cerebrovascular insufficiency have been considered. They are based on morphological characteristics - the nature of the damage and preferential localization. With diffuse bilateral damage to the white matter, leukoencephalopathic, or subcortical Biswanger, variant of discirculatory encephalopathy is distinguished. The second is the lacunar variant with the presence of multiple lacunar foci. However, in practice, mixed options are often encountered. Against the background of diffuse damage to the white matter, multiple small infarcts and cysts are found, in the development of which, in addition to ischemia, repeated episodes of cerebral hypertensive crises. In hypertensive angioencephalopathy, lacunae are located in the white matter of the frontal and parietal lobes, putamen, pons, thalamus, and caudate nucleus.

The lacunar variant is most often caused by direct occlusion of small vessels. In the pathogenesis of diffuse damage to the white matter, the leading role is played by repeated episodes of a drop in systemic hemodynamics - arterial hypotension. The cause of a drop in blood pressure may be inadequate antihypertensive therapy, a decrease cardiac output, for example, with paroxysmal heart rhythm disturbances. Persistent cough, surgical interventions, and orthostatic arterial hypotension due to autonomic-vascular insufficiency are also important. Moreover, even a slight decrease in blood pressure can lead to ischemia in the end zones of the adjacent blood supply. These zones are often clinically “silent” even with the development of infarctions, which leads to the formation of a multi-infarction state.

Under conditions of chronic hypoperfusion - the main pathogenetic link of chronic cerebral circulatory failure - compensation mechanisms can be depleted, the energy supply to the brain becomes insufficient, as a result, functional disorders first 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 (energy hunger), oxidative stress, a shift in glucose metabolism towards anaerobic glycolysis, lactic acidosis, hyperosmolarity, capillary stasis, a tendency to thrombus formation, depolarization are detected. cell membranes, activation of microglia, which begins to synthesize neurotoxins, which, along with other pathophysiological processes, leads to cell death. In patients with cerebral microangiopathy, granular atrophy of the cortical parts is often detected.

Multifocal pathological condition of the brain with predominant defeat deep sections leads to disruption of connections between cortical and subcortical structures and the formation of so-called disconnection syndromes.

A decrease in cerebral blood flow is obligately combined with hypoxia and leads to the development of energy deficiency and oxidative stress - a universal pathological process, one of the main mechanisms of cell damage during cerebral ischemia. The development of oxidative stress is possible under conditions of both oxygen deficiency and excess. Ischemia has a damaging effect on the antioxidant system, leading to a pathological pathway of oxygen utilization - the formation of active forms as a result of the development of cytotoxic (bioenergetic) hypoxia. The free radicals released mediate cell membrane damage and mitochondrial dysfunction.

Acute and chronic forms of ischemic cerebrovascular accident can transform into one another. Ischemic stroke, as a rule, develops against an already changed background. Patients are diagnosed with morphofunctional, histochemical, and immunological changes caused by a previous discirculatory process (mainly atherosclerotic or hypertensive angioencephalopathy), the symptoms of which increase significantly in the post-stroke period. The acute ischemic process, in turn, triggers a cascade of reactions, some of which are completed in the acute period, and some persist indefinitely and contribute to the emergence of new pathological conditions, leading to an increase in signs of chronic cerebral circulatory failure.

Pathophysiological processes in the post-stroke period are manifested by further damage to the blood-brain barrier, microcirculatory disorders, changes in immunoreactivity, depletion of the antioxidant defense system, progression of endothelial dysfunction, depletion of anticoagulant reserves of the vascular wall, secondary metabolic disorders, and disruption of compensatory mechanisms. Cystic and cystic-gliotic transformation of damaged areas of the brain occurs, separating them from morphologically undamaged tissues. However, at the ultrastructural level, cells with apoptosis-like reactions initiated in the acute period of stroke may persist around necrotic cells. All this leads to worsening chronic cerebral ischemia that occurs before a stroke. The progression of cerebrovascular insufficiency becomes a risk factor for the development of recurrent stroke and vascular cognitive disorders, including dementia.

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

In the residual period of ischemic stroke, depletion of the anti-aggregation potential of the vascular wall is noted, leading to thrombus formation, an increase in the severity of atherosclerosis and the progression of insufficiency of blood supply to the brain. This process is of particular importance in elderly patients. In this age group, regardless of the previous stroke, activation of the blood coagulation system, functional insufficiency of anticoagulant mechanisms, deterioration of the rheological properties of blood, and disorders of systemic and local hemodynamics are noted. The aging process of the nervous, respiratory, and cardiovascular systems leads to disruption of autoregulation of cerebral circulation, as well as to the development or increase of brain hypoxia, which in turn contributes to further damage to the mechanisms of autoregulation.

However, improving cerebral blood flow, eliminating hypoxia, and optimizing metabolism can reduce the severity of dysfunction and help preserve brain tissue. In this regard, it is very relevant timely diagnosis chronic cerebrovascular insufficiency and adequate treatment.

CLINICAL PICTURE

The main clinical manifestations of chronic cerebrovascular insufficiency are disorders in emotional sphere, polymorphic movement disorders, deterioration of memory and learning ability, gradually leading to maladjustment of patients. Clinical features of chronic cerebral ischemia - progressive course, stages, syndromicity.

In domestic neurology, for quite a long time, the initial manifestations of cerebral circulatory failure were classified as chronic cerebrovascular insufficiency along with dyscirculatory encephalopathy. Currently, it is considered unfounded to identify such a syndrome as “initial manifestations of insufficiency of blood supply to the brain,” given the non-specificity of the complaints of an asthenic nature and the frequent overdiagnosis of the vascular origin of these manifestations. The presence of headache, dizziness (non-systemic), memory loss, sleep disturbances, noise in the head, ringing in the ears, blurred vision, general weakness, increased fatigue, decreased performance and emotional lability, in addition to chronic cerebral circulatory failure, may indicate other diseases and conditions . In addition, these subjective sensations sometimes simply inform the body of fatigue. When the vascular genesis of the asthenic syndrome is confirmed using additional research methods and focal neurological symptoms are identified, a diagnosis of “dyscirculatory encephalopathy” is established.

It should be noted that there is an inverse relationship between the presence of complaints, especially those reflecting the ability to cognitive activity (memory, attention), and the severity of chronic cerebrovascular insufficiency: the more cognitive functions suffer, the fewer complaints. Thus, subjective manifestations in the form of complaints cannot reflect either the severity or the nature of the process.

The core of the clinical picture of discirculatory encephalopathy has recently been recognized as cognitive impairment, detected already in stage I and progressively increasing towards stage III. Developing in parallel emotional disorders(emotional lability, inertia, lack of emotional response, loss of interests), various motor disorders (from programming and control to the execution of both complex neokinetic, higher automated, and simple reflex movements).

Stages of dyscirculatory encephalopathy

Discirculatory encephalopathy is usually divided into 3 stages.

At stage I, the above complaints are combined with diffuse microfocal neurological symptoms in the form of anisoreflexia, convergence insufficiency, and mild reflexes of oral automatism. Slight changes in gait are possible (decreased step length, slower walking), decreased stability and uncertainty when performing coordination tests. Emotional and personal disturbances (irritability,

emotional lability, anxious and depressive traits). Already at this stage, mild cognitive disorders of the neurodynamic type appear: slowdown and inertia of intellectual activity, exhaustion, fluctuations in attention, and a decrease in the amount of RAM. Patients cope with neuropsychological tests and work that do not require time tracking. The life activity of patients is not limited.

Stage II is characterized by an increase in neurological symptoms with the possible formation of a mild but dominant syndrome. Individual extrapyramidal disorders, incomplete pseudobulbar syndrome, ataxia, central-type CN dysfunction (proso- and glossoparesis) are identified. Complaints become less pronounced and less significant for the patient. Emotional disorders worsen. Cognitive dysfunction increases to a moderate degree, neurodynamic disorders are complemented by dysregulatory ones (frontal-subcortical syndrome). The ability to plan and control one’s actions deteriorates. The performance of tasks not limited by time is impaired, but the ability to compensate is preserved (recognition and the ability to use hints are preserved). At this stage, signs of decreased professional and social adaptation may appear.

Stage III is manifested by the presence of several neurological syndromes. Severe walking and balance disorders develop with frequent falls, severe cerebellar disorders, parkinsonian syndrome, and urinary incontinence. Criticism of one’s condition decreases, as a result of which the number of complaints decreases. Severe personality and behavioral disorders may appear in the form of disinhibition, explosiveness, psychotic disorders, and apathetic-abulic syndrome. Neurodynamic and dysregulatory cognitive syndromes are accompanied by operational disorders (memory, speech, praxis, thinking, visual-spatial function defects). Cognitive disorders often reach the level of dementia, when maladjustment manifests itself not only in social and professional activities, but also in everyday life. Patients are incapacitated and in some cases gradually lose the ability to care for themselves.

Neurological syndromes in dyscirculatory encephalopathy

Most often, in chronic cerebrovascular insufficiency, vestibulocerebellar, pyramidal, amyostatic, pseudobulbar, psychoorganic syndromes, as well as their combinations, are identified. Sometimes cephalgic syndrome is isolated separately. The basis of all syndromes characteristic of dyscirculatory encephalopathy is the disconnection of connections due to diffuse anoxic-ischemic damage to the white matter.

With vestibulocerebellar (or vestibuloatactic) syndrome subjective complaints of dizziness and instability when walking are combined with nystagmus and coordination disorders. Disorders can be caused by both cerebellar-stem dysfunction due to circulatory insufficiency in the vertebrobasilar system, and disconnection of the frontal-stem tracts with diffuse damage to the white matter of the cerebral hemispheres due to impaired cerebral blood flow in the internal carotid artery system. Ischemic neuropathy of the vestibulocochlear nerve is also possible. Thus, ataxia with this syndrome There can be 3 types: cerebellar, vestibular, frontal. The latter is also called apraxia of walking, when the patient loses locomotion skills in the absence of paresis, coordination, vestibular disorders, sensitive disorders.

Pyramid syndrome in dyscirculatory encephalopathy it is characterized by high tendon and positive pathological reflexes, often asymmetrical. Paresis is mildly expressed or absent. Their presence indicates a previous stroke.

Parkinsonian syndrome within the framework of dyscirculatory encephalopathy, it is represented by slow movements, hypomimia, mild muscle rigidity, often in the legs, with the phenomenon of “counteraction”, when muscle resistance involuntarily increases when performing passive movements. Tremor is usually absent. Gait disturbances are characterized by a slower walking speed, a decrease in the size of the step (microbasia), a “sliding”, shuffling step, small and rapid trampling in place (before starting to walk and when turning). Difficulties when turning while walking are manifested not only by marking time, but also by turning the whole body with a violation of balance, which can be accompanied by a fall. Falls in these patients occur with phenomena of propulsion, retropulsion, lateropulsion and may also precede walking due to impaired initiation of locomotion (symptom of “stuck legs”). If there is an obstacle in front of the patient (a narrow door, a narrow passage), the center of gravity shifts forward, in the direction of movement, and the legs mark time, which can cause a fall.

The occurrence of vascular parkinsonian syndrome in chronic cerebral circulatory failure is caused by damage not to the subcortical ganglia, but to the corticostriatal and cortical-stem connections, therefore treatment with drugs containing levodopa does not bring significant improvement to this group of patients.

It should be emphasized that in chronic cerebrovascular insufficiency, motor disorders are manifested primarily by walking and balance disorders. The genesis of these disorders is combined, caused by damage to the pyramidal, extrapyramidal and cerebellar systems. Not the least place is given to dysfunction complex systems motor control provided by the frontal cortex and its connections with subcortical and brainstem structures. When motor control is damaged, they develop dysbasia and astasia syndromes(subcortical, frontal, frontal-subcortical), otherwise they can be called apraxia of walking and maintaining a vertical posture. These syndromes are accompanied by frequent episodes of sudden falls (see Chapter 23, “Walking Disorders”).

Pseudobulbar syndrome, the morphological basis of which is bilateral damage to the cortical-nuclear pathways, occurs in chronic cerebrovascular insufficiency very often. Its manifestations in discirculatory encephalopathy do not differ from those in other etiologies: dysarthria, dysphagia, dysphonia, episodes of forced crying or laughter and reflexes of oral automatism arise and gradually increase. The pharyngeal and palatal reflexes are preserved and even high; the tongue is without atrophic changes and fibrillary twitching, which makes it possible to differentiate pseudobulbar syndrome from bulbar, caused by damage to the medulla oblongata and/or CNs emerging from it and clinically manifested by the same triad of symptoms (dysarthria, dysphagia, dysphonia).

Psychoorganic (psychopathological) syndrome may manifest itself as emotional-affective disorders (asthenodepressive, anxiety-depressive), cognitive (cognitive) disorders - from mild mnestic and intellectual disorders to various degrees dementia (see Chapter 26, Cognitive Impairment).

Expressiveness cephalgic syndrome decreases as the disease progresses. Among the mechanisms for the formation of cephalgia in patients with chronic cerebrovascular insufficiency, one can consider myofascial syndrome against the background of osteochondrosis of the cervical spine, as well as headache Tension (TN) is a variant of psychalgia, often occurring against the background of depression.

DIAGNOSTICS

To diagnose chronic cerebral circulatory failure, it is necessary to establish a connection between clinical manifestations and pathology of cerebral vessels. For the correct interpretation of the identified changes, careful collection of anamnesis with an assessment of the previous course of the disease and dynamic monitoring of patients are very important. One should keep in mind the inverse relationship between the severity of complaints and neurological symptoms and the parallelism of clinical and paraclinical signs during the progression of cerebral vascular insufficiency.

It is advisable to use clinical tests and scales taking into account the most common clinical manifestations of this pathology (assessment of balance and gait, identification of emotional and personality disorders, neuropsychological testing).

Anamnesis

When collecting anamnesis from patients suffering from certain vascular diseases, one should pay attention to the progression of cognitive disorders, emotional and personal changes, focal neurological symptoms with the gradual formation of developed syndromes. Identification of these data in patients at risk of developing cerebrovascular accidents or who have already suffered a stroke and transient ischemic attacks, with a high degree of probability allows us to suspect chronic cerebral circulatory failure, especially in the elderly.

From the anamnesis, it is important to note the presence of coronary heart disease, myocardial infarction, angina pectoris, atherosclerosis of the peripheral arteries of the extremities, arterial hypertension with damage to target organs (heart, kidneys, brain, retina), changes in the valvular apparatus of the heart chambers, heart rhythm disturbances, diabetes mellitus and others diseases listed in the “Etiology” section.

Physical examination

A physical examination can reveal pathology of the cardiovascular system. It is necessary to determine the safety and symmetry of pulsation in the main and peripheral vessels of the limbs and head, as well as the frequency and rhythm of pulse oscillations. Blood pressure should be measured in all 4 limbs. Be sure to auscultate the heart and abdominal aorta to identify murmurs and heart rhythm disturbances, as well as the main arteries of the head (vessels of the neck), which makes it possible to determine the noise above these vessels, indicating the presence of a stenotic process.

Atherosclerotic stenoses usually develop in the initial segments of the internal carotid artery and in the area of ​​bifurcation of the common carotid artery. This localization of stenoses allows you to hear a systolic murmur during auscultation of the vessels of the neck. If there is noise above the patient's vessel, the patient should be referred for duplex scanning of the main arteries of the head.

Laboratory research

The main direction of laboratory research is to clarify the causes of the development of chronic cerebrovascular insufficiency and its pathogenetic mechanisms. Explore clinical analysis blood with reflection

Instrumental studies

The task of instrumental methods is to clarify the level and degree of damage to blood vessels and brain matter, as well as to identify underlying diseases. These problems are solved using repeated ECG recordings, ophthalmoscopy, echocardiography (according to indications), cervical spondylography (if pathology in the vertebrobasilar system is suspected), ultrasound research methods (USDG of the main arteries of the head, duplex and triplex scanning of extra- and intracranial vessels).

Structural assessment of the brain substance and cerebrospinal fluid pathways is carried out using imaging studies (MRI). To identify rare etiological factors, non-invasive angiography is performed, which makes it possible to identify vascular abnormalities, as well as determine the state of collateral circulation.

An important place is given ultrasonic methods studies that make it possible to identify both disorders of cerebral blood flow and structural changes vascular wall, which can cause stenosis. Stenoses are usually divided into hemodynamically significant and insignificant. If a decrease in perfusion pressure occurs distal to the stenotic process, this indicates a critical or hemodynamically significant narrowing of the vessel, which develops when the lumen of the artery decreases by 70-75%. In the presence of unstable plaques, which are often found with concomitant diabetes mellitus, hemodynamically significant will be the overlap of the vessel lumen by less than 70%. This is due to the fact that with an unstable plaque, the development of arterio-arterial embolisms and hemorrhages into the plaque is possible with an increase in its volume and an increase in the degree of stenosis.

Patients with such plaques, as well as with hemodynamically significant stenoses, should be referred for consultation to an angiosurgeon to resolve the issue of operational recovery blood flow through the main arteries of the head.

We should not forget about asymptomatic ischemic disorders of cerebral circulation, detected only when additional examination methods are used in patients without complaints and clinical manifestations. This form of chronic cerebral circulatory failure is characterized by atherosclerotic lesions of the main arteries of the head (with plaques, stenoses), “silent” cerebral infarctions, diffuse or lacunar changes in the white matter of the brain and atrophy of brain tissue in individuals with vascular damage.

It is believed that chronic cerebral circulatory failure exists in 80% of patients with stenotic lesions of the main arteries of the head. Obviously, this indicator can reach an absolute value if an adequate clinical and instrumental examination is carried out to identify signs of chronic cerebral ischemia.

Considering that in chronic cerebrovascular insufficiency, the white matter of the brain is primarily affected, preference is given to MRI rather than CT. MRI in patients with chronic cerebrovascular insufficiency reveals diffuse changes in the white matter, cerebral atrophy, and focal changes in the brain.

MR tomograms visualize the phenomena of periventricular leukoaraiosis (rarefaction, decreased tissue density), reflecting ischemia of the white matter of the brain; internal and external hydrocephalus(dilation of the ventricles and subarachnoid space), caused by atrophy of brain tissue. Small cysts (lacunae), large cysts, as well as gliosis, can be detected, indicating previous cerebral infarctions, including clinically “silent” ones.

It should be noted that all of the listed signs are not considered specific; It is incorrect to diagnose dyscirculatory encephalopathy only based on imaging examination data.

Differential diagnosis

The above-mentioned complaints characteristic initial stages chronic cerebrovascular insufficiency may also occur with oncological processes, various somatic diseases, be a reflection of the prodromal period or asthenic “tail” of infectious diseases, be part of the symptom complex of borderline mental disorders(neuroses, psychopathy) or endogenous mental processes (schizophrenia, depression).

Signs of encephalopathy in the form of diffuse multifocal brain damage are also considered nonspecific. Encephalopathies are usually defined by the main etiopathogenetic feature (posthypoxic, posttraumatic, toxic, infectious-allergic, paraneoplastic, dysmetabolic, etc.). Dyscirculatory encephalopathy most often has to be differentiated from dysmetabolic, including degenerative processes.

Dysmetabolic encephalopathy, caused by disorders of brain metabolism, can be either primary, resulting from a congenital or acquired metabolic defect in neurons (leukodystrophy, degenerative processes, etc.), or secondary, when disorders of brain metabolism develop against the background of an extracerebral process. The following variants of secondary metabolic (or dismetabolic) encephalopathy are distinguished: hepatic, renal, respiratory, diabetic, encephalopathy with severe multiple organ failure.

Causes great difficulties differential diagnosis discirculatory encephalopathy with various neurodegenerative diseases, in which, as a rule, cognitive disorders and certain focal neurological manifestations are present. Such diseases include multisystem atrophy, progressive supranuclear palsy, corticobasal degeneration, Parkinson's disease, diffuse Lewy body disease, frontotemporal dementia, and Alzheimer's disease. Differentiation between Alzheimer's disease and discirculatory encephalopathy is far from a simple task: discirculatory encephalopathy often initiates subclinical Alzheimer's disease. In more than 20% of cases, dementia in older people is of a mixed type (vascular-degenerative).

Dyscirculatory encephalopathy must be differentiated from such nosological forms as brain tumor (primary or metastatic), normal pressure hydrocephalus, manifested by ataxia, cognitive disorders, impaired control of pelvic functions, idiopathic dysbasia with impaired gait and stability.

One should keep in mind the presence of pseudodementia (dementia syndrome disappears during treatment of the underlying disease). As a rule, this term is used in relation to patients with severe endogenous depression, when not only mood worsens, but also motor and intellectual activity weakens. It is this fact that gave rise to the inclusion of a time factor in the diagnosis of dementia (symptoms persisting for more than 6 months), since symptoms of depression are relieved by this time. It is likely that this term can be applied to other diseases with reversible cognitive impairment, in particular, secondary dysmetabolic encephalopathy.

TREATMENT

Treatment Goals

The goal of treatment of chronic cerebrovascular insufficiency is stabilization, suspension of the destructive process of cerebral ischemia, slowing down the rate of progression, activation of sanogenetic mechanisms of function compensation, prevention of both primary and recurrent stroke, therapy of major background diseases and accompanying somatic processes.

Treatment of an acutely occurring (or exacerbation of) chronic somatic disease is considered mandatory, since against this background the phenomena of chronic cerebral circulatory failure are significantly increasing. They, in combination with dysmetabolic and hypoxic encephalopathy, begin to dominate in clinical picture, leading to incorrect diagnosis, non-core hospitalization and inadequate treatment.

Indications for hospitalization

Chronic cerebral circulatory failure is not considered an indication for hospitalization if its course is not complicated by the development of a stroke or severe somatic pathology. Moreover, hospitalization of patients with cognitive disorders and removal from their usual environment can only worsen the course of the disease. Treatment of patients with chronic cerebrovascular insufficiency is assigned to the outpatient clinic service; if cerebrovascular disease has reached stage III of discirculatory encephalopathy, home patronage is necessary.

Drug treatment

The choice of medications is determined by the main areas of therapy noted above.

The main ones in the treatment of chronic cerebral circulatory failure are considered to be 2 areas of basic therapy - normalization of brain perfusion by influencing different levels of the cardiovascular system (systemic, regional, microcirculatory) and influencing the platelet component of hemostasis. Both of these directions, optimizing cerebral blood flow, simultaneously perform a neuroprotective function.

Basic etiopathogenetic therapy, affecting the underlying pathological process, primarily implies adequate treatment of arterial hypertension and atherosclerosis.

Antihypertensive therapy

A major role in preventing and stabilizing the manifestations of chronic cerebrovascular insufficiency is assigned to maintaining adequate blood pressure. There is information in the literature about the positive effect of normalizing blood pressure on the resumption of an adequate response of the vascular wall to the gas composition of the blood, hyper- and hypocapnia (metabolic regulation of blood vessels), which affects the optimization of cerebral blood flow. Maintain blood pressure at 150-140/80 mm Hg. prevents the increase in mental and motor disorders in patients with chronic cerebrovascular insufficiency. In recent years, it has been shown that antihypertensive drugs have a neuroprotective property, that is, they protect surviving neurons from secondary degenerative damage after a stroke and/or chronic cerebral ischemia. In addition, adequate antihypertensive therapy helps prevent the development of primary and repeated acute cerebrovascular accidents, the background of which is often chronic cerebral circulatory failure.

Very important early start antihypertensive therapy, until the development of a pronounced “lacunar state”, which determines the disconnection of cerebral structures and the development of the main neurological syndromes of dyscirculatory encephalopathy. When prescribing antihypertensive therapy, sharp fluctuations in blood pressure should be avoided, since with the development of chronic cerebral circulatory failure, the mechanisms of autoregulation of cerebral blood flow are reduced, which will depend to a greater extent on systemic hemodynamics. In this case, the autoregulation curve will shift towards higher systolic blood pressure, and arterial hypotension (<110 мм рт.ст.) - неблагоприятно влиять на мозговой кровоток. В связи с этим назначаемый препарат должен адекватно контролировать системное давление.

Currently, a large number of antihypertensive drugs from different pharmacological groups have been developed and introduced into clinical practice to provide blood pressure control. However, the data obtained on the important role of the renin-angiotensin-aldosterone system in the development of cardiovascular diseases, as well as on the connection between the content of angiotensin II in the central nervous system and the volume of ischemia of brain tissue, allow today in the treatment of arterial hypertension in patients with cerebrovascular pathology to give preference to drugs that affect renin-angiotensin-aldosterone system. These include 2 pharmacological groups - angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists.

Both angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists have not only antihypertensive, but also organoprotective effects, protecting all target organs affected by arterial hypertension, including the brain. The PROGRESS (prescription of the angiotensin-converting enzyme inhibitor perindopril), MOSES and OSCAR (prescription of the angiotensin II receptor antagonist eprosartan) studies have proven the cerebroprotective role of antihypertensive therapy. The improvement in cognitive functions while taking these drugs should be especially emphasized, given that cognitive disorders are present to one degree or another in all patients with chronic cerebrovascular insufficiency and are the dominant and most dramatic disabling factors in severe stages of dyscirculatory encephalopathy.

According to the literature, it is possible that angiotensin II receptor antagonists influence degenerative processes occurring in the brain, in particular in Alzheimer’s disease, which significantly expands the neuroprotective role of these drugs. It is known that recently most types of dementia, especially in old age, are considered as combined vascular-degenerative cognitive disorders. It should also be noted the putative antidepressant effect of angiotensin II receptor antagonists, which is of great importance in the treatment of patients with chronic cerebrovascular insufficiency, who often develop affective disorders.

In addition, it is very important that angiotensin-converting enzyme inhibitors are indicated for patients with signs of heart failure, nephrotic complications of diabetes mellitus, and angiotensin II receptor antagonists can have angioprotective, cardioprotective, and also renoprotective effects.

The antihypertensive effectiveness of these groups of drugs increases when they are combined with other antihypertensive drugs, often with diuretics (hydrochlorothiazide, indapamide). The addition of diuretics is especially indicated in the treatment of elderly women.

Lipid-lowering therapy (treatment of atherosclerosis)

For patients with atherosclerotic lesions of cerebral vessels and dyslipidemia, in addition to a diet with limited animals and the predominant use of vegetable fats, it is advisable to prescribe lipid-lowering drugs, in particular statins (atorvastatin, simvastatin, etc.), which have a therapeutic and preventive effect. Taking these drugs in the early stages of dyscirculatory encephalopathy is more effective. Their ability to reduce cholesterol content, improve endothelial function, reduce blood viscosity, stop the progression of the atherosclerotic process in the main arteries of the head and coronary vessels of the heart, have an antioxidant effect, and slow down the accumulation of β-amyloid in the brain has been shown.

Antiplatelet therapy

It is known that ischemic disorders are accompanied by activation of the platelet-vascular component of hemostasis, which determines the mandatory prescription of antiplatelet drugs in the treatment of chronic cerebrovascular insufficiency. Currently, the effectiveness of acetylsalicylic acid is most well studied and proven. Enteric-soluble forms are used predominantly at a dose of 75-100 mg (1 mg/kg) daily. If necessary, other antiplatelet agents (dipyridamole, clopidogrel, ticlopidine) are added to treatment. Prescribing drugs in this group also has a preventive effect: it reduces the risk of developing myocardial infarction, ischemic stroke, and peripheral vascular thrombosis by 20-25%.

A number of studies have shown that only basic therapy (antihypertensive, antiplatelet) is not always sufficient to prevent the progression of vascular encephalopathy. In this regard, in addition to the constant intake of the above groups of drugs, patients are prescribed a course of treatment with agents that have antioxidant, metabolic, nootropic, and vasoactive effects.

Antioxidant therapy

As chronic cerebral circulatory failure progresses, there is an increasing decrease in protective sanogenetic mechanisms, including the antioxidant properties of plasma. In this regard, the use of antioxidants such as vitamin E, ascorbic acid, ethylmethylhydroxypyridine succinate, Actovegin* is considered pathogenetically justified. Ethylmethylhydroxypyridine succinate can be used in tablet form for chronic cerebral ischemia. The initial dose is 125 mg (one tablet) 2 times a day with a gradual increase in dose to 5-10 mg/kg per day (maximum daily dose - 600-800 mg). The drug is used for 4-6 weeks, the dose is reduced gradually over 2-3 days.

Use of combination drugs

Considering the variety of pathogenetic mechanisms underlying chronic cerebral circulatory failure, in addition to the above-mentioned basic therapy, patients are prescribed drugs that normalize the rheological properties of blood, microcirculation, venous outflow, and have antioxidant, angio-protective, neuroprotective and neurotrophic effects. To exclude polypharmacy, preference is given to drugs that have a combined effect, a balanced combination of medicinal substances in which eliminates the possibility of drug incompatibility. Currently, quite a large number of such drugs have been developed.

Below are the most common drugs with a combined effect, their doses and frequency of use:

Ginkgo biloba leaf extract (40-80 mg 3 times a day);

Vinpocetine (Cavinton) (5-10 mg 3 times a day);

Dihydroergocriptine + caffeine (4 mg 2 times a day);

Hexobendine + etamivan + etophylline (1 tablet contains 20 mg hexobendine, 50 mg etamivan, 60 mg etophylline) or 1 tablet forte, which contains 2 times more content of the first 2 drugs (taken 3 times a day);

Piracetam + cinnarizine (400 mg piracetam and 25 mg cinnarizine, 1-2 tablets 3 times a day);

Vinpocetine + piracetam (5 mg of vinpocetine and 400 mg of piracetam, one capsule 3 times a day);

Pentoxifylline (100 mg 3 times a day or 400 mg 1 to 3 times a day);

Trimethylhydrazinium propionate (500-1000 mg 1 time per day);

Nicergoline (5-10 mg 3 times a day).

These drugs are prescribed in courses of 2-3 months, 2 times a year, alternating them for individual selection.

The effectiveness of most drugs that affect blood flow and brain metabolism is manifested in patients with early, that is, stages I and II dyscirculatory encephalopathy. Their use in more severe stages of chronic cerebrovascular insufficiency (in stage III discirculatory encephalopathy) can give a positive effect, but it is much weaker.

Despite the fact that they all have the above-described set of properties, one can focus on some selectivity of their action, which may be important in the choice of drug, taking into account the identified clinical manifestations.

Ginkgo biloba leaf extract accelerates vestibular compensation processes, improves short-term memory, spatial orientation, eliminates behavioral disorders, and also has a moderate antidepressant effect.

Dihydroergocryptine + caffeine acts primarily at the level of microcirculation, improving blood flow, tissue trophism and their resistance to hypoxia and ischemia. The drug helps improve vision, hearing, normalize peripheral (arterial and venous) circulation, reduce dizziness and tinnitus.

Hexobendine + etamivan + etophylline improves concentration, integrative brain activity, normalizes psychomotor and cognitive functions, including memory, thinking and performance. It is advisable to slowly increase the dose of this drug, especially in elderly patients: treatment begins with 1/2 tablet per day, increasing the dose by 1/2 tablet every 2 days, bringing it to 1 tablet 3 times a day. The drug is contraindicated in epileptic syndrome and increased intracranial pressure.

Metabolic therapy

Currently, there are a large number of drugs that can influence the metabolism of neurons. These are drugs of both animal and chemical origin that have a neurotrophic effect, chemical analogues of endogenous biologically active substances, agents affecting cerebral neurotransmitter systems, nootropics, etc.

Such drugs as solcoseryl* and cerebrolysin* and polypeptides of the cerebral cortex of livestock (polypeptide cocktails of animal origin) have a neurotrophic effect. It must be taken into account that in order to improve memory and attention in patients with cognitive disorders caused by cerebral vascular pathology, fairly large doses should be administered:

Cerebrolysin * - 10-30 ml intravenously, 20-30 infusions per course;

Livestock cerebral cortex polypeptides (cortexin*) - 10 mg intramuscularly, 10-30 injections per course.

Solcoseryl(Sokoseryl) is a deproteinized hemodialysate that contains a wide range of low-molecular components of cell mass and blood serum of dairy calves. Solcoseryl contains factors that, under hypoxic conditions, help improve metabolism in tissues, accelerate reparative processes and rehabilitation periods. Solcoseryl is a universal drug that has a complex effect on the body: neuroprotective, antioxidant, activates neuronal metabolism, improves microcirculation and has an endotheliotropic effect.

At the molecular level, the following mechanisms of action of the drug are distinguished. Solcoseryl increases the utilization of oxygen by tissues under hypoxic conditions, enhances the transport of glucose into the cell, increases the synthesis of intracellular ATP, and increases the proportion of aerobic glycolysis. According to experimental data, Solcoseryl improves cerebral blood flow, leads to a decrease in blood viscosity by increasing the deformability of erythrocytes, which increases microcirculation.

The above mechanisms of action of the drug increase the functional potential of the tissue under ischemic conditions, which leads to less damage to brain tissue during ischemia.

The clinical effectiveness of Solcoseryl in patients with cerebral pathology was confirmed by double-blind, placebo-controlled studies (1, 2).

Indications: ischemic, hemorrhagic stroke, traumatic brain injury, dyscirculatory encephalopathy, diabetic neuropathy and other neurological complications of diabetes, peripheral vascular diseases, peripheral trophic disorders.

Dosage: 10-20 ml intravenously drip, 5-10 ml intravenously slowly (in saline), 2-4 ml intramuscularly (total course duration - up to 4-8 weeks), topically (in the form of ointment or gel) - for trophic disorders, damage to the skin and mucous membranes.

Bibliography

1. Ito K. et al. A double-blind study of the clinical effects of solcoseryl infusion on cerebral arteriosclerosis // Kiso to Rinsho. - 1974. - N 8(13). - P. 4265-4287.
2. Mihara H. et al. A double-blind evaluation of pharmaceutical effect of solcoseryl on cerebrovascular accidents // Kiso to Rinsho. - 1978. - N 12(2). - P. 311-343.

Domestic drugs glycine and Semax* are chemical analogues of endogenous biologically active substances. In addition to their main effect (improving metabolism), glycine can produce a slight sedative effect, and Semax * can produce an stimulating effect, which should be taken into account when choosing a drug for a particular patient. Glycine is a non-essential amino acid that affects the glutamergic system. The drug is prescribed at a dose of 200 mg (2 tablets) 3 times a day, the course is 2-3 months. Semax* is a synthetic analogue of adrenocorticotropic hormone, its 0.1% solution is administered 2-3 drops into each nasal passage 3 times a day, the course is 1-2 weeks.

The concept of “nootropic drugs” combines various drugs that can cause an improvement in the integrative activity of the brain and have a positive effect on memory and learning processes. Piracetam, one of the main representatives of this group, has the noted effects only when given in large doses (12-36 g / day). It should be borne in mind that the use of such doses by elderly people may be accompanied by psychomotor agitation, irritability, sleep disturbance, as well as provoke an exacerbation of coronary insufficiency and the development of epileptic paroxysm.

Symptomatic therapy

With the development of vascular or mixed dementia syndrome, background therapy is enhanced with agents that affect the exchange of the main neurotransmitter systems of the brain (cholinergic, glutamatergic, dopaminergic). Cholinesterase inhibitors are used - galantamine 8-24 mg/day, rivastigmine 6-12 mg/day, glutamate NMDA receptor modulators (memantine 10-30 mg/day), D2/D3 dopamine receptor agonist with a 2 -noradrenergic activity piribedil 50-100 mg/day. The last of these drugs is more effective in the early stages of dyscirculatory encephalopathy. It is important that, along with improving cognitive functions, all of the above drugs are able to slow down the development of affective disorders, which may be resistant to traditional antidepressants, and also reduce the severity of behavioral disorders. To achieve the effect, the drugs should be taken for at least 3 months. You can combine these means, replace one with another. If the result is positive, taking an effective drug or drugs for a long time is indicated.

Dizziness significantly impairs the quality of life of patients. Some of the above drugs, such as vinpocetine, dihydroergocriptine + caffeine, ginkgo biloba leaf extract, can eliminate or reduce the severity of vertigo. If they are ineffective, otoneurologists recommend taking betahistine 8-16 mg 3 times a day for 2 weeks. The drug, along with reducing the duration and intensity of dizziness, reduces the severity of autonomic disorders and noise, and also improves motor coordination and balance.

Special treatment may be required if affective disorders (neurotic, anxiety, depressive) occur in patients. In such situations, antidepressants that do not have an anticholinergic effect (amitriptyline and its analogues), as well as intermittent courses of sedatives or small doses of benzodiazepines, are used.

It should be noted that the division of treatment into groups according to the main pathogenetic mechanism of the drug is very arbitrary. For broader acquaintance with a specific pharmacological agent, there are specialized reference books; the task of this guide is to determine directions in treatment.

Surgery

In case of occlusive-stenotic lesions of the main arteries of the head, it is advisable to raise the question of surgical elimination of the obstruction of vascular patency. Reconstructive operations are often performed on the internal carotid arteries. This is carotid endarterectomy, stenting of the carotid arteries. The indication for their implementation is the presence of hemodynamically significant stenosis (overlapping more than 70% of the vessel diameter) or a loose atherosclerotic plaque, from which microthrombi can break off, causing thromboembolism of small vessels of the brain.

Approximate periods of incapacity for work

The disability of patients depends on the stage of dyscirculatory encephalopathy.

At stage I, patients are able to work. If temporary disability occurs, it is usually due to intercurrent illnesses.

Stage II of dyscirculatory encephalopathy corresponds to disability group II-III. Nevertheless, many patients continue to work, their temporary disability can be caused by both a concomitant disease and an increase in the phenomena of chronic cerebral circulatory failure (the process often occurs in stages).

Patients with stage III dyscirculatory encephalopathy are disabled (this stage corresponds to disability group I-II).

Further management

Patients with chronic cerebrovascular insufficiency require constant background therapy. The basis of this treatment is blood pressure correcting drugs and antiplatelet drugs. If necessary, substances are prescribed that eliminate other risk factors for the development and progression of chronic cerebral ischemia.

Non-drug methods of influence are also of great importance. These include adequate intellectual and physical activity, feasible participation in social life. For frontal dysbasia with disorders of gait initiation, freezing, and the threat of falls, special gymnastics are effective. Stabilometric training based on the principle of biofeedback helps reduce ataxia, dizziness, and postural instability. For affective disorders, rational psychotherapy is used.

Patient Information

Patients should follow the doctor’s recommendations for both continuous and course use of medications, control blood pressure and body weight, stop smoking, follow a low-calorie diet, and eat foods rich in vitamins (see Chapter 13 “Lifestyle Modification”).

It is necessary to carry out health-improving exercises, use special gymnastic exercises aimed at maintaining the functions of the musculoskeletal system (spine, joints), and take walks.

It is recommended to use compensatory techniques to eliminate memory disorders, write down the necessary information, and draw up a daily plan. Intellectual activity should be maintained (reading, memorizing poems, talking on the phone with friends and family, watching television, listening to music or radio programs of interest).

It is necessary to perform feasible household duties, try to lead an independent lifestyle for as long as possible, maintain physical activity while taking precautions to avoid falling, and, if necessary, use additional means of support.

It should be remembered that in older people, after a fall, the severity of cognitive impairment increases significantly, reaching the severity of dementia. To prevent falls, it is necessary to eliminate risk factors for their occurrence:

Remove carpets that could cause the patient to trip;
use comfortable non-slip shoes;
if necessary, rearrange the furniture;
attach handrails and special handles, especially in the toilet and bathroom;
Showers should be taken in a sitting position.

Forecast

The prognosis depends on the stage of dyscirculatory encephalopathy. Using these same stages, it is possible to evaluate the rate of disease progression and the effectiveness of treatment. The main unfavorable factors are severe cognitive disorders, often paralleled by an increase in episodes of falls and the risk of injury, both TBI and limb fractures (primarily the femoral neck), which create additional medical and social problems.

Cerebral circulation refers to blood circulation in the vessels that supply the central nervous system – the brain and spinal cord.

Nowadays, various types of pathologies of cerebral circulation are diagnosed more and more often, which is associated with a number of reasons. This includes poor ecology, bad habits, poor nutrition, a sedentary lifestyle and genetically determined diseases.

Why do cerebrovascular accidents develop?

The immediate causes due to which the flow of blood to the central nervous system organs is disrupted include:

• kinks of blood vessels;
• significant narrowing of the lumen of the arteries;
• (blockage of the lumen by a thrombus);
• embolism;
• aneurysms.

One of the leading reasons leading to hemorrhage into the brain tissue and the formation of a hematoma is a significant increase in blood pressure. With a sharp jump in blood pressure, a blood vessel may rupture.

Somewhat less common in clinical practice is the rupture of an arterial aneurysm - a protrusion on the vascular wall, devoid of a powerful elastic and muscular basis. Even a relatively small increase in blood pressure against the background of minor physical activity or psycho-emotional stress may well cause a rupture of a pathologically altered section of the vessel wall.

Note:if the aneurysm is localized in a vessel of the lining of the brain, then not intracerebral, but subarachnoid hemorrhage develops.

Blockage of the great vessels usually results from the separation of a blood clot or infiltrate that forms on the heart valves during inflammation. Emboli with the blood flow migrate to the cerebral vessels and clog the one whose lumen diameter is smaller than the diameter of the thrombus. An embolus may be a fragment. Blockage of the vessel leads to the fact that the supply of the brain area is stopped. In such cases, it is customary to talk about the embolic mechanism of ischemic development.

A thrombus can gradually form directly in a cerebral vessel in close proximity to an atherosclerotic plaque. Gradually, the plaque fills the lumen, which causes blood flow to slow down. The vessel wall in the area of ​​atherosclerotic lesions has an uneven surface, which additionally promotes platelet aggregation. The combination of local factors with a slowdown in blood flow becomes the cause of vessel thrombosis with the subsequent development of cerebrovascular accidents in the form of ischemic stroke.

The blood supply to the brain is often disrupted due to spasm of the muscles of the vascular walls.

Complete blockage of the main vessel is not a prerequisite for the development of cerebral infarction. In some cases, for insufficient blood flow to a certain area, a bend in the vessel is sufficient.

The mechanism of development of cerebral circulatory disorders in the form of transient ischemic attacks (“”) is similar to the mechanism of ischemic stroke, but in the first case, compensatory mechanisms work adequately within a few hours.

Symptoms of cerebrovascular accident

Depending on the individual characteristics of the patient, his age, the area that is fed by the affected vessel, as well as the mechanism and severity of the process, pathological changes in the tissues vary. Accordingly, clinical symptoms may vary.

According to the accepted classification, all morphological changes are divided into diffuse and focal.

Focal cerebrovascular accidents:

• ischemic stroke;
• hemorrhagic stroke:
• subarachnoid hemorrhages.

Important:Doctors often call ischemic stroke a “cerebral infarction.”

Diffuse cerebrovascular accidents:

• small necrotic foci;
• small focal changes in the substance;
• small hemorrhages (single and multiple);
• small cystic formations;
• gliomesodermal scar changes.

With pathologies of cerebral circulation, the patient often has only subjective signs, which include:

• varying intensity;
• dizziness;
• disturbances of sensitivity of various localizations.

Objective neurological symptoms may not be detected.

Local dysfunction of the sensory organs, the development of organic symptoms with preservation of central nervous system functions, motor disorders (for example, hyperkinesis or paralysis), epileptoform seizures, and disorders of memory or cognitive functions are also possible.

According to the nature of development, all pathologies in this category are divided into:

• slowly progressing (dyscirculatory encephalo- or myelopathy);
• initial (transient ischemic attacks and hypertensive crises);
• acute (stroke and subarachnoid hemorrhage).

Note:Transient ischemic attacks are often called “micro-strokes” by both people who are far from medicine and medical practitioners.

Signs of chronic, slowly progressive disorders

Discirculatory encephalopathy is a pathology characterized by gradual progression. It is caused by disorders of the cerebral vessels. With this disease, focal structural changes are formed in the subcortical areas.

General clinical signs of dyscirculatory encephalopathy:

• severe headaches;
• increased irritability;
• occasional dizziness;
• decreased ability to remember;
• coordination problems;
• absent-mindedness;

Discirculatory encephalopathy develops gradually; There are 3 successive stages.

Discirculatory myelopathy, which is caused by circulatory disorders in the spinal cord, also progresses gradually.

Symptoms of discirculatory myelopathy

Discirculatory myelopathy is a lesion of the spinal cord of vascular origin, manifested in the form of pelvic disorders, sensory disturbances, and various paresis. It also progresses gradually.

Disorders of spinal cerebral circulation usually occur in the form of:

• Personage-Turner syndrome, in which discirculation occurs in the area of ​​the cervicobrachial arteries, which leads to paresis of the arm muscles and pain in the cervicobrachial area.
• Preobrazhensky syndrome, characterized by dyscirculatory disorders in the area of ​​the anterior spinal artery

The development of this type of cerebrovascular accident includes 3 stages:

• compensated;
• subcompensated;
• decompensated.

At the initial stage, the patient is characterized by increased fatigue or weakness of the muscles of the arms and legs. In the second stage, pathological changes become more noticeable, impaired reflexes and paresthesia occur. The decompensated stage is characterized by the appearance of disorders of the pelvic organs (stool and urine retention), as well as the development of paresis of various localizations and paralysis.

Symptoms of initial cerebrovascular insufficiency

Initial signs of cerebral circulatory failure usually develop against a background of mental or physical stress or exposure to unfavorable conditions (lack of oxygen or high room temperature).

The main signs of initial failure include:

The appearance of such clinical signs of cerebral circulatory disorders is the basis for a comprehensive medical examination in order to identify possible atherosclerotic changes in blood vessels, arterial hypertension (high blood pressure), as well as vegetative-vascular dystonia.

Transient disturbances of cerebral blood supply are characterized by general cerebral or focal signs that persist for no more than 24 hours.

Transient ischemic attacks are transient disorders of cerebral circulation caused by insufficient blood flow to certain areas of the central nervous system.

Symptoms of transient ischemic attacks:

• speech disorders;
• problems with coordination of movements and statics;
• double vision;
• flashing “flies” before the eyes;
• paresthesia (impaired sensitivity of the limbs);
• feeling of weakness.

Important:If you notice that your friend or colleague does not answer correctly, drops objects or moves unsteadily, he probably needs urgent medical attention. Many signs of “micro-strokes” are similar to those of alcohol intoxication.

Leading to circulatory disorders in the brain, caused by an abrupt increase in blood pressure.

Symptoms of hypertensive cerebral crises:

• intense headache;
• feeling of nausea;
• (not always);
• dizziness.

If typical neurological symptoms in a patient are detected for more than 24 hours, a diagnosis of “stroke” is made, i.e. we are talking about an acute cerebrovascular accident.

Signs of acute disorders

The symptoms of ischemic and hemorrhagic strokes, thrombosis of the venous sinuses, as well as venous hemorrhages are similar to the clinic of transient cerebrovascular accidents, but neurological symptoms are diagnosed within a day or more.

Important:In most cases, strokes occur early in the morning or late at night. A patient suspected of having this acute circulatory disorder often requires hospitalization and placement in a neurointensive care unit.

Ischemic strokes are caused by a cessation of blood flow to parts of the brain due to blockage or sudden spasm of blood vessels.

Hemorrhagic is caused by bleeding into the brain tissue when the integrity of the vascular wall is violated.

Ischemic changes increase gradually, over several hours (in some cases, up to a day). Hemorrhagic stroke develops almost instantly. With it, the patient experiences intense headache and loss of consciousness.

Important:Any stroke is characterized by serious sensory impairment and paralysis, often unilateral. With a lesion localized in the right hemisphere, the left side of the body suffers and vice versa. The patient usually develops visual and articulation disturbances.

Subarachnoid hemorrhage develops against the background of rupture of an aneurysm of the arachnoid vessels. It is usually not accompanied by the appearance of neurological symptoms. A characteristic symptom is an intense headache of a “dagger” nature and loss of consciousness.