Chem disease. Chronic cerebral ischemia. Further progression of the disease

Chronic cerebral ischemia is also called cerebrovascular insufficiency. Reduced arterial blood flow through the cerebral vessels leads to oxygen deficiency in neurons and cells of brain structures. This upsets metabolic processes and leads to manifestations of ischemia.

In the International Classification of Diseases (ICD-10), the disease chronic cerebral ischemia does not exist. It can be considered a purely clinical diagnosis. Coded under subclass I67 “Cerebrovascular diseases”, fits under the heading “other” (I67.8). In cases of accurate diagnosis with an asymptomatic course, you can use the following codes:

• I65 - blockage and stenosis of precerebral arteries (vertebral, carotid, aorta, circle of Willis at the base of the skull), not leading to cerebral infarction;
• I66 - the same, but at the level of the internal vessels of the brain.

Clinicians use the term to refer to long-term progressive vascular pathology of the brain. Medical statistics assign chronic cerebral ischemia to 75% of all cerebrovascular diseases.

Causes

Signs of impaired cerebral blood flow are observed in the following diseases:

• hypertension,
• atherosclerosis,
• hypotension,
• vasculitis (inflammation of blood vessels) of allergic and infectious etiology,
• thromboangiitis obliterans,
• skull injuries,
• abnormalities of the cerebral vascular bed and aneurysms,
• disturbances in cardiac activity,
• blood diseases,
• endocrine pathology,
• kidney diseases and other diseases.

However, they are not always associated with pathology of cerebral vessels.

And coronary brain disease includes causes that solely depend on the condition of the adductor and internal arteries:

• atherosclerosis of cerebral vessels, aorta and efferent branches;
• disturbances in the direction (bends, deformations) of the external and internal sections of the carotid and vertebral arteries;
• abnormalities in the structure of blood vessels (compression due to spinal osteochondrosis, spondylarthrosis);
• inadequacy of collateral (auxiliary) blood supply;
• coronary-cerebral syndrome with coronary heart disease;
• impaired hemodynamics of the brain with general circulatory failure;
• sharp fluctuations in blood pressure;
• conditions associated with increased blood clotting;
• metabolic changes in endocrine pathology (diabetes mellitus), leading to impaired conduction through nerve synapses (neuron cell connections);
• hereditary predisposition to vascular inferiority.

The patient's stability in the Romberg position is checked not only to diagnose cerebral ischemia, but also if alcohol intoxication is suspected

Mechanism of disease

Lack of blood supply leads to hypoxia of brain neurons. First, intracellular biochemical changes cause energy loss. Then the under-oxidized waste products of cells come into play. Worsening oxygen deficiency leads to the formation of microcysts in the cerebral cortex (ischemic lacunar process).

If blood oxygen saturation is below 60% of normal, then the internal self-regulation of the lumen of the brain vessels is disrupted: they expand and stop absorbing it. As a result, hypoxic paresis of neurons develops and their connections are severed.

Clinical manifestations

Symptoms of initial changes are barely noticeable. Sensitivity, the functioning of the sense organs, the psyche, and the functions of the cerebral cortex are disrupted only during nervous overstrain, anxiety, or significant physical work.

Then the signs of impaired blood supply to the brain become permanent and are associated with the formation of multiple microinfarctions. Focal symptoms in terms of the degree of manifestation depend on the location and size of the ischemic zone.

Most common symptoms:

• headaches with a feeling of “heavy head”;
• dizziness;
• staggering when walking;
• decreased attention and memory;
• short-term visual impairment;
• emotional instability (mood changes);
• insomnia or drowsiness.

Depending on the severity of clinical manifestations, the degrees of chronic cerebral ischemia are distinguished:

1. at 1st degree (initial)- all the described symptoms are present, but there are no objective neurological signs (changes in reflexes, coordination disorders);
2. at 2nd degree (subcompensation)- symptoms progress, influence and change the personality type, the range of interests is disrupted, apathy develops, persistent depression is possible, criticism is reduced, professional skills are lost, but the ability to self-care remains, the neurologist detects the addition of focal symptoms;
3. at grade 3, signs of decompensation with severe neurological disorders such as hyperkinesis (increased tone of the limbs), epileptiform seizures, parkinsonism (tremor of the hands and head), and swallowing disorders appear.

Memory loss leads to complete dementia, dependence on caregivers, and inability to self-care.

Diagnostics

In the diagnosis of chronic cerebral ischemia, correctly collected information about the patient, analysis of the state of cardiac circulation, and complaints over time are of great importance.

An examination is carried out to exclude various pathologies (radiography of the spine, ECG), blood is checked for coagulability, lipid fractions, and glucose levels.

To study the brain and its vessels, the following are used:

• magnetic resonance imaging;
• transcranial Doppler ultrasound.

Therapeutic measures

Treatment for chronic insufficiency of blood supply to the brain is aimed at:

• development of collateral circulation;
• prevention of spasms, progression of atherosclerotic changes;
• restoration of metabolic processes in neurons;

At the same time, it is necessary to monitor the treatment of pathologies that aggravate cerebral hypoxia (osteochondrosis, diabetes mellitus, hypertension, cardiac ischemia).

A massage of the collar area is performed using high-frequency alternating current (Arsonval apparatus D) to increase blood supply to the brain

Typically, the patient is indicated for outpatient therapy, since hospitalization only intensifies all manifestations in an unfamiliar environment. In stage 3, a permanent nurse with the supervision of medical personnel is recommended.

The diet is based on the principle of anti-sclerosis: fried and spicy meat dishes are not allowed, animal fats, spicy seasonings, and canned food are limited. Dairy products, cottage cheese, boiled meat dishes, porridge with diluted milk, vegetables, and fruits are recommended.

Drug treatment includes the following.

The use of antiplatelet drugs that reduce the ability of platelets to stick together improves the patency of cerebral vessels (Clopidogrel, Dipyridamole).

To counteract the atherosclerotic process, a group of statins (Atorvastatin, Rosuvastatin, Simvastatin) is recommended.

One should take into account the possible consequences: studies have found that taking statins for 6 months increases the aggressive behavior of women. This may be due to a decrease in the blood of the “happiness” hormone (serotonin), which depends on cholesterol. Men have the opposite reaction.

Neuroprotectors improve metabolism inside brain cells, adapting them to a lack of oxygen (Actovegin, Encephabol, Piracetam).

Medicines that eliminate vitamin deficiency include Milgamma and Neuromultivit.

Cytoflavin – protects brain cells from death due to metabolic and antioxidant energy-correcting properties. The uniqueness of cytoflavin lies in its multicomponent nature (succinic acid, biboxin, nicotinamide, riboflavin), which provides an effect on different parts of the cell’s energy production, which ensures its effectiveness not only in the acute period of stroke, but also in the rehabilitation process.

In the initial stages, physiotherapy, massage of the collar area and head, and acupuncture are indicated.

If damage to the carotid artery is established, a surgical operation is performed: a stent is placed or a circumferential circulation is formed.

Cerebral vascular pathology is of social significance for society, since it causes neurological and mental disorders and leads to disability of patients and requires care. Early detection and treatment can prolong active life.

V.N.Butikov, G.O.Penina

CHRONIC BRAIN ISCHEMIA IN RESIDENTS OF NORTHERN TERRITORIES (BASED ON THE EXAMPLE OF THE KOMI REPUBLIC)

Komi branch of the State Educational Institution of Higher Professional Education "Kirov State Medical Academy",
Syktyvkar, Russia

Vascular diseases of the brain account for 30 to 59% of diseases of the cardiovascular system. Vascular pathology of the brain is a leading cause of mortality and disability in adults. The mortality rate from cerebrovascular diseases in Russia (per 100 thousand population) is 339.9, and therefore the issues of prevention and treatment of vascular pathology of the nervous system are not only of medical, but also of great social importance. Unfavorable weather and climatic conditions in the Far North create additional stress on the body's adaptation systems, primarily on the vascular system. The incidence of cerebrovascular pathology in the Komi Republic is the highest in the Northwestern Federal District, exceeding similar indicators in other regions by 1.5 - 2 times. In this regard, issues of diagnosis and treatment of conditions associated with chronic vascular diseases of the brain are also relevant for the Komi Republic. Today, data on gender, age and other characteristics of cerebrovascular pathology in the Far North are scattered and almost do not affect the situation in the European north of the Russian Federation.

The purpose of this work was to study the epidemiological, gender and age characteristics of chronic cerebrovascular pathology in the Komi Republic according to the Register of the Neurological Department of the State Institution of the Republic of Kazakhstan “Komi Republican Hospital” over a ten-year period. The register has been maintained in the department since 1998; it contains data on all cases of hospitalization in the department. Using a cross-sectional study method, we analyzed all registered cases of hospitalization of patients with cerebrovascular diseases (CVD) in the Republican Neurological Department as of December 31, 2007. We studied data on patients with an established diagnosis of initial manifestations of cerebrovascular insufficiency (IPCI) and varying degrees of chronic cerebral ischemia (CCI).

For the period from 1998 to 2007. In the neurological department, 11,426 patients were treated, of which 180 (1.56% of all hospitalized) had initial manifestations of cerebrovascular insufficiency, 1,606 (14.1% of all hospitalized) patients had chronic cerebral ischemia of varying degrees (grade 1 chronic cerebral ischemia). - 593 (5.18%), Chemical Chemistry 2nd degree - 456 (3.99%), Chemical Chemical Engineering 3rd degree - 557 people (4.87%).

Rice. 1. The ratio of different degrees of chronic cerebral ischemia among hospitalized patients with CVD (1 – CCI stage 1, 2 – CCI stage 2, 3 – CCI stage 3)

As can be seen in the figure, patients with varying degrees of CCI over the course of 10 years were hospitalized in the department with approximately equal frequency.

When analyzing the gender structure of those hospitalized in the hospital during the study period, the following distribution was revealed: the number of men with initial manifestations of cerebral circulatory disorders was 23.3% (42 people), women 76.7% (138 people). A similar gender ratio was observed in almost all groups of patients with cerebrovascular pathology. Frequency of hospitalized men with stage 1 CCI. amounted to 29.68% (176 people), women – 70.32% (417 people); men with CHI stage 2 – 30.04% (137 people), women with stage 2 CCI. – 69.96% (319 people). In the group of hospitalized patients with stage 3 CCI. men made up 60.68% (338 people), women 39.32% (219 people). Thus, there is a significant (p≤0.05) predominance of women in all groups, with the exception of patients with stage 3 CCI, in which men significantly predominate.

The average age of all hospitalized patients diagnosed with CVD and CCI was 54.83±9.25 years. At the same time, it is natural that patients hospitalized with a diagnosis of NPNMK were significantly younger - 44.89±7.63 years (p≤0.05).

When analyzing the age of hospitalized patients, a statistically significant difference was revealed in the age of onset of the disease in men and women in all groups (NPNMK, CCI). The average age of hospitalized men with a diagnosis of NPMC was 40.66±10.60, and the average age of women was 46.15±5.98 (p≤0.05)

Data on the age of patients at the time of hospitalization is presented in Table 1.

As can be seen from the table above, hospitalized women were significantly older than men in all studied groups of patients with cerebrovascular pathology. We did not find any significant differences in age between groups of hospitalized patients with chronic cerebral ischemia of varying degrees. Slightly younger age of hospitalized patients with grade 3 CCI. This is probably due to the more active referral of relatively young patients with severe impairments to the neurological hospital.

Analysis of the group of patients with a diagnosis of NPNMC revealed a significant (p≤0.001) predominance among hospitalized patients aged 41–45 years (Fig. 2).

Fig.2. Distribution of patients with initial manifestations of cerebrovascular insufficiency by age groups, in relative values

When analyzing the distribution of patients by age in the group with CCI of varying severity, a statistically significant predominance of the number of hospitalized patients with CCI stage 1 was revealed. at the age of 51 - 55 years, with CCI 2 tbsp. and CHEM 3 tbsp. at the age of 46 - 55 years. Pronounced deviation of indicators in patients with CCI grades 2 and 3. is due, in our opinion, to a more significant number of male patients in these groups compared to the group with stage 1 CCI, who are significantly younger at the time of hospitalization. All groups had a younger age of hospitalized men (p≤0.05).

Of interest is the comparative age characteristics of patients living in different climatic and geographical zones. Thus, the average age of patients with NPNMC living in the Far North is almost 5 years less than that of persons living in the southern territories of the Komi Republic (Table 2). Statistical testing revealed the significance of the differences obtained.

As follows from the table, the age of hospitalized patients with CCI living in the Far North was statistically significantly lower than the age of patients with this pathology living in the southern regions of the Komi Republic and in territories equated to the Far North (p≤0.05). We did not identify any significant differences between the age of patients living in the Southern regions and territories equated to the Far North.

Thus, the presented structure of morbidity in patients with initial manifestations of cerebrovascular insufficiency and CCI indicates a significant predominance of women in all groups of patients. The age of hospitalized men is statistically significantly lower than the age of women with the same form of cerebrovascular pathology. A significantly earlier onset of the disease was revealed in patients living in the Far North.

Bibliography.

1. Gusev E.I., Skvortsova V.I. Cerebral ischemia. M.: Medicine. 2000. – 328 p.
2. Kuzmenko V.M. Prevalence and some features of the prevention of cerebrovascular diseases in people of different ages // Probl. aging and longevity. 151; 2001. - v. 10, no. 4. - pp. 401-409.
3. Labutin N. Yu. Effect of North climate-geographical factors on cardiorespiratory system of workers of woodworking plants // Socio-economic development and health of small peoples of the North: Proc. report republic seminar, [Krasnoyarsk], November 26-28, 1990. - Krasnoyarsk, 1990. - P. 84 - 85.
4. Simonenko V.B., Shirokov E.A. Fundamentals of cardioneurology: A guide for doctors. 2nd ed. M.: Medicine, 2001. - 240 p.
5. Slonim A.D. Adaptation of humans and animals in experiments and in Northern conditions // problems of bioclimatology and climatophysiology. - Novosibirsk: SO AMS USSR, 1970. - P. 150 - 155.
6. Reducing morbidity, mortality and disability from strokes in the Russian Federation / Ed. IN AND. Skvortsova - M.: Litterra, 2008. – 192 p.
7. Hankey G.J., Warlow C.P. Treatment and secondary prevention of stroke: evidence, costs, and effects on individuals and populations/ The Lancet. 1999; 354: 1457 - 63
8. Wesnes K.A, Harrison J.E. The evaluation of cognitive function in the dementias: methodological and regulatory considerations // Dialogues Clin. Neurosci. - 2003. - v.5. - P. 77-88.

The article describes in detail such a disease as chronic cerebral ischemia. About stages, causes, symptoms. It's about proper treatment. And about how people live and how long they live with the disease.

What is chronic cerebral ischemia?

HIGM is an increasing disruption of brain activity due to the destruction of its tissues due to long-term cerebral circulatory failure.

In this case, the brain suffers due to lack of glucose and oxygen. As a result, brain functions are impaired. The person becomes forgetful, depressed, and frequent mood swings are noticed.

Thanks to the international classification of diseases, doctors can more easily navigate the huge variety of diseases of human organs. ICD code – 10 from 163.0 to 169.0.

Symptoms

Initially, the clinic is practically invisible.

A violation occurs:

1. sensitivity;
2. organs of vision, smell, touch, taste;
3. psyche;
4. if a person is overnervous, there may be a disruption in brain function.

There are a number of symptoms:

• Severe headache (heaviness in the head);
• Poor sleep;
• Lethargy;
• Mood changes;
• Memory impairment;
• Impaired coordination of movements;
• Loss of consciousness;
• Noise in the head;
• Epilepsy.

Stages

There are three stages of this disease:

1. initial stage. At this stage, subjective disturbances predominate, in the form of headaches, dizziness, lethargy, weakness, and insomnia. These disorders are followed by objective disorders: impaired coordination and memory. At this stage, neurological disorders are not observed. In this regard, with surgical treatment, it is possible to eliminate some symptoms, or even the disease itself.
2. Subcompensation stage. There is a progression of symptoms, especially from the neurological side. Loss of control over your actions, staggering when walking, walking on tiptoes or on tiptoes. Violation of the oculomotor muscles, coordination of movements.
   Slow movements are observed, the patient becomes apathetic. At this stage, it is possible to cure only some neurological disorders.
3. Stage of decompensation. There is a disruption in the normal functioning of some organs. The patient is unable to move independently and loses consciousness. Involuntary release of urine is observed, behavior becomes inappropriate.
   There are disturbances in movement regulation, as well as muscle tone, and psychotic disorders. Basically, patients with the third stage of cerebral ischemia are disabled. They may have micro-strokes.

Each stage of ischemia leads to disruption of the usual quality of life.

Diagnostics

A correctly collected patient history plays an important role in diagnosis. It is important to find out in the anamnesis: whether there was a myocardial infarction, ischemic heart disease, angina pectoris, hypertension, atherosclerosis, diabetes mellitus. It is necessary to conduct a subjective and objective examination and listen to all the patient’s complaints.

Be sure to study neuropsychological and neurological symptoms.

A number of instrumental studies are being carried out:

Laboratory research methods are also used:

• General blood analysis;
• Blood chemistry;
• Blood clotting test;
• Blood for sugar;
• Lipid fractions.

Doctors believe that left hemisphere and right hemisphere ischemia differ in the accompanying symptoms. If the foci of chronic cerebral ischemia are located on the left hemisphere, then treatment will occur faster and more effectively.

Causes of the disease

There are root and auxiliary causes.

The root causes include:

1. Incomplete cerebral blood supply, resulting in oxygen starvation. In the absence of oxygen for a long time, cells cannot function as before. If this condition lasts for a very long time, a heart attack is possible;
2. Arterial hypertension;
3. Atherosclerosis;
4. Thrombosis;
5. Damage to the vascular wall;
6. Spinal diseases such as osteochondrosis, disc herniation.

Additional reasons include:

• Ischemic kidney disease;
• Diseases of the heart and its blood vessels;
• Overweight;
• Bad habits;
• Caisson disease;
• Diabetes;
• Blood disorders such as anemia or erythrocytosis Find out the code by.
• Tumor due to compression of the artery;
• Loss of blood in large quantities;
• Elderly age;
• Venous pathology;
• Carbon monoxide intoxication, etc.

The etiology of the disease is quite large, but the main factor is circulatory disorders for various reasons.

If the disease arose as a result of the fusion of arterial hypertension and atherosclerosis, then the diagnosis is as follows: chronic cerebral ischemia of mixed origin.

Treatment

Regardless of the stage, chronic cerebral ischemia requires immediate treatment. The main goal in the treatment of CICG is to stabilize the destructive process of cerebral ischemia. And also take preventive measures against strokes, both primary and recurrent.

Hospitalization is only necessary in case of a stroke or disruption of the functioning of any organs and systems. Basically, the treatment is outpatient, since with inpatient treatment the situation can only worsen due to the fact that the unfamiliar environment has a bad effect on the patient.

Treatment of patients with CIGM should be carried out by a neurologist in the clinic. And in the third stage of ischemia, it is imperative to carry out patronage. A dairy diet is recommended. Correction of blood pressure is also necessary.

There are two treatment methods:

1. Drug therapy;
2. Surgery.

Drug therapy includes:

• Reperfusion– restoration of normal blood circulation.
• Neuroprotection, which serves as support for the metabolism of cerebral tissue, and also provides protection against structural damage.

To carry out drug therapy, the following drugs are used for treatment:

• Antiplatelet agents. These are medications that prevent the formation of blood clots. These include aspirin, dipyridamole, clopidogrel;
• Vasodilators. They improve cerebral blood circulation and dilate blood vessels. They also participate in reducing blood clotting. These are drugs containing nicotinic acid, acetylsalicylic acid, pentoxifylline and others;
• Nootropics, improving brain activity. For example: cerabralysin, piracetam, vinpocetine, actovegin, encephabol. We talk more about drugs such as here.
• ? They improve metabolism, as well as microcirculation in the blood vessels of the brain. These include: bilobil, nimodipine;
• Preparations containing satins. These are drugs such as: atorvastatin, simvastatin, rosuvastatin.
• Drugs, which eliminate vitamin deficiency. For example: milgamma, neuromultivit

These medications are usually used twice a year for two months.

In the initial stages, physiotherapeutic procedures are prescribed: acupuncture, massage of the head and collar area, physical therapy, electrophoresis.

Surgery

• This is surgery, which is used in the last stages of IGM. In case of damage to the blood vessels of the brain, and if drug treatment does not help, surgical treatment is prescribed. For example: carotid artery stenting, carotid endarterectomy, thrombectomy.
• There is another treatment method, which is carried out using stem cells. First, the germ cells are collected, then they are grown to the required volume. Next, these cells are injected using a dropper twice. The procedure itself lasts about an hour. As a result, new stem cells replace the damaged ones.
• There are also traditional methods of treatment, but using only them is very dangerous.
  Garlic recipes are popular among folk methods.
  The recipe is:
  • You need to chop the garlic and add alcohol in a one to one ratio.
  • You need to insist for two weeks, then take five drops, which are dissolved in a tablespoon of milk.

Possible complications, consequences

• In the case when the patient turned to the doctor very late, the grave consequences can no longer be avoided. Therefore, it is important to immediately contact a neurologist, because with correct diagnosis and adequate treatment, serious consequences can be avoided.
• But if the disease is still detected in the later stages, complications are possible in the form of impairment of the patient’s ability to work: weakness in the limbs, speech impairment, memory loss, stroke.
• At stage 3 disease, disability is possible due to chronic cerebral ischemia.

Forecast

Chronic cerebral ischemia is very common. Only systemic treatment of this disease can provide the necessary help for brain disorders. Proper treatment will help prevent cerebral infarction. Basically, the prognosis is good for those patients who are constantly under the supervision of their neurologist.

An unfavorable prognosis is revealed due to a late visit to the doctor.

Prevention

Prevention should be started from an early age.

You should:

1. limit yourself from stressful situations;
2. follow a diet, since obesity is one of the causes of the disease;
3. lead a healthy lifestyle;
4. give up bad habits such as smoking and alcohol;
5. move more, physical inactivity also leads to the development of this disease.

• It is imperative to urgently treat diabetes mellitus, arterial hypertension, and atherosclerosis.
• If the onset of the disease could not be avoided, you should immediately stop smoking, reduce physical activity, avoid being in the sun for a long time, drink less alcoholic beverages, and adhere to a certain diet.
• A lot depends on nutrition. If you eat improperly, salts and cholesterol are deposited in the body. As a result, plaques appear that clog the blood vessels, and he cannot fight this obstacle. As a result, oxygen stops flowing to all organs, and they begin to “suffocate.” A person must release the walls to give oxygen to the organs by contacting a neurologist.

You need to start sounding the alarm when:

1. Unpleasant phenomena constantly appear in the heart area;
2. Increased breathing or shortness of breath occurs even with minor physical exertion;
3. Suddenly weakness and fatigue appear.

Cerebrovascular diseases are one of the main problems of modern medicine. It is known that in recent years the structure of vascular diseases of the brain has changed due to the increase in ischemic forms. This is due to an increase in the proportion of arterial hypertension and atherosclerosis as the main cause of cerebrovascular pathology. When studying individual forms of cerebral circulatory disorders, chronic ischemia ranks first in prevalence.

Chronic cerebral ischemia (CHI) is a special type of vascular cerebral pathology caused by a slowly progressive diffuse disorder of the blood supply to the brain with gradually increasing various defects in its functioning. The term “chronic cerebral ischemia” is used in accordance with the International Classification of Diseases, 10th revision, instead of the previously used term “dyscirculatory encephalopathy”.

The development of chronic cerebral ischemia is promoted by a number of reasons, which are commonly called risk factors. Risk factors are divided into correctable and non-correctable. Uncorrectable factors include old age, gender, and hereditary predisposition. It is known, for example, that a stroke or encephalopathy in parents increases the likelihood of vascular diseases in children. These factors cannot be influenced, but they help to identify in advance those at increased risk of developing vascular pathology and help prevent the development of the disease. The main correctable factors in the development of chronic ischemia are atherosclerosis and hypertension. Diabetes mellitus, smoking, alcohol, obesity, insufficient physical activity, poor nutrition are the reasons that lead to the progression of atherosclerosis and the deterioration of the patient’s condition. In these cases, the blood coagulation and anticoagulation system is disrupted, and the development of atherosclerotic plaques is accelerated. Due to this, the lumen of the artery decreases or is completely blocked (Fig.). At the same time, the crisis course of hypertension is especially dangerous: it leads to an increase in the load on the blood vessels of the brain. Arteries modified by atherosclerosis are unable to maintain normal cerebral blood flow. The walls of the vessel gradually become thinner, which can ultimately lead to the development of a stroke.

The etiology of CCI is associated with occlusive atherosclerotic stenosis, thrombosis, and embolism. A certain role is played by post-traumatic dissection of the vertebral arteries, extravasal compression due to pathology of the spine or neck muscles, deformation of the arteries with permanent or periodic disturbances in their patency, hemorheological changes in the blood (increased hematocrit, viscosity, fibrinogen, platelet aggregation and adhesion). It must be borne in mind that symptoms similar to those that occur with chronic ischemia can be caused not only by vascular, but also by other factors - chronic infection, neuroses, allergic conditions, malignant tumors and other reasons with which a differential diagnosis should be made . If the described disorders are supposed to have a vascular origin, instrumental and laboratory confirmation of damage to the cardiovascular system is necessary (ECG, Doppler ultrasound of the main arteries of the head, MRA, MRI, CT, biochemical blood tests, etc.).

To make a diagnosis, one must adhere to strict diagnostic criteria: the presence of cause-and-effect relationships (clinical, anamnestic, instrumental) of brain lesions with hemodynamic disturbances with the development of clinical, neuropsychological, psychiatric symptoms; signs of progression of cerebrovascular insufficiency. The possibility of subclinical acute cerebral dyscirculatory disorders, including small-focal, lacunar infarctions, which form symptoms characteristic of encephalopathy, should be taken into account. For the main etiological reasons, atherosclerotic, hypertensive, mixed, and venous encephalopathies are distinguished, although other causes leading to chronic cerebrovascular insufficiency (rheumatism, vasculitis of other etiologies, blood diseases, etc.) are also possible.

The pathomorphological picture of CCI is characterized by areas of ischemically altered neurons or their loss with the development of gliosis. Small cavities (lacunae) and larger lesions develop. With multiple lacunae, the so-called “lacunary state” is formed. These changes are predominantly observed in the area of ​​the basal ganglia and have a typical clinical expression in the form of amyostatic and pseudobulbar syndromes, dementia, described at the beginning of the twentieth century. French neurologist P. Marie. The development of status lacunaris is most characteristic of arterial hypertension. In this case, changes in blood vessels are observed in the form of fibrinoid necrosis of the walls, their plasmatic impregnation, the formation of miliary aneurysms, and stenoses.

The so-called criblures, which are dilated perivascular spaces, are distinguished as changes characteristic of hypertensive encephalopathy. Thus, the chronic nature of the process is pathomorphologically confirmed by multiple zones of brain ischemia, especially its subcortical regions and cortex, accompanied by atrophic changes developing against the background of corresponding changes in the cerebral vessels. Using CT and MRI, in typical cases, multiple microfocal changes are detected, mainly in the subcortical zones, periventricularly, often accompanied by cortical atrophy, dilation of the cerebral ventricles, and the phenomenon of leukoaraiosis (“periventricular glow”), which is a reflection of the demyelination process. However, similar changes can be observed during normal aging and primary degenerative-atrophic processes of the brain.

Clinical manifestations of CCI are not always detected by CT and MRI studies. Therefore, the diagnostic significance of neuroimaging methods cannot be overestimated. Making a correct diagnosis for a patient requires an objective analysis of the clinical picture and instrumental examination data from the doctor.

The pathogenesis of cerebral ischemia is caused by insufficiency of cerebral circulation in its relatively stable form or in the form of repeated short-term episodes of discirculation.

As a result of pathological changes in the vascular wall, developing as a result of arterial hypertension, atherosclerosis, vasculitis, etc., autoregulation of cerebral circulation is disrupted, and there is an increasing dependence on the state of systemic hemodynamics, which also turns out to be unstable due to the same diseases of the cardiovascular system. Added to this are disturbances in the neurogenic regulation of systemic and cerebral hemodynamics. Brain hypoxia itself leads to further damage to the mechanisms of autoregulation of cerebral circulation. The pathogenetic mechanisms of acute and chronic cerebral ischemia have much in common. The main pathogenetic mechanisms of cerebral ischemia constitute the “ischemic cascade” (V.I. Skvortsova, 2000), which includes:

• decreased cerebral blood flow;
• increase in glutamate excitotoxicity;
• calcium accumulation and lactic acidosis;
• activation of intracellular enzymes;
• activation of local and systemic proteolysis;
• emergence and progression of antioxidant stress;
• expression of early response genes with the development of depression of plastic proteins and a decrease in energy processes;
• long-term consequences of ischemia (local inflammatory reaction, microcirculatory disorders, damage to the BBB).

A condition called “oxidative stress” plays a major role in damage to brain neurons. Oxidative stress is an excessive intracellular accumulation of free radicals, activation of lipid peroxidation (LPO) processes and excessive accumulation of lipid peroxidation products, aggravating overexcitation of glutamate receptors and enhancing glutamate excitoxic effects. Glutamate excitotoxicity is understood as hyperstimulation by mediators of excitation of NDMA receptors of N-methyl-D-aspartate, provoking dilatation of calcium channels and, as a consequence, massive influx of calcium into cells, with subsequent activation of proteases and phospholipases. This leads to a gradual decrease in neuronal activity, a change in the neuron-glia ratio, which causes a deterioration in brain metabolism. Understanding the pathogenesis of CCI is necessary for an adequate, optimally selected treatment strategy.

As the severity of the clinical picture increases, pathological changes in the vascular system of the brain intensify. If at the beginning of the process stenotic changes in one or two main vessels are detected, then most or even all of the main arteries of the head turn out to be significantly changed. Moreover, the clinical picture is not identical to damage to the great vessels, due to the presence in patients of compensatory mechanisms of autoregulation of cerebral blood flow. The condition of intracranial vessels plays an important role in the mechanisms of compensation for cerebral circulatory disorders. With well-developed and preserved collateral circulation pathways, satisfactory compensation is possible, even with significant damage to several great vessels. On the contrary, individual structural features of the cerebral vascular system may be the cause of decompensation (clinical or subclinical), aggravating the clinical picture. This may explain the more severe clinical course of cerebral ischemia in middle-aged patients.

Based on the main clinical syndrome, several forms of CCI are distinguished: with diffuse cerebrovascular insufficiency; predominant pathology of the vessels of the carotid or vertebrobasilar systems; vegetative-vascular paroxysms; predominant mental disorders. All forms have similar clinical manifestations. In the initial stages of the disease, all patients complain of headache, non-systemic dizziness, noise in the head, memory impairment, and decreased mental performance. As a rule, these symptoms occur during a period of significant emotional and mental stress, requiring a significant increase in cerebral circulation. If two or more of these symptoms are often repeated or exist for a long time (at least the last 3 months) and there are no signs of an organic nature, instability when walking, or damage to the nervous system, a presumptive diagnosis is made.

The clinical picture of CCI has a progressive development and, according to the severity of symptoms, is divided into three stages: initial manifestations, subcompensation and decompensation.

Stage 1 is dominated by subjective disorders in the form of headaches and a feeling of heaviness in the head, general weakness, increased fatigue, emotional lability, dizziness, decreased memory and attention, and sleep disturbances. These phenomena are accompanied, although mild, but quite persistent objective disorders in the form of anisoreflexia, discoordination phenomena, oculomotor insufficiency, symptoms of oral automatism, memory loss and asthenia. At this stage, as a rule, the formation of distinct neurological syndromes (except for asthenic) has not yet occurred, and with adequate therapy, it is possible to reduce the severity or eliminate both individual symptoms and the disease as a whole.

The complaints of patients with the 2nd stage of CCI more often include memory impairment, loss of ability to work, dizziness, instability when walking, and manifestations of an asthenic symptom complex are less often present. At the same time, focal symptoms become more distinct: revival of reflexes of oral automatism, central insufficiency of the facial and hypoglossal nerves, coordination and oculomotor disorders, pyramidal insufficiency, amyostatic syndrome, increased mnestic-intellectual disorders. At this stage, it is possible to identify certain dominant neurological syndromes - discoordination, pyramidal, amyostatic, dysmnestic, etc., which can help in prescribing symptomatic treatment.

At the 3rd stage of CCI, objective neurological disorders in the form of discoordination, pyramidal, pseudobulbar, amyostatic, and psychoorganic syndromes are more pronounced. Paroxysmal conditions—falls, fainting—are more common. In the stage of decompensation, cerebral circulation disorders are possible in the form of “small strokes” or prolonged reversible ischemic neurological deficit, the duration of focal disorders in which ranges from 24 hours to 2 weeks. At the same time, the clinical picture of diffuse insufficiency of blood supply to the brain corresponds to that of moderate encephalopathy. Another manifestation of decompensation may be a progressive “complete stroke” and residual effects after it. This stage of the process with diffuse damage corresponds to the clinical picture of severe encephalopathy. Focal symptoms are often combined with diffuse manifestations of brain failure.

In chronic cerebral ischemia, there is a clear correlation between the severity of neurological symptoms and the age of the patients. This must be kept in mind when assessing the significance of individual neurological signs that are considered normal for elderly and senile people. This dependence reflects age-related manifestations of dysfunction of the cardiovascular and other visceral systems, affecting the state and functions of the brain. To a lesser extent, this dependence is observed in hypertensive encephalopathy. In this case, the severity of the clinical picture is largely determined by the course of the underlying disease and its duration.

Along with the progression of neurological symptoms, as the pathological process develops in the neurons of the brain, an increase in cognitive disorders occurs. This applies not only to memory and intelligence, which are impaired in the 3rd stage to the level of dementia, but also to such neuropsychological syndromes as praxis and gnosis. Initial, essentially subclinical disorders of these functions are observed already in the 1st stage, then they intensify, change, and become distinct. The 2nd and especially the 3rd stages of the disease are characterized by pronounced impairments of higher brain functions, which sharply reduces the quality of life and social adaptation of patients.

In the picture of CIM, several main clinical syndromes are distinguished: cephalgic, vestibulo-ataxic, pyramidal, amyostatic, pseudobulbar, paroxysmal, vegetative-vascular, psychopathological. A feature of the cephalgic syndrome is its polymorphism, inconstancy, lack of connection in most cases with specific vascular and hemodynamic factors (excluding headaches during hypertensive crises with high blood pressure), and a decrease in the frequency of occurrence as the disease progresses.

The second most common syndrome is vestibulo-ataxic syndrome. The main complaints of patients are: dizziness, instability when walking, coordination disorders. Sometimes, especially in the initial stages, patients, complaining of dizziness, do not notice coordination problems. The results of otoneurological examination are also insufficiently indicative. In later stages of the disease, subjective and objective discoordination disorders are clearly interrelated. Dizziness and unsteadiness when walking may be partly due to age-related changes in the vestibular apparatus, motor system and ischemic neuropathy of the vestibulocochlear nerve. Therefore, to assess the significance of subjective vestibulo-ataxic disorders, their qualitative analysis during a patient interview, neurological and otoneurological examination is important. In most cases, these disorders are caused by chronic circulatory failure in the blood supply of the vertebrobasilar arterial system, so it is necessary to rely not on the subjective sensations of patients, but to look for signs of diffuse damage to the parts of the brain that are supplied with blood from this vascular system. In some cases, in patients with stages 2-3 CCI, ataxic disorders are caused not so much by cerebellar-stem dysfunction, but rather by damage to the frontal-stem pathways. There is a phenomenon of frontal ataxia, or apraxia of walking, reminiscent of hypokinesia in patients with parkinsonism. A CT examination reveals significant hydrocephalus (along with cortical atrophy), i.e., a condition similar to normal pressure hydrocephalus occurs. In general, the syndrome of circulatory failure in the vertebrobasilar system is diagnosed with CCI more often than insufficiency of the carotid system.

A feature of the pyramidal syndrome is its moderate clinical manifestation (anisoreflexia, facial asymmetry, minimally expressed paresis, revitalization of oral automatism reflexes, hand symptoms). A clear asymmetry of reflexes indicates either a previously existing cerebral stroke or another disease occurring under the guise of CCI (for example, large intracranial processes, consequences of traumatic brain injury). Diffuse and fairly symmetrical revival of deep reflexes, as well as pathological pyramidal reflexes, often combined with a significant revival of oral automatism reflexes and the development of pseudobulbar syndrome, especially in old age, indicates multifocal vascular damage to the brain (subject to the exclusion of other possible causes).

In patients with clinical manifestations of circulatory failure in the vertebrobasilar system, paroxysmal conditions are often observed. These conditions may be caused by a combined or isolated effect on the vertebral arteries of vertebrogenic factors (compression, reflex), which is associated with changes in the cervical spine (dorsopathies, osteoarthritis, deformities).

Mental disorders are quite characteristic and varied in form at different stages of CCI. If in the initial stages they are of the nature of asthenic, asthenodepressive and anxiety-depressive disorders, then in the 2nd and especially in the 3rd stage they are joined by pronounced dysmnestic and intellectual disorders, forming the syndrome of vascular dementia, which often comes first in the clinical picture .

Electroencephalographic changes are nonspecific for CCI. They consist of a progressive decrease in the β-rhythm, an increase in the proportion of slow θ- and δ-activity, accentuation of interhemispheric asymmetry, and a decrease in EEG reactivity to external stimulation.

CT characteristics undergo dynamics from normal indicators or minimal atrophic signs in the 1st stage to more pronounced small-focal changes in the brain substance and atrophic (external and internal) manifestations in the 2nd stage to sharply defined cortical atrophy and hydrocephalus with multiple hypodense foci in the hemispheres - in the 3rd stage.

A comparison of clinical and instrumental characteristics in patients with atherosclerotic, hypertensive and mixed forms of CCI does not reveal any clear differences. In severe cases of hypertension, a faster rate of increase in psychoneurological disorders, early manifestation of cerebral disorders, and a greater likelihood of developing lacunar stroke are possible.

Treatment of CCI should be based on certain criteria, including the concepts of pathogenetic and symptomatic therapy. To correctly determine the pathogenetic treatment strategy, one should take into account: the stage of the disease; identified mechanisms of pathogenesis; the presence of concomitant diseases and somatic complications; age and gender of patients; the need to restore quantitative and qualitative indicators of cerebral blood flow, normalize impaired brain functions; the possibility of preventing recurrent cerebral dysgemia.

The most important direction of CCI therapy is the impact on existing risk factors, such as arterial hypertension and atherosclerosis. Treatment of atherosclerosis is carried out according to generally accepted regimens using statins, in combination with correction of the diet and lifestyle of patients. The selection of antihypertensive drugs and the order of their prescription is carried out by a general practitioner, taking into account the individual characteristics of patients. Complex therapy for CCI includes the prescription of antioxidants, antiplatelet agents, drugs that optimize brain metabolism, and vasoactive drugs. Antidepressants are prescribed for severe asthenodepressive manifestations of the disease. Antiasthenic drugs are prescribed in the same way.

An important component of the treatment of CCI is the administration of drugs with antioxidant activity. Currently, the following drugs of this series are used in clinical practice: Actovegin, Mexidol, Mildronate.

Actovegin- a modern antioxidant, which is a deproteinized extract of the blood of young calves. Its main effect is to improve the utilization of oxygen and glucose. Under the influence of the drug, the diffusion of oxygen in neuronal structures significantly improves, which makes it possible to reduce the severity of secondary trophic disorders. There is also a significant improvement in cerebral and peripheral microcirculation against the background of improved aerobic energy exchange of vascular walls and the release of prostacyclin and nitric oxide. The resulting vasodilation and decrease in peripheral resistance are secondary to the activation of oxygen metabolism of the vascular walls (A. I. Fedin, S. A. Rumyantseva, 2002).

In case of CCI, it is advisable to use Actovegin, especially in the absence of effect from other treatment methods (E. G. Dubenko, 2002). The method of application consists of drip administration of 600-800 mg of the drug for 10 days, followed by switching to oral administration.

A constant in the treatment regimen for CCI is the use of drugs that optimize cerebral circulation. The most commonly used drugs are: Cavinton, Halidor, Trental, Instenon.

Halidor (bencyclane)- a drug that has a multidirectional mechanism of action due to phosphodiesterase blockade, antiserotonin action, and calcium antagonism. It inhibits the aggregation and adhesion of platelets, prevents the aggregation and adhesion of erythrocytes, increasing the elasticity and osmotic resistance of the latter. Halidor reduces blood viscosity, normalizes intracellular metabolism of glucose and ATP, affects phosphokinase and lactate dehydrogenase, and enhances tissue oxygenation. It has been proven that the use of this drug for 8 weeks eliminates the clinical manifestations of chronic cerebral vascular insufficiency in 86% of patients. The drug has a positive effect on a person’s emotional environment, reduces forgetfulness and absent-mindedness. Halidor is prescribed in a daily dose of 400 mg for 6-8 weeks.

Instenon- a combined drug with neuroprotective action, including a vasoactive agent from the group of purine derivatives, a substance that affects the state of the ascending reticular formation and cortical-subcortical relationships, and, finally, an activator of tissue respiration processes under hypoxic conditions (S. A. Rumyantseva, 2002; V. V. Kovalchuk, 2002).

The three components of instenon (etophylline, etamivan, hexobendine) jointly act on various parts of the pathogenesis of ischemic brain damage.

Etophylline, a vasoactive component of the purine series, activates myocardial metabolism with an increase in stroke volume. The transition from a hypokinetic type of blood circulation to a normokinetic one is accompanied by an increase in cerebral blood flow. An important effect of the component is an increase in renal blood flow and, as a consequence, dehydration and diuretic effects.

Etamivan has a nootropic effect in the form of a direct effect on the processes of memory, attention, mental and physical performance as a result of increased activity of the reticular formation of the brain.

Hexobendine selectively stimulates metabolism based on increased utilization of oxygen and glucose, due to increased anaerobic glycolysis and pentose cycles. At the same time, the physiological mechanisms of autoregulation of cerebral and systemic blood flow are stabilized.

Instenon is used intramuscularly 2.0 ml, course - 5-10 procedures. Then oral administration of instenon-forte continues, 1 tablet 3 times a day for a month (S. V. Kotov, I. G. Rudakova, E. V. Isakova, 2003). A clear regression of neurological symptoms is observed by the 15-20th day of treatment. A particularly good effect is observed with the combined use of Actovegin (drops) and instenon (intramuscular injections or oral administration). Instenon therapy has a positive effect on cognitive functions, especially on the regulation of mnestic activity and psychomotor functions.

In the complex therapy of CCI, much attention is paid to nootropic drugs that increase the resistance of brain tissue to various adverse metabolic influences (ischemia, hypoxia). The actual “nootropic” drugs include derivatives of piracetam (nootropil, lutetam), encephabol.

Piracetam increases the synthesis of high-energy phosphates (ATP), enhances aerobic metabolism under hypoxic conditions, facilitates impulse conduction, normalizes the ratio of phospholipids of cell membranes and their permeability, increases the density and sensitivity of receptors, improves interaction between the hemispheres of the brain, improves metabolic processes in the central nervous system, facilitates neuronal transmission .

Piracetam improves microcirculation due to its disaggregant properties, facilitates the conduction of nerve impulses, and improves interaction between the hemispheres of the brain. The drug normalizes the ratio of phospholipids of cell membranes and increases their permeability, prevents the adhesion of red blood cells, reduces platelet aggregation, reduces the levels of fibrinogen and factor VIII, and relieves spasm of arterioles. The drug is prescribed in a daily dose of 2.4-4.8 g for 8-12 weeks.

Encephabol- a derivative of pyritinol. The drug increases the density and sensitivity of receptors, normalizes neuroplasticity. It has a neuroprotective effect, stimulates learning processes, improves memory, memorization and concentration. Encephabol stabilizes the cell membranes of neurons by inhibiting lysosomal enzymes and preventing the formation of free radicals, improves the rheological properties of blood, increases the conformational ability of red blood cells, increasing the ATP content in their membrane. For adults, the average daily dose is 600 mg for 6-8 weeks.

Antiplatelet drugs include acetylsalicylic acid and its derivatives (cardiomagnyl, thrombo ACC). Given the presence of contraindications when prescribing acetylsalicylic acid, other drugs with antiplatelet activity (Curantil, Tiklid, Plavix) are often used.

Symptomatic therapy for CCI includes the prescription of drugs that reduce the manifestations of various symptoms of the disease. For all patients with stages 2-3 of the disease, it is advisable to prescribe anti-anxiety or antidepressant drugs. Benzodiazepine drugs are the safest for long-term use.

Grandaxin- an atypical benzodiazepine derivative, a selective anxiolytic. The drug effectively eliminates anxiety, fear, and emotional stress without sedation or muscle relaxation. The drug has a vegetative-corrective effect, which makes it possible to use it in patients with severe vegetative-vascular syndrome.

In neurological practice, a daily dose of 50-100 mg is used, the duration of use is determined individually for each patient.

The prevalence of chronic vascular pathology of the brain, the progression of its course, and the high degree of disability of patients determine the social and medical significance of the problem of CCI therapy. Currently, in clinical practice there is a trend towards increasing the use of non-drug treatment methods. This is due to the absence in patients of the phenomenon of addiction to medicinal substances with a long period of therapeutic aftereffect.

Considering the complexity of the pathogenetic mechanisms of CCI, during therapy it is necessary to achieve normalization of systemic and cerebral circulation, adjust the metabolism in the brain tissue, and the state of hemorheology. Currently, the possibilities for pharmacological correction of the manifestations of CCI are quite extensive; they allow the use of various drugs that affect all parts of the pathogenesis of post-ischemic and post-hypoxic damage to nervous tissue.

Thus, recognizing the causes, identifying risk factors and, therefore, the real possibility of effective targeted treatment and preventing the development of chronic cerebral vascular pathology requires accurate knowledge of the structural, physiological and clinical features of the manifestation of the disease. This becomes possible thanks to a systematic approach to the study of etiology, pathogenesis, clinical picture and modern methods of therapy.

M. V. Putilina, Doctor of Medical Sciences, Professor