Hypoxia, metabolic disorders and cerebral blood supply. Deterioration of blood circulation. Diagnosis of circulatory disorders of the brain. How to cure a violation of cerebral blood flow Treatment of a violation of blood circulation in the vessels of the brain

09.04.2020

Table of contents [Show]

Violation of cerebral circulation in the brain system can be associated with cardiac pathology, arterial hypotension, vasomotor dystonia, arterial hypertension, as well as aneurysm of the vessels, spinal cord and brain, lung pathology, toxic and traumatic vascular lesions of the brain, tumors, with damage to the brain and main arteries and other phenomena. Pathological changes in the tissues of the brain with disorders of cerebral circulation depend on the characteristics of the person: his age, the basin of the blood supply of the vessel. Circulatory disorders of the brain can be diffuse and focal, and focal disorders include cerebral infarction, intrathecal hemorrhage and hemorrhagic stroke. Diffuse hemorrhages are characterized by changes in the medulla of different ages; there may also be minor hemorrhages and small foci of brain necrosis. The consequences of impaired cerebral circulation can be expressed in subjective sensations such as paresthesia, numbness of the legs and arms, dizziness, headache. Other consequences can be in the form of: paralysis, impaired coordination and work of the sense organs, the development of epileptic seizures, changes in intelligence. The first manifestations of insufficient blood supply to the brain may be dizziness, decreased performance, tinnitus, which happens after strenuous physical and mental work. There are also acute circulatory disorders of the brain, which end in a cerebral stroke and they manifest themselves with cerebral and focal symptoms, and such phenomena are observed in arterial hypertension and atherosclerosis of the brain. There are also hypertensive cerebral crises and ischemic attacks, which are characterized by the appearance of focal symptoms, when a person develops diplopia or double vision, statics can also be disturbed, speech becomes difficult and limbs become numb, but there are no general cerebral symptoms. With hypertensive cerebral crises, on the contrary, cerebral symptoms appear, such as vomiting and nausea, dizziness and headache, and such phenomena can last more than a day, which is considered a stroke. A stroke of the brain is due to hemorrhage or blockage of blood vessels, so that two types of stroke can be distinguished, these are hemorrhagic and ischemic. With ischemic stroke, the blood vessels of the brain are blocked and the cause of this phenomenon is detached anti-sclerotic plaques in the large vessels of the neck, they can form in those places where the vessels are narrowed and this is the cause of ischemic stroke. Hemorrhagic stroke is somewhat different from ischemic stroke in that such a stroke can occur with a sharp increase in blood pressure and since the walls of the arteries are unevenly thinned due to atherosclerosis, rupture of these walls occurs and hemorrhage begins in the cerebral region and an intracerebral hematoma appears. After an ischemic stroke, there may be the following consequences, this is a violation of the motor functions of the limbs, their complete paralysis or a violation on one side of the body, which is called hemiplegia or hemiparesis. Swallowing can be impaired and this leads to the fact that food will not enter the esophagus, but into the windpipe and lungs, which can cause pneumonia, and malnutrition causes constipation or persistent dehydration. With ischemic stroke, speech functions are impaired due to circulatory disorders in the left hemisphere of the brain, while the patient has difficulty not only in pronouncing words, but he cannot write, count and read. When cerebral circulation is impaired during a stroke, a person sees objects, but cannot adequately assess them, even everyday objects, for example, a patient, can take a glass, pour water into it, but he does not know what to do next. Also, with a stroke, a person experiences cognitive impairments or a violation of the ability to adequately perceive and process the information received, he has almost no logical thinking, memory deteriorates, the ability to learn, practically disappears and he cannot plan something and be responsible for his actions. With a stroke, the functioning of the sacral spinal cord can be disrupted, this leads to urinary and fecal incontinence, and a number of problems associated with the work of the intestines can also occur. After a stroke, the patient may be aggressive or, on the contrary, fearful, all his emotional moods become unstable. He may start crying or laughing for no reason, or completely fall into a depressive state and not respond to others for a while, these states are accompanied by insomnia, he has low self-esteem and anxiety increases, and the patient is constantly afraid of something. Sometimes, after an ischemic stroke, the patient has various pain syndromes in the form of shooting or squeezing pains that cannot be removed with pain medications. With a hemorrhagic stroke, necrosis of brain tissue occurs and therefore the part of the body that is controlled by these parts stops working. In the event that a person does not die at the onset of a hemorrhagic stroke, which is quite rare, then he has almost the same consequences as after an ischemic stroke, the motor functions of the limbs are also impaired, the person also has a poor understanding and speech may be completely withdrawn. Thus, people who have impaired blood circulation in the brain almost always become disabled and recovery proceeds very slowly, but often these processes are absent and the person degrades more and more, complete paralysis occurs, which subsequently leads to lethal outcome.

Time is inexorably running forward and this does not have the best effect on people reaching adulthood, because it is during this period of life that many disorders and pathologies of the human body begin to manifest themselves. First of all, this concerns the functioning of the cardiovascular system, one of the disorders of which is the deterioration of cerebral circulation. Systematic headaches, frequent dizziness, fatigue, decreased performance - such symptoms are found, unfortunately, not only in the elderly. In most cases, patients do not take their health very seriously and prefer to do it on their own, without the help of a specialist doctor. Meanwhile, in this way, a violation of the blood circulation of the brain can manifest itself and the consequences in some cases are very serious. For our brain to function fully, it requires a lot of energy, which it receives from the bloodstream in the form of nutrients and oxygen. Any violations lead to a deterioration in well-being and the development of acute or chronic circulatory disorders of the brain, often to a stroke. - Acute circulatory disorders of the brain (CVA) include ischemic and hemorrhagic strokes. The cause of ischemic stroke is the blockage of a blood vessel by a thrombus, which disrupts the flow of oxygen and nutrients to a specific part of the brain. Hemorrhagic stroke is the result of rupture of the vessel wall and, as a result, hemorrhage in the brain or adjacent tissues. ACVA in most cases is a severe complication of hypertension and atherosclerotic cerebrosclerosis of the cerebral vessels. Less commonly, the causes are congenital anomalies in the development of cerebral vessels, myocardial infarction, dysfunction of heart valves, rheumatoid diseases. Almost all patients have various heart lesions with the development of cardiovascular failure. A particularly important symptom of the development of a stroke is transient cerebral circulation disorders, which usually last from several minutes to several hours and end with a complete restoration of all functions. Clinical manifestations a stroke is numbness or severe weakness, especially on one side of the body, that appears suddenly, severe headache of an unexplained nature, impaired coordination of movements when walking, dizziness, difficulty speaking or understanding, a sharp deterioration in vision. Often there is a high jump in blood pressure, sometimes a feeling of nausea, single or repeated vomiting is added. In severe cases, there may be loss of consciousness. If any of these symptoms occur, it is recommended that you promptly induce ambulance! In the diagnosis of stroke, a thorough collection of anamnesis is of paramount importance. Attention is drawn to the sudden appearance of neurological focal and / or cerebral, meningeal symptoms in a patient with vascular disease in the absence of other causes - craniocerebral or spinal trauma, alcohol, drug or drug intoxication, hypoglycemia, renal and hepatic failure. Treatment of acute cerebrovascular accident should be carried out in a hospital under constant medical supervision. Due to the fact that in the first hours of the disease, the nature of the stroke is simply impossible to determine, therapeutic measures are usually aimed at restoring cardiovascular activity, supporting breathing, normalizing blood pressure and body temperature, preventing the development of pneumonia, thromboembolism and pressure ulcers. - Chronic circulatory disorders of the brain (CBC) include cerebral circulatory failure, leading to the development of many small necrotic areas of the brain that disrupt its function, the so-called discirculatory encephalopathy. The clinic develops against the background of a lack of blood supply to the brain, as a complication of hypertension, atherosclerosis of the cerebral vessels, as a consequence of craniocerebral trauma, various intoxications, and dysmetabolic disorders (diabetes mellitus).

Found a mistake in the text? Select it and a few more words, press Ctrl + Enter

At the initial stage, HNMC is characterized by increased fatigue, emotional instability, sleep disturbance, and memory loss. With further progression of the disease, movement disorders appear, a sharp decrease in memory, attention, cerebral crises from transient transient attacks to strokes. With the development of the second stage of the disease, all the symptoms worsen - more and more often there is a headache, dizziness increases, unsteadiness when walking and tinnitus appear, a person is insecure, irritable, depressed. Decreases in working capacity, adequacy and social adaptation sick. At the third stage of HNMK, dementia (dementia), impaired consciousness and perception of the environment can develop. Stiffness of movements, lethargy, tremor of the head, arms, speech impairment appear. This stage is characterized by the development of strokes. The cause of the development of such disorders may be vascular atherosclerosis or high-grade hypertension. Moreover, the more pronounced they are, the more severe the consequences of cerebrovascular accident will be. It is clear that it is impossible to leave these diseases unattended, and even more so without appropriate treatment. In addition to these diseases, impaired cerebral circulation can occur against the background of chronic fatigue syndrome, stress, head injuries, excessive physical exertion, scoliosis, osteochondrosis, etc. Of course, at the initial stage, the symptoms of the development of the disease will be practically invisible, without letting anyone know about themselves. However, in the absence of proper treatment, the violation of cerebral circulation will rapidly progress, manifesting itself with the following symptoms: · Headache - it, as a rule, is the first signal that not everything is in order in the human body; · Pain in the eyes, aggravated by movement of the eyeballs. It is she who signals that a person's cerebral circulation is impaired to one degree or another; · Dizziness - if it occurs more than 3 times a month, then the person should immediately consult a doctor; · Congestion, noise and ringing in the ears - the more the blood circulation in the brain is impaired, the more often and longer such phenomena are; · Numbness of hands, feet or other parts of the body - it occurs suddenly and for a short time, seemingly for no apparent reason. However, this numbness is a direct consequence of impaired blood circulation in the vessels of the brain. Often in patients with impaired blood circulation in the brain, meningeal phenomena appear during an exacerbation of the disease, as well as significant tension in the muscles of the head, especially in the occipital region. In addition, a person may feel discomfort and severe weakness throughout the body. As you know, an exacerbation of cerebral circulatory disorders occurs not only with increased, but also with reduced pressure, against the background of a hypotonic crisis. The patient at this time may experience dizziness, weakness, fainting. The skin becomes pale, cold sweat appears, and the pulse rate drops significantly. Depending on the expressed neurological symptoms, the doctor can easily determine in which of the cerebral hemispheres the blood circulation is impaired. If these are the large hemispheres of the brain, then the patient often has a violation of the sensitivity of certain parts of the body - paresis, in especially severe cases, there is a decrease in sensitivity. In case of impaired blood circulation in the brain stem, a person often has dizziness, twitching of the eyelids and eyeballs, impaired coordination of movement, loss of sensitivity of the tongue, severe weakness in the limbs. Swallowing may also be impaired. By the nature of circulatory disorders of the brain, there are: 1. Initial manifestations of insufficient blood supply to the brain - clinical symptoms are dizziness, headache, noise in the head, sleep disturbance and decreased performance. 2. Acute disorders of cerebral circulation (transient circulatory disorders in the brain and strokes) - are manifested by focal or cerebral symptoms that last less than a day. 3. Chronic slowly progressive disorders of the spinal and cerebral circulation (dyscirculatory myelopathy and encephalopathy) - they are the result of progressive insufficient blood supply to the brain caused by various vascular diseases. When treating patients with impaired cerebral circulation, the main emphasis is on restoring the functions of the brain and normalizing blood circulation in it. For this, drugs are prescribed that prevent blood clotting, beta-blockers and diuretics (reduce cerebral edema). The patient lowers blood pressure and normalizes cholesterol, treats heart disease. For an accurate diagnosis, a person can be hospitalized. In the hospital, he is first examined by internal organs, and then a neurological examination will be performed. Additionally, the doctor may prescribe computed tomography and ultrasound examination of the structure of blood vessels. Acute and chronic vascular diseases of the brain occupy one of the leading places in the structure of morbidity and mortality in many countries, including Russia. Timely started correct treatment allows you to achieve a stable remission of the disease and avoid serious consequences. Constant or repeated headache, frequent high blood pressure, impaired attention, distraction, apathy - all this is a reason to immediately contact a neurologist (neurologist)! All of this can be avoided by keeping healthy image life, i.e. quit smoking and drinking alcohol, move more and maintain a normal body weight, reduce salt intake. In addition, patients with diabetes mellitus and cardiovascular diseases are recommended constant medical supervision.

The circulatory system affects the health of the entire body. A disruption in its work can lead to the fact that the tissues will no longer receive enough oxygen and nutrients. As a result, the metabolism will slow down or even hypoxia may occur. Due to such problems, serious pathologies can develop.

Clinical manifestations of the disease

On early stages hemodynamic disturbances no signs appear. And even after some time, the symptoms of this ailment are so nonspecific that it is impossible to immediately detect the disease. The main signs of poor circulation are as follows:

The lack of desire is there.
Deterioration of immunity.
Cold extremities.
Tingling and numbness in the hands.
Brittle hair and nails.
Varicose veins.
Constant tiredness.
The appearance of ulcers on the legs.
Change in skin pigmentation.
Puffiness.

Prevalence

Violation of cerebral circulation, the symptoms and treatment of which are presented in the article, is today considered the main reason disability. The number of patients with poor blood circulation is increasing every year. Moreover, such an ailment can occur not only in the elderly, but also in young people.

Types of circulatory disorders in the brain

Doctors divide cerebral blood flow disorder into two types: chronic and acute. In the first case, there is a chronic difficulty in blood circulation. Such a pathology develops for a long time, in addition, the symptoms at the first stage are poorly expressed. Only after some time, when the disease begins to progress, certain signs appear.

Acute problems of cerebral circulation are usually divided into stroke and transient disorder. In this case, strokes can be ischemic and hemorrhagic, in which hemorrhage occurs in the brain tissue due to a ruptured vessel. For a transient disturbance of blood circulation, local vascular disorders are characteristic that do not affect vital important functions... Such disorders cannot cause serious complications. Such a violation differs from an acute one in duration, for example, when symptoms are observed for less than a day, we are talking about a passing process, if more, about a stroke.

Why is there a violation of blood circulation in the brain?

Poor blood circulation in the brain in many cases results from cerebral atherosclerosis and hypertension. A person with such a pathology feels satisfactory only when he is in normal conditions. However, with an increase in blood circulation, his condition becomes worse, it can happen with physical exertion, too high temperature air or overwork. The patient begins to suffer from dizziness, noise and pain in the head, in addition, his memory and working capacity deteriorate.

In the event that such symptoms are present in a person for more than two months and are regularly repeated once a week, then we are talking about cerebral circulation failure.

After a detailed consultation and a comprehensive diagnosis, the doctor prescribes the most appropriate treatment to improve blood circulation. Accept discharged medicines the patient should immediately, without delay. Moreover, the course of such therapy involves the use of not only medications aimed at increasing blood flow to the brain, but also sedatives, as well as vitamin complexes.

Medicines that help improve poor circulation effectively combat this ailment. To eliminate such violations, agents are used that have a nootropic, vasodilating and antihypoxic effect.

In addition to drug therapy, the patient will still have to completely change their lifestyle. The patient should take regular breaks during work, sleep for at least 8 hours, and also avoid heavy physical exercise and negative emotions. It is advisable to walk in the fresh air as often as possible and ventilate the room. In addition, it is necessary to follow a diet, limit the intake of fats, carbohydrates and salt. To cure poor circulation, it is imperative to quit smoking. If you follow these recommendations, you will be able to stop the development of the disease.

Violation of cerebral circulation, the symptoms and treatment of which are interrelated, can lead to a stroke. It is for this reason, as soon as a person has the first signs of such a pathology, it is necessary to immediately consult a doctor. After all, only timely and effective therapy aimed at improving blood circulation in the brain will avoid negative consequences.

Poor blood flow in the hands

Diabetes.
Smoking.
High blood pressure.
Sedentary lifestyle.
High cholesterol.

Poor blood flow in the hands

Violation of blood circulation in the limbs leads to a deterioration in blood circulation in the body. This condition occurs due to the fact that the formed plaques clog the blood vessels.

The most common symptoms of this ailment include numbness in the fingers, headaches, swelling in the elbows and arms, tingling, cold extremity syndrome, and deterioration of the nails.

Poor blood circulation in the hands occurs, as a rule, due to the following reasons:

Abuse of caffeine, alcohol and drugs.
Diabetes.
Smoking.
High blood pressure.
Sedentary lifestyle.
High cholesterol.

People who have poor circulation in their hands need to eat more foods containing fiber, and also try to consume low-fat food, because most often it is because of such food that plaques are formed that block blood vessels. That is why, with such a disease, many patients are advised to lose weight.

Those who want to improve blood circulation in the extremities should definitely eat foods rich in vitamins E and C. You should also drink enough water with poor circulation. For this ailment, watermelon juice is especially useful.

Patients are strongly advised to maintain the body and spine in the correct position to ensure uninterrupted blood flow without difficulty or obstruction. To prevent numbness of the hands, keep them in a comfortable position during sleep.

Impaired blood circulation in the legs

Poor circulation to the extremities can lead to many health problems. If no action is taken with such an ailment, then the consequences can be serious.

The main cause of circulatory disorders in the legs is various diseases of the peripheral vessels. This problem arises when a plaque of fatty substance forms on the walls of the peripheral arteries, which hardens. Formed hardening makes it difficult for blood to move through the veins and arteries.

Often, the use of drugs and certain drugs, a sedentary and unhealthy lifestyle leads to a violation of blood circulation. Quite often, poor blood flow to the legs is observed with atherosclerosis. These problems also occur in people who are anemic, smoke a lot and eat poorly.

In case of impaired blood circulation, tingling sensations appear in the lower extremities, cramps, black and blue spots that occur most often in the calf muscles, as well as a feeling of numbness.

How to improve blood circulation in the legs?

To obtain an accurate diagnosis, the patient will have to undergo one of the following examinations: angiography of the arteries, Doppler ultrasonography, CT or MRA. Doctors compare the blood pressure levels of the ankles and hands to test how well blood is flowing through the limbs.

Therapeutic measures depend on the severity of the blockage in the veins and arteries. Mild and moderate forms of the disease are treated with medicines and various creams. Aerobics is also recommended.

Severe circulatory disorders in the legs are treated exclusively with a surgical procedure: endarterectomy, angioplasty, peripheral shunting, revascularization or atherectomy.

Consequences of poor circulation

If circulatory problems are left untreated, myocardial infarction can occur. Moreover, the risk of stroke is increased. In some cases, poor circulation leads to critical ischemia. It will be possible to avoid such complications only if you are regularly examined.

Improving blood circulation using folk methods

If poor circulation is diagnosed, what should be done in this case? To quickly eliminate the disease, the main treatment should be combined with folk remedies.

To do effective remedy, it is necessary to dissolve a small spoonful of edible salt and the same amount of sea salt in a glass of warm water. This liquid should be sucked in through the nostrils and the breath should be held for a few seconds. This solution should be treated for about 10 days.

To improve blood circulation in the legs, the following recipe will help: a pod of chopped hot pepper, a tablespoon of dry mustard and a little sea salt. All mix and pour a glass of vodka. The resulting mixture is infused for at least 10 days in a dark place. This means rubbing the limbs, after which they put on woolen socks. It is better to do the procedure before bedtime.

Nice help to get rid of this problem saline solution... To do this, 5 tablespoons of sea salt are diluted in a glass of warm water. Then a small piece of cotton wool is moistened in the solution and inserted into the nose for 20 minutes, keeping the head thrown back.

Prevention of blood flow disorders

To avoid problems with the circulatory system, it is necessary first of all to deal with lowering cholesterol, and also overcoming physical inactivity. Quitting bad habits helps to reduce the risk of developing such pathologies. In addition, it is important to timely treat infectious diseases that provoke complications.

Violation of cerebral circulation is a pathological process that leads to obstructed blood circulation through the vessels of the brain. Such a violation is fraught with serious consequences, not an exception - death. An acute process can turn into a chronic one. In this case, the risk of developing aneurysm, thrombosis and hemorrhage increases significantly. All these pathologies are fatal. In the presence of such a pathological process, you should urgently consult a doctor, treatment with folk remedies or drugs at your discretion is impossible.

Etiology

Violation of blood circulation in the brain can provoke almost any pathological process, trauma and even severe stress. Clinicians identify the following, the most common causes of cerebrovascular accident:

genetic predisposition;
head trauma;
previously carried over serious illnesses, with damage to the brain, central nervous system and nearby organs;
hypodynamia;
increased emotional excitability;
atherosclerosis;
diabetes;
hypertension;
frequent drops in blood pressure;
pathology of blood vessels and blood;
heart disease;
thrombophlebitis;
excess weight;
alcohol and nicotine abuse, drug use;
arrhythmia.

In addition, clinicians note that acute cerebrovascular accident may be due to age. In this case, people aged 50 and older are at risk. It should be understood that this violation can be caused by frequent stress, severe nervous strain, overwork of the body.

Classification

In international medical practice, the following classification of cerebrovascular accidents has been adopted:

acute form;
chronic form.

The pathologies of the chronic form include the following subspecies:

initial manifestations of insufficient blood supply to the brain (NPNMK);
encephalopathy.

The last subform is divided into the following subspecies:

hypertensive;
atherosclerotic;
mixed.

Acute disorders of cerebral circulation (ACVI) distinguish between the following subspecies:

transient violation of cerebral circulation (PNMK);
acute hypertensive encephalopathy;
stroke.

Classification of acute disorders of cerebral circulation Any of these forms is life-threatening, and at any time can provoke not only a serious complication, but also cause death. In the chronic form, the stages of development are also distinguished:

first, the symptomatology is vague. The person's condition is more indicative of chronic fatigue syndrome;
the second - significant memory impairment, social adaptation is lost;
the third - almost complete degradation of personality, dementia, impaired coordination of movements.

At the third stage of development of circulatory disorders, we can talk about an irreversible pathological process. However, the patient's age and general history should be taken into account. It is inappropriate to talk about full recovery. A classification is also used according to morphological changes:

focal;
diffuse.

Focal lesions include the following:

ischemic stroke;
hemorrhagic stroke;
subarachnoid hemorrhage.

Diffuse morphological changes include the following pathological processes:

small cystic neoplasms;
small hemorrhages;
cicatricial changes;
the formation of small-sized necrotic foci.

It should be understood that a disorder of any form of this pathological process can be fatal, so treatment must be started urgently.

Symptoms

Each form and stage of development has its own signs of cerebrovascular accident. The general clinical picture includes the following symptoms:

headaches for no apparent reason;
nausea that rarely ends with vomiting;
memory impairment;
decreased visual acuity and hearing;
dizziness;
impaired coordination of movements.

Transient cerebrovascular accidents are characterized by the following additional symptoms:

numbness of half of the body, which is opposite to the focus of pathology;
weakness of the arms and legs;
speech disorder - it is difficult for the patient to pronounce individual words or sounds;
photopsia syndrome - the visibility of luminous dots, dark spots, colored circles and similar visual hallucinations;
drowsiness;
ear congestion;
increased sweating.

Symptoms of cerebrovascular accident Since there is a symptom such as speech impairment and weakness in the limbs, the clinical picture is often confused with a stroke. It should be noted that in the case of PNMC, acute symptoms disappear in a day, which is not the case with a stroke. At the first stage of the chronic form, the following symptoms of cerebrovascular accident can be observed:

frequent headaches;
drowsiness;
increased fatigue - a person feels tired even after a long rest;
sudden mood swings, irascibility;
absent-mindedness;
memory impairment, which manifests itself in frequent forgetfulness.

During the transition to the second stage of the development of the pathological process, the following may be observed:

minor violations motor function, a person's gait may be wobbly, as if drunk;
concentration of attention worsens, it is difficult for the patient to perceive information;
frequent mood swings;
irritability, bouts of aggression;
almost constantly dizzy;
low social adaptation;
drowsiness;
efficiency practically disappears.

The third stage of chronic cerebrovascular accident has the following symptoms:

dementia;
hand tremor;
stiffness of movements;
speech impairment;
almost complete memory loss;
a person is not able to memorize information.

At this stage of the development of the pathological process, symptoms of almost complete degradation are observed, a person is not able to exist without outside help. In this case, we can talk about an irreversible pathological process. This is due to the fact that already at the initial stages, the neurons of the brain begin to die, which entails serious consequences if this process is not stopped in a timely manner.

Diagnostics

It is impossible to independently compare the symptoms and take treatment at your own discretion, since in this case, there is a high risk of complications, including those that are life-threatening. At the first symptoms, you should immediately seek emergency medical help. To find out the etiology and make an accurate diagnosis, the doctor prescribes the following laboratory and instrumental examination methods, if the patient's condition allows them:

general blood analysis;
lipid profile;
taking blood for glucose analysis;
coagulogram;
duplex scanning to identify affected vessels;
neuropsychological testing according to the MMSE scale;
MRI of the head;

In some cases, the diagnostic program may include genetic tests if there is a suspicion of a hereditary factor.

A method for diagnosing the initial manifestations of cerebrovascular accident How to treat this disorder, only a doctor can tell, after an accurate diagnosis and identification of the etiology.

Treatment

Treatment will depend on the underlying factor - depending on this, the basic therapy is selected. In general, drug therapy may include the following drugs:

sedatives;
neuroprotective agents;
multivitamins;
venotonics;
vasodilators;
antioxidants.

All drug therapy, regardless of etiology, is aimed at protecting the neurons of the brain from damage. All funds are selected only individually. In the process of undergoing drug therapy, the patient should constantly monitor blood pressure, since there is a high risk of developing a stroke, heart attack. except drug treatment, the doctor can prescribe a course of physiotherapy exercises. In some cases, such activities are used for rehabilitation. The standard program includes the following:

a set of exercises "balance", which is aimed at restoring coordination of movements;
a set of reflex exercises according to Feldenkrais;
microkinesitherapy;
exercises according to the Voight system.

The recovery program also includes a therapeutic massage and a course of treatment with a chiropractor.

Possible complications

Violation of cerebral circulation is a symptom of a serious and life-threatening pathological process. Even a slight delay in treatment can lead to the development of serious complications. In this case, the following should be highlighted:

complete disability;
dementia;
the development of pathologies from the cardiovascular system.

In the absence of timely medical care and correct treatment, a lethal outcome occurs.

Prophylaxis

Unfortunately, there are no specific methods for preventing the manifestation of such a symptom. However, if you apply in practice the elementary rules of a healthy lifestyle, you can minimize the risk of developing such a disorder. In addition, you need to systematically undergo a comprehensive preventive medical examination... At the first symptoms of the above-described clinical pictures, you need to urgently seek emergency medical help.

The human brain is responsible for coordinating most of the functions of our body. Circulatory disorders of the brain of any severity can provoke the development of various health problems - memory impairment, frequent fatigue, insomnia, decreased sex drive, poor concentration, etc.

Various factors affect blood circulation in the brain, including blood pressure, blood flow rate, the presence of diseases of the cardiovascular system, diseases of the spine, constant stress, excess weight, etc.

When there are minor disruptions or the first signs of problems with blood flow to the brain, simple changes in lifestyle, dietary habits and physical activity can help prevent the development of serious diseases.

The most frequent reasons problems with blood flow in the brain are:

Atherosclerosis- it occurs due to the accumulation of cholesterol in the vessels. With atherosclerosis, cholesterol plaques are deposited on the walls of blood vessels, which causes their blockage and narrowing of the blood flow.
Systematic stress. The state of stress negatively affects all organs and systems of a person; it can cause dangerous disturbances in the functioning of the brain.
Hypertension. With pressure drops, the heart rate is disturbed and the volume of blood pushed out by each contraction decreases, the lumen of the vessels narrows and the elasticity of the vascular wall is lost.
Head, neck and spine injuries of varying severity - in these cases, blood circulation is impaired due to hemorrhages.
Chronic fatigue syndrome. It becomes the cause of the disorder in the work of all major systems of the human body.
Unbearable physical activity. This is not only about excessive sports or hard physical work, sometimes an uncomfortable posture in which a person is for a long time is enough for circulatory disorders (for example, improper posture when working in an office).
Osteochondrosis(degenerative processes in the intervertebral discs) and scoliosis(curvature of the spine) - these diseases of the spinal column cause many pathological conditions in organism. In most cases, osteochondrosis and / or scoliosis of the cervical spine lead to impaired cerebral circulation.

Symptoms of circulatory disorders of the brain

Most often, circulatory disorders of the brain at the initial stages do not manifest themselves in any way and proceed unnoticed for a person, but with the progression of the process, alarming and very unpleasant symptoms arise.

The most common among them:

Frequent headaches. This symptom should by no means be ignored by constantly taking painkillers. It is very important to consult a specialist in time to avoid the development of dangerous consequences, including hemorrhagic stroke.
Dizziness and loss of balance indicate a serious lack of oxygen for the brain, if they occur, it is necessary to seek medical help as soon as possible.
Pain in the eyes. Most often, it increases towards the end of the day and is especially pronounced during eye movements and blinking.
Nausea and / or vomit accompanied by some or all of the above symptoms.
Convulsions(paroxysmal, involuntary muscle contraction) and numbness(decrease or complete absence of sensitivity), which appear for no apparent reason.
Change in consciousness and perception. In this case, you need to immediately contact a specialist.
Noise and ringing or ear congestion NS. The longer these symptoms are, the more serious the circulatory disorders of the brain are.
Fever or chills, increased blood pressure.

If you observe some or all of the above symptoms, you should immediately seek the advice of a specialist. In the case of disorders of the blood flow to the brain, self-medication is unproductive and can even harm. The specialist will send you for examination, and after identifying the true cause of the onset of the disease, he will prescribe a course of medications to improve blood circulation.

These may include:

drugs that prevent platelets from sticking together;
drugs to lower blood cholesterol levels;
vasodilator drugs;
drugs that prevent blood clotting;
nootropic drugs;
psychostimulants, etc.

Nutrition to improve blood circulation in the brain

For those who are wondering how to improve blood circulation in the brain or avoid aggravating the problem, it is necessary to add certain foods to their diet.

These include the following product groups:

Vegetable oils- olive, pumpkin, linseed. For the correct and "uninterrupted" work of our brain, the body needs polyunsaturated fatty acids, which can be obtained from vegetable oils... They are the nutritional basis for maintaining the proper functioning of the brain's neurons. In addition, polyunsaturated fatty acids are effective in preventing atherosclerosis.
Marine and oceanic fish species- trout, tuna, salmon, sea bass. The meat of these fish species is rich in omega-3 fatty acids, which are necessary for the membranes of brain cells and protection of blood vessels from the accumulation of cholesterol.
Berries- lingonberries, blueberries, currants, cranberries, etc. Almost all types of berries contain many antioxidants (molecules with a negatively charged electron) - natural substances that can slow down the processes of oxidation and aging of cells in the human body.
bitter chocolate with a cocoa content of at least 60%. This product contains a lot of tryptophan - an amino acid from which serotonin is formed, a hormone that prevents the development of headaches, migraines and depression.
Nuts- Greek, hazelnuts, almonds, cashews, pistachios, etc. They are rich in easily digestible proteins, healthy fats, vitamins and minerals, in addition, they contain essential amino acids necessary for the nutrition of the brain and the health of the human immune system.
Seeds- flax, pumpkin, sunflower. These foods are high in vitamin E, which has a positive effect on memory and cognitive processes. In addition, they contain a lot of omega-3 fatty acids, the benefits of which were discussed above.
Seafood- oysters, shrimps, mussels. These foods are rich in trace elements, in particular zinc and magnesium, which have a positive effect on attention and memory.
Green tea. Drinking this drink normalizes blood pressure, and the antioxidants contained in it help prevent aging of cells not only in the brain, but also in the entire body.

It must be remembered that fatty and fried foods, semi-finished products and fast food dishes provoke the accumulation of cholesterol in the vessels, which leads to their blockage and a decrease in blood flow, including to the brain.

Prophylaxis

In addition to correcting your eating habits, you can give a few more tips that will help improve blood circulation and prevent various disorders in the brain. First of all, it is necessary to avoid physical inactivity - weakening of muscle activity as a result of a sedentary lifestyle .. With the help of physical activity adequate to your gender, age, general health and weight, you can activate the blood supply to the body, including the brain.

Thermal treatments are very helpful- sauna and steam bath, as warming up the body improves blood flow throughout the body. Various means of alternative medicine are highly effective - periwinkle, propolis, tinctures on clover and other mixtures of plants that have a positive effect on the state of the cerebral vessels.

For the prevention of cerebrovascular accidents, it is necessary to avoid factors that increase the risk of vascular atherosclerosis. Overweight, smoking and high cholesterol can lead to this disease.

For people with diseases that affect blood circulation, regular visits to the doctor are shown to monitor the state of blood flow and prevent the aggravation of its disorders.

Blood supply to the brain in 60 seconds (Video)

L. MANVELOV, candidate of medical sciences, A. Kadykov, doctor of medical sciences.

Headache, noise and dizziness, memory impairment, increased fatigue, decreased performance - similar symptoms are found not only in the elderly, but also in middle-aged and even young people. Often, patients and even some medical professionals do not take such complaints very seriously. Meanwhile, they may indicate chronic cerebrovascular insufficiency.

Functional areas of the brain.

General scheme blood supply to the brain. Blood enters the brain through four large main arteries: two internal carotid and two vertebral arteries.

Brain with blood vessels (bottom view). The branches of the main vessels of the brain at its base form a vicious circle called the Willisian.

Blood clots, thrombi, develop in the area of atherosclerotic plaques that form on inner walls vessels. Blood clots can completely block even large vessels, causing serious cerebrovascular accidents.

Duplex scanning of the internal carotid artery. A formed small atherosclerotic plaque is visible, the lumen of the vessel is slightly narrowed

More late stage atherosclerosis - the lumen of the vessel of the internal carotid artery is partially blocked by a large plaque

Occlusion - complete closure of the vessel lumen by plaque.

Tortuousness of the right and left carotid arteries.

Magnetic resonance imaging of the brain. A snapshot of a healthy brain.

Changes in the medulla in Binswanger's disease - rarefaction of the white matter of the brain

Hydrocephalus - the accumulation of fluid in the brain tissue - manifests itself as an expansion of the furrows and ventricles of the brain (shown by arrows)

Multi-infarction condition - dead nerve tissue looks like small dark spots (shown by arrows)

Magnetic resonance angiography of the arteries. White arrows show: narrowing (stenosis) of the right internal carotid artery

Stenosis of the left internal carotid artery and blockage (occlusion) of the right

Left internal carotid artery occlusion

Right vertebral artery stenosis

Tortuosity of the right and left carotid arteries

BLOOD SUPPLY OF THE BRAIN

A large amount of energy is required for the normal functioning of the brain. Nutrients and oxygen are delivered to the cells of the nerve tissue through the bloodstream. Nature has taken care to create a high degree of reliability in the supply of blood to the brain. It is provided by four powerful main arteries: two carotid and two vertebral. At the base of the brain, the branches of these vessels form a vicious circle, named by Willis after the English physician and anatomist of the 17th century Thomas Willis, who first described it. Due to this, the lack of blood supply in one of the great vessels is compensated for at the expense of others. It also happens that even with serious disturbances of blood flow in three of the four main vessels, a person complains only of a slight deterioration in well-being - the compensatory capabilities of the brain are so great. Great, but, unfortunately, not unlimited. Man manages to "shake" these perfect compensation mechanisms created by nature. It all starts with the most common complaints of headache, dizziness, memory loss and fatigue. After some time, the patient develops more serious neurological symptoms, indicating multiple brain damage. The reason for this is chronic cerebral circulatory failure, or "dyscirculatory encephalopathy". This term was proposed in 1971 by well-known Russian scientists who worked at the Research Institute of Neurology of the Russian Academy of Medical Sciences, Academician of the Russian Academy of Medical Sciences E.V. Shmidt and Candidate of Medical Sciences G.A.Maksudov, and it means changes in the brain associated with disorders of its blood supply.

The main causes of the onset and development of discirculatory encephalopathy are arterial hypertension and atherosclerosis.

More than 40% of the adult population of Russia suffers from hypertension. Men and women, old people and young people get sick. Only in 5% of cases the cause of hypertension is clear. It can be renal failure, endocrine disorders, atherosclerosis and some other diseases. In 95% of cases, the cause of hypertension remains unclear, which is why it is called essential (literally - actually hypertension). In hypertensive disease, the walls of the vessels are compacted, local narrowings (stenoses) and tortuosities are formed. All this leads to circulatory disorders, including the blood supply to the brain. Sometimes it comes to occlusion - complete closure of the vessel lumen.

Unlike hypertension, the cause of atherosclerosis is known - it is a violation of lipid metabolism. In patients with atherosclerosis, the level of fat-like substances in the blood rises - cholesterol, low-density lipoproteins, triglycerides, which are deposited on the walls of blood vessels, forming lipid spots. Then the spots grow into so-called plaques. Due to the deposition of calcium salts, the plaques thicken and ultimately narrow or even close the lumen of the vessels. Then they begin to disintegrate, their particles - emboli, enter the bloodstream and sometimes clog other small and large vessels.

Sometimes osteochondrosis contributes to the development of discirculatory encephalopathy, since in this disease, due to deformation of the intervertebral discs, the vertebral arteries supplying the brain with blood can be clamped.

Violations of the blood supply lead to the gradual death of neurons in various parts of the brain, and the patient develops neurological symptoms. For discirculatory encephalopathy, emotional and personality disorders are most characteristic. At the beginning of the disease, asthenic conditions are noted: general weakness, irritability, poor sleep. Asthenia is often accompanied by depression. Gradually, such painful personality traits as egocentrism, periodically arising unreasonable excitement, which can be sharply expressed and manifest in inappropriate behavior, begin to appear. With the further development of the disease, emotional reactivity decreases and gradually turns into dullness and apathy.

Once started, the disease progresses steadily, although in its course both sharp periodic deterioration (paroxysmal course) and periods of a slow increase in the symptoms of the disease can be observed.

It should not be forgotten that discirculatory encephalopathy increases the risk of many severe brain diseases and, above all, stroke (acute circulatory disorders of the brain) (Manvelov A., Candidate of Medical Sciences; Kadykov A., Doctor of Medical Sciences. Stroke is a social and medical problem// Science and Life 2002, No. 5.). In Russia, strokes are recorded in more than 400 thousand people a year. Of these, 35% die in the first three weeks of the disease, and only half of the patients overcome the annual milestone. The possibility of epileptic seizures on the background of developing discirculatory encephalopathy should not be ruled out.

TYPES OF CHRONIC BRAIN INSUFFICIENCY

There are three main types of cerebrovascular accidents.

In Binswanger's disease, due to the thickening of the walls and narrowing of the lumen of small arteries, a diffuse lesion of the internal structures of the brain occurs - the so-called white matter. Multiple small lesions represent areas of dead neurons. In patients, there is a violation of circadian (daily) pressure fluctuations: at night it either falls too sharply, or, conversely, rises, although the pressure should slightly decrease at night. One of the main symptoms of the disease is sleep disturbance. The patient does not fall asleep well or sleeps with frequent awakenings. Other typical signs are the slow progression of memory and intelligence impairments to dementia (dementia); increasing gait disturbances, urination and defecation disorders. It is known that Binswanger's disease can overtake even at a relatively young age - up to 35 years.

Another type of discirculatory encephalopathy - the so-called multi-infarction conditions - is characterized by multiple small infarctions in the brain (micro-strokes). This means that in a certain area of the brain, due to clogging of the vessel, necrosis of the nerve tissue occurs. In this case, both superficial (gray matter) and deep (white matter) structures of the brain are affected.

The main reason for the development of multi-infarction conditions is the narrowing and thickening of the intracerebral arteries with arterial hypertension. Another common cause is heart disease accompanied by atrial fibrillation. In such patients, blood clots form in the cavities of the heart - thrombi, which can clog the vessels supplying the brain with blood. Increased blood clotting also contributes to the formation of blood clots. Another reason for the occurrence of multi-infarction conditions is atherosclerotic lesions of the intracerebral arteries.

Dyscirculatory ecephalopathy also develops when the main (carotid and vertebral) arteries are damaged, which are not inside the brain, but provide blood flow to the brain. Lesions can be of a different nature and causes - thrombosis, stenosis, bends and bends of various etiologies.

There are three stages of discirculatory encephalopathy. The duration of each of them can be different. Much depends on the degree of hypertension or atherosclerosis, lifestyle, habits, heredity, concomitant diseases, etc. At the initial stage of the disease, people often complain of headaches, dizziness, noise in the head, loss of memory (non-professional) and performance. Patients are absent-minded, irritable, tearful, their mood is often depressed. They usually find it difficult to switch from one activity to another.

At the next stage of the disease, memory disorders, including professional ones, progress. The circle of interests narrows, viscosity of thinking appears (fixation on some problem), quarrelsomeness, intellect suffers, personality change occurs. Such patients are characterized by daytime sleepiness and poor night sleep. Neurological symptoms intensify, movements slow down, their coordination is disturbed, slight speech disorders appear, staggering while walking, working capacity is significantly reduced.

At the last stage of the disease, gross changes in brain tissue make neurological symptoms even more pronounced, mental disorders intensify, up to dementia (dementia). Patients completely lose their ability to work, stop recognizing loved ones, perform inappropriate actions, and can get lost when they go out for a walk.

DIAGNOSTICS OF ENCEPHALOPATHY

When examining the overwhelming number of patients with discirculatory encephalopathy, characteristic diseases or physiological characteristics and habits are revealed. These risk factors include:

Arterial hypertension (blood pressure from 140/90 mm Hg and above);

Heart disease (coronary artery disease, rheumatic lesions, heart rhythm disturbances, etc.);

Diabetes;

Overweight;

Sedentary lifestyle;

Hypercholesterolemia (total cholesterol above 6.2 mmol / L);

Long-term and frequent neuropsychiatric stress (stress);

Complicated heredity for cardiovascular diseases (stroke, myocardial infarction or arterial hypertension in the next of kin);

Smoking;

Alcohol abuse.

Men with rapidly progressive discirculatory encephalopathy usually have a history of psycho-emotional stress, a sedentary lifestyle, alcohol abuse, lack of regular treatment, and the presence of two or more comorbidities. In women, in addition to these factors, overweight often contributes to the unfavorable course of the disease.

If patients with arterial hypertension and atherosclerosis (or representatives of other risk groups) complain of headache, dizziness, decreased performance, memory impairment, then the initial stage of discirculatory encephalopathy can be suspected. Patients with such symptoms should, first of all, constantly monitor blood pressure, undergo an electrocardiographic study, pass general blood and urine tests, blood tests for sugar and lipids. Psychological research, which assesses the state of memory, intelligence, attention and speech, does not interfere. ...

Even small nonspecific changes in the electrocardiogram can be the harbingers of cardiovascular diseases, manifested in impaired blood circulation in the brain. By the way, normal electrocardiograms or echocardiograms do not exclude the presence of the disease, since changes can be noticeable only at the time of ischemia (anemia) of the myocardium or an attack of angina pectoris. An electrocardiogram taken during exercise gives important information. Daily monitoring of the work of the heart also allows you to identify violations.

Information about the state of the fundus (the back wall of the eye), the cells of which are directly connected with the neurons of the brain, is important for the diagnosis. Changes in the vessels and nerve cells of the fundus make it possible to judge about violations of the structure of the brain tissue. In patients with discirculatory encephalopathy, hearing is often reduced, the swallowing reflex and sense of smell are impaired. Therefore, to make a diagnosis, it is necessary to conduct an otoneurological study that reveals violations of the vestibular apparatus, auditory, olfactory and gustatory perception.

Useful information is provided by the study of the rheological properties of blood - its fluidity. The main factor affecting the fluid properties of blood and the degree of its saturation with oxygen is considered to be hematocrit - the ratio of the volume of erythrocytes to the volume of plasma. Its increase contributes to an increase in blood viscosity and a deterioration in blood circulation. There is a direct link between high hematocrit and cerebral infarction.

After conducting preliminary studies, the patient is usually sent for an X-ray examination of the vessels of the brain - angiography. Doctors consider angiography to be the "gold standard" against which the results of other research methods are compared. After the introduction of a special contrast agent, X-ray images of the vessels of the brain are obtained. Angiography provides information about the duration and sequence of filling the blood vessels, about the formed "bypass" blood circulation pathways in case of blockage or narrowing of the vessels of the brain. The results of the study are important in deciding the feasibility of the operation.

Electroencephalography is an old and very common method of studying the brain, based on recording its electrical potentials. Changes in the encephalogram indicate organic changes in the brain tissue, therefore, at the initial stage of the disease with discirculatory encephalopathy, encephalography may not reveal any abnormalities.

A real revolution in brain research was made by the advent of the computed tomography method, which combines the achievements of radiography and computer methods of data processing. With its help, it is possible to obtain not indirect, but direct data on the structures of the brain and their changes. The method allows you to determine the location and size of foci of brain damage and their nature.

Recently, magnetic resonance methods have been used to diagnose circulatory disorders of the brain: nuclear magnetic resonance, magnetic resonance imaging and magnetic resonance angiography. Nuclear magnetic resonance provides information on the physicochemical properties of brain structures, so that healthy tissues can be distinguished from altered ones. Magnetic resonance imaging allows you to obtain images of the brain, determine the location, size, shape and number of foci, and study cerebral blood flow. Magnetic resonance angiography is a modification of magnetic resonance imaging. With its help it is possible to investigate the passage and "caliber" of extracranial and intracranial arteries and veins.

Currently, highly informative methods for obtaining a three-dimensional image of brain structures have been created and are successfully applied: single-photon emission computed tomography and positron emission tomography.

Ultrasound methods are widely used for examining patients not only in a hospital, but also on an outpatient basis: Doppler sonography and echotomography, duplex scanning and transcranial Doppler sonography. Doppler ultrasound is used to detect lesions of the carotid and vertebral arteries. It makes it possible to obtain information about the blood flow profile in the vessels. With duplex scanning, the color contrasting of the streams makes it possible to more clearly distinguish between moving (blood) and stationary (vessel walls) objects. The main vascular lesions detected by transcranial Doppler imaging are blockages, stenoses, spasms, and aneurysms. The most complete information about the state of the vascular system of the brain can be obtained by comparing the data of various methods of ultrasound examination. Recently appeared new method ultrasound diagnostics- transcranial sonography with color Doppler coding. It allows you to "see" the structures of the brain through the bones of the skull.

TREATMENT OF DISCIRCULATORY ENCEPHALOPATHY

Doctors have long known the so-called law of halves, based on the results of large epidemiological studies. Its essence lies in the fact that half of the patients do not know about their disease, and of those who do, half are not treated. Half of those who are being treated take medication irregularly, that is, the treatment is ineffective. Consequently, only about 12% of patients receive treatment. Such a depressing picture is taking shape because, as the French writer François de La Rochefoucauld said, "we do not have enough character to obediently follow the dictates of reason."

Meanwhile, it is known that arterial hypertension and the resulting discirculatory encephalopathy respond well to treatment. Research programs to combat arterial hypertension carried out both in our country and abroad have shown that with their help it is possible to reduce the incidence of stroke by 45-50% in five years. If the program of combating hypertension worked on the scale of the entire healthcare system in Russia, then in five years more than two million people who die from stroke would have been able to save the lives. And this is not counting the loss of patients with other lesions of the brain, heart, kidneys, eyes and other organs caused by hypertension.

1. To reduce the possibility of side effects, the antihypertensive drug is prescribed in minimal doses, and in case of insufficient decrease in blood pressure, the dose is increased.

2. To achieve the maximum effect, use combinations of drugs (to a small dose of one add a low dose of the other).

Patients with discirculatory encephalopathy against the background of severe hypertension should not strive to reduce blood pressure to normal (below 140/90 mm Hg), as this can lead to a deterioration in the blood supply to the brain; it is enough to reduce it by 10-15% from the initial level.

In addition to drug treatment, patients with hypertension must observe simple rules: limit the use of table salt (up to 5 grams per day - 1/2 teaspoon); for a long time, almost for life, to take antiplatelet agents (drugs that prevent the formation of blood clots); take vitamins and vitamin complexes containing ascorbic acid (vitamin C), pyridoxine (vitamin B 6) and niacin (vitamin PP).

With discirculatory encephalopathy caused by atherosclerosis, treatment has its own characteristics and implies a low-calorie diet (up to 2600-2700 kcal per day) with restriction of animal fats. With stable indicators of total blood cholesterol (above 6.2 mmol / l), which persist for at least six months against the background of a strict diet, drugs that lower cholesterol levels (statins) are prescribed.

Combined antiplatelet and anticoagulant therapy is used to prevent the progression of multiinfarction conditions of the brain. Anticoagulants (drugs that reduce blood clotting) are selected in accordance with the indicators of blood clotting and prothrombin and are recommended to be taken almost for life. In this case, it is necessary to control the level of prothrombin in the blood once every two weeks. Patients taking anticoagulants should report any signs of bleeding to their doctor.

In addition to treatment aimed at eliminating the causes of discirculatory encephalopathy, patients are prescribed symptomatic therapy aimed at reducing the severity of symptoms. For the prevention of memory impairment and a decrease in intelligence, agents are used that improve the metabolism in the brain. For movement disorders, therapeutic exercises, massage and other methods of restorative therapy are recommended. With dizziness, vascular drugs and drugs that affect the autonomic nervous system are prescribed.

Quite often discirculatory encephalopathy manifests itself in the form of asthenic-depressive syndrome. With his symptoms, doctors prescribe psychotherapy, psychological assistance, drug therapy: antidepressants, sedatives. But first of all, you should take care of creating a welcoming environment in the family and at work. After all, Paracelsus, an outstanding physician of the Middle Ages, noted: "The best cure for diseases is a good mood."

In patients with gross narrowing of the main vessels of the head (over 70%), the question of surgical intervention... It means three types of operations: stenting (expanding the lumen of a vessel using a special frame - a stent), reconstruction of the vascular system (connecting various vessels to each other, forming branches) or removing a part of the vessel and replacing it with a prosthesis.

For the prevention of discirculatory encephalopathy, a healthy lifestyle is of no small importance: adherence to the work schedule, diet with restriction of table salt, liquid (up to 1-1.2 liters per day), products containing animal fats (fatty meats, liver, sour cream, butter , eggs, etc.), and high-calorie foods. Besides fat, high-calorie foods include alcohol and confectionery. It is good that the diet is dominated by vegetables and fruits. You should eat at least four times a day, distributing food by calorie content as follows: breakfast before work - 30%, second breakfast - 20%, lunch - 40%, dinner - 10%. It is recommended to have dinner no later than two hours before bedtime. The interval between dinner and breakfast should not exceed ten hours.

Patients need to monitor their weight, but it should be reduced gradually. In a person leading a sedentary lifestyle, energy consumption is on average 2000-2500 kcal per day. If a woman reduces the calorie content of food to 1200-1500 kcal, and a man to 1500-1800 kcal, then in a week they will lose 0.5-1 kg. This rate of weight loss is considered optimal. An increase in physical activity gives a good preventive effect. Exercise increases the cardiovascular system's resistance to physical activity, which translates into a decrease in heart rate and blood pressure. As a result, mood improves, self-confidence appears, depression, fears, headaches, dizziness, and sleep disturbances decrease or disappear altogether. Patients become physically stronger and more enduring. A significant improvement in the condition is noted when conducting classes 3-4 times a week for 30-45 minutes. However, even after short training sessions (15-20 minutes each), the patient gets better.

Physiotherapy should be carried out regularly, with a gradual increase in the load. The intensity of the exercise is calculated using the maximum heart rate indicator (the patient's age in years is subtracted from 220). For patients who lead a sedentary lifestyle and do not suffer from coronary heart disease, choose such an intensity of exercise at which the heart rate is 60-75% of the maximum. Of course, before starting to engage in physiotherapy exercises, you should definitely consult your doctor.

Patients in the I and II stages of discirculatory encephalopathy are shown Spa treatment... It is better if it is a cardiovascular sanatorium in a familiar climate.

Timely diagnosed discirculatory encephalopathy and correctly selected complex treatment prolong an active, full life.

The polyethiology and polysystemic nature of most diseases of the brain and spinal cord necessitate a comprehensive study of cerebral functions, therefore, along with the study of energy metabolism, it is necessary to simultaneously study glucose utilization, local and global cerebral blood flow, as well as the level of cerebral oxygen metabolism. PET (positron emission tomography) meets these requirements. The PET method has shown that the functional activity of a region of the brain in animals and humans correlates with a regional increase in cerebral blood flow and glucose or oxygen metabolism, and a decrease in brain activity is reflected in their inhibition (FECamargo et al., 1991; DEKuhl et al., 1982; DEKuhl et al., 1984; EJMetter, WRHanson, 1986; MERaichle et al., 1984; D. Rougemont et al., 1983; JLTyler et al., 1988; JRWagner, 1985; K. Wienhard et al., 1989). It would be of interest to assess these parameters in infantile cerebral palsy, which is associated both with atrophic processes and with a reduction in the mediator functions of the cerebral regions concerned.

Normally (under physiological conditions), according to PET data, there is a linear relationship between the parameters of cerebral hemodynamics and metabolism. At the same time, the level of MC (cerebral blood flow) is proportional to the RCM (the volume of blood circulating in the vessels of the brain), VOC (the level of oxygen metabolism) and UOG (the level of glucose metabolism).

RCM refers to the most important parameter of cerebral hemodynamics and reflects the reaction of autoregulation of cerebral circulation in response to changes in perfusion pressure (A.G. Vlasenko, M.-K. Peti-Tabue et al., 1998, W.J. Powers, M.E. Raichle, 1985). The ability of vessels to increase the diameter is significantly limited in those blood supply basins where compensatory vasodilation has already occurred, and these areas of the brain are most susceptible to the development of ischemic damage with a further decrease in perfusion pressure due to a drop in systemic arterial pressure. Assessment of the vasodilation capabilities of the cerebral vascular system is important for the choice of treatment tactics. The reflection of the local cerebral perfusion pressure is the ratio of MK and RCM (J.M. Gibbs et al., 1984; J.W. Powers et al., 1987; U. Sabatini et al., 1991; H. Toyama et al., 1990).

With a decrease in CPP (cerebral perfusion pressure), the first compensatory response of the cerebral vascular system is vasodilation (the stage of autoregulation). At the same time, there is a gradual increase in RCM, while other indicators remain practically unchanged. When the CPP reaches the lower limit of autoregulation and the reserve capacity of vasodilation is largely depleted, MC begins to decline. Nevertheless, in this case, the SVC initially remains unchanged, which leads to an increase in the extraction of oxygen from arterial blood (the stage of oligemia), i.e. to an increase in FIK (fraction of oxygen extraction from inflowing arterial blood).

With a further decrease in CPP, a decrease in SVC develops, indicating the onset of the stage of true ischemia with impaired neuronal activity. In the future, this condition may undergo a reverse development (ischemic penumbra) or become irreversible (cerebral infarction). The presence of irreversible damage to the brain substance is evidenced by the VOC values not exceeding 1.3-1.5 ml / 100 g / min. RCM increases significantly at the stage of oligemia and remains elevated, but to a lesser extent, as ischemia progresses.

Ischemic penumbra (“ischemicpenumbra”). According to the modern concept of ischemic penumbra, it is a region of the brain with depressed functional activity, but preserved viability of nerve cells and is located on the periphery of the ischemic focus, which undergoes necrosis due to irreversible damage to the brain substance. The outcome of ischemic stroke largely depends on which part of the neurons in the ischemic penumbra "survive" and restore their functional activity. Therefore, the area of ischemic penumbra is the main target of therapeutic action. Restoration of adequate blood flow and functional activity of neurons in this area can help to reduce the size of irreversible brain damage, the volume and severity of neurological deficit, and, consequently, to improve the outcome of stroke (A.G. Vlasenko, Yu.K. Milovidov, V.V. Borisenko and V.V. cit. ed., 1998).

The area of ischemic penumbra is characterized by a sharp decrease in MC (below 20 ml / 100 g / min), a pronounced increase in FIC (over 0.80), as well as a moderate decrease in SV. A decrease in MC to 10 ml / 100 g / min causes a cascade of biochemical reactions resulting in cell death, i.e. the zone of potentially viable tissue is located between MK levels from 10 to 20 ml / 100 g / min (D. Krieger, 1998). The development of irreversible changes in the ischemic penumbra is evidenced by a sharp decrease in SVC with intact MC, as well as a rapid progressive decrease in FIC from high values to minimum values. The presence of an area of a sharp increase in FIC and a decrease in MC against the background of relative stability of the SVC, on the contrary, indicates the preservation of ischemic penumbra. As a rule, the fate of ischemic penumbra is decided already in the first few hours of a stroke, but in some cases it can exist for a longer time, at least 16 hours. recovery, thus confirming that The “survival” of the ischemic penumbra cells is the key to recovery from stroke.

According to A.G. Vlasenko, J.-C. Baron, J.-M. Derlon (1998), the fact that they (by the PET method) detected signs of ischemic penumbra up to 18 hours after the onset of a stroke indicates the need to revise the concept of a universal, limited narrow time frames (no more than 6 hours) of the therapeutic window and the advisability of an individual assessment of the state of cerebral hemodynamics and metabolism when planning treatment. Unfortunately, the concept of ischemic penumbra, “therapeutic window”, “window of hope” is not being developed in perinatal neurology, in general, and in cerebral palsy, in particular.

When studying the PET method of the distant hemodynamic and metabolic consequences of stroke, A.G. Vlasenko, J.-C. Baron, J.-M. Derlon (1998) and the authors cited by them found a decrease in MC and SV in areas of the brain located at a considerable distance from a heart attack. The identification of such areas allows mapping the disturbances in the interconnection of neurons that arise as a result of focal ischemia. Traditionally, all such phenomena are united under the general name “diachysis”, although this term sometimes hides a variety of cellular disorders - from a reversible decrease in functional activity to degenerative processes, while they have in common a similar picture of metabolic changes. It has been shown that some of these disorders can be of a purely functional nature, i.e. be potentially reversible. The phenomenon of diachysis is believed to be due to functional inactivation and deafferentation of neurons both near and at a distance from the infarction and manifests itself in the form of hypoperfusion.

The phenomenon of cross cerebellar diachysis, consisting in a decrease in SV in the cerebellar hemisphere opposite to the lesion focus, is detected (by PET) in almost half of patients with cortical or subcortical strokes. This phenomenon is most often encountered and is more pronounced with extensive heart attacks in the fronto-parietal region of the cerebral cortex, as well as with subcortical infarctions with damage to the inner capsule. According to A.G. Vlasenko, J.-C. Baron, J.-M. Derlon (1998), such a topographic relationship suggests that cross cerebellar diachysis occurs due to damage to the cortical-bridge-cerebellar pathways with transneuronal functional depression.

A decrease in metabolism in the cortical regions of the left hemisphere, revealed in patients with subcortical strokes and aphasia, suggested that speech disorders may be due to the phenomena of diachysis. The phenomena of diachysis in the form of a diffuse decrease in metabolism in the cerebral cortex of the same side as the focus are described in the case of damage to various parts of the optic tubercle and, apparently, are caused by damage to the activating thalamocortical pathways. A decrease in metabolism, although less pronounced, can also be noted in the cortex of the opposite cerebral hemisphere. Since the severity of metabolic disorders correlates with the severity of cognitive impairments, it is assumed that there is a relationship between these phenomena.

PET studies have revealed metabolic effects that propagate in the opposite direction, i.e. from the cortex to the depth of the hemisphere, for example, a pronounced decrease in metabolism in the striatum and the optic hillock on the side of the cortical-subcortical stroke.

PET studies using functional speech loads allow us to study the features of speech recovery and assess the prospects for such recovery in patients with aphasia. In this case, a favorable outcome is associated with partial preservation of speech zones in the area of cerebral infarction in the dominant hemisphere, as well as a decrease in the phenomena of diachysis in morphologically intact areas of the opposite hemisphere.

In case of progressive aphasia without dementia, a number of authors have revealed metabolic changes by PET-method, primarily in the left temporal region (P.J. Tyrrell et al., 1990). CT in these patients reveals an expansion of the subarachnoid spaces of the left frontotemporal region against the background of a general, but less pronounced, expansion of the subarachnoid space of the cerebral hemispheres and the ventricular system (P.J. Tyrrell et al., 1990). Over time, these patients develop dementia, which suggests that progressive isolated aphasia, which at the first stage of the disease corresponds to local atrophy of the cerebral cortex, is ultimately only the debut of a widespread atrophic process (A.S. Kadykov et al., 1996) ...

D. Kuhl et al. (1984) in a PET study conducted in 8 patients with Parkinson's disease and 14 healthy individuals, concluded that the patients have a decrease in the average global rate of glucose utilization (19.9 plus or minus 4.4 mmol / 100 g / min) compared with control (25.1 plus or minus 5.0 mmol / 100 g / min). The authors showed that regional differences in 18F-fluorodeoxyglucose metabolism in the temporal, parietal, frontal, occipital regions of the cerebral cortex, white matter, as well as in the caudate nucleus and thalamus do not exceed random variables... A repeated study, carried out after a 2-week course of L-DOPA therapy, showed that the level of global glucose metabolism increases insignificantly and manifests itself only as a trend, although the clinical effect was significant. Comparing the results of PET studies with the severity of clinical symptoms of parkinsonism and control parameters (volunteers of the corresponding age), it was possible to note a slowdown in the global rate of glucose utilization by up to 20% with the deepening of clinical manifestations. The expected parallelism between the decrease in the rate of glucose utilization in the striatum and the level of dopamine deficiency in the same structure, which corresponds to the severity of parkinsonism, was not found. The authors believe that degeneration of the striatum in parkinsonism does not significantly affect the rate of glucose utilization in the same structure of the brain.

This statement is consistent with the data of the study by D. Rougemont et al. (1983), in which there were no differences in local glucose metabolism in healthy individuals and in patients with parkinsonism. Changes in the content of 18F-fluorodeoxyglucose before and after treatment with L-DOPA had weak dynamics, while clinically the patients showed a significant improvement.

E. Metter and W. Hanson (1986), along with PET studies of 18F-fluorodeoxyglucose metabolism, conducted neurological, clinical and CT studies in 10 patients with symptomatic parkinsonism during speech and acoustic testing. We studied hypokinetic dysarthria, the degree of which, as it turned out, does not depend on the severity of the clinic and the variants of CT and PET manifestations.

The negative effect of hypoxia on cerebral blood flow is multicomponent: increased blood viscosity, insufficient deformability of erythrocytes, microcirculation disorders, poor tissue oxygen diffusion (G.A. Akimov, 1983). GD Dzhivelegova et al. (1983) consider the aggregation activity of platelets to be the most sensitive test for oxygen deficiency in fetuses and newborns. The specified complex of causal factors (all together or each of them separately) can, due to the difficulty of metabolic processes in the tissues of the body at the level of the microvasculature, lead to local changes in metabolism. This means that aerobic glycolysis is replaced by anaerobic, the Krebs cycle is disrupted, lactic acid accumulates, which immediately affects energy production (B.S. Vilensky, 1995). If, under conditions of aerobic glycolysis, one glucose molecule during its combustion forms 38 molecules of adenosine triphosphate (ATP), then when switching to anaerobic glycolysis, one glucose molecule forms only 2 ATP molecules... The developing acidosis, initially extracellular, further initiating intracellular, causes the disintegration of lysosomal membranes and promotes the activation of proteases. Ultimately, this "lysosomal explosion" leads to autolysis - the disintegration of cellular structures. Hence, the possibility of metabolic damage to the brain is understandable, often in the form of multiple foci of hypoxemic dysmetabolism.

§eight. Hypoxia and endothelial damage. Recently great importance attached to hypoxic damage to the endothelium. The literature (R. Kurt et al., 1995 and others) discusses the possibility that abnormal endothelial cell function may contribute to vasoconstriction by interfering with the production or action of the dilator, or by inducing the production of a constrictor.

Modern data prove that the vascular endothelium not only serves as a passive non-thrombotic interface between the blood and the vessel, but plays a dynamic role in the regulation of processes such as hemostasis, inflammation, and vascular permeability. There is more and more evidence that the endothelium plays an important, active role in vasoregulation.

In the laboratory of I.V. Gannushkina (1996) in experiments on animals and on isolated arteries of the brain, the new kind autoregulation of cerebral blood flow, which is based on the endothelium-dependent sensitivity of the cerebral vessels to the nature of the blood flow, and not only to its volume. Endothelial cells inactivate, activate and produce certain substances that can alter vascular tone (J.W. Ryan, U.S. Ryan, 1977; T.M. Griffith et al., 1984). For example, at the level of endothelial cells, 5-hydroxytryptamine, norepinephrine, bradykinin, enkephalins, acetylcholine, ATP, ADP and some prostaglandins are inactivated. Moreover, endothelial cells are also involved in the activation of angiotensin I to angiotensin II and in the production of prostacyclin (PGI2), a strong determinant of vascular reactivity in different conditions(A. L. Hyman et al., 1982; R. F. Grover et al., 1983). According to D. Davidson, S.A. Stalcup (1984), the newborn may be particularly prone to metabolic endothelial dysfunction.

Another aspect of endothelial cell function is the generation of non-prostaglandin substances that either promote or modulate the in vitro response of vascular smooth muscle to various stimuli. It has been shown (RF Furchgott, 1983; MJ Peach et al., 1985; PM Vanhoutte, VMMiller, 1985) that the endothelium plays a role in the relaxation of the arteries caused by acetylcholine, bradykinin, histamine, substance P, thrombin, PAF, ATP, ADP and etc. Conversely, the relaxations that are achieved by exogenous vasodilators such as PGI2, adenosine, atrial natriuretic factor, and exogenous agents like calcium channel blockers, nitroprusside and isoproterenol do not necessarily depend on endothelial cells, but rather directly on smooth muscles. There is additional evidence suggesting that vasoconstrictor agents such as norepinephrine and angiotensin II also stimulate endothelial cells to release a relaxing factor (different from or in addition to PGI2) that modulates direct vasoconstriction (R. F. Furchgott, 1984). Thus, the response to a given vasoconstrictor may depend on the balance between its effects on endothelial and smooth muscle cells.

In addition to the production of powerful vasodilators PGI2 and VERF by the endothelium, there are data on the generation of vasoconstrictor signals by the endothelium. Anoxia, as shown by J.G. DeMey, P.M. Vanhoutte (1982), enhances the contractile responses of isolated arteries and veins to norepinephrine. This enhancement decreases or stops after removal of the endothelium.

Summarizing these data, KR Stenmark et al. (1995) suggest that vascular responsiveness to various stimuli may be partially determined by signals arising from the endothelium. Endothelial damage can therefore cause changes in receptor-dependent endothelial cell activation, in the ability of the endothelium to release mediators, and in smooth muscle reactivity to mediators. Any or all of these changes can have a significant effect on vascular regulation.

The endothelium plays a key role in the regulation of smooth muscle cell growth and secretes growth factors for connective tissue cells. At least two major growth promoting factors have been identified in culture from intact endothelial cells in culture. These are platelet-produced growth factor (P.E.DiCorleto, 1984) and fibroblast growth factor (C.M. Gajdusek et al., 1980; P.E.DiCorleto et al., 1983).

Like the mitogenic activity determined by endothelial cells, the heparin-like inhibitor of smooth muscle cell proliferation produced by endothelial cells is of great importance (C.M. Gajdusek et al., 1980; J.J. Castello et al., 1981). This factor, under normal conditions, can prevent or limit abnormal proliferation of smooth muscle cells. When the endothelium is damaged, a decrease in the production of this inhibitor can lead to proliferation of smooth muscle cells. It is believed that hypoxia, which itself negatively affects the growth of smooth muscle cells (WEBenitz et al., 1986), is able to stimulate the proliferation of smooth muscle, either by stimulating the production of mitogenic factor from endothelial cells (RLVender et al., 1984), or a decrease in the production of a heparin-like inhibitor (DEHumphries et al., 1986), or both. These studies, therefore, show that as a result of vascular lesions, incl. and hypoxic, impairment of the production of paracrine growth factors by the endothelium may occur.

As an alternative and / or possibly a supplement, there is a possibility that endothelial damage could lead to the penetration of plasma proteins into the vascular wall. There are many possible mechanisms for altering cell phenotypes during “vascular leakage”. Extravasation of blood components into tissue structures, for example, can expose cells of the medial and adventitia layers to specific modifiers, such as peptide mitogens and differentiation factors, which can contribute to the genesis of vascular changes (R. Ross, 1986).

R. Ross (1986) summarized the data indicating that the increase in smooth muscle can occur even if the endothelium remains intact. Therefore, in the systemic circulation, the passage of plasma factors into the vascular walls, regardless of the integrity of the endothelium, may allow growth factors, including platelet-produced growth factor, to stimulate proliferation. Hypoxia, by increasing extravascular water volume and protein leakage through either damage to the endothelial barrier and / or increased pressure in the microvessels, can be a critical factor in this process, providing a driving force to push blood or endothelial cell-produced factors into vascular tissue.

J.L. Szarek, J.N. Evans (1987) showed that during chronic hypoxia the mechanical properties of large and small vessels change in different ways. Active tension decreases in both large and small vessels. In large vessels, the rigidity of the walls does not change, but in small vessels it increases. This leads to a limitation of the effect of vasodilation (K.R. Stenmark et al., 1987), an important role in which is played by hypoxic structural changes in the middle layer and the adventitia in the form of the appearance of vasodilation limiting “cuffs”.

§nine. Interrelation of hypoxia, angiopathy, circulatory disorders, BBB pathology and perivascular pathology. The main feature of the pathogenesis of intrauterine asphyxia is that, according to N.L. Garmasheva (1967), it is always preceded by fetal circulatory disorders. In these cases, conditions are often created under which the venous outflow from the region of the brain stem is disturbed (due to anatomical and physiological characteristics), which leads to secondary persistent perivascular (perivenular and pericapillary) edema of this important part of the brain, which cannot but affect the subsequent ante- and postnatal development and functioning of the nervous system and the body as a whole. I recall the question of A. Kreindler (1975): “could not, as a neurogenic factor in the emergence of acute signs of cerebral circulation insufficiency, manifest a chronic ischemic disease of the reticular formation, the more pronounced, the more frequent attacks are repeated, and lead, in the end, to the formation of irreversible nerve damage ”?

The expansion of the perivascular spaces is also associated with pulse trauma to the perivascular tissues and / or atrophy of the surrounding parenchyma (O.S. Levin, 1997). According to D.B. Bekov (1965), a feature of the outflow from the nuclear substance of the basal ganglia is the continuity of the venous networks, their transition from one nucleus to another and then the outlet of the vessels to the surface of the brain. Therefore, minor outflow disturbances in one of the cores can cause obstruction to outflow throughout the system. This is especially true for the striatum nuclei.

Disorder of the venous circulation plays an important role among the vascular diseases of the brain. It is known that 70% of the blood volume is in the veins (I.N. Dyakonova et al., 1977), and the section of small veins (venules and veins with a radius of 10-15 microns to 1-2 mm) has the greatest capacity (B. Folkov , E. Neil, 1976). Pathomorphologically increased venous pressure and obstruction of venous outflow are accompanied by venous and venular stasis and hyperemia, increased BBB permeability. In the future, there may be a proliferation of the inner membrane, thickening of the walls of the veins, the appearance of parietal thrombi and foci of periphlebitis. This leads to a thickening of the basement membrane of the capillaries, and the thickening of the basement membrane, in turn, to anoxia and a change in the tone of the vascular wall (swelling of the endothelium) and increased resistance for the flow of aggregates of erythrocytes and platelets, which are formed when venous outflow is slowed down. P. P. Nawroth, D. M. Stern et al. (1987) consider the slowing down of blood flow as a thrombogenic stimulus, and N.V. Vereshchagin (1996) indicates that hemorheological changes may have an independent significance in the origin of cerebral infarctions.

Chiange et al. (1968 - cited in: V.I.Salalykin, A.I. Arutyunov, 1978) during a histological examination of the cortical layers in those areas in which blood flow did not recover after ischemia, the following picture was found. The capillaries were compressed by edematous pericapillary glial cells, and therefore the spaces between these small vessels almost completely disappeared. In the lumens of the capillaries, numerous large endothelial “bubbles” were determined, which, due to edema, can also cause disturbances in the capillary circulation. The authors suggest that the local increase in blood viscosity as a result of the release of fluid into the pericapillary tissues during ischemia is one of the important factors causing circulatory disorders after the cessation of ischemia. In the postischemic period, the main role is played by a local circulatory disorder caused by tissue edema.

I.V. Gannushkina, V.P. Shafranova (1974), G.I. Mchedlishvili (1975) experimentally showed that with circulatory-cerebral hypoxia, blood flow is disturbed not diffusely in the entire vascular system of the zones of adjacent blood supply to the brain, but only in some of them. plots. First, blood flow slows down in individual veno-venous anastomoses and small veins, then in individual arterio-arterial anastomoses, in the intracerebral arteries and small arteries of the brain surface that extend from them. The slowdown in blood flow is accompanied by a collapse of the walls of blood vessels and a decrease in their diameter. The formed elements of the blood gradually stick together, and the formed lumps are retained in the branches of small vessels or adhere to the walls of the veins. As a result of the developing microembolism, mainly plasma begins to flow through individual sections of the vessels, which, as it were, is filtered through these lumps. Reduced blood circulation occurs, which further increases brain hypoxia in the damaged areas. In the basins of dilated arteries, intracapillary pressure increases, as a result of which filtration edema of the brain increases, leading, in turn, to compression of the microvasculature and a secondary decrease in cerebral blood flow.

GD Knyazeva et al. (1966 - cited in: V.I.Salalykin, A.I. Arutyunov, 1978) noted that a pronounced drop in pO_ in the brain leads to morphological changes in it. The earliest of these are perivascular edema, the most recent are multiple hemorrhages. As a result, two pathological changes in the microvasculature can form: stretching and occlusion of capillaries with the formation of microaneurysms and exudates and impaired BBB permeability due to changes in interendothelial structures.

According to V.I.Salalykin and A.I. Arutyunov (1978), the issues of the blood-cerebral and blood-forming barrier are only part of the problem of the permeability of the vascular walls. TF Goman, TP Sizonenko (1974) note that the most significant violations of the blood-brain barrier with high permeability (14-15%) are observed in patients with hemorrhagic strokes. In acute hemorrhages with a sudden onset, the permeability of this barrier increases moderately (6-7%).

In conditions of a disturbed BBB, the penetration of substances into the brain is facilitated, which causes general disturbances in the metabolism of neurons. Hyaline degeneration of arterioles also leads to blockage and desolation of capillaries and is accompanied by the development of collateral shunts. The resulting perivascular focal ischemia promotes the growth of functionally defective fibrovascular tissue, since viable endothelial cells tend to proliferate in a hypoxic environment (A.S. Efimov, 1989). Fibrovascular cords, similar to post-infectious or post-traumatic adhesions, have a wrinkling and / or irritative effect on the brain substance. These factors (the presence of zones of non-perfused capillaries, disseminated areas of ischemia and venous stasis) increase and prolong cerebral disorders, i.e. are a very important secondary pathogenetic link.

There is a well-known aphorism of L.O. Badalyan that vascular pathology stands “on two legs” arterial and venous. According to A.A. Shutov (1996), one should not ignore the frequency and polymorphism of venous circulatory disorders. Persistent cerebral venous dysfunction and its consequences are clearly underestimated in their importance as a link in the etiopathogenesis of perinatal encephalopathies, in general, and cerebral palsy, in particular, and one of the reasons for the steady progression of the disease, the correction of which would make it possible to achieve significant progress in prevention and treatment.

For intrauterine asphyxia, subarachnoid hemorrhages are typical. Hemorrhages under the ependymus of the lateral ventricles are also possible, followed by the formation of periventriculopathy (P.S. Gurevich, 1989). Ischemic infarctions of the subcortical parts of the brain often occur in term infants and are localized in the tegmental area, caudate nucleus and thalamus (D.A. Khodov, L.D. Molchanova, 1984). Clinically, this condition can often be detected only at the age of one year or later, when extrapyramidal insufficiency becomes noticeable (J.J. Volpe, 1975).

In practice, pure fetal hypoxia is observed relatively rarely (L.D. Mochalova et al., 1984). Z. Freud already in 1897 pointed out that asphyxia is the result of already existing brain damage. According to K.A. Semenova (1996), intrauterine hypoxia occurs a second time with any harmful effect on the brain and, which is very important, is accompanied by the phenomena of dysontogenesis.

Hypoxia disrupts the development of the vasculature and tissue of the fetal brain (B.N. Klosovsky, 1949, 1968; Yu.I. Barashnev, 1967; K.T. Nazarov, 1968; T.P. Zhukova et al., 1984). This is consonant with the views of I.A. Zambrzhitsky (1989), who believes that the canonical principle of the unity of structure and function is inconceivable without commonality in the development of cellular structures and their vascular-capillary networks, without which the structural and functional specialization of the brain cannot develop. P.S. Gurevich (1989) considers hypoxia to be one of the components of intoxication, infectious diseases and fetal malformations. According to A.D. Bedrick (1989), asphyxia is only a part of the complex of shifts that underlie many pathological conditions. Many scientists (T.P. Zhukova et al., 1984; I.N. Ivanitskaya, 1993; Yu.Ya. Yakunin et al., 1979, etc.) consider anoxia not an independent disease, but a complex multiphase process.

§ten. The relationship between the pathology of the central nervous system and the whole organism during hypoxia. Due to the developing global metabolic disorders, in hypoxic conditions of the fetus and newborn, not only the child's central nervous system is involved in the pathological process, but the entire body as a whole. The pathogenetic essence of changes caused by hypoxia and acidosis on the periphery is the degree of disturbance and reversibility of tissue perfusion (A.A. Mikhailenko, V.I. Pokrovsky, 1997).

In severe hypoxia, V.A. Tabolin et al. (1975, 1987) revealed inhibition of the ACTH-educational function of the anterior pituitary gland and a decrease in the function of the adrenal cortex, dysfunction of the pituitary-thyroid system. Under the influence of hypoxia, the function of the main vital systems of the fetus and newborn is disrupted: cardiovascular, respiratory, digestive, and immune. According to T.P.Zhukova, M. Hallman (1982), taking into account the direct effect of antenatal hypoxia on other organs (lungs, heart, etc.), all disorders of homeostasis in the neonatal period cannot be attributed only to central mechanisms. Unfortunately, when studying the etiology and pathogenesis of infantile cerebral palsy, this most important position is often not taken into account, which, obviously, affects the effectiveness of the treatment of this complex disease.

Thus, the pathological course of pregnancy, causing fetal hypoxia of varying severity, leads to imbalance and dysfunction of almost all body systems of the fetus and newborn. At the same time, there is one common pattern for all systems: with a mild degree of hypoxia in the early stages of its impact, functions are activated, with prolonged exposure to hypoxia, especially with its severe degree, functions are suppressed or depleted, especially in premature babies (N.A. Torubarova et al., 1993).

Summarizing the clinical features of the semiology of newborns with hypoxic brain damage, Yu.I. Kravtsov and F.Kh. Aminov (1994) note that, regardless of the severity of the process, there is always a diffuse lesion along the entire length of the cerebrospinal axis. T.P. Zhukova et al. (1984) also emphasize that in children with spastic forms of cerebral palsy, an important etiological factor is hypoxic damage to the neurons of the spinal cord. Of great importance is constantly concomitant hypoxia and usually long-term, if not lifelong, persistent edema of the brain tissue.

GG Goryun (1947, 1953 - cited in: N.A. Rozhansky, 1957), studying the morphological relationship of neurons, showed on a series of histological preparations that during the development of experimental edema of cat motor neurons, terminal loops (synapses in modern terminology), normally lying on the surface of the neuron, move away from it without disrupting the structure of the latter. These valuable pathomorphological data indicate deafferentation of motoneurons and, obviously, other nerve cells of both the spinal cord and the brain, and provide a convincing explanation of how clear clinical and electrophysiological signs of damage to the nervous system can be combined with normal CT and MRI images of the brain or spinal cord. ... In addition, deafferentation of a neuron is one of the inducers of apoptosis.

§eleven. Pathomorphology and pathophysiology of perinatal hypoxia (summary clinical and experimental data). Knowledge of the stages of pathophysiological and pathomorphological processes is very important, because any intervention that interrupts and disrupts the sequence of morphofunctional and neurohumoral rearrangements in the damaged central nervous system is pathogenetically unreasonable. Considering that structural brain damage is considered “evolutionarily conservative,” the adaptive responses induced by them should be considered as close to optimal. Therefore, in the search for methods and methods of treatment, one should proceed from the principle of optimizing these reactions, and not counteracting them (G.N. Kryzhanovsky, 1997).

Metabolic disturbances in the body of the fetus and newborn during hypoxia lead to significant changes in hemodynamics: the volume of circulating erythrocytes and hematocrit increases, and the degree of aggregation of blood corpuscles increases. Decompensated metabolic acidosis and hypercapnia cause disorders of microcirculation in tissues, a sharp dysregulation of peripheral vascular tone, vasospasm of the brain and heart, blood stasis, diapedetic and profuse hemorrhages with a drop in blood pressure. Due to changes in vascular and cellular permeability, as well as impaired renal function, electrolyte metabolism is significantly impaired, glucocorticoid function of the adrenal glands decreases, which increases hemodynamic disorders. These changes are similar to those in shock conditions.

Pathomorphologically, a sharp plethora of organs is revealed, accompanied by a violation of the permeability of the vascular wall, damage to the endothelium and basement membrane, followed by blood stasis, perivascular edema, hemorrhages and dystrophic changes in the parenchymal organs. Changes in organs and tissues characteristic of intrauterine fetal hypoxia, such as venous stasis, stasis, edema, create a morphological background for the development of intracranial hemorrhages. Therefore, against the background of previous fetal hypoxia, even normal childbirth can lead to extensive cerebral hemorrhage. Therefore, intracranial birth trauma and asphyxia should be considered as interdependent phenomena leading to dysfunction of the central nervous system of the newborn. Thus, functional and morphological changes in the body of the fetus and the newborn are interrelated and depend on the degree and duration of the preceding intrauterine hypoxia. Hypoxia causes a complex set of disorders in all organs and systems of the fetus. This allows (very important!) To talk about multiorgan oxygen deficiency. As a result, it is incorrect to raise the question of the consequences of hypoxia only for the central nervous system. The nervous system, affected by hypoxia, receives defective afferentation from hypoxic altered tissues, organs and systems of the body. The pathogenic effect of perverted afferentation on the trophic state, in addition to the developing central nervous system, cannot but affect its further morphogenesis.

When a neuron is damaged of any, including hypoxic, etiology under the influence of the resulting decay products, the microtubules of the dendritic-spiny apparatus disappear. Dendrites undergo dystrophic changes and show enhanced endocytosis, capturing fragments of neural structures in contact with them. Such endocytosis is interpreted as phagocytosis, which is an expression of biological disinhibition and aimed at replenishing the trophic deficit in damaged nerve cells and their processes. Not only parts of destroyed nerve cells, but also dendrites of reversibly altered nerve cells are phagocytosed. At the same time, excessive phagocytosis leads to degeneration of dendrites, and then of neurons due to the accumulation of a large amount of phagocytosed material in them. This is also facilitated by insufficient supply of trophic factors to neurons through damaged dendrites, antegrade supply of pathogenic substances from axons of pathologically altered neighboring neurons, and retrograde supply from altered dendrites (transneuronal degeneration). When neurons are damaged, glial cells and lemmocytes are disinhibited and the properties of macrophages appear in them in relation to the degenerating neuron and its processes. It is believed that such phagocytosis is essential for the "purification" of the nervous system. At the same time, pathologically enhanced phagocytosis of reversibly altered neurons and nerve terminals contributes to an increase in the territory of brain damage. In the development and prolongation of the process, peripheral immunocytes and cells of the brain's own immune system, which also include microgliocytes activated by the antigens of the damaged nervous tissue, are also involved. In addition, the decay products of the brain matter, antibodies to neurotransmitters and nervous tissue are distributed with axonal transport from neuron to neuron, the connections of which form the neural trophic network. This leads to the involvement of even distant neuronal assemblies in other parts of the central nervous system in the pathological process, thereby contributing to the progression of encephalopathy.

Brain. Little is known about the nature of structural changes in the brain of children who underwent hypoxia in the perinatal period, survived and continue to develop. It is believed that one of the leading factors in the origin of the consequences of hypoxia is the insufficiency of systemic and regional cerebral blood flow. The resulting disorders of microcirculation in the central nervous system are usually associated with general disturbances in the hemodynamics of the embryo and are expressed by dystonic changes in the vessels, mainly in the arterial bed and capillaries. Patterns of stasis and thrombosis are constantly observed, mainly in the venous part, and hemorrhages of various sizes - from diapedesic output of single erythrocytes to massive hemorrhages with rupture of the vascular wall. These circulatory disorders are persistent and generally have little dependence on the stage of development of the embryo undergoing hypoxia.

With the development of hypoxia at earlier stages of development, changes are noted in the form of venous hyperemia with symptoms of stasis and the formation of blood clots and hemorrhages, which are localized mainly in the subcortical formations, the periventricular zone and the deep layers of the white matter of the cerebral hemispheres. The earlier the embryo is exposed to hypoxia, the more often ventricular expansion is found due to destruction of the surrounding tissue and porencephalic cavities in the thickness of the white matter of the hemispheres and in the area of subcortical formations. With the development of hypoxia at later stages of development, a picture of ischemia of the cortex develops, followed by the formation of gross lesions in the form of deformation of its upper layers, the formation of scars with localization of defects symmetrically in the zones of collateral blood supply.

The act of birth, as a rule, aggravates hemodynamic disorders. Soon after birth, fresh hemorrhages appear in the brain substance, subdural hemorrhages, characteristic of intracranial birth trauma. Especially extensive and numerous hemorrhages are observed in stillborn and non-viable ones. It is essential to emphasize that hemorrhages by themselves do not yet determine the severity of the suffering of the brain of the fetus and the newborn exposed to hypoxia, because there is no parallelism between the number and size of hemorrhages, on the one hand, and the degree of impaired development of nerve cells in the future, on the other.

Arising under the influence of hypoxia, hemodynamic disturbances persist for a long time even after birth. They turn out to be not indifferent for the subsequent development of the vascular system of the brain itself. The intensity of neoplasm of blood vessels remains constantly reduced and all the more sharply, the earlier the fetus underwent hypoxia. The low values of the density of the vascular-capillary network in the cerebral cortex are explained not only by the reduced intensity of the growth of new vessels, but also by the continuing death of the existing capillaries. In the wall of the arteries of the circle of Willis, there is a significant underdevelopment of the muscle layer and fibrous frame. Similar changes are observed in most spinal and intracerebral arteries. It is natural to assume that the range of physiological reactions of the altered arteries is limited, and this is the basis for subsequent secondary hemodynamic disorders during functional loads.

Pathological changes also occur in the nerve elements after hypoxia. Some of the nerve cells in the brain die, undergoing decay. Dystrophic and atrophic changes in fetal cells are the more, the earlier in the prenatal period hypoxia acted. Moreover, sometimes normally developing cells are absent in the cerebral cortex. Pathoanatomically, in the place of many of them, only round, intensely stained nuclei are found, surrounded by a barely distinguishable rim of cytoplasm. This peculiar form of cell changes has no analogues in the histopathology of the mature brain. The fact that this kind of picture clearly predominates in sharply weakened newborns and much less often in more viable ones makes it doubtful that these changes are directly caused by primary cell damage in the process of hypoxia itself. It is assumed that they arise as a result of chronic circulatory hypoxia, which develops after the cessation of acute oxygen deficiency. Similar pictures develop in the cerebral cortex during embryonic occlusion of the Sylvian aqueduct. This confirms the great importance of disorders of general and cerebral hemodynamics in the pathogenesis of the consequences of acute hypoxia. If in the future there is a normalization of intracerebral blood circulation, then these peculiarly altered nerve cells can begin to grow and differentiate. The cells of the cerebral cortex grow and differentiate better under the action of hypoxia before birth. However, later in such neurons, pathological changes are noted in the form of depletion of cells in cytoplasm, a decrease in the number of terminal branching of dendrites and varicosities along the course of individual dendrites, especially in their distal parts. As is known, neurons, which are known to be highly sensitive to hypoxia, are characterized by selective vulnerability of dendritic processes, which are affected earlier and to a much greater extent than the cell body. It is believed that these changes indirectly indicate persistent disturbances in the relationship between cortical neurons and subcortical formations, as well as possible changes in the synaptic apparatus of neurons under the influence of antenatal hypoxia. With hypoxia, with some delay, myelination processes begin in the white matter of the brain and more actively in the stem part.

One of the reasons for the subsequent development of atrophic processes is considered to be a deficiency of glial cells in the cerebral cortex and gray matter of the nuclei of the base of the brain, resulting from the death of a significant number of matrix cells. After suffering hypoxia, there is a more rare location of astrocytic glia near the vessels of the brain with frequent hypertrophy of its processes, especially in the white matter. As a result, the nutrition of the nerve cell is disrupted, it cannot cope with the stress and is damaged again. Capillaries die at the same time. Even 8-10 years after the transferred experimental antenatal hypoxia, there is a gradual disappearance of neurons in various parts of the nervous system. This suggests that in the postnatal period of stabilization, the state of the nervous tissue does not occur, but a gradual increase in an organic defect occurs, which concerns both neurological symptoms and mental changes.

It is known that influences from the adrenergic system of the brain play an important role in the normal functioning of the central nervous system, which is involved both in compensatory processes and in the processes of morphofunctional plasticity. Currently available data indicate the diverse functions of the cerebral noradrenergic systems, which have not been fully studied. The early appearance of noradrenergic innervation of the brain during ontogenesis suggested that noradrenergic systems perform a trophic function in the development of certain areas of the central nervous system. Norepinephrine is also involved in complex mechanisms for the synthesis and release of hormones. In this regard, a certain pathology of cerebral metabolism of norepinephrine may determine the characteristics of the course of the disease in persons of different sex and age.

The noradrenergic system of the brain is the higher center or “cerebral ganglion” of the sympathetic nervous system. Noradrenergic bundles innervate almost all parts of the central nervous system, including the cerebral cortex. The nuclei giving rise to these bundles are located in different parts of the trunk. In addition, adrenergic fibers originating from the upper cervical sympathetic node, separating from the radial vessels, also innervate the gray matter. The trophic influence of the sympathetic nervous system on the cortex is carried out by means of neuroglia, on the cell membrane of which there are adrenergic receptors. When they are stimulated in glial cells, enhanced synthesis of RNA, specific enzymes and growth factor of nervous tissue begins, the formation of glucose from glycogen, etc. These and other substances are then transferred to neurons. There is also a close connection between the noradrenergic system and the hypothalamic-pituitary complex in the form of direct control of neurosecretion processes in the hypothalamic nuclei.

It is known that the sensitivity of some nuclei of the brain stem to oxygen deficiency is extremely high, and the cells of the blue spot nucleus react to the lack of oxygen first. Hypoxic disorders in the noradrenergic system of the trunk are considered to be the reason for the preservation and persistence of current and subsequent disorders in the hemostatic system.

Morphological disorders of the central link in the regulation of homeostasis are accompanied by circulatory disorders with the most severe changes in the region of the third ventricle in the form of impaired outflow into the terminal veins and the Galen vein, often accompanied by stasis, thrombosis and extensive hemorrhages. But, given the direct effect of antenatal hypoxia on other organs (lungs, heart), it is impossible to attribute all disorders of homeostasis in the neonatal period only to the central mechanisms.

In the postnatal period, at the site of the former periventricular hemorrhages, including in the hypothalamus, porencephalic cavities or cysts begin to form. Histologically, in some nuclei of the hypothalamus, hypertrophied nerve cells with numerous granules of neurosecretory are found in the cytoplasm, along the axons and near the capillaries, and in others - hypotrophied with signs of a decrease in neurosecretory activity. It is believed that such multidirectional changes are associated with a perversion of the afferent influx. In parallel, the destruction of capillaries and nerve cells continues. Thus, in the state of the hypothalamic nuclei and nuclei of the brain stem and in the subsequent, normalization is not observed. This naturally limits the capabilities of the hypothalamic-brainstem regions in maintaining homeostasis.

Analysis of the results of studying posthypoxic disorders of brain development allows us to draw a number of conclusions. The earlier in the prenatal period the embryo undergoes oxygen starvation, the more clearly expressed in the subsequent phenomena of dysgenesis, disturbances in the growth of nerve cells, destructive processes. However, regardless of the stage of intrauterine development, the conditions of oxygen deficiency act, they entail a long-term, rather complex process in terms of the mechanisms of their development, as a result of which the long-term consequences of hypoxia are formed. In this process, 4 periods are distinguished: 1 the direct effect of oxygen deficiency; 2 violation of general and cerebral hemodynamics; 3 restoration and stimulation of development (“compensation”); 4 progressive atrophic changes in the brain.

The defining moment in the deployment of the entire pathological picture in the further development of the organism, once suffered from hypoxia, is the period immediately following its termination. Circulation disorders, weakness of regulatory mechanisms, inability to restore normal relationships, are, apparently, the most important reasons determining subsequent events.

On the degree of reversibility, i.e. almost nothing is known about the prognostic significance of these changes. It is believed that different sensitivity of brain regions to the action of damaging factors is due to different levels of development, heterogeneity of structural and metabolic characteristics, peculiarities of cyto-, hemo- and angioarchitectonics. Differences can be traced when comparing different fields of the cortex, individual nuclei of the subcortical structures and the brain stem. The brain and spinal cord differ in the degree of damage. In general, from the point of view of the prevalence of changes, we can talk about diffuse lesions of the developing brain under the influence of hypoxia, taking into account the sequence of development of the pathological process outlined above.

Spinal cord. The study of the spinal cord is relevant in light of the high frequency of impaired respiratory function and movement disorders in children with the consequences of perinatal hypoxia. During the birth of a child, the spinal cord can be damaged from mechanical influences during unfavorable childbirth, for example, if it is injured by an epistropheic tooth, folds of the dura mater, or as a result of a violation of blood supply during clamping of the vertebral artery or Adamkevich's artery, etc.

Experimental and pathohistological data indicate that the development of the spinal cord can also be impaired during the prenatal period. With antenatal hypoxia and constantly after it, changes in neurons, spinal ganglia and nerve fibers of the pathways of the spinal cord are detected. The degree of damage to the spinal cord, as well as to the brain, is the greater, the earlier the factor of hypoxia acts in the earlier stages of intrauterine development. The altered neurons of the spinal cord are located mainly in the areas of collateral blood supply at the junction of the basins of different arterial systems of the gray and white matter, as well as the arteries of the anterior and posterior horns. Anomalies in the structure of the circulatory system are found both on the surface of the spinal cord and in the medulla. Changes on the surface of the spinal cord concern mainly the venous system and are most pronounced in the lumbar region. They consist in an increase in the number of venous vessels of the 3-4th order, their expansion and a large number of venous loops in the venous network, i.e. the venous network is less differentiated. All this indicates a violation of venous outflow after intrauterine hypoxia, which persists postnatally. The study of the capillary network of the gray matter of the spinal cord shows an increase in the diameter of the capillaries, which suggests a decrease in the compensatory capabilities of the vascular system of the spinal cord. In addition, a study of the permeability of the capillary bed indicates insufficient BBB function in the form of a violation of the integrity of contacts between endothelial cells of the vascular wall, a violation of the basement membrane of capillaries, etc.

Among the affected nerve cells are the neurons that innervate the diaphragm. Among motoneurons, nerve cells of the anterior-inner group of the anterior horn are most often and most affected. This group of cells forms a column along the entire length of the spinal cord and innervates the muscles of the spine. Damage to a part of these motor neurons or a violation of their blood supply is considered one of the causes of hypotension of the muscles of the spine, which leads to a violation of the child's motor activity associated with the function of these muscles, for example, holding the head, turning from abdomen to back and from back to abdomen, sitting, standing, and with its subsequent development - to poor posture, including stoop.

Along with motor neurons, small cells, which are intercalary neurons, and small cells of the lateral part of the intermediate zone, on which the fibers of the pyramidal and extrapyramidal tracts end. In the long term, after a blood supply disturbance in the lumbar spinal cord, an extensor posture of the lower extremities is noted, and electromyography data indicate the presence of spastic discharges in motor neurons. Histologically, damage to interneurons and death of synaptic endings of their fibers on motor neurons are revealed. Based on these data, it is believed that in children with spastic forms of cerebral palsy in the damaged intercalary neurons of the spinal cord, distortion of information arriving through the pyramidal-extrapyramidal tracts occurs. As a result, spastic discharges of motoneurons arise, at which the affected intercalary neurons end. As a result of this, there is an increase in the spasticity, which, as it is believed, is associated with damage to the corresponding parts of the brain.

That. the process of damage to the structures of the spinal cord, which began in utero, continues in the postnatal period. In this case, along with the nerve cells that innervate the respiratory muscles, the neurons of the spinal cord, which are part of the arc of the motor reflex, are affected. The most common damage to motoneurons of the anterior-internal group of the anterior horn can be one of the causes of hypotension of the muscles of the spine, and changes in the intercalary neurons, on which the fibers of the pyramidal and extrapyramidal tracts end, can lead to an increase in the spastic state of the muscles, associated, as is commonly believed, with the lesion of the corresponding parts of the brain.

Summary: circulatory hypoxia of the fetus or newborn entails a long-term current staged pathological process. A very special place is occupied by the stage that follows acute hypoxia and is characterized, on the one hand, by a disorder of cerebral circulation, and on the other, by profound disturbances in the growth and differentiation of the cellular elements of the brain and spinal cord. It is this stage that coincides with the most crucial periods of postnatal adaptation and maturation of the organism, especially its brain. Morphological changes in the vascular system of the brain indicate a state of chronic hypoxia during this period, which is based not only on disturbances in the delivery of oxygen and oxidation substrates, but also on deep disorganization of cellular metabolism. The state of the parenchymal elements of the nervous tissue indicates serious disorders of its trophism, primarily plastic processes.

§12. Questions of classification and terminology of hypoxic pathology. Criticism of hypoxia as a factor causing CNS pathology. There is no unified classification of CMC (cerebrovascular accidents) in newborns. In the leadership of L.O.Badalyan et al. (1980) with asphyxia of a newborn, a mild, moderate and severe degree of damage to the central nervous system is distinguished. In foreign literature, the term “hypoxic-ischemic encephalopathy” (G.M. Fenichel, 1983; R.E. Meyers, 1979) is widely used to designate small-focal, mainly ischemic lesions of the brain tissue, distinguishing three degrees of its severity - mild, severe and severe. Less commonly used the name "asphyxia stroke" and "asphyxia perinatal cerebral lesions" (J.H. Menkes, 1990; R.E. Meyers, 1979). According to E.M. Burtsev and E.N. Dyakonova (1997), CMD in a newborn is a qualitatively different condition than stroke in adults, which requires a special diagnostic approach and special rubrification, but in general, the classification of CMB in newborns is just being formed.

Domestic authors more often use the term “hemolikvorodynamic disturbance” to denote hypoxic-ischemic encephalopathy, or they are limited to the isolation of the leading neurological syndrome (hypertensive, epileptic, depression, etc.). According to E.M. Burtsev and E.N. Dyakonova (1997), from a formal point of view, this is legitimate, since even in the mild stage of hypoxic-ischemic encephalopathy, more than 1/3 of those examined with HSS (neurosonography) reveal single subependymal hemorrhages. With pronounced hypoxic-ischemic encephalopathy, hemorrhage foci are found in half of the cases, with severe - always.

EM Burtsev and EN Dyakonova (1997) consider the concepts of “hypoxic-ischemic encephalopathy”, “impaired hemoliquorodynamics” and “cerebrovascular accident” as synonyms. Nevertheless, they consider the diagnosis of “cerebrovascular accident” more preferable, especially in situations where neurosonography was not performed or was carried out several days after birth to clarify the nature of the brain damage.

On the other hand, the indication of A.Yu. Ratner (1985) is very relevant that very often the most severe birth traumas of the nervous system pass under the guise of asphyxia, and he considers it unreasonable to consider asphyxia as the main diagnosis. P.S.Babkin (1994), G.G. Shanko (1994), I.A. Skvortsov (1995) and many others remind about the widespread overdiagnosis of perinatal posthypoxic encephalopathy by neonatologists, micropaediatricians and pediatric neurologists.

According to the doctors of the Boston Children's Hospital (K. Cuban, 1997), the term “hypoxic-ischemic encephalopathy” should be used only when there is clear evidence of prenatal or postnatal hypoxia and ischemia. In other cases, it is necessary to use the term “neonatal encephalopathy”, because The criteria by which hypoxic and ischemic disorders are traditionally diagnosed are nonspecific and are found not only in hypoxia and ischemia: changes in the heart rate (heart rate) of the fetus, a low Apgar score, increased excitability or drowsiness, epileptic seizures in newborns. Frequent unreasonable use of the term "hypoxic-ischemic encephalopathy" is fraught with diagnostic errors, since the search for other causes stops (highlighted by the authors. - IS).

P.S. Babkin (1994), on the basis of many years of research obtained in the study of the fetus in 300 births and, accordingly, the same number of newborns, established some patterns. In the process of childbirth, the fetus passes into a qualitatively new state, called by the author Intranatal Fetal Hibernation (INHP), which allows it to survive the extreme conditions of childbirth and, above all, oxygen minimization and compression. This condition develops under the influence of changes in the "woman in labor - placenta - fetus" system and, first of all, in connection with rearrangements in the central nervous system, in the level of biologically active substances of the mother and fetus and is manifested by deep inhibition of the brain and spinal cord, with the exception of a number of structures associated with the mechanisms of development of IHP and some reflex reactions that are of a protective nature. The development of IPHP occurs against the background of a decrease in blood flow, activation of anaerobic and inhibition of aerobic metabolic pathways, a decrease in pO2 and pH, and an increase in pCO2 in the blood and fetal tissues. During the period of expulsion, especially at the end of it and in the first seconds after birth, when adapting to extreme conditions, the fetus can use mechanisms of relatively closed life support and functioning, which allow it to survive without damage not only oxygen minimization, but also short-term anoxia.

P.S. Babkin argues that the state of the fetus in childbirth, denoted by the term "hypoxia", and the state of the born child, denoted by the concept of "asphyxia of the newborn", in most cases are caused not by a deficiency in oxygen supply to the fetus, but by impaired autoregulation of childbirth and intrapartum adaptation of the fetus , which often develops precisely in connection with the use of various methods of obstetric activity. In a number of cases, the author writes further, the conclusion about asphyxia of a newborn is the result of overdiagnosis, when the state of IHP in the first 10-30 s after birth is mistakenly interpreted in terms of pathology.

For the blood supply to the brain, the speed of cerebral blood flow is of great importance. It depends on the state of general hemodynamics, the difference between arterial and venous pressure in the skull, resistance to cerebral blood flow in the arteries when intracranial pressure changes, changes in blood viscosity, its biochemical and gas composition, morphological changes in cerebral vessels and other factors.

Disorders of cerebral blood flow are manifested mainly in pathological changes in its intensity - weakening or strengthening.

A pathological decrease in the intensity of cerebral blood flow is possible in the following cases.

1. With a decrease in arterio-venous pressure difference due to a decrease in total blood pressure or an increase in total venous pressure. The main role is played by arterial hypotension. It weakens blood flow throughout the brain, but to a greater extent - in areas of adjacent blood supply, where intravascular pressure drops more.

2. With an increase in resistance in the vessels of the brain due to atherosclerosis, thrombosis, angiospasm of the arteries. In this case, the most pronounced changes in blood flow occur in the center of the basin of the affected vessel. An important role here is played by secondary vascular lesions - changes in their reactivity, blood flow restored after ischemia, and other factors.

3. If the outflow of blood from the skull is difficult (thrombosis of blood vessels, compression by a tumor) against the background of an increase in general pressure. In this case, the phenomena of venous stasis appear in the brain, leading to an increase in its blood supply, which is very dangerous for the brain, since it is enclosed in a hermetically closed cranium, where, in addition to it, there are incompressible blood and cerebrospinal fluid. The brain tissue itself, which is 80% water, is not compressible. Therefore, with venous congestion, due to an increase in blood volume in the cerebral vessels, intracranial pressure rises, as a result of which the brain is compressed and its functions are disrupted.

4. With intravascular aggregation of blood corpuscles.

A pathological increase in the intensity of cerebral blood flow occurs:

1. With general arterial hypertension.

2. With pathological vasodilation of the arteries. In this case, it is local in nature.

A pathological increase in the intensity of cerebral blood flow leads to an increase in pressure in the vessels of the brain, and with altered vessel walls - to hemorrhage. In the case of a violation of the blood-brain barrier, an increase in pressure in the capillaries causes a sharp increase in the filtration of water from the blood into the tissue, as a result of which cerebral edema develops. An increase in the intensity of cerebral blood flow is especially dangerous when additional factors contribute to the development of edema (hypoxia, craniocerebral trauma).

ellesilver.ru

Clinical manifestations of the disease

Prevalence

Prevalence

Types of circulatory disorders in the brain

Why is there a violation of blood circulation in the brain?

Poor blood flow in the hands

Poor blood flow in the hands

Impaired blood circulation in the legs

How to improve blood circulation in the legs?

Consequences of poor circulation

Improving blood circulation using folk methods

Prevention of blood flow disorders

Etiology

Classification

Symptoms

Diagnostics

Treatment

Possible complications

Prophylaxis

Symptoms of circulatory disorders of the brain

Nutrition to improve blood circulation in the brain

Prophylaxis

Blood supply to the brain in 60 seconds (Video)