Home Dental treatment Microangiopathy of the brain. Microangiopathy: causes, forms, manifestations, treatment Hypertensive cerebral microangiopathy

Microangiopathy of the brain. Microangiopathy: causes, forms, manifestations, treatment Hypertensive cerebral microangiopathy

Microangiopathy is a disease associated with damage to capillaries. Pathology affects vascular system and many internal organs. Often this state becomes a symptom of other independent diseases ( infectious processes, hemolysis, diabetes mellitus, oncology, liver pathologies).

Why does microangiopathy develop?

Among the causes of the disease are:

  • Hereditary pathologies accompanied by impaired vascular tone;
  • Viral infections(rubella, measles);
  • Various injuries;
  • Pathologies leading to blood damage;
  • Severe intoxication;
  • Diabetes;
  • Excessive smoking and drinking alcohol;
  • Hard work in production, leading to weakening of the body;
  • Elderly age.

Basically, pathology develops due to the following processes:

  • Necrotic damage to tissues and cells;
  • Hyalinosis - protein degeneration due to hyaline deposition;
  • Fibrinoid - increased vascular permeability. As a result, an irreversible change in structural elements and fibers occurs connective tissue;
  • Thrombosis - the formation of a blood clot in the lumen of a vessel, which leads to impaired blood flow;
  • Dysfunction of the vascular endothelium, leading to their spasm. The condition is manifested by a decrease in the production of prostacyclin, antithrombin, and an increase in the concentration of thromboxane.

Characteristic signs of the disease

Clinical manifestations determined by the specifics of tissues and organs that have been damaged, the effects of certain external factors.

Patients usually complain of decreased vision, pain and burning in the legs, the development of “intermittent” claudication, bleeding from the nose and stomach, hemoptysis, and dry skin of the feet.

Among the characteristic manifestations of the disease are:

  • Violation of the integrity of small vessels;
  • Hemostasis (blood clotting processes are disrupted);
  • Developing renal failure;
  • Subcutaneous hemorrhages may occur;
  • Damage to red blood cells.

Basic forms

In medicine, it is customary to distinguish 2 types of disease:

  • Diabetic form;
  • Cerebral form (microangiopathy of the brain).

It is worth considering each type in more detail. The cerebral form is accompanied by damage to the capillaries and their branches in the brain. This pathology may lead to thickening of the walls of arteries or capillaries of a hyaline nature.

In both cases, the disease is considered as a consequence of a chronic disease that causes damage to the white matter.

A characteristic sign of this form of the disease is damage to small blood vessels in the brain against the background of impaired circulation, atherosclerotic changes and hypertension.

The disease causes disruption of the brain and can provoke the following pathologies:

  • Lacunar infarction. Occurs during occlusion of a penetrating branch of cerebral vessels;
  • Encephalopathies leading to diffuse damage.

The diabetic form occurs when there is an increased concentration of glucose in the bloodstream. This is the most severe form of diabetes.

As a result, small vessels (capillaries, venules, arterioles), which are located near the internal organs, are damaged. The clinical manifestations of the disease will be determined by the location of the lesion.

Progressive diabetes mellitus leads to malnutrition and removal of metabolites from cells. As a result, it increases due to increased blood sugar concentrations and excess water intake.

Patients note the occurrence of edema, vascular damage due to disturbances in the metabolic processes of basic nutrients.

The disease is often characterized by the following pathologies:

  • Diabetic nephropathy (30% of patients). The condition is manifested by impaired kidney function, swelling, protein in the urine;
  • Diabetic microangiopathies of the liver;
  • Damage to the blood vessels of the legs;
  • The occurrence of diabetic angioretinopathy ().

Diagnostic measures and therapy

If the development of microangiopathy is suspected, the doctor should examine the patient’s medical history, conduct ultrasonography blood vessels and fundus. Additionally, MRI may be prescribed, X-ray examination, CT.

Therapy for the disease is determined by the location of the affected vessels and its causes.

Mainly used drug treatment, which improves blood microcirculation, as well as physiotherapy. Surgery may be required only if it is necessary to restore the patency of the vessel.

For this purpose, cryosurgical methods or laser coagulation are used.

For the cerebral form of the disease, doctors use complex therapy. Patients are prescribed medicines to lower blood pressure. To eliminate symptoms, antihypoxants are used, for example, emoxypine.

Equally important in the treatment of the disease is the normalization of lipid concentrations. Statins (atorvastatin, simvastatin) are widely used for this purpose.

To normalize brain nutrition it is used nootropic drugs: piracetam, encephabol, cerebrolysin. Medicines based on nicotinic acid (xanthinol nicotinate) help improve blood circulation.

To treat the diabetic form of the disease, it is important to normalize blood glucose levels. Modern pharmacology offers a wide choice effective drugs to achieve this effect.

As part of inpatient treatment, they use angioprotective drugs, allowing you to restore vascular walls, drugs to improve microcirculation, for example, pentoxifylline.

B vitamins, lipoic acid and antioxidants, for example, vitamin E and selenium, are very effective in the treatment of microangiopathies. For patients with the diabetic form of the disease, it is necessary to adhere to a strict diet and avoid smoking and alcohol.

The prognosis of microangiopathies is generally favorable. However, it worsens if the patient has a history of hypertension, leading to rapid progression of symptoms. Important role The age of the patient also plays a role: in an older person, the disease develops much faster.

Angiopathy of the brain is a vascular disease that is various reasons causes their tone, as a result of which brain cells cease to be supplied with blood. This is a very serious pathology that can lead to hemorrhage and even death. In some cases, we may be talking about a disease such as cerebral microangiopathy. What it is? In this case, the functioning of microscopic capillaries is disrupted. Let's look at this disease in more detail.

Characteristics of the pathology

Many have heard of, and some have even encountered, such a disease as cerebral microangiopathy. What is it? This is a pathological process that affects capillaries and small vessels, acquiring a chronic form. Blood circulation in the brain is impaired. Since oxygen and glucose are responsible for normal blood flow, a long-term lack of these substances leads to disruption of the small vessels of the brain.

Forms of microangiopathy

This brain pathology occurs as a result of disruption of the smallest vessels. This does not appear immediately, so early stage It is very difficult to diagnose such a disease.

Cerebral microangiopathy mainly occurs in older people. Those suffering from Alzheimer's disease are a particular risk group. With this disease, amyloid (glycoprotein) begins to accumulate on the walls of the veins. It is also worth noting that the pathology is difficult to diagnose and treat.

Lenticulostriate microangiopathy often affects children and is not a disease, but a feature of the circulatory system. Constant monitoring is required.

Diabetic microangiopathy occurs due to poor circulation in the brain, which provokes diabetes.

Hypertensive microangiopathy is caused by a malfunction circulatory system arising due to hypertension. It is necessary to keep blood pressure under control and avoid sudden jumps.

Causes of the disease

The development of microangiopathy occurs against the background of other diseases. This could be diabetes mellitus, oncology, liver pathology, hemolysis.

Among the main reasons are the following:

  • viral infections (measles, rubella);
  • pathologies that contribute to blood damage;
  • diabetes;
  • hypertension;
  • elderly age;
  • hereditary pathologies that cause vascular tone;
  • various injuries;
  • severe intoxication;
  • abuse of bad habits.

Most often, pathology develops as a result of the following processes:

  • Necrosis is the death of tissues and cells of the body.
  • Hyalinosis is a lack of protein due to hyaline deposition.
  • Increased vascular permeability. As a result, the fibers and structural elements of connective tissue undergo irreversible changes.
  • Thrombosis, characterized by the formation of a blood clot in the lumen of a vessel, resulting in impaired blood flow.
  • Dysfunction of the vascular endothelium, which leads to their spasm. In this condition, the production of antithrombin and prostacyclin decreases, and the concentration of thromboxane increases.

Characteristic signs of microangiopathy

Clinical manifestations of the disease depend on the specifics of organs and tissues, damage to which occurred under the influence of certain external factors. Patients most often complain of pain and burning in the legs, decreased vision, bleeding from the stomach and nose, the development of intermittent claudication, dry skin of the feet, and hemoptysis.

Thus, they highlight following signs microangiopathies:

  • the integrity of small vessels is compromised;
  • renal failure develops;
  • red blood cells are damaged;
  • the blood clotting process is disrupted;
  • there is a high probability of occurrence

Symptoms of the disease

Microangiopathy of the brain has following symptoms: the patient begins to complain of memory impairment, clouding of consciousness, causeless weakness and headaches occur. They appear due to the fact that blood circulation is disrupted in the capillaries of the brain. The resulting damage to the walls of small vessels activates the oxidative processes of lipids, free radicals are formed, which have a destructive effect on brain cells.

As the patient progresses, he becomes inattentive and forgetful. He develops convergence disorder, pupil diameters become different, and his visual functions. In addition, frequent nasal and stomach bleeding, discomfort in the legs at rest, dryness and flaking of the skin of the feet, blood clots in the urine.

Diagnostics

If there is a suspicion of brain pathology, it is important to diagnose where the foci of microangiopathy are located and what is the degree of damage to the vascular walls. For this, the following diagnostic methods are used:

  • MRI of the brain;
  • nuclear magnetic resonance;
  • Doppler ultrasound.

To get as much information as possible, they use a fairly safe procedure for the human body, such as MRI of the brain, the price of which is a little steep. This diagnostic method is considered the most popular. It allows you to identify signs of the disease such as cerebral atrophy, leukoaraiosis, microscopic hemorrhages, lacunar infarctions. MRI of the brain, the price of which depends on the amount of contrast agent used, allows you to make the correct diagnosis. If the patient weighs less than 69 kg, this figure is 2,700 rubles, from 70 to 99 kg - 3,200 rubles, from 100 kg and more - 4,400 rubles.

Method magnetic nuclear resonance allows you to study the brain tissue itself and the vascular network. In this case, signs of arterial hypoplasia are clearly visible. Foci of infarctions that arise due to vascular occlusion, cerebral hypoperfusion, and microscopic hemorrhages are easily visible.

Method Doppler ultrasound allows you to identify abnormalities in blood vessels, blockages or narrowing of the lumen.

Treatment

Patients do not always understand when they are diagnosed with cerebral microangiopathy, what it is and whether it can be cured. The doctor usually prescribes complex therapy.

First of all, the patient must take drugs that normalize blood pressure. To eliminate the lack of oxygen in the brain, antihypoxants are used, for example Emoxipin. It is also important to correct lipid levels using statins, fibrates, sequestrants bile acids. These may be the following drugs: Atorvastatin, Simvastatin, Rosuvastatin.

Also, if microangiopathy is diagnosed, treatment should be carried out using nootropics that improve brain nutrition. These are Piracetam, Nootropil, Cerebrosilin, Encephabol. To normalize blood circulation, nicotinic acid preparations are used: “Picammilone”, “Xanthylone nicotinate”.

Conclusion

Thus, we have analyzed a disease such as cerebral microangiopathy. What it is, you now know. This is a serious pathology that requires immediate intervention. The sooner it is found out where the disease is localized and what the degree of vascular damage is, the easier it will be to minimize the consequences of such an illness.

Microangiopathy is a pathology cerebral vessels small diameter (capillaries). Most often, microangiopathy serves as a secondary disease of brain diseases.

There is also microangiopathy of the retina, or pathology of the capillaries in the renal organ.

Microangiopathy of the brain, what is it?

Microangiopathy is a process of disorder in the brain when sufficient oxygen and glucose do not reach the brain cells and brain capillaries to nourish them.

This pathology manifests itself as a consequence of such diseases:

  • Necrotic death of cells of the diseased organ;
  • Blood and vascular pathologies - thrombosis. This pathology occurs from the formation of a blood plasma clot inside the vessels and disrupts the correct passage of blood in the bloodstream system;
  • Dystrophies of the hyaline type (hyalinosis). This type of disease is a protein type of vascular dystrophy, in which hyaline molecules are deposited in tissue cells;
  • Fibrinoid, which is a pathology that is expressed in irreversible consequences in increased permeability of arteries and small capillaries, and its manifestations are expressed in the destructive structure of the fibers of connective tissue cells.

With microangiopathy, the membrane molecules of the capillary membranes, as well as the intima of blood vessels, become denser, which leads to insufficient cerebral circulation.

Lack of blood in brain cells provokes the destruction of cerebral white matter, and dyscirculatory encephalopathy and stroke certainly occur.

Diabetic pathology microangiopathy manifests itself in the brain due to a high glucose index in the blood. And this condition leads to the destruction of cerebral capillaries, cerebral arterioles, as well as the destruction of cerebral venules.

The diabetic type of disease is nephropathy, as well as complete dysfunction of the renal organ.


If the capillaries of the eye organ are affected, then pathology occurs eyeball retinopathy.

Causes of microangiopathy

The main reason for the development of cerebral angiopathy in the body is a violation metabolic processes in the body, which lead to:

  • Hypoxia of tissue cells;
  • Disorders in the capillary endothelium;
  • Spasms of arteries and veins;
  • Cell adhesion of platelet molecules;
  • Activation of the renin-angiotensin process.

Pathologies in which cerebral vascular disease develops - microangiopathy:

As a secondary disease, microvascular angiopathy of the brain develops when:

  • With thrombosis of large-diameter arteries;
  • With tissue necrosis - quite often after myocardial infarction;
  • From aneurysm of blood vessels and cerebral capillaries;
  • After a cerebral stroke;
  • With ischemia of the cardiac organ.

Forms of pathology

There are 2 forms of occurrence of this pathology:

  • A form of microangiopathy caused by diabetes mellitus (diabetic);
  • Microangiopathy of cerebral vessels - cerebral.

The cerebral type of microangiopathy manifests itself in the brain capillaries and may be a consequence of the disease microangiopathic encephalopathy.

The causes of this pathology: damage and destruction of the white medulla, which occurs due to vascular pathology with impaired cerebral blood flow, in the presence of cholesterol (atherosclerotic) plaques on the brain vessels, as well as against the background of the chronic type arterial hypertension, with a constantly high blood pressure index.

Diabetic angiopathy manifests itself from the fact that the blood in the circulatory system has a constantly high glucose content. Microangiopathy of the brain reflects the most severe form of diabetes mellitus.

As a result of a high concentration of glucose, damage to the walls of the capillaries occurs, and the walls of the areolas become denser, and the integrity of the membranes of the venules, which contain both the brain and the cells of internal vital organs, is destroyed.


Signs of the degenerative diabetic form depend on the local location of the pathology focus.

Microangiopathy of cerebral type

Microangiopathy destroys cerebral vascular cells, disrupting the functioning of the entire brain, which leads to the development of the following pathologies in the body:

  • Lacunar type infarction. This type of infarction occurs during the period of occlusion in the cerebral vessels of the penetrating branch;
  • Diffuse destruction of cerebral vessels, which leads to encephalopathy.

The manifestation and development of the cerebral form of the pathology occurs slowly and against the background of chronic cerebral vascular ischemia, which is provoked by the pathology of vascular atherosclerosis and hypertension.

Both diseases primarily disrupt the functioning of the blood flow system, leading to disturbances and deviations in vascular membranes. This disorder manifests itself in the compaction of the membranes, loss of elasticity of the vessels, as well as fragility of the capillaries.

The symptoms of cerebral microangiopathy do not appear immediately, since the pathology is inherent chronic degree development (degenerative microangiopathy), and It does not begin with pronounced symptoms, from which it is difficult to determine pathology.

Manifestations of cerebral angiopathy begin with the following signs:

  • Deviations in memory occur;
  • There is dizziness;
  • Signs of headache, which can sometimes be very severe;
  • Weakness of the whole body that occurs without cause;
  • Rapid physical fatigue;
  • Intellectual ability is impaired.

As a result of disruption of the membranes of brain vessels and discirculatory actions, the process of oxidation and phosphorylation of cells occurs in the centers of the brain. Cerebral microangiopathy is inextricably linked with dementia, as well as Alzheimer's disease.

With these pathologies the following symptoms appear:

  • Sleep is disrupted, which leads to insomnia at night. Due to lack of sleep, the patient becomes irritable and sleepy during the day;
  • Motor coordination is impaired;
  • Unsteadiness in gait appears;
  • Pathological types of reflexes appear;
  • Vision is impaired;
  • An optic nerve aneurysm appears;
  • Pain in the limbs occurs during movement, as well as during rest;
  • The epidermis on the feet peels off and deep cracks appear on the heels.

Angiopathy of NK due to diabetes

Diabetic form of microangiopathy

The disease diabetes mellitus, which progresses, leads to a delay in nutrition, or to its disruption, as well as to the removal of metabolite molecules from the cells, spasms and narrowing of the membranes of blood vessels.

Osmotic pressure appears in the vessels from an excess of glucose in the blood and from an excess of water. The consequence of this condition and the chronically high concentration of glucose in the blood is damage to the capillaries and their complete destruction.

Forms of manifestation of diabetic type microangiopathy:

  • Nephropathy manifests itself, which is marked by damage to the cells and vessels of the renal organ. A severe form of nephropathy leads to a decompensated type of renal failure. Treatment requires ongoing hemodialysis procedures or kidney organ transplantation. At diabetes mellitus There is an accumulation of breakdown products of substances containing a toxic form, and intoxication of the body cells occurs. Damaged kidney organs do not have time to filter toxic elements, leading to intoxication. The initial stage of development of the pathology nephropathy manifests itself in an increase in the blood pressure index, in the general weakness of the body with nephrotic syndrome, appears severe swelling. With further progression, kidney failure occurs. The consequences of the development of nephropathy are poisoning of the body, in which the functions of all internal vital organs are disrupted, and deviations in the functioning of body systems also occur;
  • The form of development of diabetic microangiopathy is retinopathy. This type pathology affects the retina of the eye organ, which, with a progressive form of development, leads to complete blindness. At the initial stage of pathology, a violation occurs in optic nerve, unclear contours of objects, blurriness and cloudiness in the eyes, which subsequently leads to radical and abrupt manifestations of complete loss of vision. To diagnose this form, ophthalmoscopy techniques are used, biomicroscopy of the eyeball, visometry of the eye organ, and angiography of the capillaries of the retina are performed. In order to treat retinopathy, it is necessary to constantly adjust the glucose index in the blood, as well as keep this level within the normal range, or indices of the borderline type of diabetes. And also eliminate all disturbances in the body’s metabolic processes;
  • Diabetic angiopathy in a complicated form is manifested by polyneuropathy, which affects fiber cells nervous system and manifests itself as a whole complex various symptoms. The sensitivity of the whole organism increases, an increased sensation of a painful state appears, and strong pain and numbness in lower limbs, unsteadiness in gait and lameness appear. There is a problem with erection in men, signs of enuresis, and hair becomes dull and brittle. The skin becomes dry and pale. As the pathology progresses, polyneuropathy occurs more severe symptoms- difficulty swallowing, speech impairment, muscle cramps, dizziness so severe that it leads to loss of consciousness. If we normalize the concentration index in the blood and bring it closer to standard indicators, then almost all the symptoms of polyneuropathy will disappear. It is only necessary to adjust glucose immediately after the development of pathology and to do so constantly, preventing the development of the disease to such a stage when irreversible consequences begin to occur in the body.

An example of microangiopathy of amyloid etiology (due to impaired protein metabolism), directly related to vascular dementia (Alzheimer's disease)

Symptoms of cerebral microangiopathy

Symptoms depend on the site of tissue cell damage, the degree of disarmament, as well as the state of the pathology.

The first signs of microangiopathy are:

  • Decreased visual acuity;
  • Pain in the lower extremities;
  • Burning in the legs;
  • Lameness appears;
  • Stomach bleeding;
  • Nosebleeds;
  • Coughing up bloody clots;
  • Dry feet.

Also characteristic symptoms of the disease:

  • The integrity of vessels with a small diameter is compromised;
  • The hemostasis system is disrupted—poor blood plasma clotting occurs;
  • Renal organ failure develops;
  • Hemorrhages develop under the skin;
  • Cell molecules of red blood cells are destroyed.

to install accurate diagnosis, as well as the type of microangiopathy and see the picture of single supratentorial foci, it is necessary to undergo a number of instrumental studies and clinical laboratory tests:

  • MRI of the brain (magnetic resonance imaging). With this type of study, signs of hypoplasia of the cerebral arteries, as well as atrophy of the cerebral vessels, are revealed. Identify all areas of hemorrhage and heart attacks. The MRI method detects foci of gliosis of single forms of the supratentorial type;
  • Doppler ultrasound is a method for detecting pathology in the membranes of blood vessels, narrowing of vascular walls, and also determines changes in the lumen of all vessels from large diameters to small capillaries, as well as problems with thrombosis and clogging of arteries;
  • Ultrasound of the eyeball;
  • ECG (electrocardiography of the heart organ);
  • X-ray of the extremities for microangiopathy of the lower extremities;
  • CT ( CT scan).

Laboratory clinical tests when studying angiopathy:

  • General analysis of blood composition;
  • Biochemical study of blood composition;
  • Biological study of pus in discharge from diseased limbs and determination of its sensitivity to antibacterial drugs.

Diagnostic test pathologies of cerebral vessels - microangiopathy

Drug and surgical treatment of vascular microangiopathy

Treatment of brain pathology microangiopathy occurs comprehensively, using a low-cholesterol diet, as well as a diet to reduce blood glucose, as well as with the use of medications of various pharmacological groups:

pharmacological groupnames of drugs
antihypoxants to prevent hypoxia of brain cellsEmoxipin
Statinsdrug Lovastatin
febrate groupFenofibrate
nootropic medications · Nootropil;
· Piracetam;
· Pantogam
antihypertensive drugs· Tenoric;
· Kapoten
means to improve microcirculation· Pentoxifylline;
Xanthinol
group of angioprotector drugs· Dicynone;
· Complamin
medicinal group of antioxidants· Selenium;
· vitamin E;
B vitamins
group medicines antiplatelet agents· Cardiomagnyl;
· Chimes;
· Trental
coenzymes for diabetes· Flavinate;
Cocarboxylase

To restore the lumen in the vessels, surgical intervention is used using cryosurgery or laser coagulation.

Prevention

To protect yourself from cerebral vascular disease microangiopathy, you must constantly follow preventive measures:

  • Constant monitoring and adjustment of blood glucose;
  • Control of blood cholesterol levels;
  • Adhere to an anti-cholesterol diet, as well as a diet for diabetics;
  • Healthy lifestyle;
  • Do not drink alcohol;
  • Quit nicotine addiction;
  • Do not overload the body with work;
  • Avoid stressful situations.

These simple preventive measures promote proper blood microcirculation, which has a beneficial effect on the condition of blood vessels and the functioning of the entire blood flow in the body.

Life forecast

With microangiopathy, the prognosis for life is more favorable if timely diagnosis and treatment of the root cause of the pathology. The prognosis worsens with hypertension, which progresses.

In elderly people, microangiopathy develops quickly and takes on a complicated form of diabetes - the prognosis is unfavorable.

The human body is designed in such a way that organs and tissues need oxygen and various nutrients. All this is delivered to its destination through small and large vessels with blood flow. An innumerable number of metabolic processes take place in the brain and heart, where the circulatory network is most developed. For a number of reasons, small vessels appear pathological changes, leading to a deterioration in their patency. This condition is called microangiopathy. The disease received its name from the merger of three words: small “micro”, vessel “angio”, pathology “pathy”.

Description of the disease

Any organ can become a target of this disease, but the greatest concern is cerebral microangiopathy. Normal brain activity impossible without the flow of oxygen and glucose through the bloodstream. In the presence of microangiopathy, a chronic lack of these substances is observed, which in turn leads to “starvation” syndrome, expressed in impaired functioning of the smallest vessels of the brain.

The result of a decrease in the amount of blood supplied to neurons or a complete cessation of blood supply is the formation of foci of gliosis, where adhesions or “scars” are formed from rapidly growing glial cells. Over time, this condition begins to threaten a person’s life.

Causes of microangiopathy

Foci of gliosis and areas of ischemia do not appear in one hour or even a day; they form over a long time. The impetus for the onset of the disease and the appearance of syndromes can be factors such as:

  • Bad habits.
  • Traumatic lesions.
  • Blood diseases accompanied by pathology of the blood coagulation system.
  • Endocrine diseases, among which diabetes mellitus comes first.
  • Diseases of infectious origin.
  • Industrial hazards.
  • Malignant tumors.
  • Hypertonic disease.
  • Liver pathology.
  • Diseases of the urinary system.
  • Genetically inherited anomaly in the development of vascular walls.
  • Age over 50 years.
  • General exhaustion of the body. Pathology in small vessels or capillaries can develop due to tissue necrosis, lack of protein, increased vascular permeability, dysfunction of the membranes lining the vessels. Thrombotic microangiopathy occurs due to blockage of a vessel by a blood clot.

Types of disease

Microangiopathy of the brain is divided into four forms:

  • Cerebral amyloid type of disease. This form is formed in response to pathological protein deposition, and appears most often in old age.
  • Lenticulostriate appearance. At risk for this disease there are children. According to the latest data, microangiopathy of this type is a normal variant, but requires constant monitoring.
  • Diabetic form of the disease. With the progression of diabetes mellitus, an increase in the syndrome of cerebral manifestations is observed.
  • The hypertensive type of microangiopathy is typical for patients suffering from hypertension.

In one case or another, the production of collagen and glycoproteins increases, which leads to a thickening of the capillary membrane. The result is a decrease in the quality of metabolic processes, deterioration of nutrition at the site of vascular damage, and the formation of foci of gliosis.

Symptoms

The main symptoms of the presence of lesions in the brain are headaches, memory impairment, causeless weakness and clouding of consciousness. This occurs due to impaired blood circulation in small vessels, resulting in the formation of elements that destroy the white matter.

Due to the slow development of the disease, the patient does not immediately realize that something is wrong with him, because the symptoms are absent or mild, so in most cases specialized assistance addressed untimely.

At first, a person gets very tired when performing ordinary actions. Such complaints are often accompanied by medication-resistant headaches.

Characteristic is the presence of astheno-neurotic syndrome, which manifests itself in the form of:

  • bad mood;
  • irritability;
  • sleep disorders;
  • constant feeling of weakness;
  • significant decrease in performance.

Depressive syndrome is often observed during illness. As microangiopathy progresses, a person becomes distracted, inattentive and forgetful, and the ability to think also deteriorates. Focal symptoms appear, characterized by loss of coordination of movement, deterioration of vision, external different diameters pupils and other pathological reflexes.

Depending on the location and size of the areas of gliosis, the patient may develop vegetative polyneuritis syndrome, in which temperature and pain sensitivity are impaired skin in various places.
Microangiopathy of the brain is accompanied by hemorrhagic syndrome, which is manifested by frequent bleeding from the nose or stomach, hematuria (blood in the urine), as well as subcutaneous hemorrhages. The greatest danger to humans is hemorrhage in the brain matter or between the membranes of the brain.

Diagnosis of microangiopathy

Before making a diagnosis and starting treatment, it should be remembered that similar syndromes can be observed in other diseases, so it is necessary to collect an anamnesis, identify the symptoms of the disease as fully as possible and carefully examine the patient. For this purpose, studies such as:

  • general blood analysis;
  • biochemical blood test with determination of the lipid spectrum;
  • blood clotting test;
  • electrocardiogram (ECG);
  • electroencephalogram (EEG);
  • Dopplerography of blood vessels to identify narrowing, blockage and other abnormalities.

The patient needs to visit an ophthalmologist to identify pathological processes in the vessels of the fundus.

If microangiopathy is suspected, magnetic resonance imaging (MRI), computed tomography (CT), or nuclear magnetic resonance is used to identify the lesions and extent of the lesion.

Using these types of examinations, brain tissue and the vascular network are studied to detect insufficiency of the vascular walls, areas with impaired blood supply, foci of gliosis, expansion of the perivascular space, as well as microscopic hemorrhages.

Treatment

The emphasis is on conservative therapy, but it is necessary that the treatment be comprehensive, aimed at correcting the disease that caused microangiopathy and eliminating various syndromes. For diabetes mellitus, medications are used to normalize glucose levels. It is also recommended to take medications whose action is aimed at maintaining blood pressure within the age-related norm.

If there are signs oxygen starvation antihypoxants are used. Complex therapy includes various drugs to correct lipid levels, restore local blood circulation, improve nutrition of brain tissue and the condition of vascular walls. Antioxidants, antiplatelet agents and disaggregants are also used.

In addition to traditional drugs, the treatment of microangiopathy can be successfully supplemented with procedures such as massage, swimming pool, physiotherapy, acupuncture and physiotherapy. Under their influence, a person’s well-being improves, symptoms are smoothed out, and conductivity in the foci of gliosis increases. If the disease is already advanced, then to restore vascular patency it is necessary to resort to surgical intervention.

Self-medication is absolutely unacceptable; the dosage of the medication and the duration of the course of treatment are determined only by the doctor based on the information obtained as a result of the examination.

Further prognosis for microangiopathy

Microangiopathy of the brain is quite serious illness, and in the absence adequate treatment Possible deterioration of the condition to the point of disability or death. Early detection of the disease, as well as determination of the focus of gliosis and the degree of damage to the vascular walls can reduce the consequences of the disease to a minimum.

Cases of recovery from microangiopathy, as well as complete elimination of foci of gliosis, have not been recorded, but the patient is quite capable of slowing down the development of the disease on his own. It is only necessary to strictly follow the recommendations of a specialist, undergo regular treatment, prevent the progression of the underlying disease and follow the principles healthy image life.


Relevance. Modern doctors must be “instrumentally sharpened” to identify specific signs microangiopathy and proper description, due to the high prevalence of cerebrovascular pathology and the widespread use of magnetic resonance imaging (MRI).

Lacunar infarctions. Clinical evidence of recent small subcortical infarcts is lacunar stroke or lacunar syndrome, which accounts for about 25% of all ischemic strokes (Figure 1). Lacunar lesions are most often caused by local occlusion of small arteries, although the pathogenesis of these infarctions remains incompletely understood. In some patients with multiple lacunar infarctions in the deep parts of the brain without diffuse damage to the white matter (lacunar status), the process is probably associated with microatheromatosis of the initial part of the penetrating arteries going deep into the brain, or closure atherosclerotic plaque the lumen of a large vessel at the point where a penetrating branch originates from it.


Sometimes lacunar infarctions are asymptomatic and are discovered incidentally on MRI, in such cases they are asymptomatic cerebral infarctions. In contrast, for unknown reasons, 30% of patients have symptoms of lacunar stroke without visible changes on MRI, indicating that MRI techniques are not sensitive enough to detect such infarcts.

A number of studies show that small subcortical infarcts may have variable outcome on MRI, develop into lacunar cavities or white matter hyperintensity without visible cavitation on T2-weighted images, or disappear with little apparent consequence on MRI (see figure above) . The number of outcomes associated with their disappearance varies from 28% to 94% of cases (Potter GM, Doubal FN, Jackson CA, et al. 2010).

Foci of lacunar infarction are typically localized in the white matter of the cerebral sex, subcortical ganglia, internal capsule, corona radiata, centrum semiovale, pons and brainstem.


    ● 1 point - up to 2 lesions;
    ● 2 points - 3-5 lesions;
    ● 3 points - > 5 lesions.
Small (≤5 mm) and large (6-14 mm) lacunar infarcts are assessed separately. According to localization, lacunar infarctions are classified in subcortical structures (basal ganglia, thalamus, internal and external capsules, corpus callosum, deep and
periventricular white matter), in the brain stem and in the cerebellum. The diameter of the focus of lacunar infarction is usually 10 - 15 mm.

In FLAIR mode, lacunae presumed to be of vascular origin usually have a centrally hypointense signal (similar to cerebrospinal fluid) with a surrounding hyperintensity edge. At the same time, a rim is not always present, and edge hyperintensity may also surround perivascular spaces where they pass through an area of ​​white matter hyperintensity.


Perivascular spaces(criblures). Perivascular Virchow-Robin spaces are expansions of extracerebral fluid spaces around arteries, arterioles, veins and venules. They run from the surface of the brain into and through the parenchyma, following to the leptomeningeal layers. Perivascular spaces are usually microscopic and not visible on conventional neuroimaging. However, large spaces become more noticeable as the patient ages, especially when located at the base of the brain. The expansion of perivascular spaces may be associated with other morphological characteristics of cerebrovascular pathology, such as leukoaraiosis, lacunar infarctions, ! but not with atrophy. Interpretation visible expansion perivascular spaces remains clinical controversial issue. Some authors do not associate them with a pathological cause, while others find their connection with cognitive impairment.


Perivascular spaces have a signal intensity similar to cerebrospinal fluid on all sequences, since they follow the course of the penetrating vessels, they appear as linear images parallel to the course of the vessel, and they also have a round or oval shape on axial sections. Perivascular spaces tend to be most prominent in the inferior basal ganglia, where they may appear particularly enlarged and can also be seen running centripetally through the white matter hemispheres and midbrain, however, they are rarely seen in the cerebellum. Unlike lacunae, the diameter of perivascular spaces is usually no more than 3 mm, as confirmed histologically. Perivascular spaces do not have a T2-hyperintense rim around the fluid-filled space on T2-weighted or FLAIR images unless they intersect an area of ​​hyperintense white matter.

Leukoaraiosis(LA). In the genesis of PA, the leading role belongs to repeated episodes of hypoperfusion, which arise due to the interaction of a complex of causes. First of all, due to widespread microvascular pathology and systemic arterial hypotension, which can be provoked by inadequate antihypertensive therapy, orthostatic hypotension due to autonomic failure. Damage to small penetrating vessels, leading to PA, is characterized not only by their stenosis, but also, no less important, by their unresponsiveness, which may be based on endothelial dysfunction.

The predominant suffering of white matter in the periventricular and deep sections during cerebral hypoperfusion is explained by the special nature of their blood supply, provided by terminal type vessels that do not have collaterals. As a result of chronic hypoperfusion or, what may be more likely, repeated transient episodes of hypoperfusion in the deep layers of the white matter of the hemispheres, so-called incomplete infarcts develop, characterized by demyelination, death of oligodendrocytes, loss of axons, gliosis, ! but not by the formation of foci of necrosis (unlike ischemic stroke). The PA is characterized by bilateral, mostly symmetrical hyperintensity on T2-weighted images. Hyperintensity may also be present in the brainstem.

The term LA suggests a vascular origin and is common in older adults and carries clinical information about cognitive impairment as well as gait impairment. This concept excludes damage to the white matter of a different nature, with multiple sclerosis, leukodystrophy and leukoencephalopathy with.

PA of suspected vascular origin appears hyperintensity on T2-weighted sequences and may appear isointense or hypointense (although not as hypointense as CSF) on T1-weighted images. Thus, the best method for detecting PA is MRI in T2-VI mode (especially in the sequence with signal suppression from the cerebrospinal fluid - FLAIR).

To quantify the severity of this phenomenon, use the visual scale of Fazekas (1998):

Microinfarctions. Microinfarctions are small ischemic foci up to 5 mm in diameter, until recently detected only by microscopy. Published studies indicate visualization of microinfarctions on a 7 Tesla tomograph, and sometimes on a 3 Tesla tomograph. When comparing the incidence of microinfarctions in patients with Alzheimer's disease and in patients without cognitive impairment, there are conflicting data. The studies did not reveal a correlation between the frequency of microinfarctions and cognitive impairment, but did find a statistical connection between microinfarctions and the frequency of cerebral microhemorrhages. Microinfarctions often include changes characteristic of an incomplete infarction (reduction in the number of neurons, axons, gliosis) and can be localized in both the cortex and subcortical structures. Microinfarctions can be associated with arteriolosclerosis, atherosclerosis of large cerebral arteries, microembolism.


Cerebral microbleeds(CMK). CMK is an option morphological changes brain associated with damage to the small cerebral arteries, which are detected in the gradient echo mode (T2*) on MRI in the form of hypointense foci measuring 3–10 mm. SWI mode can also be used to evaluate CMB. The results of the study show that the MR-visible lesions correspond to the accumulation of hemosiderin in macrophages in the perivascular tissue during the destruction of red blood cells. Some visible CMBs on 1.5 T MRI were judged to be venules on 7 T MRI. It was found that CMBs are predominantly located near venules, which creates additional prerequisites for studying the role venous system in the pathogenesis of CMB.

By modern classification CMB localizations are distinguished:


    ● superficial or cortical;
    ● subcortical or deep (basal ganglia, internal and external capsule, thalamus, corpus callosum, periventricular white matter);
    ● located in the posterior cranial fossa, or infratentorial (brain stem and cerebellum).
The standard assessment of the frequency and location of CMB on T2* gradient echo MRI is carried out using the Microhemorrhage Anatomical Rating Scale (MARS) (Gregoire SM, 2009).

There is an algorithm for identifying CMB, since CMB can also be differentiated by foci of other origins, such as accumulation of calcium and iron, melanoma, diffuse axonal damage after injury, artifacts from the bones of the calvarium, cavernous angioma, cross section blood vessels. CMB can be distinguished from intracerebral hemorrhage by its smaller size and the absence of a cavity in the lesion, which will be visible on T1-weighted and T2-weighted or FLAIR sequences.

CMBs can be detected in cerebral microangiopathy of various origins (cerebral, hypertensive arteriopathy, vasculitis, hereditary angiopathy) and can be a predictor of macrohemorrhages.

The greatest role of CMB is discussed in cerebrovascular pathology and Alzheimer's disease. The presence or absence of strictly cortical CMBs has been included in the Boston criteria for cerebral amyloid angiopathy. Also, CMBs are a predictor of the clinical unfavorable course of cerebral amyloid angiopathy, which also increases the risk of subsequent intracerebral hemorrhages. Even a few CMBs increase the clinical significance of microvascular changes, giving them prognostic meaning. They help to differentiate hypertensive microangiopathy with their predominantly deep localization from cerebral amyloid angiopathy, in which they are detected mainly in cortical sections cerebral hemispheres (mainly occipital and parietotemporal).


Cerebral atrophy. A number of studies demonstrate a relationship between the presence and severity of cerebrovascular pathology and brain atrophy, including global cortical atrophy, atrophy corpus callosum, central atrophy (increase in ventricular size and atrophy of the basal ganglia), midbrain, hippocampus, and focal atrophy in brain areas associated with subcortical infarcts. It should be remembered that the assessment of microvascular brain damage includes the study of atrophy and vice versa.



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