Chronic cerebral ischemia. Chronic cerebrovascular disease: causes, symptoms and treatment Obtaining disability - f84.02 childhood autism due to

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Recently, failures of intracranial blood circulation have ceased to be a rarity. Experts attribute this to an improper and sedentary lifestyle, bad habits, overeating and stress.

Cerebral ischemia is manifested by the cessation of blood flow due to blockage or sharp narrowing of the arteries. Consequently, oxygen starvation develops, metabolism is disturbed, and neurons begin to die off. Such processes have an extremely negative effect on the functioning of the main organ of the central nervous system.

According to statistics, chronic ischemia accounts for the majority of diagnoses associated with cerebrovascular (cerebral) circulation. Although the development of this deviation is easy to avoid, following simple rules balanced nutrition and a healthy lifestyle.

The section of ICD-10, which includes ischemia, does not include a list of possible complications arising from oxygen starvation. Possible variations of a heart attack are divided into groups that indicate the degree of pathology:

  • a failure in blood circulation occurred in the precerebral arteries, that is, outside the vascular system of the head;
  • the vessels of the skull suffer;
  • the blockage has occurred in the veins of the brain.

For example, if a heart attack is due to a blood clot in the cerebral vessels, then a code in the range from I63.3 to I63.6 is used. When the cause of the pathology is the precerebral arteries and veins, the code changes to I63.0 - I63.2. Code I64.0 denotes a stroke without hemorrhage.

Chronic form coding options

Chronic cerebral ischemia (CCI) is not indicated in any way in the international statistical classification of diseases. This document is used in the medical community as a basis for providing a lonely approach to the diagnosis and treatment of diseases of all kinds. The classifier is rewritten every ten. The protocol of the tenth revision (2016 version) is in use today.

Chronic cerebral ischemia is absent in the ICD-10 code, since it does not belong to diseases, but is considered a clinical diagnosis. Experts classify this ailment as one or another subsection, based on the manifestations of pathology and its causes:

  • most often, such a deviation is referred to as "Cerebrovascular diseases": code I67. So designate chronic conditions that cause prolonged circulatory disorders;
  • cerebral ischemia is included in the "other" section, codes I67.8 and I67.9: all idiopathic ailments are located here;
  • blockage of internal cerebral arteries - I66;
  • aneurysms - I67.0 and I67.1;
  • atherosclerosis - I67.2;
  • encephalopathy of different etiology: I67.3 - I67.4;
  • Moyamoya's disease - I67.5;
  • inflammation in the vascular system of the head - I67.6 and I67.7.

Complications caused by cerebral ischemia are classified under the code I69.

Additional codes to indicate the reason

When making a diagnosis, the doctor must designate the ailment with a special code adopted in the international classifier, and note the circumstances that provoked chronic cerebral ischemia. Therefore, the designations of the following diseases are added:

  • high blood pressure - I95;
  • cardiac pathologies - I21 and I47;
  • in cases where there are no specific manifestations, then experts use the designation blockage of precerebral (non-cerebral) arteries: code I65;
  • cerebral hemorrhage: the code ranges from I60 to I62.

When clarifications are required in the form of clarification of complications, then codes of other subsections are assigned. For example, when it comes to dementia, the code F01 is used.

Variants of using the ICD-10

The International Classification of Diseases was created to make it easier to keep statistics. Moreover, with its help it is possible to analyze data both in a separate medical institution and on a national scale. Also, the ICD enables all doctors in the world to use the same diagnoses, thereby improving the quality of medical care.

During the treatment of ischemic pathology of the arteries or veins of the head, the doctor prescribes certain drugs that improve the patient's condition. In cases of extreme necessity, specialists make a decision on the operation.

After the completion of therapy, when it was possible to achieve positive dynamics, the doctor indicates the disease through the ICD-10 code in the discharge documents. If, in addition to cerebral ischemia, there were complications and various kinds of consequences, then the specialist also indicates them, encrypting them through ICD-10. Further, the statisticians of the medical institution, having processed the information, send it further. As a result, all the data are collected in one center, where the results will be summed up and the picture of the incidence of vascular pathologies of the head in adults or children is visible.

Ischemic conditions can really be described using ICD-10. Using the codes of the International Classifier of the tenth revision, the specialist will be able to apply diagnoses that are accepted in world medical practice. Such an approach helps to correctly assess the disease, to prescribe appropriate treatment for it according to the world standard, since therapy options are also described in ICD-10.

Diagnostics

Measures aimed at identifying chronic cerebrovascular insufficiency (CCF) include:

  • collecting anamnesis to establish symptoms of a neuropsychological and neurological nature;
  • laboratory blood tests for viscosity, lipid fractions, glucose indicators;
  • study of brain tissue: MRI and CT, duplex ultrasound, transcranial doppleography;
  • EKG, X-ray of the spine to determine possible complications.

Differential diagnosis

Cerebrovascular insufficiency or cerebral ischemia is manifested by symptoms:

  • headache;
  • dizziness;
  • irritability;
  • a person loses the ability to move normally, coordination of movements is impaired;
  • it becomes difficult for the patient to adequately perceive reality and think.

Such manifestations are characteristic not only of ischemic lesions. Similar complaints are characteristic of somatic diseases, endocrine disorders, psychological disorders, and even with malignant neoplasms, a person can experience similar sensations. Therefore, it is necessary to carry out a differentiated diagnosis.

Distinguishing ischemia is important from:

  • cognitive impairment;
  • Parkinson's and Alzheimer's disease;
  • cortico-basal degeneration;
  • differentiate with neoplasms of the brain;
  • idiopathic cell abnormalities;
  • normotensive hydrocephalus;
  • ataxia;
  • multisystem atrophy.

It is with these ailments that cerebrovascular insufficiency is usually confused.

Treatment

Cerebral ischemia requires an integrated approach. Moreover, a lot depends on the professionalism of the neurologist, since this deviation needs a special attitude.

To combat the disease, the following are used:

  • vasodilator and blood-thinning medicines: for the prevention of stroke, ischemic attacks, to normalize blood pressure indicators;
  • drugs that have a beneficial effect on blood circulation in blood vessels and saturate cells with oxygen;
  • drugs that improve brain function and blood circulation;
  • it is necessary to restore the physical condition: restorative therapy, physiotherapy exercises, massage, physiotherapy (electrophoresis, etc.).

When a disease is diagnosed with advanced ischemia, it is necessary to perform an operation, since drug therapy may not give results. Removal of sclerotic plaques and expansion of the vascular lumen is required. Neurosurgery is the most difficult type of surgical intervention, which is performed only by doctors of a certain level.

After the procedure, unpredictable complications may occur, the consequences of which are not always realistic to correct. It is for this reason that doctors take up a scalpel only in extreme cases, as a rule, after drug treatment has not had the desired effect.

Cerebrovascular diseases are pathological conditions of the brain that arise as a result of impaired blood supply to the brain due to various vascular pathologies. In accordance with the criteria of the World Health Organization, the ICD code 10 corresponds to the interval I60-I69 and belongs to class IX - "Diseases of the circulatory system".

The International Statistical Classification of Diseases and Related Health Problems 10th revision is an official classification and statistical document that is uniform for all medical institutions. Every disease must be encrypted for the formation and analysis of relevant statistics of morbidity or mortality.

Prevalence of CVD

Cerebrovascular diseases are the most important medical problem, as they are widespread and occupy a leading position in the statistics of disability and mortality. It should be noted that cerebrovascular disease according to ICD 10 and the corresponding headings I60-I62 include:

  • hemorrhagic stroke and its variations;
  • ischemic and unspecified strokes;
  • chronic stenosis of the blood vessels of the brain;
  • aneurysm, atherosclerosis of the blood vessels;
  • encephalopathy;
  • hypertensive encephalopathy;
  • passing acute disorders of cerebral circulation (hypertensive cerebral crisis, transient attacks of ischemia, which do not lead to necrotic phenomena).

The main pathogenetic factor of all these diseases is violation of blood flow to the brain arising acutely, transiently or chronically. Brain tissue is affected, leading to severe neurological symptoms and requiring immediate and ongoing treatment.

ICD 10 encryption provides invaluable assistance in monitoring these pathologies and shows the effectiveness of the therapy.

Excludes: consequences of the listed conditions (I69.8)

Excludes1: rupture of cerebral arteries (I60.7)

Brain (oops):

  • aneurysm NOS
  • acquired arteriovenous fistula

Excluded:

  • congenital cerebral aneurysm, non-ruptured (Q28.-)
  • ruptured cerebral aneurysm (I60.-)

Excludes1: subcortical vascular dementia (F01.2)

Non-suppurative thrombosis:

  • brain veins
  • intracranial venous sinus

Excludes: conditions causing cerebral infarction (I63.6)

Acute cerebrovascular insufficiency NOS

Brain ischemia (chronic)

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) has been adopted as a single normative document to take into account the incidence, reasons for the population's appeals to medical institutions of all departments, and causes of death.

ICD-10 was introduced into health care practice throughout the Russian Federation in 1999 by order of the Ministry of Health of Russia dated 05/27/97. No. 170

A new revision (ICD-11) is planned by WHO in 2017 2018.

As amended and supplemented by WHO

Processing and translation of changes © mkb-10.com

ICD-10 cerebral ischemia code

The use of the International Classification of Diseases (ICD-10) helps doctors to more easily navigate in a wide variety of pathologies human body... Modern medicine is capable of determining a mass of diagnoses that cannot be memorized or learned. This is especially true in vascular pathology: there are a lot of different variants of serious diseases associated with acute or chronic circulatory disorders of organs and systems. In particular, cerebral ischemia belongs to the "Diseases of the circulatory system" (class IX) and is located in the section "Cerebrovascular diseases". Each condition has a code that the doctor will use to diagnose and treat.

Classification of acute cerebral ischemia

Vascular pathology of the brain caused by a sudden and pronounced impairment of arterial blood flow was allocated to a separate ICD-10 group. All variants of cerebral infarction are divided into parts, each of which indicates the level of vascular pathology:

  • obstruction of blood circulation occurred at the level of vessels outside the brain (precerebral arteries);
  • impaired cerebral blood flow;
  • a thrombus formed in the cerebral veins.

ICD-10 codes from I63.0 to I63.2 denote cerebral infarction caused by thrombosis of the precerebral arteries, I63.3 to I63.6 - blockage of cerebral arteries and veins. The I64.0 code encrypts a stroke in which there is no hemorrhage in the brain structures.

This group of ICD-10 ciphers does not include complications and consequences arising from an acute ischemic attack.

Coding options for chronic cerebral ischemia

All chronic conditions leading to ischemic changes in brain structures are coded in subsection I67. The following conditions are common causes of long-term cerebral circulatory insufficiency:

  • dissecting aneurysm of cerebral arteries (I67.0);
  • cerebral aneurysm without signs of rupture (I67.1);
  • atherosclerotic vascular disease of the brain (I67.2);
  • encephalopathy due to vascular causes (I67.3);
  • encephalopathy due to arterial hypertension (I67.4);
  • rare vascular pathology of the carotid and cerebral arteries, described as Moyamoya disease (I67.5);
  • inflammatory damage to the veins and arteries of the brain, leading to impaired blood flow (I67.6 - I67.7);
  • if it is difficult to identify the main causative factor, codes I67.8 - I67.9 are used, which designate all unspecified variants of diseases.

All types of consequences of acute or chronic cerebral ischemia are coded under subsection I69.

Additional codes to indicate the reason

Often, the doctor needs not only to highlight the underlying disease with a code, but also to identify additional causal factors that led to ischemic conditions in the head. For this, ciphers from other subsections are used:

  • arterial hypotension (I95);
  • serious heart disease (I21, I47);
  • blockage of individual non-cerebral arteries (I65);
  • various variants of cerebral hemorrhage (I60 - I62).

If it is necessary to indicate complications, the doctor can use the encoding of other sections. In particular, when expressed brain disorders for the type of dementia due to vascular causes, the code F01 can be used.

Variants of using the ICD-10

If acute thrombosis or chronic cerebral ischemia is detected, the doctor conducts a course of therapy aimed at completely curing the patient from the pathology of the precerebral or cerebral arteries. Surgery can be performed if necessary. If the treatment was successful, then upon discharge, the doctor will indicate the diagnosis in the form of the ICD-10 code. The disease code will be processed by the statistical service of the hospital, sending the information to the information medical center of the region. If, in addition to the main diagnosis, there are complications and consequences that require additional examination and treatment, the doctor will indicate the coding of these conditions using the codes of the international classification.

All ischemic conditions of the brain can be encrypted using ICD-10. Applying the version of the International Classification of Diseases of the 10th revision, the doctor will always use the diagnoses used all over the world. This will make it possible to correctly assess not only the disease in a person, but also to carry out effective treatment using modern and high-tech methods of world therapy.

The information on the site is provided for informational purposes only and cannot replace the advice of your doctor.

Chronic cerebrovascular disease: causes, symptoms and treatment

A number of diseases associated with cerebrovascular accidents are called cerebrovascular. They are acute and chronic. The former include strokes and transient ischemic attacks. Chronic forms represented by vascular dementia and discirculatory encephalopathy.

Description of problems

Cerebrovascular disease is a pathological condition characterized by organic changes in the brain tissue. They arise from problems with the blood supply. Because of this, brain cells do not receive enough oxygen and other nutrients. All this becomes the reason for the appearance of such changes as a result of which cognitive disorders appear or even such a serious complication as a stroke may develop.

The main problem in most cases is diffuse or multifocal lesions of the brain. They are manifested by mental, neuropsychiatric or neurological disorders that characterize cerebrovascular disease. Dyscirculatory encephalopathy is currently absent in the international classification of diseases, established as a result of revision 10 (ICD 10), although in Russia it is this diagnosis that is most often used to designate chronic problems with cerebral circulation.

Causes of the disease

The factors that lead to a deterioration in the blood supply to the brain, experts conditionally divided into two groups. The most common cause of problems is atherosclerotic lesions of the body's major blood vessels. Cholesterol plaques form on their walls, respectively, the lumen in them decreases. Because of this, all organs with age cease to receive the required amount of oxygen and other essential substances, including glucose. This leads to the development of changes in them and to the fact that over time, chronic cerebrovascular disease can be diagnosed.

The second reason for the appearance of these problems is inflammatory processes in the cerebral vessels called vasculitis.

The risk group includes all those people who are susceptible to developing a disease such as atherosclerosis. These are patients with diabetes mellitus, smokers, as well as those who are overweight.

Types of pathologies

Cerebrovascular disease is a group of diagnoses under one name. Depending on the violations that arise and the severity of the problems, there are:

Occlusion and stenosis of cerebral vessels;

Ischemic or hemorrhagic stroke;

Transient ischemic attack;

Venous sinus thrombosis;

If you know international classification, then it is easy to find out what doctors may mean when they say that a patient has cerebrovascular disease. The ICD 10 code for this group is I60-I69.

Medical classification

It is enough for specialists to know the rubric to which the disease is attributed in order to understand what diagnosis was made to the patient. So, in order for everyone to understand that the patient has chronic cerebrovascular disease, the ICD assigned the code I67 to the pathology. For the designation of acute forms, codes I60-I66 are intended. They mean such pathologies:

  • I60 - subarachnoid hemorrhages are combined here;
  • I61 - intracerebral hemorrhage;
  • I62 - other non-traumatic intracranial effusion;
  • I63 - cerebral infarctions;
  • I64 - strokes not specified as heart attacks or hemorrhages;
  • I65-I66 - cases of blockage and stenosis of cerebral and precerebral arteries, which do not lead to cerebral infarction, but in situations where there was a lethal outcome, they are replaced by the code I63.

It is necessary to register the diagnosed diseases according to the rules established by the ICD 10. Cerebrovascular disease, the duration of which is no more than 30 days, can be classified under I60-I66. All consequences of the disease should be indicated not just under a general code, but specifically defined. For example, if there was paralysis, encephalopathy or other manifestations of cerebrovascular disease, this should be indicated.

Symptoms

Information regarding ICD 10 coding is required only by medical personnel. It is much more important for patients to figure out what symptoms to look for and when to see a doctor. So, it is important to know that cerebrovascular disease on initial stages may not show up too much. But the symptoms become more noticeable with the progression of the pathology.

Among them, the most common:

Dizziness, noise, and pain in the head;

Numbness of the limbs, impaired sensitivity in them;

Periodic visual impairment;

Short-term loss of consciousness.

In the worst cases, transient ischemic attacks and strokes occur. These conditions are the cause of a significant violation of the blood supply to the brain, as a result of which nerve cells die.

Definition of disease

In order to be diagnosed with cerebrovascular disease, it is necessary to consult a doctor in time. Statistics confirm that in the initial stages of the disease only few people turn to doctors. Many attribute their ailments to bad weather, lack of vitamins, and overwork. As a result, patients are admitted to hospitals with strokes and ischemic attacks. This can be prevented if cerebrovascular disease is detected in a timely manner. Treatment prescribed without delay will not only alleviate the patient's condition, but also reduce the risk of severe circulatory disorders in the brain.

Diagnosis of the disease is carried out as follows. First you need to pass a biochemical and general blood test. They will determine if there is a risk of developing atherosclerotic changes in the vessels. In addition to tests, it is also a good idea to do ultrasound diagnostics. With the help of duplex and triplex scanning, it is possible to reliably assess the state of the vessels.

Using such a radiopaque research method as angiography, it is possible to identify areas of narrowing and blockage of blood vessels. An EEG can be used to assess how the brain is functioning. During this procedure, changes in electrical activity are recorded.

The most reliable and accurate methods are CT, MRI or scintigraphy. All of this research is high-tech. They provide additional information about the structures of the central nervous system.

Therapy

If you have been diagnosed with cerebrovascular brain disease, then you cannot let the problem go by itself. This condition requires treatment, otherwise complications cannot be avoided. But it should be understood that for a full-fledged therapy it is necessary that the patient himself wants to recover. So, an improvement in the condition is possible only if the patient changes his lifestyle, loses excess weight, and gives up smoking and alcohol.

But, in addition to this, it is necessary to consult with your doctor and find out what kind of therapy will be optimal. In many cases, conservative methods are bypassed. But in a number of situations, it is desirable that timely surgical intervention was carried out, which will eliminate the areas of vasoconstriction that feed the central nervous system.

Conservative treatment

For chronic problems with the blood supply to the brain, conventional medication is often used. They are aimed at lowering the concentration of cholesterol in the blood, maintaining blood pressure, and improving the blood supply to tissues. Taking medications prescribed by a doctor in combination with dietary and lifestyle adjustments in general allows you to maintain brain function at the required level for a fairly long time.

For treatment, antiplatelet, nootropic, vasodilator, hypotensive, hypocholesterolemic agents are prescribed. Also, antioxidants and multivitamin complexes are recommended in parallel.

Medicines used

Thus, we have found out why it is so important for specialists to know what the code of the pathology we are considering. Cerebrovascular disease is a consequence of a number of diseases. Therefore, therapy should primarily be aimed at eliminating them.

So, with multiple cardioembolism and multi-infarction state, coalogulopathy and agniopathy, antiplatelet agents are required. The most popular among them is the common acetylsalicylic acid, which is prescribed in a dosage of 1 mg for each kg of patient weight. It may also be recommended to take medications such as "Clopidogrel" or "Dipyridamole" in a dosage of about g per day. Also in such situations, anticoagulants are prescribed, for example, "Warfarin".

Neurological disorders are treated with the use of nootropics, neurotransmitters and amino acids. Drugs such as "Glycine", "Neuromidin", "Cerebrolysin", "Actovegin" can be prescribed. In case of tinnitus and dizziness, Betahistine is often prescribed at a dosage of 24 mg twice a day.

For patients suffering from pressure surges, it is important to normalize it. Among the prescribed vasoactive drugs, such medications as Vinpocetine, Pentoxifylline are popular.

Operational methods

Traditional surgical methods allow you to get rid of ischemia of the brain tissue. For this, currently, only X-ray endovascular and microsurgical interventions are performed.

In some cases, balloon angioplasty is recommended. This is a procedure during which a special balloon is inserted into the vessel and inflated there. This helps to expand the lumen and normalize blood flow. After such an intervention - to prevent adhesion or re-narrowing of the artery - it is advisable that stenting be done. This is a procedure during which a mesh implant is placed in the lumen of the vessel, which is responsible for keeping its walls in a straightened state.

If cerebrovascular disease has been diagnosed, endarterectomy may also be performed. This is a microsurgical operation, during which all cholesterol deposits are removed from the lumen of the vessel. After that, its integrity is restored.

Folk methods

Even if you are not a supporter of alternative medicine, cerebrovascular disease is the problem that is better amenable to therapy with an integrated approach. Even doctors say that it will not work to normalize your condition without increasing physical activity, normalizing nutrition, quitting smoking and other bad habits.

In addition, you can use folk recipes in parallel with the main therapy. For example, many people recommend chopping 2 oranges and lemons in a meat grinder or blender, along with the skin, but without seeds. In the resulting gruel, add ½ cup of honey, mix and leave for a day at room temperature. After that, the mixture must be placed in the refrigerator and taken in 2 tbsp. l. up to 3 times a day. You can drink it with green tea.

Chronic cerebrovascular accident

This brochure contains a section on chronic cerebral circulation insufficiency (authored by V. I. Skvortsova, L. V. Stakhovskaya, V. V. Gudkova, A. V. Alekhin) from the book “Neurology. National leadership "ed. E.I. Guseva, A.N. Konovalov, V.I. Skvortsova, A.B. Gecht (Moscow: GEOTAR-Media, 2010)

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

Synonyms: discirculatory encephalopathy, chronic cerebral ischemia, slowly progressive cerebrovascular accident, chronic cerebral ischemic disease, cerebrovascular insufficiency, vascular encephalopathy, atherosclerotic encephalopathy, hypertensive encephalopathy, vascular paroxysmal artery disease , vascular dementia.

The term "discirculatory encephalopathy" has entered the Russian neurological practice most widely of the above synonyms, which retains its meaning to this day.

Codes according to ICD-10. Cerebrovascular diseases are coded according to ICD-10 in headings I60-I69. The concept of "chronic cerebral circulation insufficiency" is absent in the ICD-10. Dyscirculatory encephalopathy (chronic cerebrovascular insufficiency) can be coded in heading I67. Other cerebrovascular diseases: I67.3. Progressive vascular leukoencephalopathy(Binswanger's disease) and I67.8. Other specified cerebrovascular diseases, subheading "Brain ischemia (chronic)". The rest of the codes from this heading reflect either only the presence of vascular pathology without clinical manifestations(vascular aneurysm without rupture, cerebral atherosclerosis, Moyamoya's disease, etc.), or the development of acute pathology (hypertension encephalopathy).

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

Headings I65-I66 (according to ICD-10) "Occlusions or stenosis of precerebral (cerebral) arteries that do not lead to cerebral infarction" are used to encode patients with asymptomatic course of this pathology.

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

To some extent, one can judge the frequency of chronic forms of cerebrovascular diseases based on the epidemiological indicators of the prevalence of stroke, since acute cerebrovascular accident, as a rule, develops against a background prepared by chronic ischemia, and this process continues to grow in the post-stroke period. In Russia, they annually register strokes, in Moscow - more (Boyko A.N. et al., 2004). At the same time, O.S. Levin (2006), emphasizing the special importance of cognitive disorders in the diagnosis of dyscirculatory encephalopathy, suggests focusing on the prevalence of cognitive dysfunctions, assessing the frequency of chronic cerebrovascular accident. However, even these data do not reveal the true picture, since only vascular dementia is recorded (5-22% among the elderly population), not taking into account pre-dementia conditions.

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

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

The causes of both acute and chronic disorders of cerebral circulation are the same. Among the main etiological factors, atherosclerosis and arterial hypertension are considered, a combination of these 2 conditions is often revealed. Other diseases of the cardiovascular system can also lead to chronic insufficiency of cerebral circulation, especially those accompanied by signs of chronic heart failure, cardiac arrhythmias (both permanent and paroxysmal forms of arrhythmia), often leading to a drop in systemic hemodynamics. The anomaly of the vessels of the brain, neck, shoulder girdle, the aorta, especially its arch, which may not appear until the development of atherosclerotic, hypertensive or other acquired process in these vessels is also important. A large role in the development of chronic cerebral circulation insufficiency has recently been attributed to venous pathology, not only intracranial, but also extracranial. Compression of blood vessels, both arterial and venous, can play a definite role in the formation of chronic cerebral ischemia. It is necessary to take into account not only the spondylogenic effect, but also compression by altered neighboring structures (muscles, fascia, tumors, aneurysms). Low blood pressure adversely affects cerebral blood flow, especially in the elderly. This group of patients may develop lesions of the small arteries of the head associated with senile arteriosclerosis.

Another cause of chronic cerebrovascular insufficiency in elderly patients is cerebral amyloidosis - the deposition of amyloid in the vessels of the brain, leading to degenerative changes in the vascular wall with possible rupture.

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

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

Causes of chronic cerebral circulatory insufficiency

Arterial hypertension. Additional:

Heart disease with signs of chronic circulatory failure;

Heart rhythm disorders;

Vascular anomalies, hereditary angiopathies;

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

For adequate brain function, it is necessary high level blood supply. The brain, which weighs 2.0-2.5% of body weight, consumes 20% of the blood circulating in the body. The value of cerebral blood flow in the hemispheres averages 50 ml per 100 g / min, but in the gray matter it is 3-4 times higher than in the white matter, and there is also a relative physiological hyperperfusion in the anterior regions of the brain. With age, the amount of cerebral blood flow decreases, and frontal hyperperfusion also disappears, which plays a role in the development and growth of chronic cerebrovascular insufficiency. At rest, the brain's oxygen consumption is 4 ml per 100 g / min, which corresponds to 20% of all oxygen entering the body. The glucose consumption is 30 μmol per 100 g / min.

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

The main arteries of the head are the carotid and vertebral arteries, which carry blood to the brain and regulate the volume of cerebral blood flow;

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

Vessels of the microvasculature providing metabolic processes.

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

Cerebral blood flow depends on perfusion pressure (the difference between systemic blood pressure and venous pressure at the level of the subarachnoid space) and the resistance of cerebral vessels. Normally, due to the mechanism of autoregulation, cerebral blood flow remains stable, despite fluctuations in blood pressure from 60 to 160 mm Hg. With damage to cerebral vessels (lipo-hyalinosis with the development of vascular wall unresponsiveness), cerebral blood flow becomes more dependent on systemic hemodynamics.

With long-term arterial hypertension, a shift in the upper limit of systolic pressure is noted, at which cerebral blood flow remains stable and for a long time there are no violations of autoregulation. Adequate perfusion of the brain is supported by an increase in vascular resistance, which in turn leads to an increased load on the heart. It is assumed that an adequate level of cerebral blood flow is possible until there are pronounced changes in small intracerebral vessels with the formation of a lacunar state characteristic of arterial hypertension. Consequently, there is a certain margin of time when timely treatment of arterial hypertension can prevent the formation of irreversible changes in blood vessels and the brain or reduce their severity. If the basis of chronic cerebral circulation insufficiency is only arterial hypertension, then the use of the term "hypertensive encephalopathy" is legitimate. Severe hypertensive crises are always a breakdown of autoregulation with the development of acute hypertensive encephalopathy, each time aggravating the phenomenon of chronic cerebrovascular insufficiency.

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

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

The structure of the plaques is also of great importance. The so-called unstable plaques lead to the development of arterio-arterial embolism and acute disorders of cerebral circulation, often in the form of transient ischemic attacks. Hemorrhage into such a plaque is accompanied by a rapid increase in its volume with an increase in the degree of stenosis and aggravation of signs of chronic cerebrovascular insufficiency.

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

In recent years, 2 main pathogenetic variants of chronic cerebrovascular insufficiency have been considered. They are based on morphological signs - the nature of damage and predominant localization. With diffuse bilateral lesions of white matter, leukoencephalopathic, or subcortical biswanger, a variant of discirculatory encephalopathy, is isolated. The second is a lacunar variant with the presence of multiple lacunar foci. However, in practice, mixed options are often encountered. Against the background of diffuse lesions of white matter, multiple small heart attacks and cysts are found, in the development of which, in addition to ischemia, repeated episodes of cerebral hypertensive crises can play an important role. In hypertensive angioencephalopathy, lacunae are located in the white matter of the frontal and parietal lobes, shell, bridge, thalamus, caudate nucleus.

The lacunar variant is most often due to the direct occlusion of small vessels. In the pathogenesis of diffuse lesions of white matter, repeated episodes of a fall in systemic hemodynamics - arterial hypotension - play a leading role. The reason for the fall in blood pressure may be inadequate antihypertensive therapy, a decrease in cardiac output, for example, with paroxysmal heart rhythm disturbances. Persistent cough, surgical interventions, orthostatic arterial hypotension due to vegetative-vascular insufficiency are also important. In this case, even a slight decrease in blood pressure can lead to ischemia in the terminal zones of the adjacent blood supply. These zones are often clinically "mute" even with the development of heart attacks, which leads to the formation of a multi-infarction state.

In conditions of chronic hypoperfusion - the main pathogenetic link of chronic cerebral circulation insufficiency - the mechanisms of compensation can be depleted, the energy supply of the brain becomes insufficient, as a result, functional disorders and then irreversible morphological damage. In chronic hypoperfusion of the brain, a slowdown in cerebral blood flow, a decrease in the content of oxygen and glucose in the blood (energy hunger), oxidative stress, a shift in glucose metabolism towards anaerobic glycolysis, lactic acidosis, hyperosmolarity, capillary stasis, a tendency to thrombosis, depolarization of cell membranes are revealed , activation of microglia, which begins to synthesize neurotoxins, which, along with other pathophysiological processes, leads to cell death. In patients with cerebral microangiopathy, granular atrophy of the cortical regions is often revealed.

A multifocal pathological state of the brain with a predominant lesion of the deep regions leads to a violation of the connections between the cortical and subcortical structures and the formation of the so-called disconnection syndromes.

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

Acute and chronic forms of ischemic disorders of cerebral circulation can pass one into another. Ischemic stroke, as a rule, develops against an already changed background. In patients, morphofunctional, histochemical, immunological changes are revealed due to the previous discirculatory process (mainly atherosclerotic or hypertensive angioencephalopathy), the signs of which significantly increase in the post-stroke period. The acute ischemic process, in turn, triggers a cascade of reactions, some of which end in the acute period, and some remain indefinitely and contribute to the emergence of new pathological conditions, leading to an increase in signs of chronic cerebrovascular accident.

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

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

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

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

The main clinical manifestations of chronic insufficiency of cerebral circulation are disorders in the emotional sphere, polymorphic movement disorders, impairment of memory and learning ability, gradually leading to maladjustment of patients. Clinical features chronic cerebral ischemia - progressive course, staged, syndromic.

In domestic neurology, for a long time, along with discirculatory encephalopathy, the initial manifestations of cerebral circulatory insufficiency were also attributed to chronic cerebrovascular insufficiency. Currently, it is considered unreasonable to isolate such a syndrome as "the initial manifestations of insufficient blood supply to the brain", given the nonspecificity of the presented complaints of an asthenic nature and the frequent overdiagnosis of the vascular genesis of these manifestations. The presence of headache, dizziness (of a non-systemic nature), memory loss, sleep disturbances, noise in the head, ringing in the ears, blurred vision, general weakness, increased fatigue, decreased performance and emotional lability, in addition to chronic cerebral circulation insufficiency, may indicate other diseases and conditions ... In addition, these subjective sensations sometimes simply inform the body about fatigue. When confirming the vascular genesis of asthenic syndrome using additional research methods and identifying focal neurological symptoms, the diagnosis of "discirculatory encephalopathy" is established.

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

The core of the clinical picture of discirculatory encephalopathy has recently been recognized as cognitive impairments, which are detected already in stage I and progressively increasing by stage III. In parallel, emotional disorders develop (emotional lability, inertia, lack of emotional reaction, loss of interests), various movement disorders(from programming and control to the execution of both complex neokinetic, higher automated, and simple reflex movements).

Stages of discirculatory encephalopathy

Dyscirculatory encephalopathy is usually divided into 3 stages.

At stage I, the above complaints are combined with diffuse micro-focal neurological symptoms in the form of anisoreflexia, convergence failure, rough reflexes of oral automatism. Slight changes in gait (decrease in stride length, slowness of walking), decreased stability and uncertainty when performing coordination tests are possible. Emotional and personality disorders (irritability,

emotional lability, anxious and depressive traits). Already at this stage, mild cognitive disorders of the neurodynamic type appear: slowdown and inertia of intellectual activity, exhaustion, fluctuations in attention, a decrease in the volume of working memory. Patients cope with neuropsychological tests and jobs that do not require timing. Patients' livelihoods are not limited.

Stage II is characterized by an increase in neurological symptoms with the possible formation of a mild, but dominant syndrome. Separate extrapyramidal disorders, incomplete pseudobulbar syndrome, ataxia, central CN dysfunction (proso- and glossoparesis) are revealed. Complaints become less pronounced and not so significant for the patient. Emotional disorders are getting worse. Cognitive dysfunction increases to a moderate degree, neurodynamic disorders are supplemented by dysregulatory ones (fronto-subcortical syndrome). The ability to plan and control one's actions is impaired. The performance of tasks that are not limited by the time frame is violated, but the ability to compensate is preserved (recognition and the ability to use prompts are preserved). At this stage, signs of a decrease in professional and social adaptation may appear.

Stage III is manifested by the presence of several neurological syndromes. Gross violations of walking and balance with frequent falls, severe cerebellar disorders, parkinsonian syndrome, urinary incontinence develop. The criticism of one's condition decreases, as a result of which the number of complaints decreases. Severe personality and behavioral disorders may appear in the form of disinhibition, explosiveness, psychotic disorders, and apathy-abulic syndrome. Operational disorders (defects in memory, speech, praxis, thinking, visual-spatial function) join neurodynamic and dysregulatory cognitive syndromes. Cognitive disorders often reach the level of dementia, when maladjustment manifests itself not only in social and professional activity but also in everyday life. Patients are disabled, in some cases they gradually lose the ability to serve themselves.

Neurological syndromes in discirculatory encephalopathy

Most often, with chronic cerebral circulation insufficiency, vestibulocerebellar, pyramidal, amiostatic, pseudobulbar, psychoorganic syndromes, as well as their combinations, are detected. Sometimes cephalgic syndrome is isolated separately. At the heart of all syndromes inherent in circulatory encephalopathy is the disconnection of connections due to diffuse anoxic-ischemic damage to the white matter.

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

Pyramidal syndrome in discirculatory encephalopathy is characterized by high tendon and positive pathological reflexes, often asymmetric. Paresis are expressed indistinctly or absent. Their presence indicates a previous stroke.

Parkinsonian syndrome within the framework of discirculatory encephalopathy is represented by slow movements, hypomimia, rough muscle rigidity, more often in the legs, with the phenomenon of "resistance", when muscle resistance increases involuntarily during passive movements. Tremor is usually absent. Gait disorders are characterized by a slowdown in walking speed, a decrease in the size of a step (microbasia), a "sliding", shuffling step, small and fast stomping on the spot (before starting to walk and when turning). Difficulty turning while walking is manifested not only by stomping on the spot, but also by turning with the whole body in violation of balance, which may be accompanied by a fall. Falls in these patients occur with the phenomena of propulsion, retropulsion, lateropulsions and can also precede walking due to a violation of the initiation of locomotion (symptom of "stuck legs"). If there is an obstacle in front of the patient (narrow door, narrow passage), the center of gravity shifts forward, in the direction of movement, and the legs tread in place, which can cause a fall.

The emergence of vascular parkinsonian syndrome in chronic cerebrovascular insufficiency is not due to the defeat of the subcortical ganglia, but of the cortical-striatal and cortical-stem connections, therefore, treatment with drugs containing levodopa does not bring significant improvement to this contingent of patients.

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

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

The psychoorganic (psychopathological) syndrome can manifest itself as emotional-affective disorders (asthenodepressive, anxiety-depressive), cognitive (cognitive) impairments - from mild mental and intellectual disorders to various degrees of dementia (see Chapter 26 "Impairment of cognitive functions").

The severity of the cephalgic syndrome decreases with the progression of the disease. Among the mechanisms of the formation of cephalalgia in patients with chronic cerebrovascular insufficiency, myofascial syndrome can be considered against the background of osteochondrosis of the cervical spine, as well as headache stress (HDN) - a variant of psychhalgia, often arising against the background of depression.

To diagnose chronic cerebrovascular insufficiency, it is necessary to establish a connection between clinical manifestations and pathology of cerebral vessels. For the correct interpretation of the identified changes, it is very important to carefully collect anamnesis with an assessment of the previous course of the disease and follow-up of patients. It should be borne in mind the inverse relationship between the severity of complaints and neurological symptoms and the parallelism of clinical and paraclinical signs in the progression of cerebral vascular insufficiency.

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

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

It is important to note the presence of ischemic disease heart, myocardial infarction, angina pectoris, atherosclerosis of the peripheral arteries of the extremities, arterial hypertension with damage to target organs (heart, kidneys, brain, retina), changes in the valve apparatus of the heart chambers, cardiac arrhythmias, diabetes mellitus and other diseases specified in the section "Etiology ".

A physical examination reveals abnormalities in the cardiovascular system. It is necessary to determine the safety and symmetry of pulsation on the main and peripheral vessels of the limbs and head, as well as the frequency and rhythm of pulse oscillations. Blood pressure should be measured on all 4 limbs. It is imperative to auscultate the heart and abdominal aorta to detect murmurs and cardiac arrhythmias, as well as the main arteries of the head (vessels of the neck), which makes it possible to determine a noise above these vessels, indicating the presence of a stenosing process.

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

The main direction of laboratory research is to clarify the causes of the development of chronic cerebrovascular insufficiency and its pathogenetic mechanisms. Examine the CBC with reflection

A task instrumental methods- to clarify the level and degree of damage to blood vessels and brain matter, as well as to identify background diseases. These tasks are solved with the help of repeated ECG records, ophthalmoscopy, echocardiography (according to indications), cervical spondylography (with suspicion of pathology in the vertebrobasilar system), ultrasound research methods (ultrasound examination of the main arteries of the head, duplex and triplex scanning of extra- and intracranial vessels).

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

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

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

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

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

Considering that in chronic cerebral circulation insufficiency, the white matter of the brain suffers first of all, MRI is preferred over CT. MRI in patients with chronic cerebrovascular insufficiency reveals diffuse changes white matter, cerebral atrophy, focal changes brain.

On MRI tomograms, the phenomena of periventricular leukoaraiosis (rarefaction, decrease in tissue density), reflecting ischemia of the white matter of the brain, are visualized; internal and external hydrocephalus (expansion of the ventricles and subarachnoid space), due to atrophy of the brain tissue. Small cysts (lacunae), large cysts, as well as gliosis, indicating previous cerebral infarctions, including clinically "dumb" ones, can be detected.

It should be noted that all of the listed characteristics are not considered specific; it is incorrect to diagnose discirculatory encephalopathy only by the data of imaging examination methods.

The aforementioned complaints, characteristic of the initial stages of chronic cerebrovascular insufficiency, can also occur during oncological processes, various somatic diseases, reflect the prodromal period or asthenic "tail" of infectious diseases, be part of the symptom complex of borderline mental disorders (neuroses, psychopathy) or endogenous mental processes ( schizophrenia, depression).

Signs of encephalopathy in the form of diffuse multifocal lesions of the brain are also considered nonspecific. It is customary to define encephalopathy according to the main etiopathogenetic characteristic (post-hypoxic, post-traumatic, toxic, infectious-allergic, paraneoplastic, dysmetabolic, etc.). Dyscirculatory encephalopathy most often has to be differentiated from dysmetabolic, including degenerative processes.

Dysmetabolic encephalopathy caused by disorders of brain metabolism can be either primary, arising as a result of a congenital or acquired defect in neuronal metabolism (leukodystrophy, degenerative processes, etc.), and secondary, when disorders of brain metabolism develop against the background of an extracerebral process. There are the following variants of secondary metabolic (or dysmetabolic) encephalopathy: hepatic, renal, respiratory, diabetic, encephalopathy with severe multiple organ failure.

Differential diagnosis of discirculatory encephalopathy with various neurodegenerative diseases, in which, as a rule, cognitive disorders and certain focal neurological manifestations are present, cause great difficulties. Such diseases include multisystem atrophy, progressive supranuclear palsy, cortico-basal degeneration, Parkinson's disease, diffuse Lewy body disease, frontotemporal dementia, and Alzheimer's disease. Differentiation between Alzheimer's disease and discirculatory encephalopathy is not an easy task: often discirculatory encephalopathy initiates subclinical Alzheimer's disease. In more than 20% of cases, dementia in the elderly is of a mixed type (vascular-degenerative).

Dyscirculatory encephalopathy has to be differentiated from such nosological forms as a brain tumor (primary or metastatic), normotensive hydrocephalus, manifested by ataxia, cognitive disorders, impaired control over pelvic functions, idiopathic dysbasia with impaired gait and stability software.

It should be borne in mind the presence of pseudodementia (dementia syndrome disappears against the background of treatment of the underlying disease). As a rule, this term is used in relation to patients with severe endogenous depression, when not only mood worsens, but also motor and intellectual activity weakens. It was this fact that gave reason to include the time factor in the diagnosis of dementia (persistence of symptoms for more than 6 months), since the symptoms of depression by this time are stopped. Probably, this term can also be used in other diseases with reversible cognitive impairments, in particular, in secondary dysmetabolic encephalopathy.

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

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

Indications for hospitalization

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

The choice of medication is due to the main areas of therapy noted above.

The main areas in the treatment of chronic cerebrovascular insufficiency are considered 2 areas of basic therapy - the normalization of cerebral perfusion by influencing different levels of the cardiovascular system (systemic, regional, microcirculatory) and the effect on the platelet link of hemostasis. Both of these directions, while optimizing cerebral blood flow, simultaneously perform a neuroprotective function.

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

An important role in the prevention and stabilization of manifestations of chronic cerebrovascular insufficiency is assigned to the maintenance of adequate blood pressure. In the literature there is information about the positive effect of normalization of blood pressure on the resumption of an adequate response of the vascular wall to the gas composition of the blood, hyper- and hypocapnia (metabolic regulation of blood vessels), which affects the optimization of cerebral blood flow. Maintaining blood pressure at / 80 mm Hg. prevents the growth of mental and movement disorders in patients with chronic cerebral circulatory insufficiency. In recent years, it has been shown that antihypertensive drugs have neuroprotective properties, that is, they protect the preserved neurons from secondary degenerative damage after a stroke and / or in chronic cerebral ischemia. In addition, adequate antihypertensive therapy prevents the development of primary and repeated acute disorders of cerebral circulation, the background for which often becomes chronic cerebrovascular insufficiency.

Early initiation of antihypertensive therapy is very important, before the development of a pronounced "lacunar state" that determines the separation of cerebral structures and the development of the main neurological syndromes of discirculatory encephalopathy. When prescribing antihypertensive therapy, sharp fluctuations in blood pressure should be avoided, since with the development of chronic insufficiency of cerebral circulation, the mechanisms of autoregulation of cerebral blood flow are reduced, which will be more dependent on systemic hemodynamics. In this case, the autoregulation curve will shift towards a higher systolic blood pressure, and arterial hypotension (<110 мм рт.ст.) - неблагоприятно влиять на мозговой кровоток. В связи с этим назначаемый препарат должен адекватно контролировать системное давление.

Currently, a large number of antihypertensive drugs have been developed and introduced into clinical practice, allowing to ensure blood pressure control, from different pharmacological groups. However, the data obtained on the important role of the renin-angiotensin-aldosterone system in the development of cardiovascular diseases, as well as on the relationship between the content of angiotensin II in the central nervous system and the volume of cerebral ischemia, make it possible today to give preference to drugs affecting renin-angiotensin-aldosterone system. These include 2 pharmacological groups - angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists.

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

According to the literature, the influence of angiotensin II receptor antagonists on degenerative processes in the brain, in particular, in Alzheimer's disease, is not excluded, which significantly expands the neuroprotective role of these drugs. It is known that recently, most types of dementia, especially in old age, are considered as combined vascular-degenerative cognitive disorders. It should also be noted the alleged antidepressant effect of angiotensin II receptor antagonists, which is of great importance in the treatment of patients with chronic cerebrovascular insufficiency, who often develop affective disorders.

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

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

Lipid-lowering therapy (treatment of atherosclerosis)

Patients with atherosclerotic lesions of the cerebral vessels and dyslipidemia, in addition to a diet with restriction of animals and the predominant use of vegetable fats, it is advisable to prescribe hypolipidemic agents, in particular statins (atorvastatin, simvastatin, etc.), which have a therapeutic and prophylactic effect. It is more effective to take these drugs in the early stages of discirculatory encephalopathy. Their ability to reduce cholesterol content, improve endothelial functions, reduce blood viscosity, stop the progression of the atherosclerotic process in the main arteries of the head and coronary vessels of the heart, have an antioxidant effect, and slow down the accumulation of p-amyloid in the brain has been shown.

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

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

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

The use of combined action drugs

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

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

Ginkgo biloba leaf extract (pomg 3 times a day);

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

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

Hexobendin + etamivan + etofillin (1 tablet contains 20 mg hexoben-din, 50 mg etamivan, 60 mg etofyllin) or 1 forte tablet, in which the content of the first 2 drugs is 2 times more (taken 3 times a day);

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

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

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

Trimethylhydrazinium propionate (pomg 1 time per day);

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

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

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

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

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

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

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

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

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

Cerebrolysin * - intravenous drip injection, for the course of infusion;

Cattle cerebral cortex polypeptides (cortexin *) - 10 mg intramuscularly, for a course of injections.

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

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

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

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

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

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

1. Ito K. et al. A double-blind study of the clinical effects of solcoseryl infusion on cerebral arteriosclerosis // Kiso to Rinsho. - 1974. - N 8 (13). - P ..

2. Mihara H. et al. A double-blind evaluation of pharmaceutical effect of solcoseryl on cerebrovascular accidents // Kiso to Rinsho. - 1978. - N 12 (2). - P ..

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

The concept of "nootropic drugs" unites various drugs that can improve the integrative activity of the brain, which have a positive effect on memory and learning processes. Piracetam, one of the main representatives of this group, has the noted effects only when high doses are prescribed (12-36 g / day). It should be borne in mind that the use of such doses by elderly persons may be accompanied by psychomotor agitation, irritability, sleep disturbance, and also provoke an exacerbation of coronary insufficiency and the development of epileptic paroxysm.

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

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

Special treatment may be required when patients develop affective disorders (neurotic, anxious, depressive). In such situations, antidepressants are used that do not have anticholinergic effects (amitriptyline and its analogues), as well as intermittent courses of sedatives or small doses of benzodiazepines.

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

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

Approximate terms of incapacity for work

Disability of patients depends on the stage of discirculatory encephalopathy.

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

Stage II of discirculatory encephalopathy corresponds to II-III group of disability. Nevertheless, many patients continue to work, their temporary disability can be caused both by a concomitant disease and by an increase in the phenomena of chronic cerebrovascular insufficiency (the process often proceeds stepwise).

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

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

Patient information

Patients should follow the doctor's recommendations for both continuous and course medication, control blood pressure and body weight, quit smoking, follow a low-calorie diet, eat food rich in vitamins (see Chapter 13 Lifestyle Modifications).

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

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

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

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

Remove carpets that the patient can trip over;

Use comfortable non-slip shoes;

Rearrange furniture if necessary;

Attach handrails and special handles, especially in the toilet and bathroom;

Showers should be taken while sitting.

The prognosis depends on the stage of discirculatory encephalopathy. The same stages can be used to assess the rate of progression of the disease and the effectiveness of the treatment. The main unfavorable factors are pronounced cognitive disorders, often going in parallel with the increase in episodes of falls and the risk of injury, both TBI and limb fractures (primarily of the hip neck), which create additional medical and social problems.

Includes: ruptured cerebral aneurysm.

Contains 9 blocks of diagnoses.

Contains 3 blocks of diagnoses.

  • I63 - Brain infarction

    Contains 9 blocks of diagnoses.

    Includes: blockage and stenosis of cerebral and precerebral arteries causing cerebral infarction.

    Contains 6 blocks of diagnoses.

    Includes: embolism> basilar, carotid, or narrowing> of vertebral arteries, obstruction (complete)> non-infarction (partial)> cerebral thrombosis>.

    Contains 7 blocks of diagnoses.

    Included: embolism> middle, anterior and posterior narrowing> cerebral arteries and arteries obstruction (complete)> cerebellum not causing (partial)> cerebral infarction thrombosis>.

    Contains 10 blocks of diagnoses.

    The diagnosis also includes:

    CEREBROVASCULAR DISEASES (I60-I69)

    Excluded:

    • vascular dementia (F01.-)

    Excludes: sequelae of intracranial hemorrhage (I69.2)

    • embolism
    • constriction
    • thrombosis
    • embolism
    • constriction
    • obstruction (complete) (partial)
    • thrombosis

    In Russia, the International Classification of Diseases of the 10th revision (ICD-10) has been adopted as a single normative document to take into account the incidence, reasons for the population's appeals to medical institutions of all departments, and causes of death.

    ICD-10 was introduced into health care practice throughout the Russian Federation in 1999 by order of the Ministry of Health of Russia dated 05/27/97. No. 170

    A new revision (ICD-11) is planned by WHO in 2017 2018.

    As amended and supplemented by WHO

    Processing and translation of changes © mkb-10.com

    I60-I69 Cerebrovascular diseases

    with mention of hypertension (conditions referred to in I10 and I15.-)

    vascular dementia (F01.-)

    traumatic intracranial hemorrhage (S06.-)

    transient cerebral ischemic attacks and related syndromes (G45.-)

    I60 Subarachnoid hemorrhage

    Includes: ruptured cerebral aneurysm

    Excludes: sequelae of subarachnoid hemorrhage (I69.0)

    I60.0 Subarachnoid hemorrhage from carotid sinus and bifurcation

    I60.1 Subarachnoid hemorrhage from middle cerebral artery

    I60.2 Subarachnoid hemorrhage from anterior communicating artery

    I60.3Subarachnoid hemorrhage from posterior communicating artery

    I60.4 Subarachnoid hemorrhage from basilar artery

    I60.5 Subarachnoid hemorrhage from vertebral artery

    I60.6 Subarachnoid hemorrhage from other intracranial arteries

    I60.7 Subarachnoid hemorrhage from intracranial artery, unspecified

    I60.8 Other subarachnoid haemorrhage

    I60.9 Subarachnoid hemorrhage, unspecified

    I61 Intracerebral hemorrhage

    Excludes: sequelae of cerebral hemorrhage (I69.1)

    I61.0 Intracerebral hemorrhage in the subcortical hemisphere

    I61.1 Intracerebral hemorrhage, cortical

    I61.2 Intracerebral hemorrhage, unspecified

    I61.3 Intracerebral haemorrhage in the brainstem

    I61.4 Intracerebral hemorrhage in cerebellum

    I61.5 Intracerebral hemorrhage, intraventricular

    I61.6 Intracerebral hemorrhage of multiple localization

    I61.8 Other intracerebral hemorrhage

    I61.9 Intracerebral hemorrhage, unspecified

    I62 Other nontraumatic intracranial hemorrhage

    I62.0 Subdural hemorrhage (acute) (nontraumatic)

    I62.1 Non-traumatic extradural hemorrhage

    I62.9 Intracranial hemorrhage (nontraumatic), unspecified

    I63 Brain infarction

    I63.0 Cerebral infarction due to thrombosis of the precerebral arteries

    I63.1 Cerebral infarction due to embolism of precerebral arteries

    I63.2 Cerebral infarction due to unspecified blockage or stenosis of precerebral arteries

    I63.3 Cerebral infarction due to thrombosis of cerebral arteries

    I63.4 Cerebral infarction due to cerebral artery embolism

    I63.5 Cerebral infarction due to unspecified blockage or stenosis of cerebral arteries

    I63.6 Cerebral infarction due to cerebral venous thrombosis, non-pyogenic

    I63.8 Other cerebral infarction

    I63.9 Cerebral infarction, unspecified

    Excludes: conditions causing cerebral infarction (I63.-)

    I65.0 Blockage and stenosis of vertebral artery

    I65.1 Blockage and stenosis of basilar artery

    I65.2 Blockage and stenosis of carotid artery

    I65.3 Blockage and stenosis of multiple and bilateral precerebral arteries

    I65.8 Blockage and stenosis of other precerebral arteries

    I65.9 Blockage and stenosis of unspecified precerebral artery

    obstruction (complete) (partial), narrowing, thrombosis, embolism: middle, anterior and posterior cerebral arteries and cerebellar arteries that do not cause cerebral infarction

    Excludes: conditions causing cerebral infarction (I63.-)

    I66.0 Blockage and stenosis of middle cerebral artery

    I66.1 Blockage and stenosis of anterior cerebral artery

    I66.2 Posterior cerebral artery occlusion and stenosis

    I66.3 Blockage and stenosis of cerebellar arteries

    I66.4 Blockage and stenosis of multiple and bilateral cerebral arteries

    I66.8 Blockage and stenosis of other cerebral artery

    I66.9 Blockage and stenosis of cerebral artery, unspecified

    I67.0 Dissection of cerebral arteries without rupture

    Excludes: rupture of cerebral arteries (I60.7)

    I67.1 Cerebral aneurysm without rupture

    congenital cerebral aneurysm without rupture (Q28.3)

    ruptured cerebral aneurysm (I60.9)

    I67.2 Cerebral atherosclerosis

    I67.3 Progressive vascular leukoencephalopathy

    Excludes: subcortical vascular dementia (F01.2)

    I67.4 Hypertensive encephalopathy

    I67.5 Moyama disease

    I67.6 Non-suppurative thrombosis of the intracranial venous system

    Excludes: conditions causing cerebral infarction (I63.6)

    I67.7 Cerebral arteritis, not elsewhere classified

    I67.8 Other specified cerebral vascular disorders

    I67.9 Cerebrovascular disease, unspecified

    I68.0 * Cerebral amyloid angiopathy (E85 .- +)

    I68.2 * Cerebral arteritis in other diseases classified elsewhere

    I68.8 * Other cerebrovascular disorders in diseases classified elsewhere

    I69.0 Sequelae of subarachnoid hemorrhage

    I69.1 Sequelae of intracranial hemorrhage

    I69.2 Sequelae of other non-traumatic intracranial hemorrhage

    I69.3 Sequelae of cerebral infarction

    I69.4 Sequelae of stroke, not specified as hemorrhage or cerebral infarction

    I69.8 Sequelae of other and unspecified cerebrovascular diseases

    Cerebrovascular diseases

    I60 Subarachnoid haemorrhage

    I60.0 Subarachnoid haemorrhage from carotid siphon and bifurcation
    I60.1 Subarachnoid haemorrhage from middle cerebral artery
    I60.2 Subarachnoid haemorrhage from anterior communicating artery
    I60.3 Subarachnoid haemorrhage from posterior communicating artery
    I60.4 Subarachnoid haemorrhage from basilar artery
    I60.5 Subarachnoid haemorrhage from vertebral artery
    I60.6 Subarachnoid haemorrhage from other intracranial arteries
    I60.7 Subarachnoid haemorrhage from intracranial artery, unspecified
    • Subarachnoid haemorrhage from:
      • cerebral
      • communicating
    • artery NOS
    I60.8 Other subarachnoid haemorrhage
    I60.9 Subarachnoid haemorrhage, unspecified

    I61 Intracerebral haemorrhage

    I61.0 Intracerebral haemorrhage in hemisphere, subcortical
    I61.1 Intracerebral haemorrhage in hemisphere, cortical
    I61.2 Intracerebral haemorrhage in hemisphere, unspecified
    I61.3 Intracerebral haemorrhage in brain stem
    I61.4 Intracerebral haemorrhage in cerebellum
    I61.5 Intracerebral haemorrhage, intraventricular
    I61.6 Intracerebral haemorrhage, multiple localized
    I61.8 Other intracerebral haemorrhage
    I61.9 Intracerebral haemorrhage, unspecified

    I62 Other nontraumatic intracranial haemorrhage

    I62.0 Subdural haemorrhage (acute) (nontraumatic)
    I62.1 Nontraumatic extradural haemorrhage
    I62.9 Intracranial haemorrhage (nontraumatic), unspecified

    I63 Cerebral infarction

    I63.0 Cerebral infarction due to thrombosis of precerebral arteries
    I63.1 Cerebral infarction due to embolism of precerebral arteries
    I63.2 Cerebral infarction due to unspecified occlusion or stenosis of precerebral arteries
    I63.3 Cerebral infarction due to thrombosis of cerebral arteries
    I63.4 Cerebral infarction due to embolism of cerebral arteries
    I63.5 Cerebral infarction due to unspecified occlusion or stenosis of cerebral arteries
    I63.6 Cerebral infarction due to cerebral venous thrombosis, nonpyogenic
    I63.8 Other cerebral infarction
    I63.9 Cerebral infarction, unspecified

    I64 Stroke, not specified as haemorrhage or infarction

    I65 Occlusion and stenosis of precerebral arteries, not resulting in cerebral infarction

    • embolism
    • narrowing
    • thrombosis
    • of basilar, carotid or vertebral arteries, not resulting in cerebral infarction
    I65.0 Occlusion and stenosis of vertebral artery
    I65.1 Occlusion and stenosis of basilar artery
    I65.2 Occlusion and stenosis of carotid artery
    I65.3 Occlusion and stenosis of multiple and bilateral precerebral arteries
    I65.8 Occlusion and stenosis of other precerebral artery
    I65.9 Occlusion and stenosis of unspecified precerebral artery

    I66 Occlusion and stenosis of cerebral arteries, not resulting in cerebral infarction

    • embolism
    • narrowing
    • obstruction (complete) (partial)
    • thrombosis
    • of middle, anterior and posterior cerebral arteries, and cerebellar arteries, not resulting in cerebral infarction
    I66.0 Occlusion and stenosis of middle cerebral artery
    I66.1 Occlusion and stenosis of anterior cerebral artery
    I66.2 Occlusion and stenosis of posterior cerebral artery
    I66.3 Occlusion and stenosis of cerebellar arteries
    I66.4 Occlusion and stenosis of multiple and bilateral cerebral arteries
    I66.8 Occlusion and stenosis of other cerebral artery
    I66.9 Occlusion and stenosis of unspecified cerebral artery

    I67 Other cerebrovascular diseases

    I67.0 Dissection of cerebral arteries, nonruptured
    I67.1 Cerebral aneurysm, nonruptured
    • aneurysm NOS
    • arteriovenous fistula, acquired

    Excl .: congenital cerebral aneurysm, nonruptured (Q28.-) ruptured cerebral aneurysm (I60.-)

    I67.2 Cerebral atherosclerosis
    I67.3 Progressive vascular leukoencephalopathy
    I67.4 Hypertensive encephalopathy
    I67.5 Moyamoya disease
    I67.6 Nonpyogenic thrombosis of intracranial venous system
    • cerebral vein
    • intracranial venous sinus

    Excl .: when causing infarction (I63.6)

    I67.7 Cerebral arteritis, not elsewhere classified
    I67.8 Other specified cerebrovascular diseases
    I67.9 Cerebrovascular disease, unspecified

    I68 * Cerebrovascular disorders in diseases classified elsewhere

    I68.0 * Cerebral amyloid angiopathy (E85.- †)
    I68.1 * Cerebral arteritis in infectious and parasitic diseases classified elsewhere
    I68.2 * Cerebral arteritis in other diseases classified elsewhere
    I68.8 * Other cerebrovascular disorders in diseases classified elsewhere

    I69 Sequelae of cerebrovascular disease

    Not to be used for chronic cerebrovascular disease. Code these to I60-I67.

    ICD code: I60-I69

    Cerebrovascular disease

    I60-I69

    Cerebrovascular disease

    ICD code online / ICD code I60-I69 / International classification of diseases / Diseases of the circulatory system / Cerebrovascular diseases

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  • Cerebrovascular diseases (ICD code I60-I69)

    If necessary, indicate the presence of hypertension, use an additional

    Excludes: transient cerebral ischemic attacks and related syndromes (G45.-) traumatic intracranial hemorrhage (S06.-) vascular dementia (F01.-)

    Included: rupture of cerebral aneurysm Excludes: consequences of subarachnoid hemorrhage (I69.0)

    Excludes: sequelae of cerebral hemorrhage (I69.1)

    Excludes: sequelae of intracranial hemorrhage (I69.2)

    Incl .: blockage and stenosis of cerebral and precerebral arteries causing cerebral infarction Excludes: complications after cerebral infarction (I69.3)

    I64 Stroke not specified as hemorrhage or infarction

    Cerebrovascular stroke NOS Excludes: sequelae of stroke (I69.4)

    Includes: embolism> basilar, carotid or narrowing> vertebral arteries, obstruction (complete)> non-infarction (partial)> cerebral thrombosis> Excludes: conditions causing cerebral infarction (I63.-)

    Includes: embolism> middle, anterior and posterior narrowing> cerebral arteries and arteries obstruction (complete)> cerebellum not causing (partial)> cerebral infarction thrombosis> Excludes: conditions causing cerebral infarction (I63.-)

    Excludes: consequences of the listed conditions (I69.8)

    Note. Use this heading to designate conditions listed in headings I60-I67 as the cause of consequences that are themselves classified in other headings. Consequences include conditions specified as such, as residual events, or as conditions that have existed for a year or more since the onset of the causal condition.

    Cerebrovascular diseases ICD code I60-I69

    In the treatment of Cerebrovascular diseases, drugs are used:

    International Statistical Classification of Diseases and Related Health Problems - a document used as a leading framework in public health. ICD is a regulatory document that ensures the unity of methodological approaches and international comparability of materials. Currently, the International Classification of Diseases of the Tenth Revision (ICD-10, ICD-10) is in force. In Russia, health authorities and institutions made the transition of statistical accounting to ICD-10 in 1999.

    © g. ICD 10 - International classification of diseases 10th revision

    CEREBROVASCULAR DISEASES

    Included: with mention of hypertension (conditions referred to in I10 and I15.-)

    If necessary, indicate the presence of hypertension, use an additional code.

    Excluded:

    • transient cerebral ischemic attacks and related syndromes (G45.-)
    • traumatic intracranial hemorrhage (S06.-)
    • vascular dementia (F01.-)

    Subarachnoid hemorrhage

    Excludes: consequences of subarachnoid hemorrhage (I69.0)

    Intracerebral hemorrhage

    Excludes: sequelae of cerebral hemorrhage (I69.1)

    Other non-traumatic intracranial hemorrhage

    Excludes: sequelae of intracranial hemorrhage (I69.2)

    Cerebral infarction

    Includes: blockage and stenosis of cerebral and precerebral arteries (including brachiocephalic trunk) causing cerebral infarction

    Excludes: complications after cerebral infarction (I69.3)

    Stroke not specified as hemorrhage or heart attack

    Cerebrovascular stroke NOS

    Excludes: sequelae of stroke (I69.4)

    Blockage and stenosis of the precerebral arteries that do not lead to cerebral infarction

    • embolism
    • constriction
    • obstruction (complete) (partial)
    • thrombosis

    Excludes: conditions causing cerebral infarction (I63.-)

    Blockage and stenosis of cerebral arteries that do not lead to cerebral infarction

    • embolism
    • constriction
    • obstruction (complete) (partial)
    • thrombosis

    Excludes: conditions causing cerebral infarction (I63.-)

    Other cerebrovascular diseases

    Excludes: consequences of the listed conditions (I69.8)

    Vascular lesions of the brain in diseases classified elsewhere

    Consequences of cerebrovascular diseases

    Note. Heading I69 is used to designate conditions in I60-I67.1 and I67.4-I67.9 as causes of consequences that are themselves classified in other headings. Consequences include conditions specified as such, as residual events, or as conditions that have existed for a year or more since the onset of the causal condition.

    Do not use for chronic cerebrovascular diseases, use codes I60-I67.

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    International Statistical Classification of Diseases and Related Health Problems.

    Excludes: sequelae of intracranial hemorrhage (I69.2)

    I63 Brain infarction

    Includes: blockage and stenosis of cerebral and precerebral arteries causing cerebral infarction

    Excludes: complications after cerebral infarction (I69.3)

    I64 Stroke not specified as hemorrhage or infarction

    Excludes: sequelae of stroke (I69.4)

    I65 Blockage and stenosis of precerebral arteries, not leading to cerebral infarction

    Excludes: conditions causing cerebral infarction (I63.-)

    I66 Blockage and stenosis of cerebral arteries, not leading to cerebral infarction

    obstruction (complete) (partial) of the middle, anterior and constriction of cerebral arteries and thrombosis of the cerebellar arteries, not embolizing cerebral infarction

    Excludes: conditions causing cerebral infarction (I63.-)

    I67 Other cerebrovascular diseases

    Excludes: consequences of listed conditions (I69.8)

    I68 * Disorders of cerebral vessels in diseases classified elsewhere

    I69 Consequences of cerebrovascular diseases

    Note: Consequences include conditions specified as such, as residual events, or as conditions that have existed for a year or more since the onset of the causal condition.

    Chronic cerebrovascular disease: causes, symptoms and treatment

    A number of diseases associated with cerebrovascular accidents are called cerebrovascular. They are acute and chronic. The former include strokes and transient ischemic attacks. Chronic forms are represented by vascular dementia and discirculatory encephalopathy.

    Description of problems

    Cerebrovascular disease is a pathological condition characterized by organic changes in the brain tissue. They arise from problems with the blood supply. Because of this, brain cells do not receive enough oxygen and other nutrients. All this becomes the reason for the appearance of such changes as a result of which cognitive disorders appear or even such a serious complication as a stroke may develop.

    The main problem in most cases is diffuse or multifocal lesions of the brain. They are manifested by mental, neuropsychiatric or neurological disorders that characterize cerebrovascular disease. Dyscirculatory encephalopathy is currently absent in the international classification of diseases, established as a result of revision 10 (ICD 10), although in Russia it is this diagnosis that is most often used to designate chronic problems with cerebral circulation.

    Causes of the disease

    The factors that lead to a deterioration in the blood supply to the brain, experts conditionally divided into two groups. The most common cause of problems is atherosclerotic lesions of the body's major blood vessels. Cholesterol plaques form on their walls, respectively, the lumen in them decreases. Because of this, all organs with age cease to receive the required amount of oxygen and other essential substances, including glucose. This leads to the development of changes in them and to the fact that over time, chronic cerebrovascular disease can be diagnosed.

    The second reason for the appearance of these problems is inflammatory processes in the cerebral vessels, which are called vasculitis.

    The risk group includes all those people who are susceptible to developing a disease such as atherosclerosis. These are patients with diabetes mellitus, smokers, as well as those who are overweight.

    Types of pathologies

    Cerebrovascular disease is a group of diagnoses under one name. Depending on the violations that arise and the severity of the problems, there are:

    Occlusion and stenosis of cerebral vessels;

    Ischemic or hemorrhagic stroke;

    Transient ischemic attack;

    Venous sinus thrombosis;

    If you know the international classification, then it is easy to find out what doctors may mean when they say that a patient has cerebrovascular disease. The ICD 10 code for this group is I60-I69.

    Medical classification

    It is enough for specialists to know the rubric to which the disease is attributed in order to understand what diagnosis was made to the patient. So, in order for everyone to understand that the patient has chronic cerebrovascular disease, the ICD assigned the code I67 to the pathology. For the designation of acute forms, codes I60-I66 are intended. They mean such pathologies:

    • I60 - subarachnoid hemorrhages are combined here;
    • I61 - intracerebral hemorrhage;
    • I62 - other non-traumatic intracranial effusion;
    • I63 - cerebral infarctions;
    • I64 - strokes not specified as heart attacks or hemorrhages;
    • I65-I66 - cases of blockage and stenosis of cerebral and precerebral arteries, which do not lead to cerebral infarction, but in situations where there was a lethal outcome, they are replaced by the code I63.

    It is necessary to register the diagnosed diseases according to the rules established by the ICD 10. Cerebrovascular disease, the duration of which is no more than 30 days, can be classified under I60-I66. All consequences of the disease should be indicated not just under a general code, but specifically defined. For example, if there was paralysis, encephalopathy or other manifestations of cerebrovascular disease, this should be indicated.

    Symptoms

    Information regarding ICD 10 coding is required only by medical personnel. It is much more important for patients to figure out what symptoms to look for and when to see a doctor. So, it is important to know that cerebrovascular disease in the initial stages may not particularly manifest itself. But the symptoms become more noticeable with the progression of the pathology.

    Among them, the most common:

    Dizziness, noise, and pain in the head;

    Numbness of the limbs, impaired sensitivity in them;

    Periodic visual impairment;

    Short-term loss of consciousness.

    In the worst cases, transient ischemic attacks and strokes occur. These conditions are the cause of a significant violation of the blood supply to the brain, as a result of which nerve cells die.

    Definition of disease

    In order to be diagnosed with cerebrovascular disease, it is necessary to consult a doctor in time. Statistics confirm that in the initial stages of the disease only few people turn to doctors. Many attribute their ailments to bad weather, lack of vitamins, and overwork. As a result, patients are admitted to hospitals with strokes and ischemic attacks. This can be prevented if cerebrovascular disease is detected in a timely manner. Treatment prescribed without delay will not only alleviate the patient's condition, but also reduce the risk of severe circulatory disorders in the brain.

    Diagnosis of the disease is carried out as follows. First you need to pass a biochemical and general blood test. They will determine if there is a risk of developing atherosclerotic changes in the vessels. In addition to tests, it is also a good idea to do ultrasound diagnostics. With the help of duplex and triplex scanning, it is possible to reliably assess the state of the vessels.

    Using such a radiopaque research method as angiography, it is possible to identify areas of narrowing and blockage of blood vessels. An EEG can be used to assess how the brain is functioning. During this procedure, changes in electrical activity are recorded.

    The most reliable and accurate methods are CT, MRI or scintigraphy. All of this research is high-tech. They provide additional information about the structures of the central nervous system.

    Therapy

    If you have been diagnosed with cerebrovascular brain disease, then you cannot let the problem go by itself. This condition requires treatment, otherwise complications cannot be avoided. But it should be understood that for a full-fledged therapy it is necessary that the patient himself wants to recover. So, an improvement in the condition is possible only if the patient changes his lifestyle, loses excess weight, and gives up smoking and alcohol.

    But, in addition to this, it is necessary to consult with your doctor and find out what kind of therapy will be optimal. In many cases, conservative methods are bypassed. But in a number of situations, it is desirable that timely surgical intervention was carried out, which will eliminate the areas of vasoconstriction that feed the central nervous system.

    Conservative treatment

    For chronic problems with the blood supply to the brain, conventional medication is often used. They are aimed at lowering the concentration of cholesterol in the blood, maintaining blood pressure, and improving the blood supply to tissues. Taking medications prescribed by a doctor in combination with dietary and lifestyle adjustments in general allows you to maintain brain function at the required level for a fairly long time.

    For treatment, antiplatelet, nootropic, vasodilator, hypotensive, hypocholesterolemic agents are prescribed. Also, antioxidants and multivitamin complexes are recommended in parallel.

    Medicines used

    Thus, we have found out why it is so important for specialists to know what the code of the pathology we are considering. Cerebrovascular disease is a consequence of a number of diseases. Therefore, therapy should primarily be aimed at eliminating them.

    So, with multiple cardioembolism and multi-infarction state, coalogulopathy and agniopathy, antiplatelet agents are required. The most popular among them is the common acetylsalicylic acid, which is prescribed in a dosage of 1 mg for each kg of patient weight. It may also be recommended to take medications such as "Clopidogrel" or "Dipyridamole" in a dosage of about g per day. Also in such situations, anticoagulants are prescribed, for example, "Warfarin".

    Neurological disorders are treated with the use of nootropics, neurotransmitters and amino acids. Drugs such as "Glycine", "Neuromidin", "Cerebrolysin", "Actovegin" can be prescribed. In case of tinnitus and dizziness, Betahistine is often prescribed at a dosage of 24 mg twice a day.

    For patients suffering from pressure surges, it is important to normalize it. Among the prescribed vasoactive drugs, such medications as Vinpocetine, Pentoxifylline are popular.

    Operational methods

    Traditional surgical methods allow you to get rid of ischemia of the brain tissue. For this, currently, only X-ray endovascular and microsurgical interventions are performed.

    In some cases, balloon angioplasty is recommended. This is a procedure during which a special balloon is inserted into the vessel and inflated there. This helps to expand the lumen and normalize blood flow. After such an intervention - to prevent adhesion or re-narrowing of the artery - it is advisable that stenting be done. This is a procedure during which a mesh implant is placed in the lumen of the vessel, which is responsible for keeping its walls in a straightened state.

    If cerebrovascular disease has been diagnosed, endarterectomy may also be performed. This is a microsurgical operation, during which all cholesterol deposits are removed from the lumen of the vessel. After that, its integrity is restored.

    Folk methods

    Even if you are not a supporter of alternative medicine, cerebrovascular disease is the problem that is better amenable to therapy with an integrated approach. Even doctors say that it will not work to normalize your condition without increasing physical activity, normalizing nutrition, quitting smoking and other bad habits.

    In addition, you can use folk recipes in parallel with the main therapy. For example, many people recommend chopping 2 oranges and lemons in a meat grinder or blender, along with the skin, but without seeds. In the resulting gruel, add ½ cup of honey, mix and leave for a day at room temperature. After that, the mixture must be placed in the refrigerator and taken in 2 tbsp. l. up to 3 times a day. You can drink it with green tea.

    Disruption of the normal functioning of the cerebral vessels is a serious problem. One of these diseases is cerebrovascular disease of the head. It leads to hypoxia, and disruption of the normal functioning of the body.

    To answer the question of what is cerebrovascular disease of the brain, it is necessary to start with a classification.

    This is a large complex of symptoms that includes several diseases:

    • ischemic and hemorrhagic nature;
    • Prolonged violation of circulation in the vessels of the brain - occlusion and spasm, arteritis and aneurysm;
    • Diseases associated with increased pressure in the vessels of the brain - atherosclerotic or hypertensive encephalopathy.

    ICD code -10 cerebrovascular disease I60-I69, since this concept includes several diseases.

    The reasons

    The main causes of cerebrovascular brain disease are:

    • ... Cholesterol begins to be deposited in the lumens, gradually forming plaques, which lead to a decrease in the lumen of the artery. As a result, blood supply and oxygen supply are disrupted;
    • , increased thrombus formation;
    • Spasm of the artery wall in hypertension;
    • Autoimmune diseases such as vasculitis;
    • Osteochondrosis of the cervical spine.

    All the reasons appear in the body for a reason. Certain predisposing factors lead to their development:

    • The presence of a negative effect on microcirculation in general;
    • Age over 60;
    • Disorders of cholesterol metabolism;
    • Obesity;
    • Coronary artery disease;
    • Chronic stress
    • Injuries to the skull and brain;
    • Long-term use of oral contraceptives;
    • Continuous smoking;
    • Hereditary predisposition.

    Symptoms

    The symptoms of cerebrovascular disease are very diverse. In the early stages of development, you can find following signs stroke:

    • Excessive tiredness;
    • Excessive nervousness, bad mood;
    • Unrelated fussiness;
    • Sleep disturbance;
    • A constant feeling of heat without a rise in temperature;
    • Feeling of dryness in the mouth;

    When 2 or 3 of the above symptoms appear, you need to consult a doctor for a timely diagnosis. Cerebrovascular head disease at this stage lends itself well to drug correction.

    With the progression of hypoxia, more formidable disorders begin to appear: impairment of memory, logic and coordination of movements, worries, which is not eliminated by painkillers. Development of depressive states, egocentrism is also possible.

    The diagnosis of cerebrovascular disease cannot be called simple. It is necessary to conduct a large number of studies and exclude all other pathologies.

    The main diagnostic methods that are used first:

    • and urine;
    • Determination of blood clotting;
    • Electrocardiography;
    • X-ray examination of the chest organs.

    Of the specific research methods, the following will be effective:

    • ... This method allows you to quickly and effectively determine the presence of abnormalities in the vessels;
    • Angiography. A special contrast agent is injected into the bloodstream, which on X-ray displays the course of the vessels, the quality of their work and the presence of narrowing of the lumen;
    • Scintigraphy of cerebral vessels;
    • vessels of the brain.
    • The use of CT and MRI will also be quite informative.

    Treatment of cerebrovascular disease of the cerebral vessels should be carried out exclusively under the supervision of a specialist doctor. Self-medication is unacceptable.

    All therapy is based on the restoration of all functions of the brain and the prevention of deterioration in its work. For the patient, first of all, it is very important to adjust the lifestyle. A complete rejection of cigarettes and alcohol is required. Fatty and fried foods are excluded. In the presence of excess weight, its correction is carried out.


    Drug treatment cerebrovascular disease begins with the elimination of the factor that provoked the disruption of the vascular function. Treatment is carried out, the amount of cholesterol in the blood is normalized, drugs are introduced that reduce the risk of thromboembolism and blood clots in general.

    Only after treatment of the underlying disease can one proceed to the treatment of cerebrovascular insufficiency of the disease. Drugs are prescribed that improve blood flow in the vessels of the brain. If necessary, resort to surgical treatment... In severe cases, they resort to the use of stents, cutters or balloons, which will restore the lumen of the vessel.

    Prophylaxis

    Prevention of cerebrovascular disease is quite simple.

    It consists in timely treatment provoking factors, namely:

    • Blood pressure should always be within the normal range;
    • Elimination of bad habits;
    • Balanced;
    • Sufficient rest;
    • Elimination of excess weight.

    Sometimes for prevention, platelet antiplatelet agents and drugs that improve cerebral blood flow can be used.

    Forecast

    Cerebrovascular disease is a very serious medical condition that requires attention. When the first signs appear, you should immediately consult a doctor. Timely diagnosis will not allow the development of formidable complications. Any disease can be eliminated at the initial stages of its development.