Chronic cerebral ischemia symptoms. Neurology. Video: cerebral ischemia

State budget educational institution

Higher professional education

Northwestern State Medical University named after I.I. Mechnikov

Ministry of Health of Russia

Department of Neurology named after Academician S.N. Davidenkova

Cerebrovascular diseases. Classification. Chronic cerebral ischemia. Encephalopathy.

Teacher

Zuev Andrey Alexandrovich

MPF student 425gr.

Medvedev A.A.

Saint Petersburg 2013

Cerebrovascular diseases- a group of brain diseases caused by pathological changes in cerebral vessels with impaired cerebral circulation.

ICD 10 proposes a classification of vascular diseases of the nervous system, the purpose of which is to provide statistical data on the frequency of causes of death and hospitalizations and on the assessment of the quality of medical care. The classification of vascular lesions of the brain adopted in the Russian Federation divides cerebrovascular accidents into acute and chronic forms.

Chronic forms include:

Initial manifestations of insufficiency of blood supply to the brain (NPNKM);

Dyscirculatory encephalopathy (hypertonic, atherosclerotic and mixed).

Acute forms include:

Transient cerebrovascular accident;

Acute hypertensive encephalopathy;

Stroke.

Chronic cerebral ischemia

Slowly progressive dysfunction of the brain resulting from diffuse and/or small-focal damage to the brain tissue in conditions of long-term cerebral blood supply insufficiency.

The concept of "chronic cerebral ischemia" includes:

encephalopathy,

chronic ischemic brain disease,

vascular encephalopathy,

cerebrovascular insufficiency,

atherosclerotic encephalopathy,

vascular (atherosclerotic) parkinsonism,

vascular dementia,

vascular (late) epilepsy.

Of the above names, the most common in modern medicine is the term "dyscirculatory encephalopathy".

Etiology and pathogenesis

Among the main etiological factors are considered atherosclerosis and arterial hypertension often reveal a combination of these two conditions. Other causes of chronic cerebrovascular ischemia cardiovascular diseases, especially those accompanied by signs of chronic heart failure, cardiac arrhythmias (both permanent and paroxysmal forms arrhythmias), often leading to a drop in systemic hemodynamics. An anomaly of the vessels of the brain, neck, shoulder girdle, aorta (especially its arch) is also important, which cannot manifest itself before the development of atherosclerotic, hypertonic or other acquired process in these vessels. Recently, a large role in the development of chronic cerebral ischemia is assigned to venous pathology, not only intracranial, but also extracranial. Compression of blood vessels, both arterial and venous, can play a certain role in the formation of chronic cerebral ischemia. It is necessary to take into account not only the spondylogenic influence, but also compression by altered neighboring structures (muscles, tumors, aneurysms). Another cause of chronic cerebral ischemia may be cerebral amyloidosis (in elderly patients).

Clinically detectable encephalopathy is usually of mixed etiology. In the presence of the main factors in the development of chronic cerebral ischemia, the rest of the variety of causes of this pathology can be interpreted as additional causes. Identification of additional factors that significantly aggravate the course of chronic cerebral ischemia is necessary to develop the correct concept of etiopathogenetic and symptomatic treatment.

The main causes of chronic cerebral ischemia:

atherosclerosis;

arterial hypertension.

Additional causes of chronic cerebral ischemia:

cardiovascular diseases (with signs of CHS);

violation of the heart rhythm;

vascular anomalies, hereditary angiopathy;

venous pathology;

vascular compression;

arterial hypotension;

cerebral amyloidosis;

systemic vasculitis, diabetes;

blood diseases.

In recent years, 2 main pathogenetic variants of chronic cerebral ischemia have been considered, based on the following morphological features: the nature of the damage and the predominant localization. With bilateral diffuse lesions of the white matter, a leukoencephalopathic (or subcortical Biswanger) variant of dyscirculatory encephalopathy is isolated. The second is a lacunar variant with the presence of multiple lacunar foci. However, in practice, mixed options are very common.

The lacunar variant is often due to direct occlusion of small vessels. In the pathogenesis of diffuse lesions of the white matter, the leading role is played by repeated episodes of a drop in systemic hemodynamics - arterial hypotension. The cause of the fall in blood pressure may be inadequate antihypertensive therapy, a decrease in cardiac output. In addition, persistent cough, surgical interventions, orthostatic hypotension (with vegetative-vascular dystonia).

In conditions of chronic hypoperfusion - the main pathogenetic link of chronic cerebral ischemia - the compensation mechanisms are depleted, the energy supply of the brain is reduced. First of all, functional disorders develop, and then irreversible morphological disorders: a slowdown in cerebral blood flow, a decrease in the level of glucose and oxygen in the blood, oxidative stress, capillary stasis, a tendency to thrombosis, and depolarization of cell membranes.

Chronic cerebral ischemia is one of the most common vascular diseases of the central nervous system, from the occurrence of which no one is immune. Let us consider in more detail what it is, why it develops and how this disease manifests itself.

Chronic cerebral ischemia (CCI) is the international name for a disease known as dyscirculatory encephalopathy. Both of these names describe the essence of the disease in a very accessible way: due to chronic circulatory disorders, the brain constantly suffers from ischemia, which leads to the occurrence of small focal lesions of the brain tissue and the appearance of various psycho-neurological disorders.

Causes of HIM

The most relevant causes of the development of CCI today are atherosclerosis and hypertension, which lead to damage to the arteries of the brain. Much less common are cases of disease caused by pathological changes in the venous bed, the blood coagulation system and autonomic regulation of the functioning of the body. In addition to the main causes, provoking factors (risk factors) play an important role in the development of CCI. They can be divided into two large groups: those that can be corrected and those that cannot be corrected. Uncorrected factors include:

• hereditary predisposition. If someone in the family suffered from cerebrovascular accidents, the risk of CCI is much higher in the offspring.
• Elderly age. The older the person, the more likely it is to develop HIM.

The following risk factors can be adjusted:

• Bad habits. Everyone can quit smoking and limit alcohol consumption. Moreover, it is most important to give up cigarettes, since it is from them that the vessels narrow and become more brittle.
• Excess weight.
• Diabetes. It is necessary to detect this disease in a timely manner and treat it.
• Inactivity.
• Wrong nutrition.

Why is CHEM dangerous?

Perhaps so much would not have been said about chronic cerebral ischemia if this disease had not been one of the leaders among those that lead to disability. People who have the last stage of this disease become absolutely helpless, they cannot take care of themselves, cannot adequately respond to the world around them, and in some cases they cannot move normally (as a rule, they are given a disability of the first group). In addition, against the background of chronic circulatory disorders and cerebral ischemia, an acute disorder may develop - ischemic or hemorrhagic stroke. These pathological conditions are deadly.

How to recognize HIM?

At the initial stages of the development of the disease, the symptoms are rather indicative, since they also occur with other diseases, as well as with banal overwork. For example:

• Irritability and mood lability.
• Frequent headaches.
• Memory deterioration.
• Sleep disorders.

The appearance of these signs should not be ignored, especially if there are such concomitant diseases and pathological conditions as arterial hypertension, diabetes mellitus, obesity, dyslipidemia, increased blood clotting, previous strokes, etc.

CHEM stages

There are three stages (degrees) of chronic cerebral ischemia:

• CHIM 1 degree is characterized by various subjective disorders, that is, health disorders that the patient complains about. These are dizziness, and headaches, and memory impairment, and noise in the head, and deterioration in performance, and unmotivated weakness. Objectively, the doctor can identify some neurological disorders and signs of asthenic syndrome in the patient.
• HIM of the 2nd degree already has more serious manifestations - the patient's ability to work not only worsens, but is completely lost. All the symptoms described above are aggravated, and emotional-volitional disorders are added to them. In addition, neurological disorders become pronounced, the neuropathologist can already identify the dominant syndrome - discoordinating, amyostatic, pyramidal, or others.
• HIM grade 3 is a stage of dementia (dementia), which joins all of the above symptoms. People are upset intellect, memory, cognitive activity is disturbed, criticism is reduced. Quite often, such patients experience fainting and epileptic seizures.

At the first stage of the disease, with the help of complex drug therapy, it is possible to stop the progression of the pathology and improve the patient's well-being. The prognosis for the second stage is somewhat worse, but the third stage is already irreversible changes that cannot be eliminated even by the most modern methods.

Treatment for grade 3 CCI is carried out only symptomatic, allowing at least somehow alleviate the patient's condition. Based on this, we can conclude that any deterioration in well-being cannot be ignored, since only timely detected dyscirculatory pathologies of the brain can be treated.

Diagnostics

When the first signs of CCI appear, it is necessary to contact a neurologist who will be able to examine and determine exactly what it is: overwork or really a violation of cerebral circulation and chronic cerebral ischemia. To identify the cause of the development of CCI, the patient is prescribed a series of studies:

• X-ray of the skull and cervical spine.
• Rheoencephalography.
• Doppler study of blood vessels supplying the brain.
• Head CT.
• Extended biochemical blood test (with mandatory determination of lipid profile and glucose).
• ECG and echocardiography.

In addition, if there are symptoms of CCI, the patient is referred for a consultation with a psychiatrist, ophthalmologist, therapist, cardiologist and other specialists, if necessary.

Cerebral ischemia is a dangerous damage to brain structures that occurs against the background of insufficient blood supply to one or another part of the brain. When such a condition develops due to a sharp blockage of the main arteries, there may be a loss of function of a part of the brain or even the death of all cells. The longer the brain remains without blood, the more destructive.

Chronic cerebral ischemia has long-term consequences, since it does not completely block the arterial bed. Long-term relative insufficiency of blood flow in the brain tissues leads to this form of ischemia. In the process of such a disease, there is a gradual loss of functions of higher nervous activity.

Cerebral ischemia can be localized and extensive. In the first case, the lack of blood flow is detected only in certain areas of the organ, so there is a loss of specific functions. Extensive ischemia is much more severe and manifests itself in almost everything.

They control all processes in the body: from the ability to see, hear and think to maintaining the heartbeat and breathing. The lack of blood flow can affect any functional part of the brain, and the consequences will always differ in the degree of life threat.

Damaged nerve cells are not replaced by new ones and are not repaired. An ischemic attack in any part of the brain will lead to a natural dysfunction. Chronic ischemia is quite insidious in that the cells do not die immediately. A person with this disease may not feel anything for months or years, although his brain will gradually deteriorate.

Symptoms of the disease

Patients with chronic cerebral ischemia suffer from a wide range of symptoms. Symptoms may vary slightly from patient to patient. The prevalence of ischemic damage plays a role, since a localized violation of the blood supply to the brain will manifest itself with specific symptoms associated with the functions of the affected area.

The most common symptoms include incoordination, unsteady gait, numbness of body parts. Clarity of thinking may be disturbed, loss of short-term and even long-term memory may occur. Almost all patients also experience dizziness.

Other clinical signs of the disease:

• : bifurcation, blurring, loss of visual field, sudden blindness
• hearing loss
• feeling of fog in the head
• involuntary urination during sleep
• nausea and vomiting not related to digestive disorders
• fast fatiguability
• loss of concentration
• slowness
• mental disorders
• loss of labor skills and social adaptation

Symptoms vary greatly at different stages of the disease, since the process of ischemia affects more and more functional areas of the brain.

Many of the symptoms listed above are not specific, so doctors need to rule out other diseases of the nervous system. For example, various types of dementia are similar in their manifestations to the initial stages of cerebral ischemia.

Causes of chronic cerebral ischemia

As noted above, the causes of chronic cerebral ischemia differ from acute ischemia. Vascular disorders can take years to develop and gradually reduce the intensity of cerebral blood flow. Chronic ischemia does not lead to sudden brain death against the background of clinical well-being.

It is one of the most common causes of cerebral ischemia. First, a lipid spot forms on the damaged vessel wall, then a plaque grows on the lipid spot. This structure gradually blocks the blood flow. In addition, the growing plaque can break away from the vessel wall and move through the bloodstream to a narrower branch of the artery, where a blockage occurs. With atherosclerosis, small arterioles of brain tissue can become blocked, which leads precisely to the chronic course of ischemia.

Pseudotuberculosis: treatment and proven methods for diagnosing the stages of the disease

Any cardiovascular pathology also contributes to the development of the disease. The most significant factors include:

• high blood pressure
• cardiac arrhythmia
• venous insufficiency leading to reduced blood flow from the brain
• dissections or vascular aneurysms
• dissection of the walls of blood vessels

Who can have it?

The presence of risk factors should be an incentive to prevent the disease. Patients with diabetes should have their sugar levels monitored and regularly examined for vascular lesions. With obesity and atherosclerosis, a strict diet is required. Smoking cessation is recommended.

Pathophysiology of the disease

The pathophysiology of chronic cerebral ischemia is not limited to anatomical changes in the arteries. This is a complex sequential process of destruction, equally manifesting itself at the cellular and tissue levels. The main mechanism of the pathophysiology of ischemia is associated with metabolic dysfunction of individual cells against the background of hypoxia.

The blood supply to the brain is arranged somewhat differently than the blood supply to other organs. The brain is fed by extracranial and intracranial arteries, branching into a huge number of arterioles. Arterioles of different calibers penetrate all parts of the brain and deliver blood to literally every cell. The need for such a device is due to the fact that nerve cells do not retain nutrients inside themselves, everything is consumed at once.

During ischemia, nerve cells lose their ability to provide aerobic metabolism due to the lack of oxygen and nutrients. The brain cannot switch to anaerobic metabolism because the structure of nerve cells does not allow for the storage of energy substrates. Resource depletion occurs as early as the fourth minute of hypoxia. Against the background of the absence of biological energy, cells lose the ability to maintain their electrochemical gradients, that is, they cease to isolate their contents from the external environment. A massive influx of calcium into nerve cells blocks protein synthesis and the removal of decay products. After that, the cell structures begin to collapse.

Stopping blood flow in the brain tissue for 10 seconds leads to loss of consciousness. After twenty seconds, electrochemical activity in the cells stops completely. In essence, nerve cells in the first stages lose contact with each other and only then die.

Stages of development of the disease

We found that chronic ischemia develops gradually, and the symptoms get worse and worse over time. Let's try to consider the manifestations of the disease at different stages of development:

1. First stage. At this stage, first of all, violations of cognitive activity occur: memory impairment, mental clarity, loss of concentration. Emotional distress is connected to cognitive pathologies, which is expressed in unstable mood, apathy, depression and irritability. Fine motor skills of the hands are significantly deteriorating - a person loses writing skills and drops small objects. There is a violation of coordination of movement, orientation in space. Close people of the patient may pay attention to changes in gait: it becomes lethargic and sweeping.
2. Second stage. The peculiarity of this stage of the disease is that some cognitive functions improve against the background of compensatory mechanisms and psychological adaptation. Sometimes this is mistaken for the process of recovery, although the disease, on the contrary, progresses. The emotional state worsens, depression develops. The damage to auditory and visual functions increases. Speech and facial expressions of the patient are severely affected due to nerve damage. There may be violent laughter or crying. The ability to plan one's actions is significantly reduced, because of which the patient sometimes loses domestic independence.
3. Third stage. It is characterized by a pronounced degradation of gait and coordination in space. The patient may lose balance even on level ground. Urinary and fecal incontinence is also observed during wakefulness. They are connected to emotional distress, possibly the development of dementia.

Treatment of sore throat when swallowing in traditional and folk ways

Stages of compensation and decompensation

In the clinical picture of any disease, the stages of adaptation and loss of organ functions are distinguished. At the first stages of the development of pathology, the functions of the affected organ can be compensated by various protective mechanisms. With an increase in the intensity of the pathological process, the work of protective mechanisms becomes insufficient, and the affected organ loses its functions.

There is a special terminology:

• Compensation is the process of preserving the functions of the affected organ through the involvement of special mechanisms.
• Subcompensation is a stage of gradual depletion of the body's compensatory functions against the background of an increasing organ damage.
• Decompensation is the loss of function of the affected organ.

The compensatory stage of chronic cerebral ischemia falls on the first and second stages of the disease. Insufficient blood supply is compensated by additional collaterals of the vasculature; some cerebral regions are able to functionally replace the affected areas. This stage corresponds to mild manifestations of the disease, which are often difficult to diagnose.

The processes of subcompensation and decompensation occur at the third stage of the disease. Collaterals become insufficient, brain cells die from lack of oxygen and nutrients. This is manifested by the most severe clinical manifestations - dementia occurs, subcortical zones are affected.

Diagnosis of chronic cerebral ischemia

Each stage of the disease is characterized by specific symptoms, so the doctor first of all conducts a survey and examination of the patient. Vivid signs of impaired cognitive activity, gait and coordination in space immediately catch the eye of the diagnostician. The examination includes the determination of reflexes - this is a productive method for diagnosing the second and third stages of cerebral ischemia.

sugar level at a particular moment and in the last months of observation.

The main stage in the diagnosis of cerebral ischemia is the appointment of instrumental methods. Doctors prescribe the following studies:

• Electrocardiogram to detect pathologies of the heart
• Echocardiography for structural and functional diagnostics of the heart
• Ultrasound dopplerography of the vessels of the head and neck
• Ophthalmoscopy to detect visual lesions
• Computed and magnetic resonance imaging for in-depth analysis of the state of the brain
• Angiography

It is extremely important for a doctor to isolate the specific symptoms and clinical manifestations of cerebral ischemia, since some neurological diseases have a similar spectrum of manifestations.

Early manifestations of the disease

This point deserves special mention. Diagnosis of the first stage of chronic cerebral ischemia is significantly hampered by fuzzy symptoms. The disease in most cases occurs in older people with other chronic diseases, which is why the symptoms of ischemia do not attract attention.

If a person suffers from chronic cardiovascular diseases for a long period, it is necessary to carefully monitor the neurological condition. The first stage can be manifested even by minor changes in gait and. People (especially the elderly) may not attach any importance to minor cognitive impairments.

Principles of treatment

Treatment of chronic cerebral ischemia is to restore adequate blood supply and maintain the result. This usually involves lifelong therapy. Most lesions of the nervous system are not subject to recovery, so it is necessary to conduct adequate therapy with the appearance of the first signs of the disease.

Commonly used methods to restore blood flow:

• drugs that prevent thrombosis
• drugs that reduce the workload of the heart
• oxygen therapy
• physiotherapy
• surgical methods for removing blood clots
• surgical methods for creating bypass routes of blood flow
• thrombolytic drugs

In domestic practice, drugs of the nootropic spectrum are often used to restore some damaged brain structures.

Etiological treatment is essential. If chronic cerebral ischemia was caused by cardiovascular and other diseases, then treatment of the underlying cause is necessary. It is especially important to carry out treatment in connection with high blood pressure, diabetes and atherosclerosis.

Neurosurgical measures are used in complicated cases. For example, sometimes it is necessary to artificially create vascular collaterals or restore the patency of an intracranial artery.

Forecast

The prognosis is related to the degree of development of the disease. Therapy, started at the initial stage of the disease, gives positive results and improves vital signs. Treatment options for the second and third stages of chronic cerebral ischemia are limited. As a rule, only adequate blood flow to the brain can be restored. Damaged nerve structures are almost never restored. In advanced cases, compensatory therapy helps - for example, with severe hearing loss, hearing aids can help.

Chronic cerebral ischemia in the long term. Timely diagnosis of brain blood filling pathologies allows applying the most effective methods of treatment.

Jul 14, 2017 Violetta Doctor

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

What is chronic cerebral ischemia?

HIGM- this is an increasing violation of the activity of the brain, due to the destruction of its tissues, due to long-term insufficiency of cerebral circulation.

In this case, the brain suffers due to a lack of glucose and oxygen. As a result, brain function is impaired. The person becomes forgetful, depressive, frequent mood changes are noticed.

Thanks to the international classification of diseases, doctors are much easier to navigate in a huge variety of diseases of human organs. ICD code - 10 from 163.0 to 169.0.

Symptoms

Initially, the clinic is almost invisible.

Violation occurs:

1. sensitivity;
2. organs of vision, smell, touch, taste;
3. psyche;
4. if a person is nervous, perhaps a violation of the functions of the brain.

There are a number of symptoms:

• Violent headache (heaviness in the head);
• Bad sleep;
• lethargy;
• Mood changes;
• memory impairment;
• Violation of coordination of movements;
• Loss of consciousness;
• Noise in the head;
• Epilepsy.

stages

There are three stages of this disease:

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

Each stage of ischemia leads to a violation of the usual quality of life.

Diagnostics

An important role in the diagnosis is played by a correctly collected patient history. In the anamnesis, it is important to find out whether there was a myocardial infarction, coronary artery disease, angina pectoris, hypertension, atherosclerosis, diabetes mellitus. It is necessary to conduct a subjective and objective examination, listen to all the complaints of the patient.

Be sure to study the neuropsychological and neurological symptoms.

A number of instrumental studies are being carried out:

And also apply laboratory methods of research:

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

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

Causes of the disease

Distinguish between root and auxiliary causes.

The root causes include:

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

Supporting reasons include:

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

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

If the disease arose as a result of the fusion of arterial hypertension and atherosclerosis, then the diagnosis sounds like this: chronic cerebral ischemia of mixed genesis.

Treatment

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

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

Therapy of patients with CCI should be carried out by a neurologist in a polyclinic. And in the third stage of ischemia, it is imperative to carry out patronage. A milk diet is recommended. It is also necessary to correct blood pressure.

There are two methods of treatment:

1. drug therapy;
2. Surgery.

Medical therapy includes:

• reperfusion- Restoration of normal blood circulation.
• Neuroprotection, which serves as a support for the metabolism of cerebral tissue, and also provides protection against structural damage.

For the implementation of drug therapy, the following drugs are used to treat:

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

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

At the initial stages, physiotherapeutic procedures are prescribed: acupuncture, massage of the head and collar zone, physiotherapy exercises, electrophoresis.

Surgery

• This is an operation, which is used in the last stages of IGM. In case of damage to the vessels of the brain, and if drug treatment has not helped, surgical treatment is prescribed. For example: carotid stenting, carotid endarterectomy, thrombectomy.
• There is another treatment carried out using stem cells. First, germ cells are taken, then they are grown to the desired volume. Further, these cells are injected with a dropper twice. The procedure itself takes about an hour. As a result, new stem cells replace the damaged ones.
• There are also folk remedies., but using only them is very dangerous.
  Garlic recipes are popular among folk methods.
  The recipe is this:
  • it is necessary to chop the garlic and pour alcohol in a ratio of one to one.
  • you need to insist for two weeks, then take five drops, which are dissolved in a tablespoon of milk.

Possible complications, consequences

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

Forecast

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

An unfavorable prognosis is revealed in connection with a late visit to the doctor.

Prevention

Prevention should be taken from an early age.

Should:

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

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

You need to start sounding the alarm when:

1. Constantly there are unpleasant phenomena in the region of the heart;
2. There is an increase in breathing or shortness of breath even with slight physical exertion;
3. Suddenly there is weakness and fatigue.

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2014

Other specified lesions of cerebral vessels (I67.8)

Neurology

general information

Short description

Approved

At the Expert Commission on Health Development

Ministry of Health of the Republic of Kazakhstan

Chronic cerebral ischemia (CCI)- slowly progressive brain dysfunction resulting from diffuse and / or small-focal damage to the brain tissue in conditions of a long-term cerebral blood supply insufficiency

The concept of "chronic cerebral ischemia" includes: "dyscirculatory encephalopathy", "chronic ischemic brain disease", "vascular encephalopathy", "cerebrovascular insufficiency", "atherosclerotic encephalopathy". Of the above names, the most common in modern medicine is the term "dyscirculatory encephalopathy"

I. INTRODUCTION

Protocol name: Chronic cerebral ischemia

Protocol code:

ICD-10 code(s):

I 67. Other cerebrovascular diseases

I 67.2 Cerebral atherosclerosis

I 67.3 Progressive vascular leukoencephalopathy (Binswanger's disease)

I 67.5 Moyamoya disease

I 67.8 Cerebral ischemia (chronic)

I 67.9 Cerebrovascular disease, unspecified

Abbreviations used in the protocol:

AG - arterial hypertension

BP - blood pressure

AVA - arteriovenous aneurysm

AVM - arteriovenous malformation

ALAT - alanine aminotransferase

ASAT - aspartate aminotransferase

BA - bronchial asthma

GP - general practitioner

HBO - hyperbaric oxygen therapy

BBB - blood-brain barrier

DS - duplex scanning

GIT - gastrointestinal tract

IHD - ischemic heart disease

CT - computed tomography

LDL - low density lipoproteins

HDL - high density lipoproteins

MDP - manic-depressive psychosis

INR - international normalized ratio

MRI - magnetic resonance imaging

MRA - magnetic resonance angiography

NPCM - initial manifestations of insufficiency of blood supply to the brain

OGE - acute hypertensive encephalopathy

ONMK - acute cerebrovascular accident

TCM - transient cerebrovascular accident

PST - anticonvulsant therapy

PTI - prothrombin index

PET - positron emission tomography

PHC - primary health care

ESR - erythrocyte sedimentation rate

SAH - subarachnoid hemorrhage

SLE - systemic lupus erythematosus

CCC - cardiovascular system

UZDG - ultrasonic dopplerography

Ultrasound - ultrasonography

FEGDS - fibroesophagogastroduodenoscopy

CHEM - chronic cerebral ischemia

CN - cranial nerves

ECG - electrocardiography

EchoCG - echocardiography

EMG - electromyography

EEG - electroencephalography

Protocol development date: year 2014.

Protocol Users: neuropathologist, internist, general practitioner (family doctor), emergency medical doctor, psychotherapist, speech therapist, physiotherapist, physical therapy and sports doctor, psychologist, social worker with higher education, social worker with secondary education, paramedic.

Classification

Clinical classification

CHEM classification(Gusev E.I., Skvortsova V.I. (2012):

According to the main clinical syndrome:

With diffuse cerebrovascular insufficiency;

With a predominant pathology of the vessels of the carotid or vertebrobasilar systems;

With vegetative-vascular paroxysms;

With predominant mental disorders.

By stages:

Initial manifestations;

subcompensation;

Decompensation.

By pathogenesis(V. I. Skvortsova, 2000):

Decreased cerebral blood flow;

Increase in glutamate excitotoxicity;

calcium accumulation and lactate acidosis;

Activation of intracellular enzymes;

Activation of local and systemic proteolysis;

The emergence and progression of antioxidant stress;

Expression of early response genes with the development of plastic protein depression and a decrease in energy processes;

Long-term consequences of ischemia (local inflammatory reaction, microcirculatory disorders, damage to the BBB).

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

The main (mandatory) diagnostic examinations carried out at the outpatient level:

General blood analysis;

General urine analysis;

Coagulogram (INR, PTI, determination of blood clotting, hematocrit);

Ultrasound of extra/intracranial vessels of the head and neck.

Additional diagnostic measures carried out at the outpatient level:

EEG video monitoring (with paroxysmal disorder of consciousness);

MRI of the brain with perfusion assessment;

MRI tractography.

The minimum list of examinations that must be carried out when referring to planned hospitalization:

General blood analysis;

General urine analysis;

Biochemical analyzes (ALT, AST, urea, creatinine, bilirubin, total protein, cholesterol, LDL, HDL, triglycerides, glucose);

Coagulogram: prothrombin time with subsequent calculation of PTI and INR in blood plasma, determination of blood clotting time, hematocrit;

Determination of glycosylated glucose.

The main (mandatory) diagnostic examinations carried out at the hospital level:

General blood analysis;

General urine analysis;

Wasserman reaction in blood serum;

X-ray of the chest organs (2 projections);

Biochemical analyzes (ALT, AST, urea, creatinine, bilirubin, total protein, cholesterol, LDL, HDL, triglycerides, glucose);

Coagulogram (prothrombin time followed by calculation of PTI and INR in blood plasma, determination of blood clotting time, hematocrit);

Additional diagnostic examinations carried out at the hospital level:

Ultrasound diagnostics is complex (liver, gallbladder, pancreas, spleen, kidneys), exclude somatic and volumetric formations;

X-ray of the chest organs (2 projections);

Ultrasound of the vessels of the brain and brachiocephalic trunk.

Diagnostic measures taken at the stage of emergency care:

Diagnostic criteria:

The clinical picture of CCI is characterized by a combination of disorders:

Cognitive disorders (violation of the ability to memorize, retain new information, decrease in the pace and quality of mental activity, violation of gnosis, speech, praxis);

Emotional disorders: the predominance of depression, loss of interest in what is happening, narrowing the circle of interests;

Vestibular-atactic syndrome;

Akinetic-rigid syndrome;

pseudobulbar syndrome;

pyramidal syndrome;

oculomotor disorders;

Sensory disturbances (visual, auditory, etc.).

Complaints and anamnesis

Complaints: headaches, non-systemic dizziness, noise in the head, memory impairment, decreased mental performance, impaired speech, gait, weakness in the limbs, short-term loss of consciousness (drop attacks), tonic-clonic convulsions, ataxia, dementia.

Anamnesis: myocardial infarction, ischemic heart disease, angina pectoris, hypertension (with damage to the kidneys, heart, retina, brain), atherosclerosis of the peripheral arteries of the extremities, diabetes mellitus, infectious and allergic diseases, intoxication.

Physical examination:

Motor disorders (hemiparesis, monoparesis, tetraparesis, asymmetry of reflexes, the presence of pathological hand and foot reflexes, symptoms of oral automatism, protective symptoms);

cognitive disorders;

Violation of behavior (aggression, delayed reaction, fearfulness, emotional instability, disorganization);

hemianesthesia;

Speech disorder (aphasia, dysarthria);

Visual disorders (hemianopsia, anisocoria, diplopia);

Violations of the cerebellar and vestibular functions (statics, coordination, dizziness, tremor);

Disturbances of bulbar functions (dysphagia, dysphonia, dysarthria);

Damage to the oculomotor cranial nerves;

Paroxysmal disturbance of consciousness (loss of consciousness, bite marks on the tongue);

Violation of urination and defecation;

Paroxysmal conditions (with circulatory failure in the basin of the vertebrobasilar system).

Laboratory research:

Complete blood count: elevated ESR and leukocytosis;

Prothrombin index - an increase in the values ​​of the indicator;

Hematocrit (hematocrit number) - decrease or increase in the values ​​of the indicator;

Determination of blood glucose levels: hypo/hyperglycemia;

Determination of urea, creatinine, electrolytes (sodium, potassium, calcium) - identification of electrolyte imbalance associated with the use of dehydrating therapy.

Instrumental research:

- CT scan of the brain: detection of focal changes in the substance of the brain

- Brain MRI in T1, T2, Flair mode: the presence of "silent" heart attacks, damage to the periventricular and deep white matter (leukoareosis);

- Ultrasound of cerebral vessels and brachiocephalic trunk(extra and intracranial vessels of the head and neck): detection of stenosis of intracranial arteries, spasm of cerebral vessels, SAH;

- EEG: with a first-time epileptic seizure, especially with partial seizures, with suspicion of Todd's syndrome, to identify a non-convulsive epilepticus, which is manifested by sudden confusion;

- Fundus examination: determination of congestive manifestations, or edema of the optic nerve, or changes in the vessels in the fundus;

- Perimetry: detection of hemianopsia;

- ECG: detection of CVS pathology;

- Holter ECG monitoring: detection of embolism, asymptomatic attack of atrial fibrillation;

-Chest X-ray(2 projections): changes in the configuration of the heart in valvular disease, expansion of the boundaries of the heart in the presence of hypertrophic and dilated cardiomyopathy, the presence of pulmonary complications (congestive, aspiration pneumonia, thromboembolism, etc.).

Indications for consultation of narrow specialists:

Consultation of a therapist in the presence of concomitant somatic pathology;

Consultation with an ophthalmologist: in order to identify hemianopsia, amaurosis, strabismus, disturbances of accommodation, pupillary reactions; changes characteristic of a brain tumor, hematoma, chronic venous encephalopathy;

Consultation with a cardiologist: in the presence of hypertension, coronary artery disease (sudden cold clammy sweat, a sharp drop in blood pressure), rhythm disturbances (atrial and paroxysmal and other types of arrhythmias), detection of changes in the ECG or ECG Holter monitoring;

Consultation with an endocrinologist: if there are signs of diabetes and diabetes insipidus, thyroid diseases;

Consultation of a speech therapist: the presence of aphasia, dysarthria;

Consultation of a psychotherapist: for the purpose of psychocorrection;

Consultation of a psychiatrist: with severe dementia, manic-depressive psychosis.

Consultation of a neurosurgeon: the presence of a hematoma, stenosis of the vessels of the head and neck, AVA, AVM, tumor or brain metastases;

Consultation of a vascular surgeon: the presence of severe stenosis of the vessels of the brain and neck, the solution of the issue of further surgical treatment;

Cardiac surgeon's consultation: the presence of a cardiac pathology requiring surgical intervention;

Audiologist consultation: in the presence of hearing impairment, noise, whistling in the ears and head.

Differential Diagnosis

Differential Diagnosis:

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Treatment

Treatment goals:

Slow down the progression of the disease;

Improve the quality of life;

In the presence of epileptic seizures, the selection of adequate anticonvulsant therapy (PST).

Treatment tactics:

Normalization of blood pressure, lipids, cholesterol and blood glucose levels;

The use of vasoactive, neuroprotective and neurotrophic drugs.

Non-drug treatment:

Semi-bed (ward).

2) Diet: table number 10 (restriction of salt, liquid).

Medical treatment

Nootropic drugs:

Phenotropil - 100 - 200 mg 1-2 times / day (up to 15 hours of the day);

Piracetam - 20% solution in ampoules in / in or / m, 5 ml per day, followed by transfer to tablet intake of 0.6-0.8 g / day for a long time;

A complex of peptides obtained from the brain in / in 5-10 ml in ampoules.

Antiplatelet agents:

Acetylsalicylic acid (film-coated tablets) - 75-150 mg / day under the control of PTI, coagulogram.

Membrane protectors:

Citicoline: 500 - 2000 mg/day IV or IM; further 1000 mg / day - in sachets (level A);

Neuroprotection:

Magnesium sulfate, 25% solution 30 ml/day (level A);

Glycine, 20 mg/kg body weight (average 1-2 g/day) sublingually for 7-14 days

Inosine + nicotinamide + riboflavin + succinic acid:

20 ml/day intravenously drip slowly (60 drops per minute) for 10 days, then oral tablets of 300 mg - 2 tablets 2 times a day for 25 days (level c);

Ethylmethylhydroxypyridine succinate, infusion at 100 mg/day, followed by transfer to the tablet intake of the drug at a dose of 120-250 mg/day (level B);

Tocopherol acetate (vitamin E): 1-2 ml / m 1 time / day for 7-10 days, then 1 tablet 2 times / day for 2 months.

Vasoactive drugs:

Vinpocetine infusion - 2-4 ml / day in / in - 7-10 days with a transfer to oral administration of 5-10 mg / day for a month;

Nicergoline - 2-4 mg / m or / in 2 times / day, and then tablets of 10 mg 3 times / day for a month;

Benciclane fumarate - at a dose of 100 mg/day IV with the transition to tablet intake at a dose of 100 mg 2 times a day for 2-3 months, the maximum daily dose is 400 mg (level B).

Pentoxifylline at a daily dose of 400-800 mg 2-3 times / day (level B).

Muscle relaxants:

Baklosan, orally 5-20 mg/day for a long time (depending on muscle tone);

Tolperisone hydrochloride, 50-150 mg 2 times a day for a long time (under the control of blood pressure).

For nociceptive pain:

Non-steroidal anti-inflammatory drugs (meloxicam 7.5-15 mg IM or orally, lornoxcam 4-8 mg for pain IM or orally; ketoprofen 100-300 mg IV, IM or orally);

For neuropathic pain:

Pregabalin 150 - 600 mg/day;

Gabapentin 300-900 mg/day.

Lipid-lowering therapy:

Atorvastatin 10-20 mg/day - long-term; the maximum daily dose is 80 mg.

Antihypertensive drugs:

Medical treatment provided on an outpatient basis

1.Basic medicines

Neuroprotective Therapy:

Magnesium sulfate, 25% - 10.0 ml ampoule;

Cortexin -10 mg/day IM for 10 days, vials;

A complex of peptides obtained from the brain of a pig 5-10 ml IV, in ampoules.

Membrane protectors:

Citicolines, 500-2000 mg/day IV or IM; further 1000 mg / day - in sachets;

Choline alfoscerate - 400 mg 2-3 times / day.

Antiplatelet agents:

Acetylsalicylic acid - 75-150 mg / day, film-coated tablets (under the control of PTI, coagulogram);

Nootropic drugs:

Phenotropil - 100 - 200 mg 1-2 times / day (until 15 pm), tablets 100 mg

Piracetam - 10 ml / day - ampoules (5 ml), tablets 0.4 g 3 times a day, ampoules of 5 ml or tablets of 400 mg, 800 mg, 1200 mg.

Antioxidants and antihypoxants:

Inosine + nicotinamide + riboflavin + succinic acid - 1-2 g / day IV - 5.0 ml ampoules; 600 mg / day - tablets. Ampoules of 5.0 ml, tablets of 200 mg;

Ethylmethylhydroxypyridine succinate - 100 mg/day IV, at a dose of 120-250 mg/day - tablets. Ampoules of 100 mg, 2 ml.

Vasoactive agents:

Vinpocetine - 5-10 mg tablets 3 times a day / day; Tablets 5.10 mg, 2 ml ampoules;
- nicergoline - 10 mg tablets 3 times a day, tablets; ampoules 5 mg, tablets 5, 10 mg;
- benziklan fumarate - in / in slowly 50-100 mg / day, ampoules; 100 mg 2 times / day for 2-3 months, tablets. Ampoules of 2 ml, tablets of 100 mg.

Pain relief medications:

Meloxicam - 7.5-15 mg intramuscularly or tablets; tablets of 7.5 and 15 mg, ampoules of 1-2 ml.

Lornoxekam - 4-8 mg - in / m, ampoules; when taken orally - 4 mg 2-3 times / day - tablets; tablets of 4, 8 mg, ampoules of 4 mg.

Ketoprofen 100-300 mg IV, IM or 1 tablet 2 times a day - tablets, capsules. Tablets and ampoules of 100 mg.

Muscle relaxants:

Baclofen - 5 mg tablets - 5-20 mg per day;

Tolperisone - 100 mg / day - ampoules, tablets of 50 mg - 50-150 mg / day.

Oral indirect anticoagulants(antivitamins K):

Warfarin, orally 2.5-5 mg per day under the control of INR. 2.5 mg tablets

Preparations that improve microcirculation:

Pentoxifylline - tablets - 400 mg - 800 mg per day; Tablets 100 mg, 4000 mg, ampoules 100 mg.

Nimodipine - 30 mg tablets 2-3 times a day (level B). Tablets of 30 mg.

Pain relief drugs(neuropathic pain):

Pregabalin - start with a dose of 150 mg to 600 mg / day, capsules; Tablets of 150 mg.

Gabapentin - at a dosage of 300-900 mg per day, capsules of 100, 300, 400 mg. Tablets of 300 mg.

Antioxidants:

Tocopherol acetate (vitamin E) - 1-2 ml / day 5%, 10%, 30% solution in / m - ampoules; 1-2 pills 2-3 times / day for 1-2 months - capsules, pills. Ampoules of 20 ml of 5% and 10% solution in oil.

Lipid-lowering therapy:

Atorvastatin 10-20 mg / day - long-term (2-3 months); the maximum daily dose is 80 mg (tablets). Tablets of 5-10 mg.

Antihypertensive drugs:

Correction of blood pressure is carried out according to the clinical protocol "Arterial hypertension".

Antiepileptic therapy:

The relief of an epileptic seizure or status epilepticus is carried out according to the clinical protocol “Epilepsy. epileptic status.

Medical treatment provided at the inpatient level

1.Basic medicines:

Neuroprotective Therapy:

Magnesium sulfate, solution 25% 10.0 ml; ampoules;

A complex of peptides obtained from the brain of a pig in / in 5-10 ml, ampoules.

Cortexin - in / m 10 mg / day for 10 days, vials.

Membrane protectors:

Citicolines: 500-2000 mg/day IV or IM; further 1000 mg/day in sachets (level A);

Choline alfoscerate - 400 mg 2-3 times / day, tablets.

Nootropic drugs:

Phenotropil - tablets 100 mg.

Piracetam - 5 ml ampoules.

Antioxidants and antihypoxants:

Inosine + nicotinamide + riboflavin + succinic acid - ampoules 5.0-10 ml; 200 mg tablets.

Ethylmethylhydroxypyridine succinate - ampoules of 2 ml, 5 ml, tablets of 125 mg.

Vasoactive agents:

Vinpocetine - 2 ml ampoule;

Nicergoline - 2 ml ampoules;  benziklan fumarate - 2 ml ampoules, 100 mg tablets.

Antihypoxants:

A complex of peptides obtained from the brain of a pig 10-30 mg / day by infusion; ampoules.

Pain relief medications:

In the presence of nociceptive pain: non-steroidal anti-inflammatory drugs:

Meloxicam - 7.5-15 mg per tablet;

Lornoxekam - 4-8 mg tablets; vial 8 mg

Ketoprofen tablets and ampoules 100 mg.

For neuropathic pain:

Pregabalin -150 mg capsules;

Gabapentin - capsules of 100, 300, 400 mg.

Muscle relaxants:

Baclofen - Tablets 10, 25 mg;

Tolperisone - tablets 50 mg.

2. Additional medicines:

Antiplatelet agents:

Acetylsalicylic acid (film-coated tablets) - 75-150 mg;

Antioxidants:

Tocopherol acetate (vitamin E) - Ampoules of 20 ml of 5% and 10% solution in oil.

Lipid-lowering therapy:

Atorvastatin tablets 5-10 mg.

Antihypertensive drugs.

Correction of blood pressure is carried out according to the clinical protocol "Arterial hypertension".

Antiepileptic therapy.

The relief of an epileptic seizure or status epilepticus is carried out according to the clinical protocol “Epilepsy. epileptic status.

Drug treatment provided at the stage of emergency emergency care:

Treatment of arterial hypertension (see the clinical protocol "Arterial hypertension").

Epileptic seizures (see the clinical protocol "Epilepsy", "Epileptic status").

Other treatments

Other types of treatment provided at the outpatient level:

1) Physiotherapy:

electrophoresis;

Electrical muscle stimulation;

Heat treatment (ozokerite treatment; "salt" chamber);

Physiopuncture;

Oxygen cocktail;

Massage;

Ergotherapy;

Hydrokinesitherapy;

Mechanotherapy;

Classes in the Montessori system;

Classes on analytical simulators with the biofeedback program (training on EMG and EEG parameters);

Posturography (robotic);

Proprioceptive correction;

Information

Sources and literature

1. Minutes of the meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2014
   1. 1) Schmidt E.V. Classification of vascular lesions of the brain and spinal cord // Zhurn. Neurologist and psychiatrist. 1985. No. 9. pp. 1281-1288. 2) The European Stroke Initiative Executive Committee and the EUSI Writing Committee: European stroke initiative recommendations for stroke management – ​​update 2003. Cerebrovascular Disease 2003;16:311-337. 3) Skvortsova V.I., Chazova I.E., Stakhovskaya L.V., Pryanikova N.A. Primary prevention of stroke. M., 2006. 4) Maiti R, Agrawal N, Dash D, Pandey B. Effect of Pentoxifylline on inflammatory burden, oxidative stress and platelet aggregability in hypertensive type 2 diabetes mellitus patients. Vascul Pharmacol 2007; 47(2-3):118-24. 5) Gusev E.I., Belousov Yu.B., Boyko A.N. General principles of pharmacoeconomic research in neurology: Guidelines. M., 2003. 56 p. 6) A guide to neurology by Adams and Victor. Maurice Victor, Allan H. Ropper - M: 2006. - 680 p. (S. 370-401). 7) Stock V.N. Pharmacotherapy in neurology: A practical guide. – 4th ed., revised. and additional – M.: 2006. – 480 p. 8) Medicines in a neurological clinic: A guide for doctors / E.I. Gusev, A.S. Nikiforov, A.B. Gekht. - M: 2006. - 416 p. Evidence-based medicine. Directory / Edited by S.E. Baschinsky. Moscow, 2003. 9) OS Levin The main medicines used in neurology. Handbook, Moscow, 6th edition. MED press-inform. 2012. 151 p. 10) Schmidt E.V. Vascular diseases of the nervous system. - Moscow. - 2000. - S. 88-190. 11) Adams H., Hachinski V., Norris J. Ischemic Cerebrovascular Disease // Oxford University press. - 2001. - P. 575. 12) Akopov S., Whitman G.T. Hemodynamic Studies in Early Ischemic Stroke Serial Transcranial Doppler and Magnetic Resonance Angiography Evaluation //Stroke. 2002;33:1274–1279. 13) Flemming K.D., Brown R.D. Jr. Cerebral infarction and transient ischemic attacks. Efficient evaluation is essential to beneficial intervention // Postgrad. Med. - 2000. - Vol. 107, no.6. – P. 55–62. 14) Guidelines for the Early Management of Adults with Ischemic Stroke // Stroke. - 2007. - Vol. 38. - P. 1655. 15) Stroke. Principles of treatment, diagnosis and prevention / Ed. Vereshchagina N.V., Piradova M.A., Suslina Z.A. - M.: Intermedica, 2002.- 189 p. 16) P.V. Voloshin, V.I. Taitslin. Treatment of vascular diseases of the brain and spinal cord / 3rd ed., add. - M.: MEDpress_inform, 2005. - 688 p. 17) Stefano Ricci, Maria Grazia Celani, Teresa Anna Cantisani et al. Piracetam for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2006. - No. 2. 18) Ziganshina LE, Abakumova T, Kuchaeva A Cerebrolysin for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2010. - No. 4 19) Muir KW, Lees KR Excitatory amino acid antagonists for acute stroke // Cochrane Database of Systematic Reviews. - 2003. - No. 3. 20) Gandolfo C, Sandercock PAG, Conti M Lubeluzole for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2010. - No. 9. 21) Horn J, Limburg M Calcium antagonists for acute ischemic stroke // Cochrane Database of Systematic Reviews. - 2010. - No. 9. 22) Asplund K Haemodilution for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2002. - No. 4. 23) Bath PMW, Bath-Hextall FJ Pentoxifylline, propentofylline and pentifylline for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2004. - No. 3. 24) Bennett MH, Wasiak J, Schnabel A et al. Hyperbaric oxygen therapy for acute ischaemic stroke // Cochrane Database of Systematic Reviews. - 2010. - № 9. 25) Diseases of the nervous system. A guide for doctors // Ed. N.N. Yakhno, D.R. Shtulman, M., 2011, T.I, T.2. 26) O.S. Levin The main drugs used in neurology. Handbook, Moscow, 6th edition. MEDpress-inform. 2012. 151 p. 27) "Neurology"

Information

III. ORGANIZATIONAL ASPECTS OF PROTOCOL IMPLEMENTATION

List of protocol developers with qualification data:

1) Nurguzhaev Erkyn Smagulovich - Doctor of Medical Sciences, Professor of the RSE on REM "Kazakh National Medical University named after S.D. Asfendiyarov" Head of the Department of Nervous Diseases

2) Izbasarova Akmaral Shaimerdenovna - RSE on REM "Kazakh National Medical University named after S.D. Asfendiyarov" Associate Professor of the Department of Nervous Diseases

3) Raimkulov Bekmurat Nametovich - Doctor of Medical Sciences, Professor of the RSE on REM "Kazakh National Medical University named after S.D. Asfendiyarov" Professor of the Department of Nervous Diseases

Conflict of interests: In relation to the drug "Actovegin", a justification with an evidence base is given in the Cochrane Community Library, where there are 16 clinical studies on the use of this drug with presented clinical efficacy.

Reviewer:

Tuleusarinov Akhmetbek Musabalanovich - Doctor of Medical Sciences, Professor of the Department of Traditional Medicine of JSC "Kazakh Medical University of Continuing Education"

Conditions for revision of the protocol: revision of the protocol after 3 years and / or when new methods of diagnosis / treatment with a higher level of evidence appear.

Attached files

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