Transient ischemic attack(TIA) is neurology: according to international classification diseases of the tenth revision of ICD-10 is a transient (temporary) acute dysfunction of the central nervous system and deformation of the blood flow of certain areas of the spinal cord and brain or the inner lining of the eye.

This condition goes away along with neurological symptoms. The attack manifests itself within 24 hours, which is a critical period for it, after which all symptoms disappear completely (this creates additional difficulty for the doctor in determining the diagnosis).

If the symptoms of an ischemic attack continue after a day, cerebral failure is regarded as an acute stroke.

Therefore, it is important to carry out competent prevention, preventing the aggravation of the manifestations of a transient ischemic attack, than to be content with a long recovery.

What is a transient ischemic attack?

Pathology in most cases pursues people after 45 years of age (more often after 65 years). A transient ischemic attack from a stroke is distinguished by the short-term development and recovery of the former.

Experts warn people who have undergone TIA to be more careful, because it is a harbinger of a stroke.

Acute trans ischemic attack occurs as a result of local disturbances... Cerebral symptoms such as dizziness, nausea, vomiting are a manifestation of acute encephalopathic hypertension when blood pressure rises.

According to the Institute of Neurology of the Russian Academy of Medical Sciences, almost 50% of those who have undergone a transient heart attack have an increase blood pressure... And these pathologies exacerbate each other.

Transient ischemic attacks are regarded by doctors as a warning signal of an acute ischemic stroke.

Therefore, as medical practice shows, you need to be most careful in the treatment of a microstroke.

For this, enhanced antiplatelet, vascular, neurometabolic and symptomatic therapy is carried out in order to eliminate severe consequences.

International statistical classification ICD-10

A transactional ischemic attack does not have pronounced signs, with which one goes to a doctor. It is not possible to independently determine the development of pathology, which means that it is not possible to determine the number of such attacks. ... Epidemiologists suggest that in Europeans, the disease occurs in 5 out of 10 thousand people.

The incidence of diseases in persons over 45 years old is only 0.4%, and also prevails in men 65-70 years old and in women aged 75-80 years.

For 5 years before the onset of stroke, half of the patients have an ischemic attack.

According to the ICD-10 classification, such TIA and related syndromes are distinguished (G-45.)

Vertebrobasilar arterial system syndrome (G45.0) when the skin turns pale and sweaty, eyeballs by themselves begin to move in horizontal direction, oscillating from side to side and it becomes impossible to independently touch the tip of your nose with your index finger.

Temporary occlusion due to low blood supply to the carotid artery (hemispheric) (G45.1)- for a few seconds, in the direction of the localization of the attack, the eye becomes blind, and on the opposite side it grows numb, loses sensitivity or is seized by a convulsive limb, there is a temporary violation of the speech apparatus, drowsiness, weakness, fainting.

Bilateral multiple symptoms of cerebral (cerebral) arteries (G45.2): short-term disturbances in speaking, decreased sensitivity and motor functions in the limbs, along with temporary loss of vision on the opposite side of the TIA and convulsions.

Transient blindness Amaurosisfugax (G45.3).

Transient global amnesia- transient memory disorder with sudden loss of ability to memorize (G45.4).

Other TIA and manifestations transient with attacks (G45.8).

If TIA spasm is present, but the reasons for it are not specified and then the diagnosis is indicated with the G45 code.

This is a classification of a transient ischemic attack, depending on the area in which the thrombus is formed.

Symptoms

Depending on the vascular basin, where ischemia is manifested, transient ischemic attacks occur in the carotid and vertebro-basilar basins (VVB).

Carotid and vertebrobasilar basin

Depending on the affected area, determine the place of the brain, which receives less blood supply.

And here neurologists divide symptoms into two types:

• General- nausea, pain and weakness, dizziness and lack of coordination, short-term loss of consciousness;
• Local- individual, depending on the affected area.

According to local manifestations, the area affected by the thrombus is determined.

TIA in IVB is the most common occurrence of short-term ischemia (occurs in 70 cases out of 100).

Accompanied by:

TIA in the carotid pool occurs:

• With visual impairment, monocular blindness (in the right or left eye) and disappears as the attack disappears (lasts a few seconds);
• With paroxysmal vestibular and sensory disorders - it is impossible to control the body due to loss of balance;
• Vascular visual disorders - occur in the form of a decrease in sensitivity or complete paralysis of one side of the body, and warns of a micro-stroke in this area;
• With convulsive syndromes, during which convulsions in the limbs, without loss of consciousness, bend and unbend the arms and legs on their own.

TIA in the local area of ​​the blood flow of the retinal artery, ciliary or orbital artery is prone to stereotypical recurrence and is accompanied by:

• Transient blindness- visual acuity suddenly drops, clouding, distortion of colors occurs, a veil appears on one eye.
• Hemianesthesia, a decrease in muscle tone, the occurrence of convulsions, paralysis, which informs about a transient ischemic attack of the carotid arteries.
• Transit global amnesia- occurs after a strong nervous shock or painful sensation... Short-term amnesia of new information is noted in the presence of very old, absent-mindedness, a tendency to repeat, vestibular ataxia. TGA lasts up to half an hour, after which the memories are fully restored. Similar attacks of TGA may recur in a few years. A patient in a coma may have a sail symptom, which is called so because of the outward resemblance of inflation during breathing of the cheek on the side opposite to the paralyzed one.

The difficulty in determining the diagnosis is that the attack symptoms are short-lived and the neuropathologist is forced to diagnose TIA only from the patient's words, which will depend on the pathological zone of cerebral blood flow.

Despite the reversibility of the symptoms, it must be remembered that at the time of the onset of the spasm, the arteries carrying oxygen and vital substances stop the processes.

Energy is not produced, and cells suffer from oxygen starvation (temporary hypoxia is observed).

Symptoms in humans with brain hypoxia

The damage to the body from an attack will depend on the area of ​​the affected area, but even small local attacks will bring considerable harm to health.

Signs of aortic-cerebral attacks

The emergence of pathological processes in the blood circulation in the aortic zone before the bifurcation of the carotid and vertebral vessels are marked by symptoms:

• Photopsia, diplopia;
• Noise in the head;
• Vestibular ataxia;
• Drowsiness and decreased physical activity;
• Dysarthria.

Violation can appear with congenital heart disease.

And if there is an increase in blood pressure, then there are:

• Headache;
• Vestibular ataxia;
• Weakness in the limbs;
• Nausea and vomiting.

Attack symptoms become more pronounced if the patient begins to change head positions and the risk of TIA increases (Table 1).

Risk of ischemic stroke after TIA (on the AVSD scale)
Index	Signs	Grade
HELL	above 140/90 Hg	1
Age	over 65 years old	1
Manifestation	weakness, numbness of one of the limbs	2
	dysarthria without limb disorders	1
	other	0
Duration of symptoms	over 1 hour (severe, occurs due to irreversible cerebral deformity)	2
	up to 1 hour (moderate, in the absence of any residual effects after paroxysm)	1
	less than 10 minutes (mild)	0
For a patient who has previously been diagnosed with diabetes mellitus		1
The maximum number of points on the scale: 7 points.

The main causes of transient ischemic attacks

Can be defined as:

These factors are the reason for the insufficient supply of oxygen and vital substances by the vessels of the brain, which increases the load on them.

And instead of blood flow, a spasm occurs in one of the areas, which violates the proportions between the necessary and received nerve cells.

Diagnostics

Diagnosis of a transient ischemic attack is complicated by the transience of the attack, the doctor learns about the attack that has occurred only from the patient's words, which may be completely inaccurate.

For diagnostics, consider the following:

• Similar signs occur with irreversible cerebral disorders, because of this, it is worth using all kinds of methods for diagnosing TIA;
• After an attack, the patient is likely to have a stroke;
• A clinic with full-fledged technical equipment of a neurological direction is the best hospital for hospitalization and appropriate examination of a patient who has had an attack.

During emergency hospitalization, the patient undergoes: spiral computed tomography or MRI (magnetic resonance imaging).

From laboratory methods studies of a patient after a transient ischemic attack are carried out as follows:

• Clinical analysis of peripheral blood (circulating through the vessels outside the hematopoietic organs);
• Biochemical studies (antithrombin III, protein C and S, fibrinogen, anticardiolipin antibodies and others), which provide a complete analysis of liver and kidney function and the presence of tissue death;
• Expanded hemostasiogram to determine the blood clotting index;
• General analysis of blood and urine (determination of liver and kidney function, urinary tract, identifying pathologies);

To examine the patient, the following is prescribed:

• Electroencephalogram (EEG)- allows you to diagnose neurological diseases and determine the presence of lesions of brain tissue;
• 12-lead electrocardiography (ECG)- determines the development of arrhythmia, heart failure;
• Daily (Holter) ECG monitoring- if there are relevant indications;
• Echocardiography (EchoCG)- method of examination and assessment of the heart and its contractile activity;
• Lipidogram- a comprehensive study that determines the level of lipids (fats) of various blood fractions;
• Angiography of cerebral arteries It is used to study the vessels of the circulatory and lymphatic systems, the development of the network of auxiliary vessels, the presence of thrombosis (carotid, vertebral and selective).

In addition to a neuropathologist, a patient who has had an ischemic attack should be examined by doctors such as a cardiologist, ophthalmologist, and therapist.

Also, differential diagnostics is carried out to exclude the occurrence of other diseases, such as:

• Epilepsy;
• Fainting;
• Ocular migraine;
• Inner ear pathology;
• Myasthenia gravis;
• Panic attacks;
• Horton's disease.

By excluding diseases that are not suitable for symptoms and factors, the only correct diagnosis will be determined and assigned correct treatment.

Treatment

The main task of treatment after a transient ischemic attack is to prevent the ischemic process, to restore normal blood circulation and metabolism of the ischemic cerebral region.

When a transient cerebrovascular accident occurs, doctors recommend hospitalization of the patient in order to early stage TIA prevent future complications.

Hospitalization is required if you have frequent of the above symptoms that prevent you from functioning properly.

If symptoms are extremely rare, then you can treat at home., but only under the supervision of a doctor and following all his prescription.

The set of measures taken to restore blood flow, eliminate oxygen starvation in the area of ​​impaired vascularization and drug protection of the brain is presented in Table 2.

activity	Medications
The main
thinning blood and restoring blood circulation	Aspirin, ThromboAss, Acetylsalicylic acid, Dipyridamole, Clopidogrel, Cardiomagnyl, metabolites (Cytoflavin), and in case of stomach diseases - Tiklopedin
restoration of capillary blood flow	under stationary conditions, intravenously, a plasma-substituting antishock drug Reopolyglyukin is injected
lowering blood cholesterol levels and delaying the development of atherosclerosis	statin drugs, such as Atorvastatinum, Simvastatinum, Pravastatinum), but they are used with extreme caution (if the result exceeds the danger from side effects as they can cause mental disturbances
removal of angiospasm	coronary artery disease like papaverine, nicotinic acid, Nikoverin
restoration of microcirculation of cerebral vessels	Cavinton, Vinpocetinum
preservation of brain cells and their supply of additional energy	smart dredges such as Piracetamum, Nootropil, Cerebrolysin
Additional
electrophoresis and drugs against muscle spasms, light massage of the cervical-collar zone, Darsonval therapy
oxygen, coniferous, radon baths based on mineral radon waters
therapeutic physical activity to restore blood flow, the development of additional vessels

It is necessary to keep under control the intake of drugs that affect the level of blood pressure. These may include diuretics.

Diabetics with transient ischemic attack need drugs that lower glucose levels by lowering blood sugar.

Patients who have thrombus formation, upon detection of the initial phenomena of thrombus formation in stationary conditions, are given fibrinolytic therapy to reduce the size of the intracoronary thrombus.

You can use the funds traditional medicine for overall increase immune system and protection against atherosclerosis. These can be teas, decoctions and tinctures from clover, hawthorn, lemon, garlic and fish oil supplements. But such methods cannot replace medical treatment.

Prognosis for TIA

Usually, after such an attack, the likelihood of developing the next is high. Moreover, such attacks can become systematic... A timely response to symptoms plays an important role in predicting the consequences of TIA.

If the patient himself and his relatives quickly noticed the characteristic clinical manifestations and realized that an ischemic attack had begun, then there is an opportunity to take immediate measures to prevent its consequences.

The transient ischemic attack itself takes place in a relatively short period of time. But the forecasts for the further development of the situation are quite serious.

In this case, rapid hospitalization of the patient and appropriate therapy are required. Such actions not only reduce the negative impact of the attack on the body, but also provide an opportunity for their reverse development.

Is it possible to predict the likelihood of stroke in TIA?

One of the most common predictions after TIA is stroke. According to statistics, it develops in 10% of patients affected by an attack within the first 24 hours. In 20% of patients, a stroke occurs within three months after the attack, in 30% this period can reach five years.

The occurrence of strokes is closely associated with ischemic attacks. Therefore, after the occurrence of such an attack, a person automatically falls into a risk group.

It is receiving greater scrutiny from doctors and is encouraged to devote more time to stroke prevention and compliance healthy way life. Preventive therapeutic procedures can also be performed.

It is important to monitor the state of health and observe the dynamics. In this case, we can more accurately talk about the possibility of a stroke after an ischemic attack.

Prevention

Primary and secondary prevention of transient ischemic attack in this case consists of:

Prevention is complemented by traditional medicine.

Which doctor should I go to?

In the event of a TIA, the patient must be hospitalized. The specialized department will be neurological.

After the main crisis period is over, the cardiologist and neurologist will become the main attending physicians of the patient who has had an attack.

Since the solution of the problem requires the treatment of blood vessels and the accompaniment of possible neurological consequences. Also, it is the cardiologist who gives recommendations on how to prevent possible recurrences of such conditions.

conclusions

Timely TIA treatment prevents stroke. Anti-ischemic therapy restores blood supply to the brain, improves metabolism and oxygenation of cells.

In the event of a transient ischemic attack, the doctors' requirements for hospitalization for a month are fully justified.

Since the attending doctor, due to the transience of the symptoms, cannot see them himself, he directs them to diagnostics in order to clarify the diagnosis and prescribe adequate treatment.

Video: Transient ischemic attack - a harbinger of stroke.

Some patients presenting with suspected stroke are diagnosed with transient ischemic attack (TIA). The term sounds incomprehensible to many and seems less dangerous than the well-known stroke, but this is a mistake. Consider what effect transient ischemic attacks have on the brain and how dangerous this condition is.

General information about TIA

A transient attack is a short-term violation of the blood supply to certain areas of the brain tissue, which leads to hypoxia and cell death.

Consider the main difference between a transient ischemic attack and a stroke:

• Development mechanism. With stroke lesions, there is a complete cessation of blood flow to the brain tissue, and during transient ischemia, insignificant blood flow to the part of the brain remains.
• Duration. Symptoms in TIA after a few hours (maximum - a day) gradually subside, and if a stroke has occurred, the signs of deterioration remain the same or progress.
• The possibility of spontaneous improvement in well-being. The ischemic attack gradually stops, and healthy structures begin to perform the function of dead brain cells, and this is one of the main differences from a stroke, in which, without medical care, the foci of necrosis increase, and the patient's condition gradually worsens.

It may seem that a transient ischemic attack of the brain is less dangerous than a stroke damage to the brain tissue, but this is a misconception. Despite the reversibility of the process, frequent oxygen starvation of brain cells causes irreparable harm.

Reasons for the development of short-term ischemia

It is clear from the description of the mechanism that transient attacks of ischemic origin provoke partial vessel overlap and a temporary decrease in cerebral blood flow.

Cholesterol plaques in blood vessels

The provoking factors for the development of the disease are:

• hypertonic disease;
• cardiac pathologies (coronary artery disease, atrial fibrillation, CHF, cardiomyopathy);
• systemic diseases affecting the internal vascular wall (vasculitis, granulomatous arthritis, SLE);
• diabetes;
• cervical osteochondrosis, accompanied by changes in bone processes4
• chronic intoxication (alcohol and nicotine abuse);
• obesity;
• advanced age (50 years and older).

In children, pathology is often provoked by congenital features of the cerebral vessels (underdevelopment or the presence of pathological bends).

The presence of one of the above reasons for a transient ischemic attack is not enough; for the appearance of the disease, the influence of 2 or more factors is necessary. The more provoking causes a person has, the higher the risk of an ischemic attack.

Symptoms depend on localization

With a transient ischemic attack, symptoms may vary slightly depending on the location of the temporarily developed ischemia. In neurology, the signs of the disease are conventionally divided into 2 groups:

General

These include general cerebral signs:

• migraine headache;
• disorder of coordination;
• difficulty in orientation;
• nausea and not relieving vomiting.

Despite the fact that similar signs occur in other diseases, the symptoms listed above suggest that an ischemic attack of the brain has occurred and a medical examination is necessary.

Local

The neurological status is assessed in a medical institution by specialists. By the nature of the deviations that have arisen in the patient, the doctor will be able to suggest the approximate location of the pathological focus even before the apparatus examination. According to the localization of ischemia, there are:

• Vertebrobasilar. This form of the pathological process is observed in 70% of patients. A transient ischemic attack in the vertebrobasilar basin develops spontaneously and is often provoked by a sharp turn of the head to the side. When a focus is found in the VBB, the total Clinical signs and to them are added visual impairment (it becomes indistinct), slurred speech, motor and sensory disorders.
• Hemispheric (carotid artery syndrome). The patient will develop migraine-like pains, dizziness, difficulty in coordination and fainting. The provoking factor will almost always be changes in the vertebrae in the cervical spine.
• SMA (spinal muscular atrophy). With damage to the carotid pools of the brain in humans, there is a one-sided decrease in motor activity and sensitivity of one or both limbs, and vision impairment in one eye is possible. A distinctive feature of this form of pathology is that with ischemia in the right carotid pool, the right eye suffers, and paresis occurs on the left. If the focus is located in the left basin, MCA develops on the right.

In some cases, with mild to moderate ischemic attack of the brain, the symptoms are not characteristic. Then, before identifying the localization of the pathology with the help of special equipment, they say that an unspecified TIA has occurred.

Diagnostic methods

The acute phase of the pathology is diagnosed on the basis of the patient's symptoms (local status) and clinical and laboratory examination. This is necessary in order to exclude diseases with similar symptoms:

• brain tumors;
• meningeal lesions (infections or toxic lesions of the meninges);
• migraine.

For differential diagnostics, use:

These types of hardware examination help to identify foci of ischemia and necrosis of areas of brain tissue.

MRI room in the clinic

Additionally, to clarify the etiology of the disease, the patient is prescribed:

• examination of peripheral blood;
• biochemistry;
• blood clotting testing;
• lipid tests (cholesterol and triglyceride content);
• urine test (provides additional information about metabolic processes).

In addition to laboratory tests, a person is carried out:

• Doppler ultrasonography. Determine the speed of blood flow and the nature of the filling of the vessels. It makes it possible to identify areas of the brain with reduced blood supply.
• ECG. Allows you to detect cardiac pathologies.
• Angiography. The introduction of a contrast agent and a series of X-ray images can determine the nature of the distribution of blood flow in the vessels of the brain.
• Fundus examination by an ophthalmologist. This check is necessary even if there are no signs of visual impairment. If the carotid pool is affected, then the fundus blood circulation from the side of the lesion always suffers.

With the onset of violations, signs of a transient ischemic attack are easy to identify if you immediately call an ambulance or deliver a person to medical institution.

A distinctive feature of a transient attack is that the arising disorders are transient and a day after the attack, the patient almost does not feel discomfort and can lead a full-fledged lifestyle, but short-term ischemia does not pass without a trace.

If such patients seek medical help and report that yesterday they had signs of visual impairment, sensitivity or physical activity, the examination is carried out using the same method. This is due to the fact that the brain tissue is sensitive to hypoxia, and even with a short oxygen starvation, the death of cellular structures occurs. The foci of the resulting necrosis can be identified using instrumental research.

With a transient ischemic attack, diagnostics helps not only to identify the affected necrotic foci, but also to predict the possible course of the disease.

First aid and treatment

At home, it is impossible to provide full assistance to the patient - qualified actions of medical workers are needed.

First aid to a patient before the arrival of doctors will consist of 2 points:

• Calling an ambulance or delivering a person to a medical facility.
• Providing maximum rest. The victim of a transient attack is disoriented and frightened, so you need to try to calm the patient down and lay him down, always with his head and shoulders raised.

When can you get up after a transient ischemic attack if the victim could not be taken to the doctor during the attack? There are no strict restrictions here, but doctors recommend limiting physical activity a day after the attack (the patient should lie down more, and when changing posture, do not make sudden movements).

In transient ischemic attack, the standard of care is as follows:

• Restoration of full blood flow in the cerebral vessels (Vinpocetine, Cavinton).
• Reducing the number of damaged brain cells (Nootropil, Cerebralizin, piracetam).
• Reduction of intoxication caused by a lack of blood circulation (Rheopolyglucin infusion).

• Signs of thrombosis or blood clots. Apply Cardiomagnet, Aspirin or Thrombo ACC.
• Development of vascular spasm. Use Nicotinic acid, Papaverine, or Nikoverine.

With elevated cholesterol levels, statins are prescribed to prevent the formation of atherosclerotic plaques.

Patients in the acute phase must be admitted to the hospital, where the treatment necessary for a transient ischemic attack will be carried out.

If a person goes to a medical institution some time after an attack, then therapy is allowed on an outpatient basis.

Most patients are interested in the duration of treatment, but only the attending doctor can answer this question, but it is important to tune in to a long course of therapy and strictly follow clinical recommendations.

Despite the fact that specific rehabilitation is not needed in this condition, it should be remembered that during the attack, a small number of neurons died and the brain becomes vulnerable to the development of serious complications.

Preventive actions

In transient ischemic attack, prevention is the same as for other conditions associated with vascular disorders:

• Elimination of risk factors. Bringing blood parameters back to normal (cholesterol, coagulation).
• Increased physical activity. Moderate exercise normalizes blood circulation throughout the body, boosts immunity, and reduces the risk of developing TIA. But when playing sports, you must observe moderation. If a person has already developed transient ischemia or is at risk for the development of pathology, then swimming, yoga, walking or medical gymnastics should be preferred.
• Diet. With high blood clotting, hypercholesterolemia or diabetes mellitus nutritionists select a special nutrition program. General recommendations for making a menu include: limiting "harmful delicacies" (smoked, fatty, pickles, canned food and semi-finished products), as well as adding vegetables, fruits and cereals to the diet.
• Timely treatment of exacerbations of chronic pathologies. Above was a list of diseases that provoke an ischemic attack. If they are not started and the complications that have arisen are treated in a timely manner, the likelihood of pathology is greatly reduced.

Knowing what TIA is, you should not neglect preventive advice. Medical recommendations that are not difficult to follow will help to avoid serious consequences.

Prediction of ischemic attacks

After a single transient ischemic attack, the consequences are invisible and the clinic disappears after a day, but the further prognosis is not always favorable - the tendency to re-development of TIA increases, and, with the influence of additional unfavorable factors, the following complications may appear:

• Transient ischemic stroke. Disrupted blood flow is not restored after an hour and irreversible death of cellular structures occurs.
• Hemorrhagic stroke. With weakness of the wall, the partially blocked vessel cannot withstand the increased blood pressure below the site of blood flow disturbance and its rupture occurs. The leaked blood infiltrates the brain structures, making it difficult for cells to work.
• Visual impairment. If the focus is localized in the vertebrobasilar system, then visual field disturbance or a strong decrease in acuity is possible. When the impairment is located in the basin of the right artery, the MCA will be left-sided, but there is a high probability that visual function on the right will suffer and vice versa (vision in one eye will be preserved).

The prognosis is aggravated by the patient's bad habits, the presence of concomitant diseases and risk factors, as well as old age.

Who to contact

When the first signs of a transient ischemic attack are detected, an ambulance should be called. The arrived medical team will provide the necessary assistance to the patient and take the person to the necessary specialist.

If the transportation is carried out independently, then the patient must be shown to a neurologist.

Having studied the necessary information about TIA diagnosis - what it is and how dangerous it is, it becomes clear that this condition cannot be ignored. Despite the fact that the resulting disorders are reversible and do not affect the person's lifestyle, they cause the death of part of the brain structures and, under unfavorable circumstances, become the cause of disability.

Cerebral ischemia is a short-term dysfunction of the central nervous system as a result of impaired blood circulation in certain areas of the brain. It is important to provide first aid correctly so that the ischemic attack does not develop into a stroke in the future.

Transient ischemic attack is a transient or dynamic disorder of the blood supply, which is accompanied by focal disorders of the brain functions. It lasts no more than 24 hours. If, after an ischemic attack of the brain, minor changes are detected, the patient's condition is defined as ischemic stroke.

Causes of ischemic attack of the brain

Cerebral ischemia is not a separate disease. It develops against the background of diseases associated with disorders of the heart and other organs. The causes of a transient ischemic attack are:

• Atherosclerosis - vascular disease, manifested in deposits on the walls of blood vessels of the brain, cholesterol plaques, narrowing the lumen. This leads to impaired blood circulation, creates an oxygen deficiency. It manifests itself in memory impairments, frequent headaches.
• Arterial hypertension- a disease associated with increased blood pressure. It is important to always control the pressure.
• IHD - acute or chronic damage to the heart muscle as a result of changes in the coronary arteries. The main cause of cardiac ischemia, as well as cerebral ischemia, is the blockage of blood vessels.
• Atrial fibrillation is the most common disease associated with heart rhythm disturbances. It manifests itself as unpleasant sensations in the region of the heart, sudden attacks of heartbeat, severe weakness.
• Cardiomyopathy is a myocardial disease accompanied by cardiac dysfunction. It appears as heaviness in the region of the heart, tingling, shortness of breath and swelling.
• Diabetes mellitus - the basis of the disease is a deficiency in the formation of insulin and an excess of production of glucose in the blood. The consequence is the slow destruction of the vessel walls.
• Osteochondrosis of the cervical vertebrae reduces blood flow due to inflammation of the intervertebral joints of the tissues.
• Obesity creates an additional burden on the work of all organs, including blood vessels.
• Bad habits
• Elderly age- in men, the age of 60-65 is critical. In women, symptoms of an ischemic attack of the brain begin to appear after 70 years.

Symptoms of cerebral ischemia

The onset of the disease is asymptomatic. The vessels do not have nerve endings, so the disease sneaks up unnoticed. The main symptoms of an ischemic attack are manifested in a short-term speech disorder, vision problems, fatigue, increasing weakness, memory loss, and nervous excitement. Insomnia or, conversely, drowsiness is observed. There may be severe headaches and dizziness, nausea, vomiting, numbness of the extremities, a feeling of cold, cerebral ischemia, accompanied by loss of consciousness.

Diagnostics

It is necessary to study all the patient's complaints in order to correctly diagnose. Studies such as blood tests for cholesterol and glucose, general analysis, cardiography, electroencephalography, ultrasound of the head arteries, duplex scanning of blood vessels, MRI and CT angiography are carried out.

Treatment

Treatment of a transient ischemic attack should be prescribed by a neurologist. In the fight against cerebral ischemia, therapeutic, surgical, non-drug methods are used.

Therapeutic method

The therapeutic method for the treatment of transient ischemic attack is reperfusion - restoration of blood circulation in the zone of impairment. It is carried out by prescribing special drugs to affect the thrombus, if there are no contraindications to this.

Another therapeutic method is neuroprotection - maintaining the brain tissue from structural damage. There are primary and secondary neuroprotection. The primary method of treatment is to interrupt the impending cell death. It is carried out as an emergency aid from the first minutes and within three days after ischemia. The secondary method is to interrupt delayed cell death, reduce the consequences of ischemia. Begins 3 hours after identifying signs of ischemia. Lasts about 7 days.

The therapeutic method of treatment is accompanied by the intake of the following drugs:

• Antiaggregates prevent blood clots. The most commonly used drug is aspirin.
• Angioprotectors improve the process of blood circulation in the vessels, reduce capillary fragility. These include: Bilobil, Nimodipin.
• Vasodilators help improve cerebral circulation by expanding the passage in the vessels. The main disadvantage of this drug- a decrease in blood pressure, which leads to a deterioration in the supply of blood to the brain. The medicine should be selected individually, taking into account the patient's age. The most common drugs in this group are Mexidol, Actovegin, Piracetam.
• Nootropic drugs improve brain activity, stimulate metabolism in nerve cells, protect them from oxygen starvation. Piracetam, Glycine, Vinpocetine, Cerebrolysin are nootropics.

All drugs prescribed by a doctor must be taken in courses: twice a year for two months.

Surgical methods

Surgery is an emergency treatment. They are used in the later stages, when therapeutic treatment does not bring results. One of these methods is carotid endaterectomy, aimed at removing the inner wall of the carotid artery, affected by atherosclerosis, which destroys it. This operation has a long lasting effect. It is usually done under local anesthesia and lasts no more than two hours. An incision is made in the neck area, the carotid artery is isolated, in which an incision is made in the place of the plaque, and the inner wall is scraped out. Then sutures are applied.

Transient ischemic attack (TIA) is one of the types of acute circulatory disorders in the brain tissue, which is manifested by cerebral and focal signs of brain damage and lasts from a couple of minutes to 24 hours. If the signs persist for more than the specified time, then this condition should be regarded as an ischemic stroke.

The manifestations of TIA depend on the location of the lesion, the duration and severity of the attack. A transient ischemic attack is a serious harbinger of a stroke, a kind of warning to the body of an impending disaster. If we turn to the statistics, we can make sure that during the first month after TIA, stroke develops in 20% of patients, and during the first year after the incident - in 42%.

Causes and risk factors for TIA

Most often, transient ischemic attacks occur in patients with cerebral atherosclerosis, high blood pressure and their combination. A much lesser role is given to such etiological factors as diabetes mellitus, vasculitis, compression of arteries by osteophytes in osteochondrosis of the cervical spine.

Other, more rare, causes of TIA development include:

• thromboembolic disorders in the vessels of the brain, which arise as a result of cardiac arrhythmias, congenital and acquired heart defects, bacterial endocarditis, atrial fibrillation, prosthetics of the heart valve apparatus, intracardiac tumors, etc.;
• a sudden drop in blood pressure, which leads to acute hypoxia of the brain tissue (shock of any genesis, Takayasu's disease, orthostatic hypotension, bleeding);
• damage to cerebral arteries of an autoimmune nature (systemic vasculitis, Buerger's disease, Kawasaki syndrome, temporal arteritis);
• pathological disorders in the cervical spine (osteochondrosis, spondyloarthrosis, spondylosis, intervertebral hernia, spondylolisthesis);
• disorders in the blood system, which are accompanied by an increased tendency to thrombosis;
• migraine, especially clinical variant with an aura (the risk of this type of TIA is significantly increased in women who take oral contraceptives);
• stratification (dissection) of the cerebral arteries;
• congenital defects of the vascular apparatus of the brain;
• malignant neoplasms of any localization;
• Moya-Moya disease;
• deep vein thrombosis lower limbs.

Risk factors for developing TIA:

• atherosclerosis and hyperlipidemia;
• diabetes;
• hypodynamia;
• overweight;
• bad habits;
• all the above-described diseases and pathological conditions.

Important to remember! People who are at risk of developing TIA, and therefore ischemic stroke, should be informed about possible risk and take all possible preventive measures.

The essence of the disease

There are several mechanisms for the development of acute disorders of cerebral circulation and, in particular, TIA. But the most common is the following.

Microemboli and atheromatous masses that form in the carotid and vertebral arteries (they are the result of the breakdown of atherosclerotic plaques) with the blood flow can move into the vessels of a smaller caliber, where they cause blockage of the arteries. Most often, the terminal cortical branches of arterial vessels are affected. In addition to blocking the lumen of the arteries, they cause irritation and spasm of the vascular walls. Since such masses by themselves can rarely cause a complete cessation of blood circulation distal to the site of localization, the second mechanism plays a major role in the development of TIA symptoms.

These platelet and atheromatous masses are very soft in structure and therefore quickly dissolve. After that, the spasm of the artery is eliminated and the blood flow in this area of ​​the brain is normalized. All symptoms disappear. Also, these microemboli can be of cardiogenic origin or be the result of problems in the blood coagulation system.

This process itself lasts only a few seconds or minutes, but pathological signs sometimes last up to 24 hours. This is due to the edema of the vascular wall due to its irritation, which disappears for several hours after the acute period.

But, unfortunately, the development of the disease is not always so favorable. If the dissolution of blood clots and vasospasm are not eliminated on their own within 4-7 minutes, but in the neurons that are in hypoxia, irreversible changes occur, and they die. A stroke develops. But, fortunately, such strokes have a relatively favorable prognosis, as they are never extensive.

TIA symptoms

Signs are most often manifested by focal nerve signs. Much less common are cerebral symptoms such as headache, vertigo, bouts of nausea with vomiting, impaired consciousness.

TIA symptoms depend on the localization of atherosclerotic plaques - in the carotid or vertebro-basilar vascular bed.

TIA in the vertebrobasilar vascular basin

This type of TIA occurs most often and accounts for up to 70% of transient ischemic attacks.

TIA symptoms:

• attacks of systemic dizziness;
• vegetative-vascular disorders;
• noise and ringing in the head and ears;
• headache of a bursting character in the back of the head;
• bouts of lingering hiccups;
• pallor of the skin;
• increased sweating;
• visual disturbances - dots, zigzags in front of the eyes, loss of visual fields, double vision, fog in front of the eyes;
• signs of bulbar syndrome (impaired swallowing, pronunciation of words, loss of voice);
• nystagmus;
• violation of statics and coordination of movements;
• drop attacks - attacks of a sharp fall without losing consciousness.

TIA in the carotid vascular basin

It is manifested mainly by focal neurological symptoms, most often these are sensitive disorders. Sometimes the symptoms are so scanty that the patient does not even understand that something is wrong with his body.

TIA symptoms:

• numbness of some parts of the body, most often from one limb, but it can also proceed as hemianesthesia (damage to the arm and leg on one half of the body);
• development movement disorders in the form of monoparesis or hemiparesis (damage to one limb or arms and legs on one half of the body);
• if the lesion is localized in the left hemisphere, then problems with speech develop - aphasia, cortical dysarthria;
• seizures;
• blindness in one eye.

The duration and reversibility of TIA symptoms is different, from a few seconds to 24 hours. But, nevertheless, an accurate diagnosis can be made only after some time. The fact is that with TIA, according to additional methods studies (MRI and CT) do not find any pathological foci. If this happens, then we should talk about a stroke, even if all the signs have disappeared during the first day after the start. In medicine, there is a special term for this type of circulatory disorders in the brain tissue - "minor stroke".

Video transmission and signs of stroke:

TIA severity

Depending on the dynamics of the disease, there are 3 degrees of severity of a transient ischemic attack:

1. Easy- focal neurological signs are present for up to 10 minutes, go away on their own, no consequence remains.
2. Medium severity- signs last from 10 minutes to several hours, disappear on their own or under the influence of therapy without consequences.
3. Heavy- neurological symptoms are present from several hours to 1 day, pass under the influence of specific therapy, but after an acute period, there are consequences in the form of minor neurological symptoms that do not affect the quality of life, but are detected during examination by a neurologist.

Depending on the frequency of attacks, a distinction is made between:

• rare TIAs - no more than 1-2 times a year;
• with an average frequency - 3-6 times a year;
• frequent - once a month or even more often.

Diagnostics

Diagnosis of an ischemic transient attack presents some difficulties. First, people do not always pay attention to the symptoms of a disorder, considering them a common condition. Secondly, differential diagnosis between ischemic stroke and TIA in the first hours presents very great difficulties, since the symptoms are very similar, and there may not be any changes on tomography, as a rule, with a stroke, they are clearly visible only 2-3 days from the development of the pathology.

For diagnostics, use:

• detailed objective examination of the patient, collection of complaints and study of the medical history, determination of risk factors for the development of TIA;
• a full range of laboratory tests of blood and urine, which must necessarily include a lipid profile, a study of blood coagulation, a biochemical blood test;
• ECG and ultrasound of the heart to identify cardiopathology;
• Ultrasound of the vessels of the head and neck;
• magnetic resonance imaging or computed tomography of the brain;
• electroencephalography;
• blood pressure monitoring;
• other methods necessary for making the main diagnosis.

Important to remember! Since the exact diagnosis of a transient ischemic attack is retrospective, all patients with focal neurological symptoms are subject to hospitalization and treatment according to stroke protocols, because these conditions can be distinguished only after 2-3 days.

Treatment principles

First, it is necessary to determine whether a transient ischemic attack requires treatment. Many experts argue that TIA therapy is not necessary at all, because all symptoms go away on their own. This is true, but there are 2 controversial points.

First... TIA is not an independent disease, but a consequence of primary pathology. Therefore, all therapeutic measures should be aimed at the therapy of the diseases that caused the violation, as well as at the primary and secondary prevention of the development of acute cerebrovascular accidents.

Second... TIA treatment should be carried out in accordance with all medical protocols for the management of patients with ischemic stroke, since, as already mentioned, it is simply impossible to distinguish between these two conditions in the first hours.

Main therapeutic measures:

• compulsory hospitalization in a specialized neurological department;
• specific thrombolytic therapy (administration of drugs that can dissolve existing blood clots) is used in the first 6 hours from the onset of the disease in patients who still suspect a stroke;
• anticoagulant therapy - the administration of drugs that thin the blood and prevent the formation of blood clots (heparin, enoxaparin, deltaparin, fraxiparin, etc.);
• medicines that normalize blood pressure when it rises (beta-blockers, ACE inhibitors, sartans, diuretics, calcium channel blockers);
• antiplatelet agents that prevent platelets from sticking together and the formation of blood clots (clopidogrel, aspirin);
• drugs that have neuroprotective abilities - they protect nerve cells from damage, increase their resistance to hypoxia;
• antiarrhythmic drugs for cardiac arrhythmias;
• medicines that lower blood cholesterol levels - statins (atorvastatin, rosuvastatin, simvastatin, etc.);
• symptomatic therapy and restorative agents.

Surgery

Surgery can be prescribed for atherosclerotic lesions of extracranial vessels, in particular carotid. There are three types of surgical interventions:

proper nutrition;

normalization of body weight;

elimination of bad habits;

treatment of concomitant diseases - hypertension, diabetes mellitus, arrhythmias, atherosclerosis, etc.;

sufficient physical activity;

taking blood-thinning drugs for people at risk;

surgical correction of narrowing of the arteries.

Video transmission about ischemic attack - a harbinger of stroke:

Making a conclusion, it is necessary to remember that although a transient ischemic attack does not pose a direct threat to human life, it is a warning to the body that irreparable may happen in the near future. Therefore, in no case should this state be ignored, but it is necessary to take all measures to prevent a catastrophe.

RCHRH (Republican Center for Healthcare Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols MH RK - 2013

Transient cerebral ischemic attack, unspecified (G45.9)

Neurology

general information

Short description

Approved by the minutes of the meeting
Expert Commission on the Development of Healthcare of the Ministry of Health of the Republic of Kazakhstan

No.23 on 12/12/2013

Transient neurological disorders with focal symptoms that develop as a result of short-term regional cerebral ischemia, but do not lead to the development of infarction of the ischemic area are designated as transient ischemic attacks .

I. INTRODUCTORY PART

Protocol name: Transient ischemic attack

Protocol code:

ICD-10 codes: G45

G45 Transient transient cerebral ischemic attacks [attacks] and related syndromes

G45.0 Vertebrobasilar arterial system syndrome

G45.1 Carotid artery syndrome (hemispheric)

G45.2 Multiple and bilateral cerebral artery syndromes

G45.3 Transient blindness

G45.4 Transient global amnesia

Excludes: amnesia NOS (R41.3)

G45.8 Other transient cerebral ischemic attacks and associated syndromes

G45.9 Transient cerebral ischemic attack, unspecified

Cerebral artery spasm

Transient cerebral ischemia NOS

G46 * Vascular cerebral syndromes in cerebrovascular diseases G46.0 * Middle cerebral artery syndrome (I66.0)

G46.1 * Anterior cerebral artery syndrome (I66.1)

G46.2 * Posterior cerebral artery syndrome (I66.2)

G46.3 * Stroke syndrome in the brain stem (I60-I67)

G46.4 * Cerebellar stroke syndrome (I60-I67)

G46.5 * Purely motor lacunar syndrome (I60-I67)

G46.6 * Purely sensitive lacunar syndrome (I60-I67)

G46.7 * Other lacunar syndromes (I60-I67)

G46.8 * Other vascular syndromes of the brain in cerebrovascular diseases (I60-I67)

Abbreviations used in the protocol:

BP - blood pressure;

APTT - activated partial thrombin time;

BIT - intensive care unit;

HIV - Human Immunodeficiency Virus;

DWI - diffusion-weighted images;

AI - ischemic stroke;

Ischemic heart disease - ischemic heart disease;

CT - computed tomography;

CPK - creatine phosphokinase;

HDL - high density lipoproteins;

LDL - low density lipoproteins;

MRI - magnetic resonance imaging;

MSCTA - multispiral computed angiography;

MRA - magnetic resonance angiography;

INR - international normalization ratio;

ONMK - acute cerebrovascular accident;

AMI - acute myocardial infarction;

PHC - primary health care;

TKDG - rancranial doplerography;

TIA - transient ischemic attack;

USDG - Doppler ultrasound;

Ultrasound - ultrasound examination;

HR - heart rate;

ECG - electrocardiogram;

EEG - electroencephalography;

NIHSS - National Institutes of Health Stroke Scale

Protocol development date: May 2013

Protocol users: neurologists, neurorenimatologists, cardiologists, general practitioners, rehabilitologists, radiation diagnostics doctors, functional diagnostics doctors, neurosurgeons, angiosurgeons.

No Conflict of Interest Statement: no.

Classification

Clinical classification TIA

By the severity of clinical manifestations TIA is subdivided into:

Light (up to 10 minutes);

Moderate (up to several hours);

Severe (up to 24 hours).

By frequency TIA is subdivided into:

Rare (1-2 times a year);

Medium frequency (3-6 times a year);

Frequent (once a month or more).

Diagnostics

II. METHODS APPROACHES AND PROCEDURES OF DIAGNOSTICS AND TREATMENT

List of basic and additional diagnostic activities:

At the stage of the emergency room, the patient is assessed somatic and neurological status, general clinical examinations are carried out (complete blood count with platelet count, coagulogram, glucosometry, ECG), urgent ultrasound examinations extra and intracranial vessels of the head. The maximum time a patient can be in the emergency room should not exceed 40 minutes.

Diagnostic criteria

Complaints and anamnesis

The neurologist on duty collects complaints and anamnesis, specifying the exact time of onset and regression of neurological symptoms.

Possible complaints upon admission:

Headache

Dizziness

Unsteadiness, unsteadiness when walking

Facial asymmetry

Speech impairment

Weakness in the limbs

Numbness in the limbs

Seizure

Nausea

Visual impairment

Pain in the region of the heart

Palpitations

Breathing disorder

Medical history... Clarify point by point.

Disease onset time: (hours, minutes)

Preceding factors:

Emotional stress

Alcohol intake

Reception drugs

Reception medicines before the ambulance arrives

Anamnesis of life... Clarify point by point.

ONMK postponed earlier

Ischemic stroke (when?)

Hemorrhagic stroke (when?)

TIA earlier (when?, How often?)

Previously identified stenoses, occlusions of the main arteries of the head (carotid, vertebral arteries)

Previously identified arterial aneurysms, vascular malformations

Cardiac diseases

Arterial hypertension, how long

Maximum rise in blood pressure

Average numbers of blood pressure

Taking basic antihypertensive drugs (names of drugs, doses, frequency of administration)

Acute myocardial infarction (when? Types of treatment)

Violations heart rate:

Atrial fibrillation (form)

Extrasystole

Cardiac conduction disorders

Other heart rhythm disorders

The presence of prosthetic heart valves

Rheumatic heart disease

Bacterial endocarditis

Diabetes mellitus, how long

Taking oral hypoglycemic drugs (drug names, doses, frequency of administration)

Insulin intake (drug names, doses)

Systemic diseases connective tissue:

Systemic lupus erythematosus

Periarteritis nodosa

Nonspecific aortoarteritis

Fibromuscular dysplasia

Other vasculitis

Blood diseases:

Erythremia

Thrombocytopenia

Antiphospholipid syndrome

Thrombocytosis

Hemophilia

Leukemia

Vasculitis

Other blood disorders

Taking anticoagulants (name of drugs, duration of administration, dose)

Postponed operations, injuries, infectious diseases

Availability chronic diseases

Smoking (experience, number of cigarettes smoked per day)

Alcohol abuse, drug use.

Hereditary history (presence of acute cerebrovascular accident, AMI, arterial hypertension, atherosclerosis, diabetes mellitus and other diseases of the heart, blood and blood vessels in close relatives), allergic history

Physical examination: Neurological examination with an assessment of the neurological status according to the NIHSS scale (Appendix 1)

Laboratory research

Basic:

1. Complete blood count with hematocrit and platelet count

2. General urine analysis

3. INR, APTT, PO, PT fibrinogen

4. Blood glucose

5. Total cholesterol, HDL, LDL, beta-lipoproteins, triglycerides

6. Blood electrolytes (potassium, sodium, calcium, chlorides)

7. Hepatic transaminases, total, direct bilirubin

8. Urea, creatinine

9. Total protein

Additional:

1. Determination of the antinuclear factor of antibodies to cardiolipins, phospholipids, LE-cells;

2. MV-CPK, troponin test according to indications

3. D dimer according to indications;

4. Proteins C, S;

5. Protein fractions according to indications;

6. Blood test for HIV, syphilis, hepatitis B, C.

Instrumental research:

Basic:

2. Urgent ultrasound examinations of the vessels of the head and neck:

3. Doppler ultrasound of the extracranial vessels of the head or duplex scanning

4. Transcranial doplerography of the cerebral arteries

5. MSCTA or MRA for the diagnosis of occlusion or stenosis of extra- and (or) intracranial arteries of the head

Additional:

1. Cardiac ultrasound is indicated for patients with a history of cardiac pathology, revealed by objective examination or according to ECG data, with suspected cardioembolic genesis of TIA;

2. CT or MRI of the brain in diagnostically unclear cases to exclude others possible reasons transient neurological disorders (brain tumor, small intracerebral hemorrhage, traumatic subdural hematoma, etc.);

3. Cerebral angiography is performed in cases when hemodynamically significant stenosis of the internal carotid artery is detected and surgical treatment is planned to confirm the results of non-invasive ultrasound research methods and assess intracerebral circulation;

4. EEG in the presence of convulsive syndrome;

5. Holter daily ECG monitoring according to indications;

Daily monitoring of blood pressure according to indications;

Fundus examination, perimetry according to indications.

TIA symptoms:

1. Numbness or weakness of the face, arms or legs, often on one side of the body

2. Sudden onset of speech or understanding problems

3. Sudden onset of vision problems

4. Dizziness, lack of coordination of movements and balance

5. The appearance of a severe headache for an unknown reason

The main symptoms are:

Clinical picture transient ischemic attacks are characterized by transient focal neurological symptoms and depends on the basin of the circulatory disorders of the brain (carotid or vertebro-basilar). In most cases, the diagnosis of TIA is made retrospectively, since at the time of the patient's examination by a specialist, focal neurological symptoms are absent. In this regard, a thorough history taking and knowledge of the clinical manifestations of TIA are required.

TIA in the basin of the carotid arteries are manifested by transient mono- or hemiparesis, sensory disturbances, and speech disorders. Sometimes there is a transient visual impairment in one eye on the side of the affected internal carotid artery. Patients may complain of a "shadow falling in front of the eye" or a "white veil".

TIA in the vertebrobasilar basin is most often manifested by transient vestibular and cerebellar disorders (systemic dizziness, nausea, ataxia), slurred speech (dysarthria), facial numbness, diplopia, unilateral or bilateral

Movement and sensory disorders. Sometimes hemianopsia or transient visual impairment in both eyes is observed.

Isolated dizziness, nausea, or vomiting are not common with TIAs and are most often accompanied by other stem symptoms. A number of symptoms previously attributed to TIA in the vertebrobasilar basin (syncope, epileptic seizures) are considered by many researchers to be unusual for this pathology.

Transient blindness (transient monocular blindness (TMS), or amaurosis fugax) is a condition that is more often unilateral, sudden, short-term (usually within a few seconds) loss of vision due to transient ischemia in the area of ​​blood supply to the orbital, posterior ciliary arteries or retinal arteries. Visual impairment is often described by the patient as a "curtain" or "shutter", which has moved from top to bottom or bottom to top. Sometimes vision loss is limited to the upper or lower half of the visual field. Usually TMS occurs spontaneously, without provoking factors, but sometimes it can be caused by bright light, changes in body position, physical exercise or a hot bath. Painful sensations are not typical for TMS. Monocular blindness may not be the only complaint. Other symptoms are also observed: contralateral hemiparesis and hemihypesthesia to the corresponding hemisphere in severe lesions of the carotid artery. TMS may recur (usually stereotypically), but the area of ​​visual impairment varies depending on the area of ​​ischemia.

Transient global amnesia (TGA) is a unique syndrome in which a patient, more often middle-aged, suddenly loses short-term memory with a relative preservation of memory for distant events. The patient's consciousness and orientation in his own personality are not violated, but there is an incomplete orientation in space and environment, repetition of stereotyped questions, confusion. The etiology of this dramatic syndrome remains unknown; attempts are made to explain it by ischemia of the hippocampal-fornic system. Some authors consider this pathology to be an epileptic phenomenon or a variant of migraine. TGA episodes are often triggered by certain factors such as emotional distress, pain, and intercourse. Attacks usually last from several tens of minutes to several hours. Memory recovery is complete. In this case, there is no neurological deficit. The tendency to repeat is small, the frequency is rare - once every few years. Such patients have risk factors for the development of cerebrovascular pathology, especially arterial hypertension.

TIA diagnosis
Patients who have undergone TIA require examination to determine the cause of transient cerebral ischemia in order to prevent ischemic stroke and other diseases of the cardiovascular system.

The examination plan includes angiological examination (palpation and auscultation of the vessels of the neck and extremities, measurement of blood pressure

On both hands), a detailed general blood test, a biochemical blood test with the determination of cholesterol and its fractions, a study of hemostasis, ECG, non-invasive ultrasound methods for examining the precerebral and cerebral arteries (preferably duplex scanning of the precerebral arteries and TCD of the cerebral arteries), MSCTA, MR angiography.

If there is a suspicion of a cardioembolic genesis TIA, a consultation with a cardiologist and a more in-depth examination of the heart (echocardiography, Holter monitoring) are indicated. In cases unclear genesis TIA, as in ischemic stroke, shows in-depth studies of blood plasma: determination of coagulation factors and fibrinolysis, the level of lupus anticoagulant and anticardiolipin antibodies.

In cases where hemodynamically significant stenosis of the internal carotid artery is detected and surgical treatment is planned, cerebral angiography is usually performed beforehand to confirm the results of non-invasive ultrasound research methods and assess intracerebral circulation.

CT or MRI of the head is desirable in all cases of TIA, but it is necessary in diagnostically unclear cases to exclude other possible causes of transient neurological disorders (brain tumor, minor intracerebral hemorrhage, traumatic subdural hematoma, etc.). In most patients with TIA, CT and MRI of the head do not show focal changes, however, in 10-25% of cases (more often in cases where neurological disorders persisted for several hours), cerebral infarction is detected, which indicates a certain convention of the term TIA.

Indications for specialist consultation:

Consultation with a cardiologist in case of arterial hypertension, cardiac arrhythmias, with suspected acute coronary syndrome, as well as for the development of a program of secondary individual prevention;

Consultation of a vascular surgeon in case of revealed stenosing lesions of the great vessels of the neck in order to determine the indications for reconstructive operations;

Consultation of an endocrinologist for the purpose of correcting hyperglycemia and for developing a program of secondary individual prophylaxis in patients with diabetes mellitus;

Consultation with a hematologist in the presence of coagulopathies.

Differential diagnosis

Differential diagnosis:

Specifications	Seizure	Debut multiple sclerosis	Transient ischemic attack
Onset of the disease 13-18 years old	13-18 years old	More often 15-30 years	Typically over 45
Provoking factors	Disturbed night sleep, alcohol intake	Postponed ARVI, solar insolation, hot bath.	Hypertension, blood diseases, atherosclerosis.
Cause	Changes functional state brain (hereditary burden), organic defeat brain (tumors, cysts, post-stroke foci)	Autoimmune process	Arterial hypertension, heart rhythm disturbances, heart pathology, blood diseases, vascular atherosclerosis.
Duration of an attack	5-10 minutes	More than 24 hours	At least 24 hours
Start	Sudden	Gradual	Sudden
Associated symptoms	The presence, in addition to paresis of the limbs, the attachment of twitching in them. With Todd's paralysis, this symptomatology is accompanied by impaired consciousness. With a partial sensory seizure, a combination of numbness and tingling of the extremities, a feeling of warmth, and internal movement is characteristic.	Hemiparesis, paraparesis, monoparesis, atactic syndrome, pelvic dysfunctions.	Transient: impaired consciousness, visual impairment, bulbar syndrome, hemiparesis and monoparesis of the extremities, anisoreflexia, sensory disturbances, vestibulocochlear syndrome.
EEG	Epileptic activity	No change	No change
MRI	High-resolution MRI allows detecting cases of mesialtemporal sclerosis, hippocampal atrophy, sclerosis, combined pathology is noted (hamartomas, cortical dysplasias, gray matter heterotopies)	Focuses of demyelination in the head and / or spinal cord	No focal changes

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Treatment

Treatment goals is the prevention of the development of stroke, the restoration of neurological deficits in the shortest possible time.

Treatment tactics

Non-drug treatment
Observation in the neuroresuscitation unit for at least 4 hours, subject to bed rest. Longer observation of the patient in the BIT is carried out according to indications (atrial fibrillation, an increase in neurological deficit, a history of cardiorespiratory diseases, etc.)

Drug therapy:

Maintaining an adequate level of blood pressure

If necessary, decrease in blood pressure is carried out by 15-20% of the initial values: by 5-10 mm Hg. Art. per hour in the first 4 hours, and then by 5-10 mm Hg. Art. for every 4 hours. It is important to exclude fluctuations in blood pressure!

Antihypertensive drugs:

1. ACE inhibitors

Captopril is the drug of choice for lowering blood pressure. It is administered orally at an initial dose of 12.5 mg if the systolic blood pressure is not higher than 200 mm Hg, or 25 mg if the systolic blood pressure is higher than 200 mm Hg. If necessary, it is applied repeatedly at the same or twice as much dose, depending on the established hypotensive effect. If after 30-40 minutes. after taking 12.5 mg. Captopril blood pressure decreased by 15% from the initial, repeat the introduction of the drug in the same dose after 3 hours. If blood pressure has not changed or increased, 25 mg is prescribed. urgently.

Enalapril is used when emergency parenteral administration of the drug is required. The dose is titrated under the control of blood pressure and is usually 1.25 mg. intravenously slowly (within 5 minutes) for physical. solution. It is considered effective to reduce systolic blood pressure by 15% from the initial after 30-60 minutes. The frequency of administration, if necessary, every 6 hours.

Perindopril is administered orally at 2-4 mg. 1-2 times a day.

2. Antagonists of AT II receptors

Eprosartan is administered orally at 600 mg once a day

Candesartan is administered orally at an initial dose of 4-8 mg. Once a day, in case of impaired liver and kidney function, the initial dose is reduced to 2 mg per day.

3. Beta-blockers

Propranolol is prescribed in a dose of 20-40 mg by mouth. For an urgent decrease in blood pressure, an intravenous dose of 1 mg is used. within 1 min (0.4 ml. 0.25% solution in 20 ml. physical solution). If necessary, injections are repeated at 2 minute intervals, the maximum dose is 10 mg.

Esmolol is used to urgently lower blood pressure in the form of intravenous infusion: loading dose of 0.5 mg / kg for 1 minute, then 0.05 mg / kg / min. within the next 4 minutes. It is possible to re-enter the loading dose and increase the rate of administration to 0.1 mg / kg / min. The usual maintenance dose is 0.025-0.3 mg / kg / min

4. Alpha-Beta-blockers

Proxodolol is used for emergency parenteral lowering of blood pressure. It is prescribed in / in 1-2 ml. 1% solution within 1 min. If necessary, repeat this dose at 5 min intervals. before the effect appears. Possibly in / in drip injection of 5 ml. 1% solution in 200 ml. isotonic sodium chloride solution or 5% glucose solution at a rate of 0.5 mg (2 ml solution) in 1 min. In total, no more than 5-10 ml of a 1% solution (50-100 mg) is injected. With SBP more than 220 mm Hg, DBP 121-140 mm Hg vlabetalol 10-20 mg. every 10 minutes - 20 minutes

5. Agonists of central alpha-adrenergic receptors

Clonidine is prescribed 0.075-0.15 mg sublingually. For an emergency decrease in blood pressure in / in 0.1-0.2 mg (1-2 ml of a 0.01% solution) slowly. The maximum daily dose is 0.75 mg.

6. Alpha-1-blockers

Ebrantil is used for hypertensive crisis, severe arterial hypertension, including those resistant to therapy. Intravenous injection of 25 mg of the drug is carried out. If blood pressure decreases after 2 minutes, then to maintain it at the achieved level, intravenous infusion is performed. If after 2 min. after intravenous injection, the pressure remains the same, repeated intravenous injection of 25 mg of ebrantil is performed. If blood pressure decreases after 2 minutes. after repeated injection, intravenous infusion is carried out with an initial dose of up to 6 mg in 1-2 minutes. If after 2 minutes. after repeated intravenous injection, blood pressure remains at the same level, then the drug ebrantil is injected intravenously slowly at a dose of 50 mg.

7. Vasodilators

Sodium nitroprusside is used for an emergency controlled decrease in blood pressure with an increase in diastolic blood pressure above 140 mm Hg. The initial dose is 0.5-10 mcg / kg per minute, then the dose is selected depending on the hypotensive effect. The effect is immediate but short-lived. It has a cerebral vasodilator effect, which may be accompanied by an increase in intracranial pressure. First-line agent for lowering blood pressure in acute hypertensive encephalopathy.

With a decrease in blood pressure

Dopamine is used to maintain blood pressure. 50-100 mg. the preparation is diluted with 200-400 ml. isotonic solution and administered intravenously, preferably using an infusion pump (initial up to 5 μg / kg / min). The initial rate of administration is 3-6 drops per minute. Under strict control of blood pressure and pulse rate, the rate of administration can be increased to 10-12 drops per minute. The infusion is continued until the average blood pressure rises within 100-110 mm Hg.

Glucocorticosteroids. Prednisolone is administered once intravenously at a dose of 120 mg. or dexamethasone once in / in a dose of 16 ml. The subsequent mode of administration of corticosteroids is determined by the degree of stabilization of the mean blood pressure in the range of 100-110 mm Hg.

Hyper HAES(if necessary, correction of hypovolemia) 250 ml. within 30 minutes.

Correction of glucose levels

An absolute indication for insulin prescription short acting the blood glucose level is more than 10 mmol / l. Patients with diabetes should be transferred to subcutaneous injections short-acting insulin, blood glucose control after 60 minutes.

Intravenous drip of insulin is carried out at a plasma glucose level of more than 13.9 mmol / l. The initial dosage of insulin for intravenous drip injection is calculated by the formula: (blood plasma glucose level (mmol \ L) * 18-60) * 0.03 = ______ UNITS per 1 hour intravenously. The insulin dose is changed every hour using this formula.

In case of hypoglycemia below 2.7 mmol / l-infusion of 10-20% glucose or bolus in / in 40% glucose 30.0 ml.

Neuroprotective therapy:

Magnesium sulfate (glutamate receptor antagonist) 25% solution 30 ml per day

10 ml / drip

IV or IV 500-1000 mg 1-2 times a day, depending on the severity of the condition

The maximum daily dose for parenteral administration is 2000 mg, for oral administration is 1000 mg.

Gliatilin (choline alfoscerate-cholinomimetic central action) increases cerebral blood flow, enhances metabolic processes and activates the structures of the reticular formation of the brain.

Cytoflavin (inosine + nicotinamide + riboflavin + succinic acid). A metabolic drug with antioxidant activity. It has a positive effect on the processes of energy production in the cell, reduces the production of free radicals and restores the activity of antioxidant enzymes. The drug activates cerebral blood flow, stimulates metabolic processes in the central nervous system... Introduce intravenously drip slowly at a dose of 10 ml diluted in 200 ml of 5% glucose or saline twice a day for 10 days.

After 4-24 hours of a patient with TIA staying in the neuroreanimation unit, subject to clear consciousness, absence (or minimal) neurological symptoms, absence of severe somatic pathology, stable respiratory parameters and central hemodynamics, the patient can be transferred to the early neurorehabilitation unit.

Other treatments

Surgery

The decision to perform surgical interventions in the acute period of TIA (the first 24 hours) should be made individually in each case as a result of a discussion with the participation of neurologists, anesthesiologists, resuscitators and surgeons (neurosurgeon and (or) vascular surgeon).

If there is a clinical TIA or minor stroke and the presence of critical stenosis / acute occlusion of the great arteries within 24 hours, an attempt at thrombendarterectomy is recommended.

In other cases, the decision to carry out neuroangiosurgical intervention is made routinely after the necessary examinations and consultations of specialists.

Indications for vascular reconstructive surgery or endovascular interventions are similar to those for ischemic stroke.

Preventive actions

Primary prevention TIA is at the same time the primary prevention of ischemic stroke, due to the common etiology and pathogenetic mechanisms, and is aimed at eliminating risk factors. Risk factors - various clinical, biochemical, behavioral and other characteristics inherent in to an individual(individual populations), as well as external influences, the presence of which indicates an increased likelihood of developing a certain disease.

Risk factors for TIA:

1. Corrected:
- arterial hypertension
- smoking
- heart pathology
- pathology of the main arteries of the head
- lipid metabolism disorders
- diabetes

Hemostatic disorders
- alcohol and drug abuse
- taking oral contraceptives
- migraine

2. Uncorrectable:
- floor
- age
- ethnicity
- heredity

The main directions of primary prevention of TIA and ischemic stroke
Modification of behavioral risk factors (smoking cessation, alcohol abuse, intensification of physical activity (Class III, level B), normalization of body weight (Class III, level B), restriction of salt intake (Class III, level B).

Smoking cigarettes increases the risk of stroke by almost 40% in men and 60% in women. Smoking cessation is accompanied by a gradual significant reduction in the risk of stroke, and after 5 years of abstinence from smoking, the risk of stroke in a former smoker is not much different from the risk of stroke in a never-smoker (Class III, Level B).

Women with risk factors for stroke (arterial hypertension, dyslipidemia, migraine, TIA) are not recommended to use oral contraceptives with a high content of estrogen; it is advisable to use contraceptives with a low content of estrogen or switch to other methods of preventing pregnancy. Alcohol abuse (regular consumption of more than 70 g of pure ethanol per day, alcoholic binges) increases the risk of stroke; cessation of alcohol abuse gradually reduces this risk (Class III, Level B).

Moderate alcohol consumption (no more than 20-30 g of pure ethanol per day) is discussed as a means of preventing atherosclerosis and reducing the risk of ischemic stroke. The use of many drugs (heroin, cocaine, etc.) also increases the risk of stroke, and stopping them gradually reduces the risk.

Diabetes mellitus treatment

Active identification and adequate treatment of hypertensive patients. Continuous adequate antihypertensive therapy, carried out for several years, reduces the risk of stroke in patients with hypertension by 2 times (Class IV, GCP). As part of primary prevention, it is recommended to achieve a target blood pressure level of less than 140/90 mm Hg, calcium antagonists have the maximum advantage.

In sick arterial hypertension and diabetes mellitus, it is recommended to achieve and maintain an ideal body weight, which in most cases requires a decrease in the total calorie content of food.

Reducing excess body weight by only 5-10 kg can lead to a significant reduction in high blood pressure. In addition to diet, regular physical activity (sports, walking) is important to reduce body weight, the intensity of which is individual and should be agreed with the doctor.

The use of antithrombotic drugs in patients with atrial fibrillation reduces the risk of cardioembolic stroke. The use of warfarin reduces the risk by 68%, aspirin by 21%. The choice of antithrombotic agent is determined by the patient's age and the presence of other risk factors for stroke. For patients in moderate and high risk groups, it is preferable to prescribe warfarin with a mandatory achievement of the target INR level of 2.5.

The use of aspirin in patients with coronary artery disease, ischemia of the lower extremities. Along with aspirin, the first line is clopidogrel (75 mg per day). It is usually used for aspirin intolerance. Clopidogrel is also advantageous in cases of multivessel disease.

Correction of lipid metabolism disorders. LDL has the main atherogenic potential, especially if they are modified under the influence of glycans (in diabetes mellitus) or peroxidation. HDL plays a key role in the transport of lipids, in the removal of their "excess" and have antiatherogenic properties. high density lipoprotein levels less than 0.9 mmol / l), a stricter diet is recommended (reducing fat intake to 20% of the total calorie intake and cholesterol to less than 150 mg per day). For atherosclerotic lesions of the carotid and vertebral arteries, a very low fat diet (reducing cholesterol intake to 5 mg per day) can be used to prevent the progression of atherosclerosis. If within 6 months of the diet it is not possible to significantly reduce hyperlipidemia, then antihyperlipidemic drugs (lovastatin, simvastatin, pravastatin, etc.) are recommended in the absence of contraindications to their use (Class I, level A).

The use of statins in patients with coronary artery disease reduces the risk of stroke by 30%. When stenosis of the internal carotid artery is detected, surgical treatment is discussed - carotid endarterectomy. Currently, the effectiveness of this operation has been proven in severe (narrowing 70-99% of the diameter) stenosis of the internal carotid artery in patients who have undergone TIA or minor stroke. When deciding on surgical treatment, one should take into account not only the degree of stenosis of the carotid artery, but also the prevalence of atherosclerotic lesions of the precerebral and cerebral arteries, the severity of the pathology of the coronary arteries, the presence of concomitant somatic diseases... Carotid endarterectomy is recommended in a specialized clinic in which the complication rate during surgery does not exceed 3-5% (Class I, Level A).

Secondary prevention of TIA
In the conditions of the department of early neurorehabilitation, according to the results of examinations and consultations, measures for individual prevention of stroke are started. Patient stratification by risk of recurrent stroke allows different treatment regimens to be selected.

Re-stroke risk assessment scale

Risk factors	Points
Age less than 65 years	0
Age 65-75 years old	1
Over 75 years old	2
Arterial hypertension	1
Diabetes	1
Myocardial infarction	1
Other cardiovascular diseases (IHD, heart failure, ventricular arrhythmia), excluding myocardial infarction and atrial fibrillation)	1
Peripheral artery disease	1
Smoking	1
Transient ischemic attack or stroke in addition to the event being assessed	1
Points total

Scores from 0 to 2 - low risk (less than 4% per year).
Scores from 3 to 9 - high risk (more than 4% per year).

Antihypertensive therapy

Calculation of target values ​​of blood pressure
Most patients have less than 140/90 mm Hg (Class I, Level A).

With concomitant diabetes mellitus and kidney disease less than 130/80 mm Hg (Class IV, level C).

In the presence of hemodynamically significant stenoses, it is impossible to reduce blood pressure too much!

The drugs of choice are ACE inhibitors, angiotensin receptor blockers (since they have angio-, organoprotective, antiatherogenic effects, and reduce the risk of stroke in normotonic patients). In addition, diuretics and small doses of B-blockers can be used.

Lipid-lowering therapy

Necessarily prescribed for high risk of stroke (generalized atherosclerosis) when there is concomitant coronary artery disease or atherosclerosis of the peripheral arteries or diabetes mellitus, as well as severe stenosis of the brachiocephalic arteries (critical and subcritical stenosis) without ischemic events (Class I, level A).

If there is concomitant coronary artery disease or atherosclerosis of the peripheral arteries, the target LDL cholesterol level is less than 2.6 mmol / l.

If there are multiple risk factors (very high risk of stroke), the target LDL cholesterol level is less than 1.8 mmol / L.

It is necessary to start therapy within the first 6 months, once every 3 months, monitor the lipid profile, liver function tests and CPK. The basis for the abolition of statins: an increase in CPK by more than 10 times and liver function tests by more than 5 times.

Antithrombotic therapy(Class I, Level A).

Small doses (25 mg) of aspirin + 200 mg of slow-release dipyridamole in capsules 2 times a day (agrenox).

Clopidogrel 75 mg / day (Plavix, Egithromb) is the first choice drug with a high risk of recurrent stroke.

With intolerance to aspirin or with concomitant myocardial infarction, angina pectoris or obliterating atherosclerosis of the vessels of the lower extremities, diabetes mellitus, after carotid endarterectomy, coronary artery bypass grafting, balloon angioplasty and stenting.

Aspirin -75-325 mg (cardiomagnyl, thrombosis, cardio ASK, aspirin cardio, etc.)

Clopidogrel 75 mg + Aspirin 50 mg. (This combination is not recommended for recent stroke as it doubles the risk of bleeding) (Class I, Level A), it is only used for concomitant acute coronary syndrome ( unstable angina, myocardial infarction without Q wave), recent stenting.

Duration of admission is at least 1 year, followed by switching to other antiplatelet agents.

Antiplatelet therapy in the form of small doses (50-100 mg) aspirin-containing monopreparations can be recommended 1-2 months after hemorrhagic stroke if there is concomitant significant vascular atherosclerosis and there is a high risk of ischemic events.

Anticoagulant therapy
Warfarin. It is used only for cardiogenic etiology of stroke (especially with non-valvular atrial fibrillation) for a long time (Class I,

Level A)., And in case of cardioembolic stroke against the background of acute myocardial infarction, at least 3 months. Also, anticoagulant therapy may be preferred in patients with aortic atheroma, fusiform aneurysm of the main artery, or neck artery dissection. The initial dose is 2.5 mg to the level of INR = 2-3 (once a week, monitor the INR, increase the dose by 1.25 mg at a time). After dose titration, control INR once a month or PTI (target level 50-60%).

Frequent falls

Low adherence to therapy,

Uncontrolled epilepsy

GI bleeding

Older age is not a contraindication for oral anticoagulant therapy (Class I, Level A). If it is impossible to prescribe warfarin, it is recommended to prescribe agrenox, in extreme cases, aspirin 100 mg.

With transient ischemic attacks and minor stroke, anticoagulant therapy is started immediately, and if more than 1 \ 3-1 \ 2 of the middle cerebral artery basin is affected, it should be started after 2-3 weeks.

Surgery

Carotid endarterectomy shown at:

Symptomatic stenosis of the carotid artery is more than 70%, in centers where the risk of perioperative complications is less than 6% (Class I, Level A).,

With symptomatic stenosis of the carotid artery 50-69% (more effective in men who have had hemispheric stroke), where the risk of perioperative complications is less than 3%,

Stenosis of the carotid artery is less than 50% in the presence of an atherosclerotic plaque with an uneven embologic surface.

Before, during and after carotid endarterectomy, antiplatelet agents are required!

Carotid angioplasty and stenting of the main arteries is indicated for:

With contraindications to carotid endarterectomy or stenosis in a surgically inaccessible area,

With restenosis after carotid endarterectomy.
After surgery, a combination of clopidogrel + aspirin for at least 1 year, followed by a switch to other antiplatelet agents (Class I, level A) ..

Further management
Patients who have undergone TIA are subject to dispensary observation at a neurologist at the polyclinic at the place of residence. At the outpatient stage, under the supervision of PHC specialists (neurologists, cardiologists, therapists, general practitioners, endocrinologists, vascular surgeons, etc.), the necessary examinations are carried out to identify the causes and pathogenetic mechanisms of TIA (if they were not performed at the previous stage), and the activities are continued. for individual stroke prevention, developed in the conditions of a stroke center.

Treatment efficacy indicators
In a patient who has undergone TIA, the criteria for the effectiveness of treatment are:
1. Complete stabilization of vital functions (respiration, central hemodynamics, oxygenation, water and electrolyte balance, carbohydrate metabolism).
2. Regression of neurological deficits
3. Normalization of laboratory parameters (complete blood count, urine analysis, blood biochemical parameters, coagulogram).
4. Basic correction of blood pressure with the achievement of target values.
5. Restoration of blood flow in a stenotic (occluded) vessel, confirmed by the results of angiographic studies (cerebral angiography, MSCTA, MRA) and ultrasound methods (USDG of extracranial vessels, TCDG).