What is a wbb of the brain. Consequences of onmc by ischemic type. Causes of difficulty in the outflow of blood from the brain

In general, stroke occurs due to an episode of ischemia (80-85% of patients), hemorrhage (15-20% of patients).

A number of risk factors for stroke are listed below:

• Advanced age
• Family history
• High blood pressure
• Cardiac ischemia
• Diabetes
• Smoking cigarettes
• Heart diseases
• Obesity
• Hypodynamia
• Alcoholism

The onset and duration of the symptoms of vertebral stroke depends, to a large extent, on the etiology. Patients with thrombosis of the basilar artery usually have an increase and decrease in a group of symptoms, as many as 50% of patients experience transient ischemic attacks (TIA) for several days to several weeks before the onset of occlusion.

In contrast, emboli are sudden, without a prodromal stage, with an acute and dramatic presentation.

Common Symptoms Associated with Vertebrobasilar Stroke

• Dizziness
• Nausea and vomiting
• Headache
• Decreased level of consciousness
• Abnormal oculomotor signs (eg, nystagmus, diplopia, pupil changes)
• Ipsilateral weakness of the muscles innervated by the cranial nerves: dysarthria, dysphagia, dysphonia, weakness of the muscles of the face and tongue.
• Loss of sensitivity in the face and scalp
• Ataxia
• Contralateral hemiparesis, tetraparesis
• Loss of pain and temperature sensitivity
• urinary incontinence
• blurring of visual fields
• neuropathic pain
• hyperhidrosis in the face and limbs

Features of the symptoms of stroke in VBD in the embolic variant

• rapid onset - from the appearance of the first symptoms to their maximum development no more than 5 minutes
• movement disorders: weakness, awkwardness of movements or paralysis of the limbs of any combination, up to tetraplegia;
• sensory disorders: loss of sensation OR paresthesia of the extremities in any combination or spreading to both halves of the face or mouth;
• homonymous hemianopsia, or cortical blindness;
• disorders of coordination of movements; imbalance, instability;
• systemic and non-systemic dizziness in combination with double vision, swallowing disorders and dysarthria.

Symptoms that can also be seen in patients

• Horner's syndrome
• nystagmus (especially vertical)
• rarely hearing impairment.

Dizziness, ataxia and visual disturbances form the characteristic

pathology triad indicating ischemia of the brain stem, cerebellum and occipital lobes of the brain.

Sometimes the typical syndrome of vascular lesion in VBD can be combined with impairment of higher cerebral functions, for example, with aphasia, agnosia, acute disorientation.

Alternating syndromes with clearly localized foci within the VBD, for example, Weber, Miyard-Gubler, Wallenberg-Zakharchenko syndromes, rarely occur in their pure form.

A special form of acute cerebrovascular accident

in VBB there is an “archer's” stroke associated with mechanical compression of the vertebral artery at the C1-C2 level during extreme turn of the head.

At present, the mechanism of such a stroke is explained by the tension of the artery at the C1-C2 level when turning the head, accompanied by a tear in the intima of the vessel, especially in patients with pathological changes in the arteries. In the case of compression of the dominant PA, there is no sufficient compensation of blood flow in the VBP. due to hypoplasia of the opposite vertebral artery or its stenosis, as well as the failure of the posterior connecting arteries, is a factor contributing to the development of an "archer's" stroke. One of the predisposing factors of this pathology is the presence in patients of the Kimmerli anomaly - an additional bone half-ring arch, which can compress the vertebral arteries above the arch of the first cervical vertebra.

ACVE in VBB is an urgent condition requiring hospitalization in a specialized vascular neurological department, treatment of ischemic stroke in VBB occurs in a hospital setting in a number of cases of the neuroreanimation department.

Rehabilitation after a stroke in the vertebrobasilar basin

Stroke rehabilitation plays a critical role in restoring brain function. Doctors and nurses play a critical role in rehabilitation.

nurses are often the first to offer initiation of therapy services because they have the widest possible involvement with the patient. Prior to discussing specific disciplines of therapy, addressing nursing issues in the care of patients with vertebrobasilar stroke.

may vary depending on the symptoms and the severity of the brain damage. Initial interventions include caring for the patient, maintaining the integrity of the skin, regulating bowel and bladder function, maintaining nutrition, and keeping the patient safe from injury.

Other important issues, in consultation with the attending physician, include the restoration of self-care swallowing function. In some patients, the severity of the neurological deficit makes it impossible to stand up, however, patients should be activated, including their active participation in physical rehabilitation (physiotherapy exercises) and occupational therapy.

Positioning in bed and in the chair ensures patient comfort and prevents pressure sores complications. If the upper limb is flaccid or paretic, correct posture is critical to prevent shoulder subluxation and pain.

Nursing staff should train family members in caring for a stroke survivor. The patient's family members may not be familiar with stroke and its consequences. Education aims to educate the patient and family members about the importance of continuing rehabilitation and prevention of recurrence, about appropriate precautions, and continuing therapy after being discharged home.

Some patients have fluctuating signs and symptoms that are often related to position. Because of this possibility, precautions are necessary with measures that can be taken until the symptoms have stabilized.

The physical therapist is responsible for adjusting gross motor skills such as walking, maintaining body balance, the ability to move and change posture within a bed or wheelchair.

The exercise therapy physician also develops an exercise program and instructs the patient in order to generally strengthen and increase movement. Education of the patient's family members and the use of lower limb prosthetics may be necessary to ensure functional mobility. Also shown is vestibular gymnastics.

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Features of ischemic stroke in the vertebrobasilar basin

Violations of the blood supply to the brain (stroke) remain the most urgent problem in the world medical practice of neuropathologists.

According to medical statistics, up to 80% of all cases of diagnosed strokes had an ischemic nature of their occurrence.

Of these, up to 30% falls on the localization of a negative focus in the vertebrobasilar vascular basin, but

the probability of death is much higher than with other localizations of the lesion.

Experts have also reliably established that up to 70% of the formation of a cerebral catastrophe was preceded by transient ischemic attacks. In the absence of adequate treatment, subsequently, an ischemic stroke with severe consequences was necessarily formed.

Characteristics of the vertebrobasilar system

It is this vascular structure that accounts for up to 30% of the total intracranial blood flow.

This is possible due to the peculiarities of its structure:

• paramedial arteries branching directly from the main arterial trunks;
• the bending arteries designed to supply blood to the lateral areas of the brain;
• the largest arteries located in the extracranial and intracranial cerebral regions.

It is this abundance of vessels and arteries with different lumen diameters, with a varied structure and anastomotic potential that determines the widest clinic of discirculation.

Along with the formation of clinical manifestations typical for transient ischemic attacks, a specialist can also detect atypical forms of ischemic stroke, which significantly complicates the diagnosis.

Reasons for development

Experts today are talking about the following most significant reasons for the formation of ischemic stroke:

1. Atherosclerotic lesion of intracranial vessels;
2. Features of the structure of the vascular bed of a congenital nature;
3. Formation of microangiopathies against the background of hypertensive pathology, diabetes and other diseases;
4. Severe compression of the arteries by pathologically altered cervical structures of the spine;
5. Extravasal compression, formed as a result of hypertrophied scalene muscle or hyperplastic transverse processes of the cervical segments of the spine;
6. Trauma;
7. Lesions of the vascular wall by inflammatory phenomena - various arteritis;
8. Changes in rheological parameters of blood.

It is customary to distinguish between the following types of stroke in the vertebro-basilar region:

• in the basilar artery itself;
• in the region of the posterior cerebral artery;
• right-sided variant of ischemic lesion;
• left-sided variant of cerebral catastrophe.

For the reason identified, the violation can be:

Symptoms

Most victims, upon careful questioning, can recall that the state of stroke was preceded by symptoms of transient ischemic attacks: previously uncharacteristic dizziness, unsteadiness when walking, pain in the head of a local nature, memory impairment.

If a person does not contact a specialist on time or in the absence of treatment, the symptoms of a stroke increase many times over. Their severity is largely determined by the localization of the negative focus, the extent of damage to the brain structures, the initial state of human health, and the adequacy of collateral blood supply.

1. Illusory perception by the patient of his own and external movements due to severe dizziness;
2. Inability to maintain an upright position - static ataxia;
3. Various severity of pain in the occipital region of the head, sometimes with irradiation to the region of the neck, eye sockets;
4. Some visual disorders;
5. The possibility of the formation of drop attacks - a person suddenly feels the maximum severity of weakness in the lower extremities and falls;
6. Significant memory impairment.

In the presence of one symptom or their combination, it is recommended to immediately consult a neurologist and the necessary list of diagnostic procedures. Ignoring the previous transient ischemic attack of a cerebral accident can lead to very serious complications in the future.

Diagnostics

In addition to carefully collecting anamnesis and conducting a diagnostic study, the specialist makes a diagnosis. Mandatory diagnostic procedures:

• dopplerography;
• duplex scanning;
• angiography;
• CT or MRI of the brain;
• contrast panangography;
• radiography;
• a variety of blood tests.

Only the entire completeness of the data allows for an adequate differential diagnosis of stroke in the vertebrobasilar basin.

Treatment

Stroke requires mandatory transportation of the victim to the conditions of a neurological hospital for complex treatment

1. Thrombolytic therapy - modern drugs are injected into the bloodstream, contributing to the fastest dissolution of the embolus that blocked the lumen of the intracranial vessel. The decision-making lies with the specialist, who takes into account all the variety of indications and contraindications to the procedure.
2. To lower the parameters of blood pressure in the case of a hypertensive crisis, a person is administered antihypertensive medications.
3. Neuroprotective agents are called upon to maximally improve blood circulation in the brain and accelerate their recovery.
4. Antiarrhythmic drugs are prescribed to restore an adequate heart rate.

In the absence of positive dynamics from the ongoing conservative therapy of stroke, the neurosurgeon decides to conduct a surgical intervention - to remove the thrombotic mass directly from the damaged vessel site.

Prophylaxis

As you know, the disease is easier to prevent than to deal with the treatment of its complications later. That is why the main efforts of specialists are aimed at promoting preventive measures to prevent strokes:

• correction of the diet;
• daily intake of the recommended antihypertensive and antiarrhythmic drugs, anticoagulants;
• constant monitoring of pressure parameters;
• taking modern statins;
• an annual full range of diagnostic procedures for persons at risk for the formation of a stroke;
• in the event of a blockage of an intracranial vessel with atherosclerotic or thrombotic masses - the appropriate surgical tactics of treatment.

The prognosis of stroke in the vertebrobasilar basin in the case of adequate therapeutic measures is very favorable.

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Ischemic brain stroke

Ischemic cerebral stroke is an acute disturbance of the blood supply to the brain resulting from the interruption or obstruction of blood supply. The disease is accompanied by damage to the brain tissue, disruption of its work. Acute circulatory disorders of the brain by ischemic type account for 80% of all strokes.

Stroke poses a serious threat to able-bodied and elderly people, leads to prolonged hospitalization, severe disability, high financial costs of the state, deterioration in the quality of life of affected people and their family members.

Stroke is a disease of the century

Stroke affects about 6 million people in the world every year, about 4 million of them die, half of them remain disabled. The number of patients in Russia is at least 450 thousand people per year. Worst of all, the incidence is increasing and the age of sick people is getting younger.

There are 5 types of ischemic stroke, depending on the mechanism of its origin, that is, pathogenesis:

• Thrombotic. The cause (or etiology) is atherosclerosis of the large and medium arteries of the brain. Pathogenesis: an atherosclerotic plaque narrows the lumen of the vessel, then, after exposure to certain factors, a complication of atherosclerosis occurs: the plaque ulcerates, platelets begin to settle on it, forming a thrombus, which blocks the inner space of the vessel. The pathogenesis of thrombotic stroke explains a slow, gradual increase in neurological symptoms, sometimes the disease can develop within 2-3 hours in several acute episodes.

Thrombotic stroke usually develops against the background of atherosclerosis

• Embolic. Etiology - blockage of a vessel by a thrombus coming from internal organs. Pathogenesis: a thrombus forms in other organs, after which it breaks off and enters the cerebral vessel with the blood flow. Therefore, the course of ischemia is acute, rapid, the lesion focus is impressive in size. The most common source of blood clots is the heart, cardioembolic stroke develops with myocardial infarction, cardiac arrhythmias, artificial valves, endocarditis; less often, atherosclerotic plaques in large major vessels are the source of blood clots.

A common cause of cerebral obstruction is a cardiogenic embolus.

• Hemodynamic. At the heart of the pathogenesis is a violation of the movement of blood through the vessels. Etiology - low blood pressure, this phenomenon can be observed with a slow heart rate, ischemia of the heart muscle, during sleep, prolonged standing in an upright position. The onset of symptoms can be rapid or slow, and the disease occurs both in calmness and during wakefulness.
• Lacunar (the size of the focus does not exceed 1.5 cm). Etiology - lesion of small arteries in hypertension, diabetes mellitus. The pathogenesis is simple - after a cerebral infarction, small cavities-lacunae appear in its depths, a thickening of the vascular wall occurs or the lumen of an artery is blocked due to compression. This explains the peculiarity of the course - only focal symptoms develop, there are no signs of general cerebral disorders. Lacunar stroke is more often recorded in the cerebellum, the white matter of the brain.

Lacunar stroke, as a rule, is a consequence of arterial hypertension

• Rheological. Etiology is a blood clotting disorder that is not associated with any diseases of the blood and vascular system. Pathogenesis - the blood becomes thick and viscous, this condition prevents it from entering the smallest vessels of the brain. During the course of the disease, neurological disorders come to the fore, as well as problems associated with blood clotting disorders.

The most common causes of ischemic stroke are thrombosis and embolism.

Types of stroke according to the rate of increase in neurological symptoms

Depending on the rate of formation and the duration of the persistence of symptoms, 4 types are distinguished:

• Microstroke or transient ischemic attack, transient cerebral ischemia. The disease is characterized by mild severity, all symptoms disappear without a trace within 1 day.
• Small stroke. All symptoms persist for more than 24 hours but less than 21 days.
• Progressive ischemic stroke. Differs in the gradual development of the main neurological symptoms - over several hours or days, sometimes up to a week. After that, the health of the sick person is either gradually restored, or neurological abnormalities persist.
• Completed stroke. Symptoms persist for more than 3 weeks. A cerebral infarction usually develops, after which severe physical and mental health problems sometimes persist. With extensive stroke, the prognosis is poor.

Clinic

• Movement disorders of varying severity. Disorders of the cerebellum: lack of coordination, decreased muscle tone.
• Violation of the pronunciation of one's own and the perception of someone else's speech.
• Visual impairment.
• Sensitive disorders.
• Dizziness, headache.
• Violation of the processes of memorization, perception, cognition. The severity depends on the size of the lesion.

The clinic depends on the cause of the disease, the size and location of the lesion. It is worth distinguishing between lacunar infarction, lesions of the carotid, anterior, middle, posterior and villous cerebral arteries, special attention is paid to ischemia of the vertebro-basilar basin.

Ischemic stroke of the vertebrobasilar basin (VBB)

The vertebral arteries merge at the base of the brain into the basilar artery

Two vertebral arteries, merging, form one basilar, that is, the main one. With vascular insufficiency of these arteries, two important parts of the brain suffer at once - the trunk and the cerebellum. The cerebellum is responsible for the coordination, balance and tone of the extensor muscles. The dysfunction of the cerebellum can be called "cerebellar syndrome". The brain stem contains 12 cranial nerve nuclei, which are responsible for swallowing, eye movement, chewing, and balance. After a stroke in the brain stem, these functions can be impaired to varying degrees. In ischemic strokes, focal dysfunctions of the cerebellum in combination with symptoms of brain stem damage predominate.

Symptoms of acute vascular insufficiency of the vertebral arteries: as a result of damage to the cerebellum, an imbalance and coordination of movements occurs, with damage to the cerebellum, muscle tone decreases, as a result of damage to the cerebellum, a violation of the coordination of muscle movements is observed. If the trunk is damaged, oculomotor disorders, facial nerve palsy, paresis of the extremities (alternating syndrome), chaotic movement of the eyeballs, combined with nausea, vomiting and dizziness, appear, a person has poor hearing. The trunk also regulates the reflexes of chewing and swallowing.

With simultaneous damage to the basilar or both vertebral arteries, the course of the disease worsens, there is paralysis of both arms and legs, coma.

The course of TIA with damage to the intracranial part of the vertebral artery and the posterior cerebellar artery is not severe, manifested by nystagmus, dizziness with vomiting and nausea, impaired facial sensitivity, changes in the perception of pain and temperature.

Diagnostics

Treatment tactics are determined by the type of stroke

To select a treatment regimen, it is very important to establish the form of an acute vascular disorder, because medical tactics for hemorrhages and ischemia have serious differences.

Diagnosis of cerebrovascular accident by ischemic type begins with a medical examination, the main symptoms of the disease and the existing risk factors are taken into account. The doctor listens to the heart, lungs, measures the pressure on both hands and compares the indicators. To clarify neurological disorders, to determine the severity, it is imperative to undergo a neurological examination.

For an urgent diagnosis and clarification of the cause of the disease, an ultrasound examination of the vascular bed of the brain, an electroencephalogram is carried out, angiography allows you to more accurately see changes in the vascular system of the brain - contrast is injected into the vessels and an X-ray is taken, often it is necessary to do MRI and CT of the brain. In addition, the diagnosis of ischemic stroke should include a finger and vein blood test, a coagulation test, and a general urinalysis.

Prophylaxis

Prevention of ischemic cerebral circulation disorders is aimed at eliminating risk factors and treating concomitant diseases. Primary prevention is aimed at preventing the first seizure in life, secondary prevention of recurrent stroke.

The International Health Organization has established a list of preventive measures:

• Refusal from cigarettes. After quitting active and passive smoking, the risk of stroke is reduced significantly even in older people who have smoked their entire adult life.
• Avoiding alcohol. It is not recommended to drink alcohol even in moderation, because each person has his own individual concept of moderation. It is completely necessary to give up alcohol for people who have already suffered an acute disturbance of cerebral blood supply in their lives.
• Physical activity. Regular physical activity at least 4 times a week will have a positive effect on weight, the state of the cardiovascular system, and the fatty composition of the sick person's blood.
• Diet. The diet consists in moderate consumption of fats, it is recommended to replace animal fats with vegetable fats, eat fewer simple carbohydrates, eat more fiber, pectins, vegetables, fruits and fish.
• Reducing excess body weight. Weight loss should be achieved by reducing the calorie content of food, establishing 5-6 meals a day, increasing physical activity.
• Normalization of blood pressure is the most effective prevention of ischemic stroke. With a healthy blood pressure, the risk of developing a primary and repeated stroke is reduced, and the work of the heart is normalized.
• It is necessary to adjust the blood sugar level in diabetes mellitus.
• It is necessary to restore the work of the heart.
• Women are advised to stop using contraceptives that contain large amounts of estrogen.
• Drug prophylaxis. Secondary prevention of ischemic stroke must necessarily contain antiplatelet and anticoagulant drugs - Aspirin, Clopidogrel, Dipiradamol, Warfarin.

Secondary prevention medication

Observing the listed preventive measures for a long time, you can reduce the risk of developing any diseases of the cardiovascular system.

75% of strokes are primary, which means that by observing preventive measures, it is possible to reduce the overall incidence of stroke.

Forecast

The chances of a favorable outcome for each person are different and are determined by the size and location of the lesion. Patients die after the development of cerebral edema, displacement of the internal structures of the brain. The chances of surviving are 75–85% of patients by the end of the first year, 50% after 5 years, and only 25% after 10 years. Mortality is higher in thrombotic and cardioembolic strokes, and very low in lacunar type. Low survival rate in elderly people, hypertensive patients, smokers and drinkers of alcohol, people after a heart attack, with arrhythmias. The chances of a good recovery decrease rapidly if neurologic symptoms persist for more than 30 days.

In 70% of the surviving people, disability persists for a month, after which the person returns to his usual life, 15-30% of patients after a stroke remain stable disabled, the same number of people have every chance of developing a second stroke.

Patients who have had a microstroke or a minor stroke have a chance to leave for work early. People with extensive strokes may or may not return to their previous jobs after a long recovery period. Some of them can return to their original place, but for an easier job.

With timely assistance, properly selected treatment and rehabilitation, it is possible to improve the patient's quality of life and restore the ability to work.

Stroke is not a hereditary, chromosomal and inevitable disease. For the most part, a stroke is the result of chronic human laziness, overeating, smoking, alcoholism and irresponsibility to doctor's prescriptions. Enjoy life - run in the morning, go to the gym, eat natural light food, devote more time to your children and grandchildren, spend the holidays with delicious non-alcoholic cocktails and you will not have to learn about the causes and statistics of stroke.

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Stroke in the vertebro-basilar basin

Vertebrobasilar insufficiency: clinical picture and diagnosis

Acute (ACVA) and chronic disorders of cerebral circulation remain one of the urgent problems of modern medicine. According to various authors, up to 20% of stroke patients become deeply disabled, up to 60% have a pronounced disability and need long-term and costly rehabilitation, and only less than 25% of patients return to their usual work activities.

Among the survivors, 40-50% have a second stroke within the next 5 years.

It has been established that up to 80% of all strokes are ischemic in nature. And although only 30% of strokes occur in the vertebrobasilar basin. mortality from them is 3 times higher than from strokes in the carotid pool. More than 70% of all transient ischemic attacks occur in the vertebrobasilar basin. Every third patient with a transient ischemic attack subsequently develops an ischemic stroke.

The prevalence of pathology of the brachiocephalic arteries is 41.4 cases per person. Of these, 30-38% is the pathology of the subclavian and vertebral arteries.

Wide spread, constant increase in morbidity, high mortality in patients of working age, a high percentage of disability among patients put the problem of cerebrovascular ischemia in the socially significant group.

The vertebrobasilar system accounts for about 30% of all cerebral blood flow. It supplies blood to various formations: the posterior parts of the cerebral hemispheres (occipital, parietal lobes and mediobasal parts of the temporal lobe), the optic tubercle, most of the hypothalamic region, the legs of the brain with a quadruple, the pons varoli, the medulla oblongata, the reticular formation, the cervical spinal cord.

From the anatomical and functional point of view, 4 segments are divided along the subclavian artery: V 1 - from the subclavian artery to the transverse segment C VI. V 2 - from vertebra C VI to vertebra C II. V 3 - from the vertebra C II to the dura mater in the area of ​​the lateral occipital foramen, V 4 - to the fusion of both vertebral arteries into the main one (see Fig.).

Vertebrobasilar insufficiency is a condition that develops due to insufficient blood supply to the region of the brain fed by the vertebral and basilar arteries and causes the appearance of temporary and permanent symptoms. In ICD-10, vertebrobasilar insufficiency is classified as "Vertebrobasilar arterial system syndrome" (section "Vascular diseases of the nervous system"); and is also classified in the section "Cerebrovascular diseases". In the domestic classification, vertebrobasilar insufficiency is considered within the framework of discirculatory encephalopathy (cerebrovascular pathology, the morphological substrate of which is multiple focal and (or) diffuse brain lesions), “vertebral artery syndrome”. Other synonyms are "irritation syndrome of the sympathetic plexus of the subclavian artery", "posterior cervical sympathetic syndrome", "Barre-Lieu syndrome". In foreign literature, along with the term "vertebrobasilar insufficiency", the term "circulatory failure in the posterior cranial fossa" (posterior circulation ischemia) is gaining popularity.

Various etiological factors lead to the development of vertebrobasilar insufficiency. They can be conditionally divided into 2 groups: vascular and extravascular.

Table. Etiological factors of vertebrobasilar insufficiency and frequency of their occurrence

Stroke with lesion localization in the vertebrobasilar basin

As acute, in its form, violations of the usefulness of cerebral circulation, so, in fact, its chronic forms today remain one of the most pressing, burning problems of world modern medicine. According to the estimates of various authors, about 18, 20% of all patients who once survived a stroke turn out to be deeply disabled, about 55, 60% of such patients retain pronounced disabilities or need constant exercise for a rather long and often very costly rehabilitation.

At the same time, only about 20 or 25% of all patients who have undergone a state of stroke pathology, in one form or another (ischemic or hemorrhagic cerebral stroke in history), are able to return to their usual work activity after discharge from the hospital. These statistics are more clearly shown in the diagram below:

At the same time, doctors found that almost 80% of all emerging stroke pathologies are ischemic in nature or the nature of their occurrence. And, although no more than about 30% of stroke conditions are localized in the so-called vertebrobasilar basin, the development of a fatal outcome after such events is almost three times higher than from the more common stroke pathologists with the localization of the focus of brain tissue damage in the carotid basin.

In addition, more than 70% of all emerging transient ischemic attacks (or other transient disorders of cerebral blood flow) preceding the state of full-fledged stroke damage occur precisely in the vertebrobasilar basin mentioned above. At the same time, every third such patient who has undergone a transient ischemic attack with a similar localization of the problem subsequently develops a very difficult ischemic stroke.

What is our vertebrobasilar system?

It should be understood that the share of the so-called physicians, the vertebrobasilar system usually accounts for about 30% of the total cerebral blood flow. It is the vertebrobasilar system that is responsible for the blood supply of a wide variety of cerebral organ formations, such as:

• The posterior parts of the cerebral hemispheres (these are the occipital and parietal lobes and the so-called medio-basal parts of the temporal lobes).
• The visual hillock.
• Most of the vital hypothalamic area.
• The so-called legs of the brain with its quadruple.
• Oblong part of the brain.
• Pons.
• Or the cervical region of our spinal cord.

In addition, in the system of the described vertebrobasilar basin, physicians distinguish three groups of different arteries. This is about:

• The smallest arteries, or about the so-called paramedial arteries, extending directly from the main trunks of both the vertebral and main arteries, from the anterior spinal artery. This also includes deeply perforating arteries that originate from the larger posterior cerebral artery.
• The short type of circumflex (or circular) arteries, which are designed to wash the lateral areas related to the brain stem with arterial blood, as well as the long type of circumflex arteries.
• The largest or largest arteries (which include the vertebral and main arteries) located in the extracranial and intracranial cerebral regions.

Actually, the presence in the standard vertebrobasilar basin of such a number of arteries with different calibers, with different structures, with different anastomotic potential and with different zones of blood supply, usually determines the localization of a particular focus of stroke, its specific manifestations, as well as the clinical course of the pathology.

Nevertheless, the possible individual peculiarities of the location of such arteries, the diversity in the pathogenetic mechanisms, quite often, predetermine the differences in the neurological clinic in the development of such pathologies as acute ischemic stroke with localization in the vertebrobasilar zone.

And this means that along with the development of neurological syndromes typical for stroke pathology, physicians can often note not only the standard clinical picture during the development of pathologists in the vertebrobasilar zone, which is described by clinical guidelines, but rather an atypical course of such stroke pathology. This, in turn, often significantly complicates the diagnosis, determination of the nature of a specific stroke pathology and the subsequent choice of adequate therapy for it.

Why does this type of brainstroke occur?

The state of primary vertebrobasilar insufficiency, often preceding the same-name stroke pathology, has the ability to develop due to one degree or another of the severity of insufficient blood supply to the regions of brain tissue fed by the vertebrates or the main arteries. In other words, a wide variety of etiological factors can lead to the development of such a pathology, which are conventionally divided into two groups:

• This is a group of vascular factors.
• And a group of extravascular factors.

It is customary to refer to the first group of factors that often become the reasons for the development of such a stroke pathology: atherosclerosis, stenosis or occlusion of the subclavian arteries, their developmental anomalies (say, pathological tortuosity, the same anomalies of the entrance to the bone cocoa, numerous hypoplasias, etc.). pathologies of an extravascular nature are usually referred to: embolism of different etiology in the vertebrobasilar zone or extravasal compression of the subclavian artery itself.

In rare cases, fibromuscular dysplasia, damage to the subclavian artery after neck injuries or after non-professional manipulations during manual therapy can lead to a brainstroke of this type.

Symptoms

Most authors write about the polysymptomatic manifestations of stroke pathology with a similar localization of the lesion of brain tissue, the severity or severity of which, as a rule, is determined by the specific location and extent of arterial lesions, the general position of hemodynamics, the real level of blood pressure, the state of the so-called collateral circulation and etc. The disease can manifest itself as persistent focal neurological disorders and some general cerebral symptoms. These symptoms include:

International Neurological Journal 3 (3) 2005

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Heart attacks in the vertebrobasilar basin: clinical picture and diagnosis

Authors: S. M. Vinichuk, I. S. Vinichuk, National Medical University, Kiev; T.A. Yalynska, Clinical Hospital "Feofania", Kiev

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In this work, a clinical neuroimaging analysis was carried out in 79 patients with a clinical picture of ischemic infarction in the vertebrobasilar basin (VBB). The features of the neurological clinic of lacunar and non-acunar posterior circulatory infarctions are described. To verify them, we used the method of magnetic resonance imaging (MRI). The technique of diffusion-weighted magnetic resonance imaging (DW MRI) turned out to be more informative for the diagnosis of acute lacunar and nonacunar infarctions in the brainstem.

Occlusive lesion of the arteries in the vertebrobasilar basin (VBB) leads to the development of posterior circulation infarcts with localization in various parts of the brain stem, thalamus, occipital lobes and cerebellum. The frequency of their development takes second place (20%) after a heart attack in the basin of the middle cerebral artery (MCA) (Kamchatov P.R. 2004) and is 10-14% in the structure of all ischemic strokes (Vinichuk S.M. 1999; Evtushenko S. K. 2004; Toi H. et al, 2003). According to other authors, in Europeans, the pathology of intracranial arteries in the VBD occurs more often than in the carotid basin (Vorlow Ch.P. et al. 1998).

The posterior vertebrobasilar system is evolutionarily more ancient than the anterior - carotid. It develops completely separately from the carotid system and is formed by arteries that have different structural and functional characteristics: vertebral and main arteries and their branches.

In the system of the vertebrobasilar basin, there are three groups of arteries (Vorlow Ch.P. et al. 1998) (Fig. 1):

Small arteries, the so-called paramedian, extending directly from the trunks of the vertebral and main arteries, from the anterior spinal arteries, as well as deep perforating arteries originating from the posterior cerebral artery (PCA);

Short enveloping (or circular) arteries supplying blood, respectively, to the lateral areas of the brainstem, the tegmental area, as well as long enveloping arteries - the posterior inferior cerebellar artery (PICA), the anterior inferior cerebellar artery (PNMA), the superior cerebellar artery (VMA), PCA with its branches and anterior villous artery;

Large or large arteries (vertebral and main) in the extra- and intracranial sections.

The presence in the posterior vertebrobasilar basin of arteries of different caliber with differences in their structure, anastomotic potential and with different zones of blood supply of small, deep perforating arteries, short and long circumflex arteries, as well as large arteries in most cases determine the localization of the lesion, its size and clinical course of posterior circulatory infarction. At the same time, individual differences in the location of arteries, a variety of pathogenetic mechanisms very often determine the individual characteristics of the neurological clinic in acute ischemic strokes in VBD. Therefore, along with the presence of typical neurological syndromes, doctors often note not the clinical picture of vertebrobasilar stroke, which is described in clinical guidelines, but its atypical course, which makes it difficult to determine the nature of the stroke and the choice of adequate therapy. In such a clinical situation, only brain imaging techniques can help.

Materials and research methods

A comprehensive clinical and neuroimaging examination was carried out in 79 patients (48 men and 31 women) aged 37 to 89 years (on average 65.2 ± 1.24 years). The study included all those admitted with a clinical picture of acute ischemic stroke to the VBB. Patients were admitted within 6-72 hours after the onset of the first symptoms of the disease. The main cause of ischemic cerebral circulation disorders (CMC) was arterial hypertension in combination with vascular atherosclerosis (74.7%), in another 22.8% of the examined it was combined with diabetes mellitus; in 25.3% of patients, the main etiological factor of the disease was atherosclerosis. Patient information was recorded in standard protocols, which included demographic indicators, risk factors, clinical symptoms, laboratory and neuroimaging studies, outcome, etc.

The degree of impairment of neurological functions was assessed during hospitalization of patients, during treatment, and at the end of therapy using the NIHSS scale (National Institutes of Health Stroke Scale, USA). At the same time, we used the scale of B. Hoffenberth et al. (1990), which suggests a more adequate assessment of clinical parameters in acute CCD in VBD. To assess the degree of recovery of neurological functions, a modified Rankin scale was used (G. Sulter et al. 1999). Ischemic stroke subtypes were classified according to the Special Report from the National Institute of Neurological Disorders and Stroke (1990) Classification of cerebrovascular diseases III. Stroke 21: scale; TOAST criteria (Trial of ORGin Acute Stroke Treatment - a study of low molecular weight heparin ORG in the treatment of acute stroke) (AJGrau et al. 2001) The definition of lacunar syndromes was based on data from clinical studies by K. Miller Fisher (CM Fisher, 1965; 1982) and neuroimaging methods.

Standard laboratory tests were carried out: a study of the level of glucose, urea, creatinine, hematocrit, fibrinogen, acid-base balance, electrolytes, lipids, indicators of blood coagulating properties.

All patients underwent ultrasound Doppler ultrasound of the great vessels of the head in the extracranial section (USDG) and transcranial Doppler (TCD), in some cases, duplex scanning; 12-electrode ECG was performed, blood pressure (BP) was monitored; the volumetric MC was determined by the internal carotid (ICA) and vertebral arteries (PA).

Spiral computed tomography (SCT) of the brain was performed in all cases immediately upon admission to the hospital. It allowed to determine the type of stroke: ischemia or hemorrhage. At the same time, the use of SCT did not always allow detecting a brain stem infarction in the acute period of the disease. In such cases, the technique of routine magnetic resonance imaging (MRI) was used, since magnetic resonance images of the posterior fossa are more informative than SCT. MRI of the brain was performed using a Magnetom Symphony (Siemens) apparatus with a magnetic field strength of 1.5 T and a Flexart apparatus (Toshiba) with a magnetic field strength of 0.5 T. A standard scanning protocol was used, including TIRM (Turbo Inversion Recovery Magnifucle) and T 2 -weighted images (T 2 -BI) in the axial plane, T 1 -weighted images (T 1 -BI) in the sagittal and coronary planes. However, in the presence of several pathological foci using the MRI technique, it was difficult to determine the degree of their prescription, to verify the foci of infarction in the medulla oblongata, especially in the acute period. In such cases, a more sensitive neuroimaging technique was used - diffusion-weighted magnetic resonance imaging (DW MRI).

With the help of diffusion-weighted images (DWI), it is possible to determine the area of ​​acute cerebral ischemia within a few hours after the development of a stroke, which is manifested by a decrease in the measured diffusion coefficient (CDI) of water and an increase in the MR signal on DWI. Restriction of water diffusion occurs due to insufficient energy (loss of tissue ATP, weakening of the sodium-potassium pump function) and the onset of cytotoxic edema of ischemic brain tissue (Neumann-Haefelin T at al. 1999). Therefore, it is believed that DWI is especially sensitive in identifying an ischemic focus with a reduced ATP content and a high risk of irreversible damage to neurons (von Kummer R. 2002). The brain tissue after acute focal ischemia with a high MR signal on DWI and a low ICD corresponds to the infarction focus.

Another modern sensitive technique for brain imaging, perfusion-weighted (PV) MRI, which is used in clinical practice, provides information on the hemodynamic state of brain tissue and can reveal perfusion disorders both in the ischemic nucleus zone and in the surrounding collateral areas. Therefore, during the first hours after the onset of a stroke, the areas of perfusion disorders on the perfusion-weighted image (PVI) are usually more extensive than on DWI. It is believed that this zone of diffusion-perfusion mismatch (DWI / PVI) reflects the ischemic penumbra, i.e. “Tissue at risk” of functional impairment (Neumann-Haefelin T at al. 1999).

We performed DW MRI in the axial plane when examining 26 patients (32.9%): 12 patients were examined within 24 hours after the development of a heart attack, including 1 - within 7 hours, 2 - up to 12 hours from the onset of the disease. The rest of the patients underwent DWI on days 2-3 and in the dynamics of the disease: 4 patients were examined 3 times, 2 times - 14.1 times - 8.

Magnetic resonance angiography, which allows visualizing large extra- and intracranial arteries, was performed in 17 patients (30.4%) with non-acunar ischemic infarction.

The aim of our study is to assess the importance of clinical and neuroimaging methods in the diagnosis of lacunar and non-acunar posterior-circular infarctions.

Results and its discussion

Clinical and neuroimaging examination of 79 patients (48 men and 31 women, aged 60 to 70 years) with a clinical picture of ischemic stroke in VBB made it possible to identify such clinical forms of acute ischemic cerebrovascular accidents: transient ischemic attacks (TIA) (n = 17) , lacunar TIA (n = 6), lacunar infarction (n = 19), non-acunar infarction in VBP (n = 37). In patients with TIA and lacunar TIA, neurological deficit regressed within the first 24 hours from the onset of the disease, although in patients with lacunar TIA, small foci of lacunar infarction were detected on MRI. We analyzed them separately. Therefore, the main study group consisted of 56 patients.

Taking into account the causes and mechanisms of the development of acute CCD, the following subtypes of ischemic infarctions were identified: lacunar infarction (n = 19), atherothrombotic (n = 21), cardioembolic (n = 12) infarctions and infarction of unknown cause (n = 4).

The frequency of localization of the detected ischemic infarction in VBD, verified by neuroimaging, was different (Fig. 2). As can be seen from the data presented, most often infarction foci were detected in the area of ​​the bridge (32.1%), thalamus (23.2%), less often in the area of ​​the cerebral pedicles (5.4%). In many surveyed (39.4%) posterior-circular infarctions were caused by multifocal lesions: the medulla oblongata and cerebellar hemispheres (19.6%); various parts of the brain stem and cerebellar hemisphere, occipital lobe of the brain; cerebellar hemispheres and thalamus; occipital lobes of the brain.

Although on the basis of clinical data it was not possible to accurately determine the arterial localization of the lesion, neuroimaging methods made it possible to conduct a clinical description of an infarction in VBB, taking into account the vascular territory of the blood supply and, according to TOAST criteria, classify all posterior circulatory ischemic infarctions into lacunar and nonacunar.

Classification of ischemic infarctions in VBD according to etiological and pathogenetic characteristics:

Lacunar infarctions due to lesions of small perforating arteries caused by microangiopathies against the background of arterial hypertension and diabetes mellitus, provided that there are no sources of cardioembolism and stenosis of large vertebrobasilar arteries (n = 19);

Non-lacunar infarctions due to lesions of short and / or long enveloping branches of the vertebral and basilar arteries in the presence of sources of cardioembolism and the absence of stenosis of large vertebrobasilar arteries (n = 30);

Non-lacunar infarctions due to occlusive lesions of large arteries (vertebral and main), in the extra- or intracranial regions, i.e. due to macroangiopathies (n = 7).

As can be seen from the above data, the defeat of small branches was the cause of lacunar infarctions in 33.9% of cases; the defeat of the short or long enveloping branches of the vertebral or basilar arteries was the most frequent (53.6%) cause of the development of non-acunar infarction; occlusion of large arteries also led to the occurrence of non-acunar infarction and was detected in 12.5% ​​of the subjects. The localization of the lesion on MRI and DW MRI of the brain was relatively often correlated with the neurological clinic.

I. Lacunar infarctions in VBB

Clinical characteristics and outcomes of 19 patients with lacunar infarction (LI) in VBD, verified by neuroimaging methods, are shown in Table. 1. LI lesions usually had rounded outlines, about 0.5-1.5 cm in diameter. If during the first study the LI diameter was more than 1 cm, it more often increased with repeated MRI.

Lacunar infarctions occurred as a result of damage to a separate paramedian branch of the PA, OA, or one perforating thalamogenicular artery - a branch of PCA against the background of arterial hypertension, which was often combined with hyperlipidemia, and in 6 patients - with diabetes mellitus. The onset of the disease was acute, sometimes accompanied by dizziness, nausea, and vomiting. The background neurological deficit on the NIHSS scale corresponded to 4.14 ± 0.12 points, on the B. Hoffenberth scale - 5.37 ± 0.12 points, i.e. responded to mild neurological dysfunctions.

More often (n = 9) purely motor infarction (PDI) was detected, caused by damage to the motor pathways in the area of ​​the base of the bridge, which are supplied with blood by small paramedian arteries extending from the main artery. It was accompanied by paresis of the facial muscles and arms, or the arm and leg were completely affected on one side. Complete motor syndrome was detected in 3 patients, partial - in 6 (face, arm or leg), they were not accompanied by objective symptoms of sensitivity disorders, obvious disorders of the brain stem function: loss of visual fields, hearing loss or deafness, tinnitus, diplopia, cerebellar ataxia and gross nystagmus. For illustration, we present the patient's MRI (Fig. 3), performed 27 hours after the onset of the disease, T 2 TIRM - weighted tomogram in the axial projection, which revealed a lacunar infarction in the right parts of the pons. The diagnosis of LI is confirmed by DW MRI data and a diffusion map (Fig. 4). PDI was clinically determined.

Lacunar infarctions in the thalamus in 5 patients caused the development of a purely sensory syndrome (HR), which was caused by damage to the lateral thalamus due to occlusion of the thalamogenicular artery (Fig. 5, 6). Hemisensory syndrome was complete in 2 patients and incomplete in 3. Complete hemisensory syndrome was manifested by a decrease in superficial and / or deep sensitivity or numbness of the skin according to the hemitype in the absence of homonymous hemianopsia, aphasia, agnosia and apraxia. In incomplete hemisensory syndrome, sensory disorders were recorded not on the entire half of the body, but on the face, arm or leg. In 2 patients, cheiro-oral syndrome was detected, when sensory disturbances occurred in the area of ​​the corner of the mouth and palm homolaterally; in one patient the cheiro-oral-pedal syndrome was determined; it was manifested by hypalgesia of pain sensitivity in the area of ​​the corner of the mouth, palms and feet on one side without motor disorders.

In 2 patients, lacunar thalamic infarction was accompanied by the spread of ischemia towards the inner capsule, which led to the development of sensorimotor stroke (SM) (Fig. 7, 8). Neurological symptoms were caused by the presence of a lacuna in the lateral nucleus of the thalamus, but there was an effect on the adjacent tissue of the inner capsule. In neurological status, sensory and movement impairments were determined, but sensory impairments preceded motor impairments.

Two patients were diagnosed with "atactic hemiparesis". Gaps were found at the base of the bridge. The neurological clinic was manifested by hemiataxia, moderate leg weakness, and mild arm paresis. The syndrome of dysarthria and clumsy hands (dysarthria-clumsy - hand syndrom) was detected in one patient, was due to the localization of the lacuna in the basal parts of the pons and was accompanied by dysarthria and severe dysmetry of the arm and leg.

Lacunar infarctions in VBB were characterized by a good prognosis, restoration of neurological functions occurred on average on 10.2 ± 0.4 days of treatment: 12 patients had complete recovery, 7 had insignificant neurological microsymptoms (dysesthesia, pain), which did not affect the performance of their previous duties and daily life activity (1 point on the Rankin scale).

II. Non-lacunar infarction in VBB

The clinical characteristics of patients with non-acunar infarction in VBD of various etiologies are given in table. 2. As evidenced by the above data, the most common neurological symptoms in patients with acute ischemic infarction due to damage to short or long circumflex branches of the vertebral (PA) or main (OA) arteries were: systemic dizziness, headache, hearing impairment with noise in the same ear , motor and cerebellar disorders, sensory disturbances in Zelder's zones and / or according to mono- or hemitype. The clinical and neurological profile of posterior circulatory infarctions due to damage to large arteries (vertebral and main) in all patients was manifested by a defect in the visual field, movement disorders, impaired statics and coordination of movements, palsy gaze, less often - dizziness, hearing impairment.

Analysis of the background neurological deficit in patients with non-acunar infarctions due to lesions of short or long circumflex arteries of PA or OA indicates that impairments of neurological functions according to the NIHSS scale corresponded to moderate severity (11.2 ± 0.27 points), and according to the B. Hoffenberth scale - severe disorders (23.6 ± 0.11 points). Thus, the scale of B. Hoffenberth et al. (1990) compared with the NIHSS scale in assessing acute vertebrobasilar stroke more adequately reflected the impairment of neurological functions, the severity of the patient's condition. At the same time, in case of heart attacks in VBP due to damage to large arteries and the development of a gross neurological defect, the scales used unidirectionally reflected the volume of neurological deficit, probably because the patients were dominated by extensive ischemic infarctions.

The baseline blood pressure level in patients with occlusion of large arteries of VBP was significantly lower than in patients with lesions of short or long circumflex branches of the vertebral or basilar artery. In some patients with occlusion of large arteries, which caused the development of large-focal brainstem infarction, arterial hypotension was recorded upon admission. On the other hand, arterial hypertension on the first day after a stroke in patients with lesions of the short or long circumferential branches of PA and OA could be a manifestation of a compensatory cerebrovascular reaction (Cushing's phenomenon), which arose in response to ischemia of brain stem formations. Attention was drawn to the lability of blood pressure during the day, with an increase in the morning hours after sleep.

The clinical picture of nonacunar infarctions caused by lesions of short and / or long circumflex branches of the vertebral and basilar arteries in the presence of sources of cardioembolism and the absence of stenosis of large vertebrobasilar arteries was heterogeneous with different clinical course. All other things being equal, the development of focal changes in the posterior parts of the brain depended on the level of the lesion, the arterial bed and the size of the heart attack.

Blockage of the posterior inferior cerebellar artery was manifested by the alternating Wallenberg-Zakharchenko syndrome. In the classical version, it manifested itself as systemic dizziness, nausea, vomiting, dysphagia, dysarthria, dysphonia, impaired sensitivity on the face according to the segmental dissociated type in the Zelder zones, Berner-Horner syndrome, cerebellar ataxia on the side of the focus and movement disorders, hypesthesia of pain and temperature sensitivity trunk and limbs from the opposite side. The same neurological disorders were characteristic of the blockage of the intracranial section of the PA at the level of the posterior inferior cerebellar artery and paramedian arteries branching from it.

Variants of the Wallenberg-Zakharchenko syndrome were often observed, which arose with occlusive lesions of the paramedian arteries of the PA, medial or lateral branches of PICA and were clinically manifested by systemic dizziness, nystagmus, and cerebellar ataxia. On MRI of the brain, they revealed foci of infarction in the medial or lateral regions of the medulla oblongata and the lower regions of the cerebellar hemispheres.

In the case of cardioembolic occlusion of the paramedian or short circumflex branches of the basilar artery, non-acunar infarctions occurred in the pons (Fig. 9, 10). Their neurological clinic was polymorphic and depended on the level of arterial lesions and the localization of the heart attack. Blockage of the pons paramedian arteries was manifested by alternating Fauville syndromes - peripheral paresis of the facial muscles and the external rectus muscle on the side of the focus with contralateral hemiparesis or Miyara-Gubler: peripheral paresis of the facial muscles on the side of the focus and hemiparesis on the opposite side.

When the branches of the basilar artery supplying the midbrain were blocked, paresis of the muscles innervated by the oculomotor nerve occurred on the side of the focus and hemiplegia on the opposite side (Weber's syndrome) or hemiataxia and athetoid hyperkinesis in the contralateral limbs (Benedict's syndrome) or intentional hemitremoric muscle hypotonia with hemiplegia (Claude syndrome). With a heart attack in the quadruple artery basin, paralysis of the upward gaze and failure of convergence (Parino's syndrome) occurred, which was combined with nystagmus.

Bilateral infarctions in the pool of paramedian and short circumflex arteries of OA were characterized by the development of tetraparesis, pseudobulbar syndrome, and cerebellar disorders.

Cerebellar infarction occurred acutely as a result of cardiac or arterio-arterial embolism of the anterior inferior cerebellar artery or superior cerebellar artery and was accompanied by cerebral symptoms and impaired consciousness. Blockage of PNMA led to the development of a heart attack in the region of the lower surface of the cerebellar hemispheres and pons. The main symptoms were dizziness, tinnitus, nausea, vomiting and, on the side of the lesion, paresis of the facial muscles of the peripheral type, cerebellar ataxia, and Berner-Horner syndrome. In the case of occlusion of the IAV, the infarction focus was formed in the middle part of the cerebellar hemispheres and was accompanied by dizziness, nausea, and cerebellar ataxia on the side of the focus (Fig. 11). Cerebellar ischemic strokes have also occurred when the vertebral or basilar arteries are blocked.

Blockage of the internal auditory (labyrinth) artery, which in most cases originates from the anterior inferior cerebellar artery (can also branch off from the main artery) and is terminal, arose in isolation and manifested itself as systemic dizziness, unilateral deafness without signs of damage to the brain stem or cerebellum.

Blockage of the PCA or its branches (spur and parieto-occipital artery) was usually accompanied by contralateral homonymous hemianopsia, visual agnosia, with preserved macular vision. In the case of left-sided localization of the heart attack, amnestic or semantic aphasia and alexia occurred. The defeat of the branches of the PCA, which supply blood to the cortex of the parietal lobe on the border with the occipital, manifested itself as cortical syndromes: disorientation in place and time, visual-spatial disturbances. Large-focal infarctions of the occipital lobe of the brain were accompanied by hemorrhagic transformation of the infarction (Fig. 12).

Thalamic infarctions occurred as a result of damage to the thalamo-subthalamic (thalamoperforating, paramedian branches) and thalamogenicular arteries, which are branches of the posterior cerebral artery. Their occlusion was accompanied by depression of consciousness, paresis of gaze upward, neuropsychological disorders, memory impairment (anterograde or retrograde amnesia), contralateral hemihypesthesia. More severe disorders (depression of consciousness, paresis of gaze upward, amnesia, thalamic dementia, akinetic mutism syndrome) occurred in bilateral thalamic infarction, which developed as a result of atheromatous or embolic occlusion of the common leg of the thalamo-subthalamic artery, the paramedian branches of which supply the thalamic artery with blood supply to the posterior medial arteries. 13). Occlusion of the thalamo-genicular artery caused the development of infarction in the ventrolateral region of the thalamus and was accompanied by Dejerine-Russi syndrome: transient hemiparesis, hemianesthesia, choreoathetosis, ataxia, hemialgia and paresthesia were detected on the side opposite to the lesion focus.

Blockage of the posterior villous arteries, which are branches of the PCA, led to the development of a heart attack in the posterior thalamus (cushion), geniculate bodies and was manifested by contralateral hemianopsia, sometimes by impaired mental activity.

Vertebral artery (VA) occlusion occurred at both the extracranial and intracranial levels. With occlusion of the extracranial part of the PA, short-term loss of consciousness, systemic dizziness, visual impairments, oculomotor and vestibular disorders, impaired statics and coordination of movements were noted, paresis of the extremities, and impaired sensitivity were also detected. Often there were attacks of sudden falls - drop attacks with impaired muscle tone, autonomic disorders, respiratory disorders, cardiac activity. MRI of the brain revealed infarction foci of the lateral regions of the medulla oblongata and the lower regions of the cerebellar hemispheres (Fig. 14, 15).

The occlusion of the intracranial part of the PA was manifested by the Wallenberg-Zakharchenko alternating syndrome, which in the classical version was also detected with blockage of the PICA.

Blockage of the main artery was accompanied by damage to the pons, midbrain, cerebellum, characterized by loss of consciousness, oculomotor disorders caused by the pathology of pairs III, IV, VI of cranial nerves, the development of trismus, tetraplegia, impaired muscle tone: short-term decerebrational rigidity, hormone-tonic muscle cramps, which were replaced - and atony. Acute embolic occlusion of OA in the area of ​​the fork led to ischemia of the ristral parts of the brainstem and bilateral ischemic infarction in the blood supply of the posterior cerebral arteries (Fig. 16, 17). Such a heart attack was manifested by cortical blindness, oculomotor disorders, hyperthermia, hallucinations, amnesia, sleep disorders and, in most cases, was fatal.

Thus, posterior circulatory ischemic infarctions are etiologically different, heterogeneous in their clinical course and with different outcomes.

The results of our study show that the MRI technique is sensitive for the detection of acute ischemic posterior circulatory strokes. At the same time, it did not always allow visualizing an acute lacunar infarction or ischemic foci in the brain stem, especially in the medulla oblongata. To identify them, the diffusion-weighted MRI technique was more informative.

The sensitivity of DWI in detecting acute brainstem infarction in the period up to 24 hours after the onset of stroke was 67%, the infarction focus during this time was not detected in 33% of patients, i.e. a third of those examined with clinical symptoms of a brain stem infarction had false negative results. Repeated examination of patients after 24 hours using DW MRI of the brain revealed an infarction zone.

The lack of information content of the DWI technique in determining acute infarction when localized in the brain stem can be explained by two factors. First, the presence of small ischemic foci, since perforating arteries vascularize very small areas of the brainstem. Second, neurons in the brain stem are more resistant to ischemia than neurons in the evolutionarily younger cerebral hemispheres. This could be one of the reasons for their higher tolerance to ischemia and the later development of cytotoxic edema of the brain stem tissue (Toi H. et al. 2003).

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Many people ask the question of what ONMK is and what the consequences are after it. This article will analyze the main reasons for the manifestation of CVA and the consequences.

ONMK - what is it

Many people who have nothing to do with medicine probably do not know what ACVA is. So, an acute circulatory disorder in the brain is a stroke that causes damage and death of brain cells. The cause of this disease is the formation of a blood clot in the blood vessels of the brain or the rupture of some blood vessels, which causes the death of a huge number of nerve cells and blood cells. According to statistics, it is ONMK that is in first place among diseases that cause human death. Every year all over the world, as indicated by the federal registry of patients with stroke, 14 percent of people die from this disease, as well as 16 from other types of diseases of the circulatory system.

Reasons why ACVE may appear

In order to prevent the appearance of this disease, it is necessary to pay attention to your lifestyle from an early age. For example, constant sports activities can significantly reduce the possibility of CVA manifestations. What it is, you already know, some of the causes of this ailment will be considered further.

As a rule, this disease does not come suddenly, very often the diagnosis of "stroke" can be established as a consequence of certain diseases. Often the cause of this condition can be:

• hypertension;
• obesity is the most common cause indicated by the federal registry of a patient with stroke;
• diabetes;
• high cholesterol;
• heart disease;
• alcohol and smoking;
• various kinds of medicines;
• high hemoglobin levels;
• according to the federal register ONMK, another reason is age;
• traumatic brain injury;
• genetic predisposition and so on.

Now it is clear what ONMK is. These are the consequences of a wrong lifestyle. Therefore, it is very important to monitor your health and physical condition.

Ischemic stroke

Ischemic stroke is a stroke caused by damage to brain tissue and impaired blood flow to one or another of its parts.

In the majority of ischemic stroke patients, general diseases of the cardiovascular system are found. Such diseases also include arteriosclerosis, heart disease (arrhythmia, rheumatic defect), diabetes mellitus.

ACVA of this type is characterized by sharp and frequent manifestations of pain, the consequence of which is a deterioration in blood circulation in the cerebral cortex. As a rule, such attacks can make themselves felt several times per hour and last for 24 hours.

CVA is included in the international classification of diseases 10 revision

ONMK codes (ICD 10):

1. I63.0. Human cerebral infarction as a consequence of thrombosis of the precerebial blood arteries.
2. I63.1. Human brain infarction after embolism of the precerebral blood arteries.
3. I63.2. Cerebral infarction as a consequence of stenosis of the precerebral blood arteries or non-thinning blockage of the cerebral arteries.
4. I63.3. ACVA as a consequence of thrombosis of the blood arteries of the brain.
5. I63.4. Stroke due to embolism of cerebral blood vessels.
6. I63.5. ACVA as a consequence of stenosis of blood arteries or their non-thinning blockage.
7. I63.6. Non-pyogenic cerebral infarction as a consequence of cerebral blood vein thrombosis.
8. I63.8. Brain infarction for other reasons.
9. I63.9. Unrefined ONMK.
10. I64.0. Unsophisticated stroke, which manifests itself as a hemorrhage or heart attack.

CVA codes (ICD 10) allow doctors to quickly establish the classification of the disease, the true cause of its appearance and determine the necessary treatment. Therefore, this classification is the main tool in the hands of a doctor, which allows you to save the life of a person.

Causes of ischemic stroke ACVA

The main reason for the manifestation of ischemic stroke is a decrease in blood flow to the brain. Very often, this is why an ischemic stroke becomes the cause of death of a person.

So, we found out the features of ischemic stroke, what it is and what are its symptoms.

This, as a rule, is the result of damage to the vessels of the neck and some arteries of the brain in the form of occlusive lesions and stenosis.

Let's find out the main reasons for its occurrence. The main factors that can affect the decrease in blood flow include the following:

1. Occlusions and stenoses of the main arteries of the brain and vessels of the neck.

2. Thrombotic layers on the surface of an atherosclerotic plaque.

3. Cardiogenic embolism, which occurs when there are artificial valves in the human heart.

4. Stratification of the great arteries of the cervical spine.

5. Hyalinosis of small arteries, as a result of which microangiopathy develops, which leads to the formation of lacunar infarction of the human brain.

6. Hemorheological changes in blood composition, which occurs with vasculitis, as well as coagulopathies.

Very rarely, the cause of the manifestation of this disease can be external trauma of the carotid arteries and various inflammatory processes, which can significantly impair the permeability of blood through the vessels.

Also, very often, the main cause of cerebral stroke can be osteochondrosis of the cervical spine, during which the blood vessels are significantly pinched, which can lead to a decrease in blood flow. Patients with osteochondrosis are constantly advised to massage the cervical spine and smear it with various warming drugs that can significantly expand blood vessels and improve blood circulation.

ACMC symptoms

Signs of this disease can very often appear sharply or increase gradually. As a rule, the main symptoms of this disease include a disorder of speech and vision in a patient, disturbances in various reflexes, coordination of movement, headaches, disorientation, sleep disturbance, noise in the head, memory impairment, paralysis of the face, tongue, lack of sensation of some limbs, and so on. Further.

In acute disturbance of cerebral circulation, the following consequences are characteristic - cerebral stroke, circulatory disturbance in the cerebral cortex during the formation of blood clots in the vessels and main blood arteries of the head, etc.

With symptoms of acute cerebrovascular accident, which last more than a day, a stroke is diagnosed. At the first stage of this disease, severe headache, dizziness, nausea, gag reflexes, and so on may also appear. If you do not immediately pay attention to these manifestations, this can lead to the death of a person.

According to the registry of patients with stroke, according to statistics, the main cause of these manifestations can be high blood pressure, which can be observed during intense physical exertion. A sharp increase in blood pressure can cause rupture of blood vessels in the brain, followed by hemorrhage and internal cerebral hematoma.

In most cases, the above symptoms are observed before ischemia. As a rule, they can last several hours or several minutes. As a rule, with the manifestation of stroke ischemic type, the symptoms constantly become more active. According to experts, with the manifestation of these symptoms, most people experience disorientation, as a result of which a person loses vigilance, coordination of movements worsens, so many patients simply fall asleep. According to statistics, 75 percent of ischemic-type infarction attacks occur during sleep.

Diagnosis of acute cerebrovascular accident by ischemic type

To identify the problem, it is necessary to carry out diagnostics and various studies on the ICD system. Doctors will be able to diagnose ONMK after carrying out the following procedures:

• glucose, hemostasis, antiphospholipid antibodies.
• Electrocardiography of changes in blood pressure.
• the cerebral cortex, as a result of which it will be possible to detect the affected parts of the brain and the resulting hematomas without any problems.
• Cerebral angiography and so on.

Treatment of acute cerebrovascular accident in ischemic type

The most common cause of death is ONMK. Treatment should therefore be supervised by experienced doctors. With this disease, the following therapy is carried out:

1. Maintenance of vital functions of the human body. The patient should use antihypertensive drugs when the blood pressure in the body is 200 to 120 mm. rt. Art. The use of anticoagulants is also prescribed (they are used for concomitant pathologies and are used for a long time after the normalization of the condition), vasoactive drugs, antiplatelet agents, decongestants, neuroprotectors, and so on.
2. Various sets of exercises are performed - speech therapy classes and breathing exercises.
3. The issue of thrombolysis upon admission of a patient to a medical facility within 3-6 hours from the moment of manifestation of the disease is considered.
4. Secondary prevention of the disease.
5. Various rehabilitation measures are being carried out, and so on.

As a rule, the main points of treatment will be prescribed only by a doctor, who will familiarize himself in more detail with the victim's illnesses.

In the event that there are suspicions of an acute violation of cerebral circulation, it is necessary to contact highly qualified specialists in this field of activity. As a rule, first of all, it will be necessary to undergo magnetic resonance imaging, which can accurately determine all pathologies of the cerebral cortex. Thus, it will be possible to prevent the possibility of complications of the disease and begin treatment even before it fully manifests itself. A specialized department of ONMK, as a rule, should have special equipment that will significantly improve treatment.

Disease statistics among population groups

This disease very often worries not only elderly people, but also young people. This disease today attracts the attention of tens of thousands of scientists from all over the world, as it very often worries people of different age groups. A lot of cases were recorded when ACVA began to progress already in young people, and even in infants. Scientists cite statistics according to which it turned out the following number of diseases per 100,000 population at different ages.

The number of stroke patients at different ages is shown in the table.

Federal register of a patient with stroke

The federal register keeps records of the number of patients with a particular disease. He studies the progression of certain diseases and the reasons for their development. CVA is a disease that is also accounted for. This register contains all information about patients and their history.

The Federal Register states that mortality due to diseases of the vascular system of the body is in the first place today. As a rule, 50 percent of deaths are associated precisely with acute circulatory disorders of the brain (ACVA), that is, the main cause of death is precisely a stroke. Every year in the Russian Federation, an average of 400-450 thousand cases of stroke are recorded, that is, every one and a half minutes a person develops this disease. Of the total number of patients, approximately 40 percent die.

Every year the number of patients with acute cerebrovascular accident is growing significantly. Thus, according to the federal register of the ONMK department, in 1996 in the Moscow region 16 thousand victims were registered, and in 2003 this figure increased to 22 thousand patients. From this it can be concluded that acute cerebrovascular accident is one of the most progressive diseases today.

According to the federal register of ONMK, about a million people live in our country who have already survived this disease, while it is worth noting that a third of the victims are people of working age. After illness among people of this age, only 25 percent of the victims were able to return to work. Based on these data, it can be determined that stroke is one of the most progressive and dangerous diseases.

The federal register of patients with acute cerebrovascular accidents every day is replenished with a huge number of patients, but the number of cases remains unchanged. This is justified by the fact that the life expectancy after the disease is significantly reduced. Therefore, it is worth constantly monitoring your health in order to prevent the manifestations of this disease.

Consequences of acute cerebrovascular accident

The consequences of stroke can be very different - from mild to severe. Very often, after an acute violation of cerebral circulation, people receive the following consequences:

• Loss of sensitivity in a specific area of ​​the body. Very often, the sensitivity of the hands, feet, fingers, the right or left side of the body, the muscles of the face, the tongue, and so on is lost.
• Weakness or complete paralysis of the arm or arms, leg or legs, an individual part of the body, or the right or left side of the body.
• Very often victims lose hearing, vision, taste, sensitivity of certain nerve endings of the limbs of the body.
• Often after stroke, patients feel dizziness, double vision, noise in the head, and so on.
• Confused speech.
• Difficulty in pronunciation and word selection when speaking.
• Lack of ability to recognize specific parts of the body.
• Involuntary urination.
• Lack of ability to move.
• Lack of orientation in space and loss of balance.
• Unexpected fainting spells and so on.

Departments of ONMK conduct constant rehabilitation sessions for patients. As a rule, under the supervision of experienced doctors, it is possible to eliminate these consequences and completely restore the sensitivity of the body. After a certain period of time after the manifestation of ischemic attacks or stroke, a person will be able to fully return to a normal lifestyle. It is worth considering that the so-called can last for a long period of time. If they are observed throughout the day, this will lead in most cases to a full stroke. They can also occur over a period of time. Thus, some people experience these symptoms several times a year. And after each such manifestation, a certain period of rehabilitation is required.

The consequences of stroke can be very different, since the area of ​​brain damage can be different.

First aid for stroke

The very first thing to do when symptoms of this disease are detected is to call an ambulance. In no case should the patient be disturbed without reason during the manifestation of the symptoms of this disease, therefore, immediately after the first signs, it is necessary to isolate him.

At the next stage, all patients with stroke should lie in such a way that the upper body and head are raised, and it is also necessary to grind the collar zone of the body in order to facilitate breathing for the patient. It is also necessary to provide fresh air to the room where the patient is located (open the window, doors, and so on).

In the event that the patient has vomiting spasms, it is necessary to turn his head to the left side and clean the oral cavity with gauze or just a clean napkin. This is done to prevent vomit from entering the lungs when breathing, which can lead to additional problems.

One of the most common symptoms of stroke is an epileptic seizure - a person completely loses consciousness, after a few seconds a wave of convulsions sweeps through the body, which can last for several minutes. It is also worth noting that such attacks can be repeated several times.

Everyone can ask a question about what needs to be done in this case. The patient should be turned on his side, put a pillow under his head. Holding your head, it is necessary to constantly wipe the secretions from the mouth so that they do not enter the respiratory organs. To prevent the patient from biting his tongue, it is necessary to insert a comb or a stick into his mouth. It is worth noting that under no circumstances should you press the patient's arms and legs or lean on him with the whole body. Such actions can significantly increase seizures or cause various kinds of injury - dislocations, fractures. It is only necessary to slightly hold the patient's legs so that he cannot injure himself or others. Do not use ammonia, as it can cause respiratory arrest in the patient.

If, after an attack, the victim's heart stops beating or breathing stops completely, it is necessary to urgently do direct heart massage and mouth-to-mouth breathing or mouth-to-nose breathing.

Now you know the basic exercises and ACVA standards that can save a person's life during seizures.

How to prevent the occurrence of stroke diseases

Based on the above statistics, it can be seen that this disease manifests itself even in children. It is easy to guess that every year there are more and more people who suffer from this disease. All this is associated with unhealthy diet, inactive lifestyle and high mental stress.

If a person does not lead an active lifestyle and constantly spends time at the computer, he has a good chance of contracting this disease. Obesity, as it was said, is the main cause of this disease, which is why the issue of maintaining physical fitness is very relevant today for the younger generation.

Heavy loads are also very often a source of problems, since with an increase in blood pressure there is a risk of rupture of blood arteries and veins, which will also lead to stroke. Therefore, it is necessary to constantly go in for sports, lead an active lifestyle, eat right - and the risk of stroke will significantly decrease.

The most deadly and terrible disease in our time is precisely ONMK. You already know what it is and why this disease occurs, so you must adhere to the above recommendations in order to prevent the disease in the future.

In recent years, 2 main pathogenetic variants of chronic cerebrovascular insufficiency have been considered. An important role in the development of chronic cerebral circulation insufficiency has recently been attributed to venous pathology, not only intracranial, but also extracranial.

The pathogenesis of cerebrovascular insufficiency in VBD can cover an extremely wide range of changes. Along with the pathology of the vessels of the vertebrobasilar system (stenosis and occlusion) due to atherosclerosis, extravasal factors are of great importance. Other causes also include pathological tortuosity, congenital developmental disorders in the form of hypo- and aplasia of the vertebral artery, Kimmerly's anomaly.

Mechanical compression of the vertebral artery at the level of the cervical spine, which underlies the development of the “archer's” stroke. Treatment of vertebro-basilar insufficiency is one of the services offered by the multidisciplinary clinic Doctor. Here you will find out what vertebro-basilar insufficiency is, how the treatment is carried out, the cost of the procedure.

Moreover, some of them, short-term and transient, are detected only during the attack, while others, long-term, may remain after an attack of circulatory disorders. In VBB, both transient ischemic attacks (TIA) and ischemic strokes and microstrokes can occur.

With such lesions, dizziness is often combined with tinnitus or hearing loss, is paroxysmal, and lasts a few seconds. Such dizziness can be classified as benign and quickly correcting conditions.

The main symptoms of circulatory disorders in VBB:

Compression of blood vessels, both arterial and venous, can play a definite role in the formation of chronic cerebral ischemia. Low blood pressure adversely affects cerebral blood flow, especially in the elderly. This group of patients may develop lesions of the small arteries of the head associated with senile arteriosclerosis. Quite often, chronic cerebral circulation insufficiency is detected in patients with diabetes mellitus, they develop not only micro-, but macroangiopathies of various localization.

In the presence of the main factors in the development of chronic cerebrovascular insufficiency, the rest of the variety of causes of this pathology can be interpreted as additional causes.

Cerebral blood flow depends on perfusion pressure (the difference between systemic blood pressure and venous pressure at the level of the subarachnoid space) and the resistance of cerebral vessels. Adequate cerebral perfusion is maintained with an increase in vascular resistance, which in turn leads to an increased load on the heart.

Clinic (manifestations and symptoms):

Severe hypertensive crises are always a disruption of autoregulation with the development of acute hypertensive encephalopathy, each time aggravating the phenomenon of chronic cerebrovascular insufficiency. But cerebral blood flow depends not only on the severity of stenosis, but also on the state of collateral circulation, the ability of cerebral vessels to change their diameter.

However, even with hemodynamically insignificant stenosis, chronic cerebral circulation insufficiency will almost certainly develop. When the main arteries of the head are damaged, cerebral blood flow becomes very dependent on systemic hemodynamic processes. They are based on morphological signs - the nature of damage and predominant localization. In this case, even a slight decrease in blood pressure can lead to ischemia in the terminal zones of the adjacent blood supply.

However, at the ultrastructural level around necrotic cells, cells with apoptosis-like reactions, triggered in the acute period of stroke, can persist.

Each vertebral artery (there are two in total, right and left) is conventionally divided into 4 segments:

The progression of cerebrovascular insufficiency becomes a risk factor for the development of recurrent stroke and vascular cognitive disorders up to dementia. The core of the clinical picture of discirculatory encephalopathy has recently been recognized as cognitive impairments, which are detected already in stage I and progressively increasing by stage III. At stage I, the above complaints are combined with diffuse micro-focal neurological symptoms in the form of anisoreflexia, convergence failure, rough reflexes of oral automatism.

At this stage, signs of a decrease in professional and social adaptation may appear. At the heart of all the syndromes inherent in circulatory encephalopathy is the disconnection of connections due to diffuse anoxic-ischemic damage to the white matter. In the vestibulocerebellar (or vestibuloatactic) syndrome, subjective complaints of dizziness and instability when walking are combined with nystagmus and coordination disorders.

Pyramidal syndrome in discirculatory encephalopathy is characterized by high tendon and positive pathological reflexes, often asymmetric. Difficulty turning while walking is manifested not only by stomping on the spot, but also by turning with the whole body in violation of balance, which may be accompanied by a fall.

The genesis of these disorders is combined, due to the defeat of the pyramidal, extrapyramidal and cerebellar systems. To diagnose chronic cerebral circulatory insufficiency, it is necessary to establish a connection between clinical manifestations and pathology of cerebral vessels. Atherosclerotic stenosis usually develops in the initial sections of the internal carotid artery and in the area of ​​the bifurcation of the common carotid artery. The main direction of laboratory research is to clarify the causes of the development of chronic cerebrovascular insufficiency and its pathogenetic mechanisms.

An important place is given to ultrasound research methods, which make it possible to detect both disorders of cerebral blood flow and structural changes in the vascular wall, which are the cause of stenosis.

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

If at the heart of chronic cerebral circulatory insufficiency lies only arterial hypertension, then the use of the term "hypertensive encephalopathy" is legitimate. With the progression of chronic insufficiency of cerebral circulation, there is an increasing decrease in the protective sanogenetic mechanisms, including the antioxidant properties of plasma.

Dyscirculatory encephalopathy and its main symptoms

Dyscirculatory encephalopathy is a disease that is accompanied by organic changes in nerve tissues. It should be noted that in the absence of treatment, the disease progresses, leading to unpleasant and dangerous consequences. That is why it is so important to seek the help of a specialist on time.

In most cases, the disease occurs against the background of chronic vascular insufficiency in the tissues of the brain. Due to impaired blood circulation and, accordingly, a deficiency of oxygen and nutrients, a change in structures is observed, which leads to serious disruptions in the work of the whole organism. The causes of vascular insufficiency can be different. Most often, discirculatory encephalopathy is the result of atherosclerosis (blockage) of the vessels of the brain. But chronic hypertension, rheumatism and other problems can lead to the same result.

Dyscirculatory encephalopathy: symptoms

The main signs of the disease directly depend on the stage of its development. In modern medicine, it is customary to distinguish three main stages, each of which is accompanied by different symptoms:

At the first stage (stage of compensation), changes in the mental state and behavior of a sick person are mainly observed. As a rule, during this period, patients become emotionally unstable - they are too excitable, unrestrained and irritable. Often, this condition also affects the quality of sleep, which becomes alarming, as a result of which a person simply cannot rest normally. Sometimes headaches and dizziness are observed, as well as a decrease in memory and concentration.

The second stage is accompanied by more persistent organic changes in the tissues of the brain, which cannot but be reflected in the patient's condition. Recurrent headaches become persistent. The increased excitability disappears - the person becomes lethargic, depressed, gets tired quickly, does not sleep well. As the disease progresses, other disorders are observed, for example, some reflexes disappear, memory is significantly impaired, hearing decreases, tremors in the limbs, and seizures appear.

Dyscirculatory encephalopathy in the third stage is accompanied by more pronounced symptoms, because during this period the morphological changes in the meninges are already easy to notice during tomography. All of the above symptoms remain, but become even more pronounced. In addition, other disorders appear, which depend on which particular area of ​​the brain was damaged. Often, the disease is accompanied by paresis or paralysis, speech disorders and serious mental disorders are observed.

Therapy directly depends on the stage of the disease and the symptoms present. Patients are usually prescribed drugs that improve blood flow, as well as those drugs that strengthen the walls of blood vessels and eliminate their spasm. In some cases, drugs are used that regulate the activity of the brain. With increased excitability, sedatives are indicated, while with high blood pressure, antihypertensive drugs are used.

KhNMK - chronic cerebrovascular accident

It is customary to distinguish the initial manifestations of cerebrovascular accidents as an early stage of chronic cerebrovascular accident and DE (discirculatory encephalopathy) - multifocal brain damage caused by chronic circulatory failure.

In turn, the following forms of DE are distinguished:

Causes and pathogenesis of HNMC

As a rule, chronic impairment of cerebral circulation is a consequence of cardiovascular pathology. Usually KhNMK develops against the background of:

• vegetative-vascular dystonia;
• atherosclerosis, hypertension;
• diabetes;
• heart diseases of various etiologies;
• vasculitis;
• diseases of the blood, accompanied by a violation of its rheological properties.

These pathologies alter the general and cerebral hemodynamics and lead to a decrease in cerebral perfusion (less than / 100 g per minute). The most important factors involved in the pathogenesis of CCI include:

• changes in the extra-, intracranial parts of the vessels of the head;
• lack of collateral circulation capabilities;
• violation of blood circulation autoregulation;
• violation of rheology.

Obesity, physical inactivity, alcohol abuse and smoking play a significant role in the progression of CNI.

Symptoms of chronic cerebrovascular accident

In the early stages of CCI, the picture is characterized by patients' complaints of a feeling of heaviness in the head, mild dizziness, unsteadiness when walking, noise in the head, rapid fatigue, decreased attention and memory, as well as sleep disturbance. The initial manifestations of circulatory failure occur after psychoemotional and / or physical overstrain, against the background of alcohol consumption, under unfavorable meteorological conditions. Patients have signs of vegetative-vascular and emotional lability, a certain slowdown in thinking processes, and a lack of convergence is possible. The progression of the initial manifestations of circulatory failure leads to the formation of the next stage - DE.

Depending on the severity of manifestations, there are three stages of chronic cerebrovascular accident. In stage I, the symptoms are insignificant, patients usually remain functional; in stage II, the symptoms are moderately expressed, and in stage III, patients become disabled.

With atherosclerotic encephalopathy, that is, with DE caused by atherosclerotic lesions of the vessels that provide blood supply to the brain, in stage I, a decrease in attention and memory is noted, especially for current events, it is difficult to memorize new information, it is difficult for the patient to switch from one activity to another. At the same time, mild cognitive impairments, as a rule, are compensated for by the preserved everyday and professional skills, as well as intellectual capabilities. Often, patients complain of increased fatigue and decreased performance, often there is emotional lability with a decrease in the psycho-emotional background. Diffuse headaches, noise in the head are noted. Complaints of patients about instability when walking are characteristic. In the neurological status, insignificant disseminated symptoms are revealed in the form of moderate signs of pseudobulbar syndrome, tendon hyperreflexia and anisoreflexia, as well as postural instability.

In stage II, clinical manifestations progress, cognitive impairment increases, performance decreases, patients become touchy and irritable. Narrowing of interests is noted, memory disorders are increasing. Dull headaches, dizziness, and unsteadiness when walking are often present. In the neurological status, anisoreflexia, pseudobulbar symptoms, vestibulo-cerebellar disorders, and subcortical symptoms are detected.

In stage III, there is a further aggravation of neurological manifestations. Patients show significant diffuse neurological symptoms in the form of an increase in pyramidal insufficiency, pseudobulbar disorders, cerebellar and extrapyramidal symptoms, as well as disorders of control of the pelvic organs. Epileptic seizures are possible. Stage III is characterized by pronounced disorders of higher mental functions: significant cognitive disorders before dementia, the development of apatoabulic syndrome is likely, pronounced emotional and personal changes. In the later stages, patients lose the skills for self-care. For atherosclerotic encephalopathy, sleepiness after eating, the Windsheid triad, is typical. In stage III, Hackebusch's disease, or pseudo-Alzheimer's form of atherosclerosis, is a symptom complex, the main manifestation of which is dementia. At the same time, a decrease in memory, confabulations, a pronounced narrowing of the range of interests, uncriticality, speech disorders, gnosis and praxis are noted. In addition, in the late stage of atherosclerotic encephalopathy, the formation of the Demage-Oppenheim syndrome is possible, which is characterized by gradually developing central tetraparesis.

Chronic hypertensive encephalopathy is a form of DE caused by arterial hypertension. Arterial hypertension leads to diffuse damage to the brain tissue, the disease progresses rather quickly with significant fluctuations in blood pressure, repeated hypertensive crises. The disease can manifest itself at a fairly young age, on average. In the initial stages, the clinical picture of hypertensive encephalopathy is characterized by sufficient dynamism and reversibility of symptoms. Characterized by a neurosis-like syndrome, frequent headaches, mainly occipital localization, noise in the head. In the future, signs of bilateral pyramidal insufficiency, elements of akinetic-rigid syndrome, tremors, emotional and volitional disorders, decreased attention and memory, and a slowdown in mental reactions may appear. As the progression progresses, personality disorders arise, the range of interests narrows, speech intelligibility is impaired, anxiety increases, and weakness is noted. Patients are characterized by disinhibition.

In the III stage of hypertensive encephalopathy in patients, as a rule, severe atherosclerosis occurs, the condition is characterized by features typical for atherosclerotic encephalopathy - developing dementia. In a far advanced stage, patients lose the ability to self-care, control of pelvic functions, signs of apato-abulic or paranoid syndromes may appear.

A variant of hypertensive encephalopathy in combination with atherosclerotic brain damage is Binswanger's encephalopathy (progressive vascular leukoencephalopathy). It usually manifests itself at the age of 50 and is characterized by memory impairment, cognitive impairment, motor impairment in chronic subcortical cerebrovascular accident. Epileptic seizures sometimes occur. As a rule, encephalopathy in chronic cerebrovascular accident develops gradually, although stepwise progression associated with vascular crises, fluctuations in blood pressure and heart disorders is possible.

Venous DE is characterized by venous congestion in the skull, chronic hypoxia and intracranial hypertension. Venous DE more often develops in patients with cardiopulmonary diseases, as well as with arterial hypotension.

Diagnostic procedures for chronic cerebrovascular accident include the collection of anamnesis, taking into account information about somatic pathology (especially about cardiovascular diseases), analysis of patient complaints, neurological, neuropsychological examination. Instrumental examination involves Doppler ultrasound (USDG), rheoencephalography, CT) or MRI, ophthalmoscopy and angiography. As a rule, an examination of the heart is necessary (electrocardiography - ECG, echocardiography), as well as a study of the rheological properties of blood.

Treatment of chronic cerebrovascular accident

Arterial hypertension is one of the most important risk factors for CIU, however, episodes of hypotension are also unfavorable for patients with DE. In the process of correction, it is advisable to maintain blood pressure at a stable level slightly exceeding the "optimal" indicators: mm Hg. It is necessary to select medications for chronic disorders of cerebral circulation, taking into account the characteristics of the patient, his reaction to the prescribed medications. For the treatment of arterial hypertension, angiotensin-converting enzyme inhibitors are used - ACE (captopril, perindopril, enalapril, enalaprilat), angiotensin II receptor antagonists (candesartan, eprosartan), β-blockers (in particular, atenistolol, labetolol, metolopol central α-adrenergic receptors (clonidine), slow calcium channel blockers (nifedipine). Diuretics as antihypertensive therapy are used only according to indications (for example, heart failure, ineffectiveness of other antihypertensive drugs) due to a possible deterioration in blood rheology.

Forecast

Usually, chronic cerebrovascular accident is characterized by a slowly progressive course, although a stepwise progression is possible (usually after vascular crises). In stage I, the ability to work and household adaptation of patients in most cases is preserved, in stage II there is a slight or moderate decrease in working capacity, in stage III patients are disabled, often unable to self-service.

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Chronic cerebrovascular accident (CCI): what is it?

1. Blood supply to the brain 2. Causes of the disease 3. Mechanisms of development 4. Clinical manifestations 5. Diagnostics 6. Treatment

Cerebrovascular pathology occupies a leading position among all neurological diseases. If the identification of acute hemodynamic disorders most often does not present difficulties due to vivid clinical manifestations, chronic dyscirculation may not be diagnosed for a considerable time. Such nonspecific symptoms as recurrent headaches, fatigue, distraction of attention are sometimes harbingers of a gradual increase in the disease. At the same time, chronic cerebrovascular accident (CVC) often leads to disability and significantly reduces the patient's quality of life.

CNMC is a gradually progressive disease of the brain, which is based on its diffuse discirculatory process, leading to ischemia of the nervous tissue. Depletion of cerebral blood flow changes biochemical reactions in nerve cells, disrupts their nutrition and subsequently causes neuronal death. With significant hemodynamic changes, neurological symptoms appear associated with the lack of adequate blood supply to certain areas of the brain.

The term "chronic cerebrovascular accident" in the international classification of diseases ICD 10 is absent. Chronic cerebral ischemia (code I 67.9) and cerebrovascular disease not specified (code I 67.9) are considered the closest in terms of the clinical picture and pathogenesis of the disease. In addition, in ICD 10 you can find similar concepts - progressive vascular leukoencephalopathy, cerebral atherosclerosis and hypertensive encephalopathy.

Blood supply to the brain

The structures of the brain receive blood supply from the vertebrobasilar vascular basin (VBV) and the carotid system.

The carotid system gives the anterior and middle cerebral arteries that feed:

• frontal, parietal and temporal lobes;
• striopallidal subcortical structures;
• inner capsule.

Areas of blood supply to the vertebrobasilar basin:

The predominant discirculation in the vertebrobasilar system is often associated with the anatomical features of the vertebral arteries, which are located in the canal of the cervical vertebrae. Osteochondrosis of this section, neck injuries and displacement of the vertebrae deform blood vessels and impede adequate blood supply to the brain.

The two blood supply basins are connected by connecting arteries that complete the circle of Willis. It is believed that such a closed system is a manifestation of compensatory mechanisms necessary when one of the arteries is excluded from the bloodstream. If the communicating vessels do not function fully or are completely absent, the circle of Willis is considered open or open.

Causes of the disease

Failure of cerebral circulation is mainly found in the elderly. Recently, however, there has been a sad tendency towards the "rejuvenation" of the disease. Moreover, the causes of the development of the disease often do not depend on the patient's age. The main predisposing factors include:

• instability of blood pressure (hypertension, hypotension);
• atherosclerosis;
• cardiac pathology;
• vasculitis;
• disorders of blood rheology;
• diabetes;
• chronic intoxication;
• hypodynamia;
• obesity;
• stressful situations.

The causes of pathology can also be hidden in a person's genetic predisposition to the development of etiological components of the disease (hereditary forms of hypertension, diabetes mellitus, hyperlipidemia).

Development mechanisms

Insufficient cerebral blood flow provokes a number of morpho-functional disorders that play a major role in the development of the disease. Lack of adequate oxygen supply to cells:

• reduces the activity of redox processes;
• inhibits the synthesis of adenosine phosphate;
• inhibits the aerobic form of glycolysis;
• activates the anaerobic pathway for glucose utilization;
• disrupts the activity of ion transport through the cell wall.

These processes lead to the formation of small punctate foci of ischemia, diffusely scattered in the brain tissue. The degree of hypoxic damage to the nervous tissue determines the causes of the pathological process, the severity of these factors, the duration of their effect and the state of the organism itself (acid-base balance, blood gas level).

Clinical manifestations

The clinical picture of the disease depends on the duration of the disease and the vascular basin, where discirculation predominantly occurs. Due to the fact that ischemic foci are most often diffusely localized, the symptoms of the disease can include several components.

Currently, a three-degree gradation of chronic cerebrovascular pathology is used. This division reflects the severity of the main manifestations and the severity of the disease.

The lack of blood supply to the brain of the 1st degree is characterized by the presence of disseminated neurological symptoms, which does not allow identifying the leading neurological syndrome. As a rule, in this case, there is a small number of small foci of ischemia, which are not capable of leading to pronounced functional impairments. Patients report complaints of general weakness, recurrent headaches, dizziness, distraction of attention, memory loss, rapid fatigability. Neurological examination reveals pyramidal insufficiency with asymmetry of tendon and periosteal reflexes, symptoms of mild dysfunction of the vestibulocerebellar system, and autonomic manifestations.

II degree of chronic cerebrovascular pathology is diagnosed when a focal symptom complex of the disease is detected. At this stage, most often formed:

• cerebellar syndrome. It is manifested by static and dynamic ataxia, instability in the Romberg position, dysmetria and impaired performance of coordination tests.
• pyramidal disorders. Revealed in the presence of paresis of the extremities with the manifestation of pathological reflexes;
• strio-pallidal disorders. Most often, vascular parkinsonism is diagnosed with a specific tremor such as "coin counting" or "pill rolling", increased muscle tone in the extrapyramidal variant and hypokinesias;
• syndrome of sensitive disorders. It occurs when the cerebral conductors are damaged, superficial and deep sensitivity. Symptoms of hypesthesia, perversion of sensitivity, hyperpathy, and a decrease in two-dimensional spatial feeling are formed.
• cognitive dysfunction. It is manifested by the pathology of memory, attention, thinking. For the II degree of chronic cerebral ischemia, gross cognitive decline is not typical.

III degree of chronic brain failure is diagnosed with severe cognitive pathology with the development of dementia. At the same time, patients are usually disoriented, not critical. This period is characterized by symptoms of emotional disorders in the form of apatho-abulic syndrome and aggressive behavior. Extensive zones of ischemia can act as an epileptic focus with the development of periodic somatomotor or somatosensory paroxysms. Symptoms of the disease at this stage are practically not amenable to medication control. Her treatment is reduced to social rehabilitation and environmental adaptation of the patient.

Patients with grade III chronic cerebral hemodynamic impairment require constant monitoring by relatives and doctors.

Cerebral blood flow is directly related to the quality of peripheral circulation. With a decrease in cerebral perfusion, a clinical manifestation of a symptom complex of vascular disorders in the periphery is possible. So, chronic forms of cerebral dyscirculation can be associated with the development of peripheral Raynaud's syndrome.

There is a concept of "initial manifestations of cerebral circulatory failure." Such a diagnosis is valid in the presence of subjective complaints typical of cerebral dyscirculation, in the presence of a normal neurological status.

Diagnostics

A number of diagnostic procedures are required to confirm the diagnosis. On the one hand, this makes it possible to clarify the presence of the main morphological substrate of the disease (ischemic foci), as well as to identify the predisposing factors and the degree of their manifestations. On the other hand, additional instrumental examination methods can exclude other brain pathologies that can manifest themselves with a similar neurological deficit.

The standards for the diagnosis of chronic cerebrovascular insufficiency include:

• neuroimaging;
• angiography;
• ultrasound scanning of the vessels of the head and neck;
• daily monitoring of indicators of peripheral blood pressure;
• electrocardiogram;
• X-ray examination of the cervical spine;
• analysis of the lipid spectrum of blood;
• coagulogram;
• glycemic profile.

Treatment

Chronic forms of cerebral blood flow disorders, as a rule, are subject to outpatient treatment. Decompensated types of pathology with an increased likelihood of developing acute cerebrovascular complications are hospitalized in the hospital.

Treatment of insufficient blood supply to the brain should correct risk factors for the disease and prevent its progression. For this, it is necessary to activate compensatory mechanisms aimed at restoring blood flow. The main treatment is directed at the causes of the disease and the restoration of cerebral perfusion.

To normalize the background of the development of chronic cerebrovascular insufficiency, the following are prescribed:

• antihypertensive drugs;
• lipid-lowering treatment;
• antiplatelet agents.

Treatment with these drugs involves their constant intake. Etiotropic therapy of chronic cerebral ischemia is not used as a course of treatment.

To stabilize the patient's condition, use:

• antioxidants;
• neurotrophics;
• vascular protectors to improve both central and peripheral blood flow;
• nootropic drugs;
• metabolic agents.

Basic treatment is supplemented with symptomatic agents for leveling individual components of the clinical manifestations of the disease (analgesics, anticonvulsants).

The complex treatment of I and II degrees of chronic cerebrovascular pathology, as well as the initial manifestations of cerebral dyscirculation, include physiotherapy, massage, psychotherapy, allowing to stop moderate symptoms of the disease.

Chronic cerebral ischemia is a serious neurological pathology that has adverse consequences without timely treatment. The prognosis directly depends on the duration of the disease, the degree of its progression and the adequacy of the prescribed therapy. Avoiding the development of acute cerebrovascular disorders and vascular dementia will allow competent treatment and adherence to the basic rules of prevention (correct diet, moderate physical activity, regular medical examination).

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Khnmk in vbb what is it

One of the common causes of dizziness is cerebral circulation failure in the vertebrobasilar basin (VBB), which can occur in the form of chronic ischemia, transient cerebrovascular accidents or strokes.

Pathogenesis. The main causes of ischemic changes in this pathology are factors that limit blood flow to the vertebrobasilar system or contribute to excessive outflow from it to other vascular basins. The pathogenesis of cerebrovascular insufficiency in VBD can cover an extremely wide range of changes. Along with the pathology of the vessels of the vertebrobasilar system (stenosis and occlusion) due to atherosclerosis, extravasal factors are of great importance. For example, thrombosis of the vertebral artery is possible due to dissection of the artery in case of a whiplash or other neck injury, inadequate manual manipulations on the cervical spine.

Other causes also include pathological tortuosity, congenital developmental disorders in the form of hypo- and aplasia of the vertebral artery, Kimmerly's anomaly. In the presence of the latter, when turning the head, bending and compression of the vertebral artery occurs, with its possible trauma

Also, pathological conditions such as Klippel-Feil-Sprengel anomaly, non-closure of the posterior arch of the Atlas, saddle hyperplasia of the lateral Atlas masses, underdevelopment of the articular processes of the cervical vertebrae, cervical ribs, “steal” syndrome ( subclavian-vertebral robbery) and a number of others. In addition, there is often a blockage of blood vessels by a thrombus that has formed and migrated into the basin of the vertebral or basilar artery from the heart cavity.

However, it should be noted that most of the listed factors are significant precisely for an acute vascular catastrophe, manifesting dizziness - transient cerebrovascular accidents or strokes. Systemic vertigo (i.e., when a person has a feeling of falling, moving in space, accompanied by nausea and vomiting) with chronic cerebral circulation insufficiency never occurs, and anxiety, depression, orthostatic hypotension, metabolic disorders ( hypo-, hyperglycemia), drug dizziness, impaired attention, vision, etc., which require adequate diagnosis and treatment.

Clinical manifestations. The core of the clinical picture in transient disorders of cerebral circulation in the vertebrobasilar basin are episodes of dizziness, often accompanied by nausea, vomiting, instability when walking and standing, noise, a feeling of stuffiness in the ears, autonomic disorders in the form of profuse sweating, blanching or vice versa, redness facial skin, lasting from several minutes to several hours. There may also be hearing impairments (mainly loss) and vision ("flies" in front of the eyes, "blurred vision", "blurred picture"). Sudden falls without loss of consciousness ("drop attacks", Unterharnscheidt syndrome) are extremely dramatic for patients, which are acute circulatory disorders in the reticular formation of the brain stem and usually occur with sharp turns or throwing the head back.

Strokes in the vertebrobasilar basin are characterized by a rapid onset (from the onset of the first symptoms to their maximum development, it takes no more than 5 minutes, usually less than 2 minutes), as well as the following neurological symptoms:

1. movement disorders: weakness, awkwardness of movement, or paralysis of the limbs;
2. sensitivity disorders: loss of sensitivity or paresthesia of the limbs and face;
3. visual impairment in the form of double vision, loss of visual fields;
4. imbalance, instability
5. violation of swallowing and speech clarity.

A special form of acute cerebrovascular accident in VBB is a bowhunter’s stroke, associated with mechanical compression of the vertebral artery at the level of the cervical spine during extreme turn of the head to the side.

Mechanical compression of the vertebral artery at the level of the cervical spine, which underlies the development of the “archer's” stroke.

The mechanism of development of such a stroke is explained by the tension of the artery when turning the head, accompanied by a tear in the intima of the vessel (dissection), especially in patients with pathological changes in the arteries.

Diagnostics. When diagnosing cerebral circulation insufficiency in VBB, it is necessary to take into account that the symptoms of the disease are often nonspecific and may be the result of another neurological or other pathology, which requires a thorough collection of patient complaints, study of the anamnesis of the disease, physical and instrumental examinations to identify the main cause of its development. The leading role in the diagnosis of clinically significant changes in blood flow in the vertebrobasilar basin is currently played by neuroimaging methods for examining the brain (MRI and CT), as well as Doppler ultrasound and duplex scanning with CDC, which allow non-invasive and relatively cheap assessment of the structure and patency of the vascular bed.

It is important to note that the differential diagnosis between vertigo caused by damage to the cerebellum and / or brain stem (central) and arising from dysfunction of the vestibular apparatus or vestibular nerve (peripheral) is not always easy. On the one hand, very often conditions such as benign paroxysmal positional vertigo are taken for a stroke, at the same time, sometimes patients with acute vascular insufficiency in VBD are mistakenly treated for “cervical osteochondrosis with vestibulopathic syndrome” by chiropractors and osteopaths with the development of corresponding complications ...

Treatment. In the case of acute neurological deficits (alternating syndromes, cerebellar insufficiency, "negative" cattle, etc.), the patient should be urgently hospitalized at the regional vascular center or neurological department to exclude stroke in the VBD. If confirmed, the treatment is carried out according to the current guidelines and recommendations.

In case of dizziness against the background of chronic cerebral circulation insufficiency, the VBB focuses on drugs that improve blood circulation in the brain due to vasodilating and rheopositive action (vinpocetine, cinnarizine, betahistine, etc.). Adequate correction of blood pressure, prevention of thrombus formation in various cardiac arrhythmias is of great importance.

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Elderly people are familiar with such a disease, the name of which is ONMK - acute cerebrovascular accident or just a stroke. Almost every older person experienced this ailment on himself. It is very important to understand the causes of stroke and proper treatment of the disease.

What it is?

Stroke is a clinical symptom manifested by sharp disruptions in the normal operation of the existing options of the brain of the head, the duration of which is more than one day.

The main symptoms of stroke are:

1. The inability of the patient's body to move normally;
2. Disorders of the organs responsible for sensitivity;
3. Violations of the proper functioning of the speech apparatus;
4. The inability of the patient to make swallowing movements;
5. Frequent headache;
6. Loss of consciousness.

An unexpectedly appeared violation of the speech apparatus, loss of body sensitivity and problems with coordination of movement disappear over the next day. Then they talk about a transistor ischemic attack. This is not such a dangerous disease as a stroke, but it also applies to stroke.

If the disease refers to disorders in the work of the circulatory system, then it is characterized as "ACV by the type of ischemia." In the case when a specialist confirms bleeding, then the disease has the characteristic of "CVA of hemorrhagic type."

A stroke that ends in stroke is the stage when blood flow to some part of the brain stops. This phenomenon is caused by a decrease in the tone of the walls of the arteries of the brain and is accompanied by a disorder of the neurological system, which is a consequence of the destruction of part of the nerve tissue.

ONMK - code according to ICD-10

In the tenth international classification of diseases, ACVA has several codes that differ from each other according to the disorders that caused the disease.

Prevention and therapy of this disease are considered at the state level, since ACVA is fatal in one third of cases. Sixty percent of patients who have had the disease turn out to be disabled, who cannot do without social assistance.

Causes of ACVA

ACVA, which is related to the ischemic type, develops as a result of existing pathologies in the patient's body.

Such diseases include:

ACVA occurs not only in the adult population, but also in children. This is due to the fact that the vessels of the child's brain have any abnormalities in their development. A high risk of developing stroke is observed in children who have congenital heart disease.

When stroke occurs, only 30% of children fully recover. About fifty percent have incurable disorders in the neurological system. Twenty percent of cases of development of acute circulatory disorders of the brain in children are fatal.

In what cases can ONMK be suspected?

The diagnosis of stroke is made if the patient has the following disorders in the body:

1. A sharp lack of sensitivity in the limbs;
2. Loss of vision up to blindness;
3. Inability to recognize the opponent's speech;
4. Loss of balance, coordination problems;
5. Very severe headaches;
6. Clouding of consciousness.

An accurate diagnosis can be made only after a diagnosis has been made.

Stages of cerebral infarction

ONMK has several stages of development. Let's consider each of them in more detail.

Ischemic stroke

ACVA of this type is accompanied by a complete cessation of blood flow delivery to specific areas of the brain tissue, which are accompanied by the destruction of brain cells and the termination of the work of its main functions.

Causes of ischemic stroke

ACVA of this type is caused by the obstruction of blood flow to any brain cell. As a result, the normal functioning of the brain stops. Plaque, which is made up of cholesterol, can also interfere with normal blood flow. More than 80% of all diseases are caused by this.

Risk group

ACVA is most often manifested in a population category that has the following pathologies:

• Vascular disorders of an atherosclerotic nature;
• A sharp increase in blood pressure;
• Previous extensive myocardial infarction;
• Stretching an artery;
• Acquired or congenital heart defects;
• Increased blood density caused by diabetes:
• Reduced blood flow rate, which is a consequence of cardiac insufficiency;
• Overweight;
• Transistor ischemic attacks previously suffered by the patient;
• Excessive consumption of products of the alcoholic and tobacco industry;
• Reaching the age of sixty;
• Use of oral contraceptives that can cause blood clots.

Symptoms of the disease

Neurologists distinguish several intervals in the development of ischemic stroke according to the severity of the disease:

1. The sharpest. Lasts up to five days;
2. Spicy. The duration is 21 days;
3. Early recovery. From the moment the elimination of acute symptoms takes six months;
4. Recovery at a later stage. The rehabilitation period lasts for two years;
5. Elimination of traces. More than two years.

In addition to general symptoms, ischemic cerebral stroke is characterized by local symptoms. It depends on the zone in which the disease occurred.

And so, if amazed , then the following symptoms appear:

• Disorder of the visual system in the side where the vessel was blocked;
• The sensitivity of the limbs disappears from the opposite side of the lesion focus of the disease;
• In the same area, muscle tissue paralysis occurs;
• Disorders in the work of the speech apparatus are observed;
• The inability to realize your illness;
• Body orientation problems;
• Loss of visual field.

With narrowing of the artery of the spine, other symptoms are noticeable:

• Decreased hearing;
• Twitching of the pupils when moving in the opposite direction;
• Objects look double.

If defeat happened on area of ​​alignment with an unpaired blood vessel, then the symptomatology manifests itself in a more severe form:

In case of defeat anterior cerebral artery:

• Loss of sensitivity in the opposite side, usually in the leg area;
• Slowness in movement;
• Increased tone of muscle-flexor tissue;
• Lack of speech;
• The patient cannot stand and walk.

If disruptions prevent normal patency of the middle cerebral artery:

• The consequence of a complete blockage of the main trunk is a state of severe coma;
• In half of the body, there is a loss of sensitivity;
• The locomotor system refuses;
• The inability to fix the gaze on the subject;
• Fields of vision drop out;
• There is a failure of the speech apparatus;
• The patient is unable to distinguish the right limb from the opposite.

In case of violation patency of the posterior cerebral artery the following clinical picture is observed:

Blockage of the optic-geniculate artery accompanied by the following symptoms:

• Lack of tactile sensations on the opposite side of the face and body;
• If you touch the patient's skin, then he experiences severe pain;
• Wrong perception of light and knocking;
• The forearms and shoulder joints are flexed. The fingers are also bent at the base.

Defeat at the site visual hillock characterized by the following symptoms:

• The patient's movements have a wide range;
• There is a strong tremor;
• Loss of coordination occurs;
• Half of the body loses sensitivity;
• Excessive sweating is characteristic;
• Bedsores develop.

The most severe case of ACVA is the process of breaking through an intracerebral hematoma. Hemorrhage occurs in the cerebrospinal fluid pathways, fills the cerebral stomachs with blood. This ailment is called "ventricular tamponade".

This case of acute cerebrovascular accident is the most severe and in almost all cases is fatal. The explanation for this lies in the unobstructed flow of blood to the patient's brain.

Treatment of stroke by ischemic type

The above symptoms may appear unexpectedly in a loved one. It is very important to provide first aid to the patient.

After calling an ambulance, it is necessary to alleviate the patient's condition using the following techniques:

1. Put the patient on the side so that the vomiting leaves the victim's mouth without hindrance;
2. The head should be slightly raised;
3. If you have a tonometer, then you need to measure your blood pressure. If a sharp increase in pressure to critical values ​​is noticed, then a drug should be placed under the patient's tongue to reduce it;
4. Provide the patient with an amount of fresh air;
5. Free the patient's neck from any compressive things.

Inpatient treatment

After arriving at a medical facility, the victim is placed in an intensive care unit. Further, the patient is assigned a special diet, in which the emphasis is placed on the balance of all the necessary trace elements. Nutrition is adjusted so that fatty, spicy, salty foods are not observed in the diet.

Mayonnaise and other condiments should also be avoided. Vegetables and fruits are limited only during the acute stage of the disease. If the patient's consciousness is absent, then food intake is carried out through a medical probe no earlier than two days later.

After confirmation of CVA, inpatient treatment continues for a month. The consequences after transferring this ailment are extremely severe.

Strong decrease in strength in muscle tissue on the opposite side of the brain, the site of which was affected. A certain category of patients practically learns to walk again and perform normal movements;

... The decrease in strength occurs only in the area of ​​the mouth, cheeks and lips. The patient is unable to properly eat and drink;

Quite often, impaired work of the speech apparatus is found.... It is caused by damage to the speech center in the human brain. The patient either completely loses speech, or does not perceive the words of another person;

Movement coordination disorder th is caused by damage to the parts of the central nervous system that are responsible for the normal functioning of the human motor system. In severe cases, violations can persist for several months;

Malfunctions of the visual system are of a different nature and depend on the size and location of the stroke lesion. Usually they are expressed in the loss of visual fields;

Sensory impairment is expressed in the loss of pain, sensations of warmth and cold.

Rehabilitation

A very important stage on the path of recovery after stroke.

Quality therapy includes the following categories of treatment:

1. Physiotherapy. It is necessary to return the patient to normal movement of the limbs. The set of exercises is selected by the attending physician;
2. Visit to a speech therapist. It is prescribed if the patient has speech and swallowing disorders;
3. Physiotherapy. The most affordable type of therapy, which is located in every clinic;
4. Medication therapy. The main stage in the recovery process. Drugs mitigate complications after illness and prevent the risk of relapse;
5. Training for the mind. It is advisable for the patient to read as much literature as possible, memorize poetry or excerpts of works.

Stroke by hemorrhagic type

The components that provide nutritional action, which include oxygen, enter the brain through the carotid arteries. Located in the cranial box, they form a network of vessels, which is the root of the blood supply to the central nervous system. When the destruction of the artery tissue occurs, then the flow of blood rushes to the brain.

Causes of occurrence

Hemorrhagic stroke occurs in the case of cerebral hemorrhage from a vessel whose integrity has been compromised. As a result, a hematoma occurs in the patient's brain, which is limited to the brain tissue. Also, blood from a ruptured vessel can enter the area surrounding the brain.

Risk group

Particular attention should be paid to the state of your health of the following category of citizens:

• Suffering from congenital dilation of blood vessels;
• Having anomalies in the development of arteries and veins;
• Suffering from inflammatory diseases of the walls of blood vessels;
• With pathologies of connective tissues of a systemic nature;
• Having lesions of blood vessels, accompanied by a violation of protein metabolism;
• Abuse of drugs that stimulate the nervous system.

Symptoms

1. Acute headache;
2. Constant gagging;
3. Frequent loss of consciousness over a long period;
4. In almost all cases, there is an increase in blood pressure;
5. Increasing sensations of weakness in the limbs;
6. Disorder in the work of the organs responsible for sensitivity or complete loss of sensitivity;
7. Violation of the motor system;
8. Disorder of the visual system;
9. Strong nervous excitement;
10. When tested, a small amount of blood is observed in the cerebrospinal fluid;

Treatment of stroke by hemorrhagic type

Drug therapy consists in the use of drugs, the action of which is aimed at stopping bleeding, reducing the size of the cerebral edema, and calming the nervous system. Antibiotics and beta blockers are used.

Medicines can cause a relapse of stroke, so it is advisable to eliminate the problem through surgery. First of all, the neurosurgeon removes the lesion, and then eliminates the malfunction in the vessel.

Reversibility of pathology

During diagnostic studies, it is essential whether the symptomatology of stroke is reversible. When the stage is reversible, the brain cells exist in the paralysis phase, but their integrity and full-fledged work are not disturbed.

If the stage is irreversible, then the brain cells have died and cannot be restored in any way. This area is called the "ischemic zone". But therapeutic treatment is possible in this case.

Its meaning is to provide neurons with all nutrients in the ischemic zone. With proper treatment, cell functions can be partially reanimated.

It was found that a person does not use all the resources of his body in the process of his life, including not all brain cells are involved. Cells that are not involved in work can replace the killed cells and ensure their full functioning. The process is rather slow, so full rehabilitation continues for three years.

Transistor ischemic attack (TIA)

This disease is also a stroke, but unlike ischemic and hemorrhagic stroke, it is temporary. For a certain period of time, there is a sharp disturbance of blood flow in the large vessels of the brain, as a result of which its cells suffer from a lack of oxygen and nutrients. Symptoms of TIA, a transistorized ischemic attack, last for 24 hours and are similar to those of a stroke.

If more than 24 hours have passed, but the disease has not receded, then most likely an ischemic or hemorrhagic stroke has occurred.

Symptoms

Consider the symptoms of transistor ischemic attack:

• There is a decrease in sensitivity in one of the sides of the face, body, lower or upper limbs;
• Weakness in the body that is mild to moderate;
• Violations in the work of the speech apparatus, up to the complete absence of speech or problems with understanding the words of the opponent;
• Dizziness and lack of coordination;
• Sudden noise in the ears and head;
• Headache and heaviness.

These symptoms appear abruptly and disappear after 3-4 hours. The deadline that distinguishes a transistor ischemic attack from a stroke is no more than a day.

What diseases can cause TIA?

TIA can be caused by the following conditions:

1. Persistent increase in blood pressure, which is chronic;
2. Chronic vascular disease of the brain;
3. Changes in blood clotting;
4. A sudden drop in blood pressure;
5. Impossibility of normal blood flow through the artery caused by a mechanical obstacle;
6. Pathology of the structure of the vessels of the brain.

Transistor ischemic attack can and should be treated! Despite the fact that her symptoms go away rather quickly, this ailment already signals a malfunction in the body and, in case of relapse, can turn into a stroke!

Risk group

A transistor ischemic attack is no less dangerous than a stroke. Up to 8% of TIA patients in the future suffer from a stroke that occurs within a month after the attack. In 12% of patients, stroke occurs within a year and in 29% within the next five years.

Treatment of transistor ischemic attack

It is carried out in a hospital.

Diagnostic tests include the following procedures:

1. Visit to a cardiologist, angiologist and ophthalmologist. The patient is prescribed a consultation with a medical psychologist;
2. For laboratory analysis, the patient must pass a general blood and urine test, as well as blood for biochemical analysis;
3. Electrocardiography;
4. Computed tomography of the brain;
5. X-rays of light;
6. Constant blood pressure check.

The victim is allowed to go home only if the recurrence of TIA is excluded or the patient has the opportunity to be immediately hospitalized in the event of a second attack.

Treatment for transistor ischemic attack consists of taking the following oral medications:

• The action of which is aimed at thinning the blood;
• Vasodilatation agents;
• Lowering blood cholesterol levels;
• Aimed at normalizing blood pressure.

It is good to combine drug therapy with balneotherapy and physiotherapy.

Prophylaxis

To avoid the occurrence and recurrence of a transistor ischemic attack, a set of preventive measures should be followed:

1. Go in for sports, having previously drawn up a lesson plan with your specialist;
2. Correct your diet by reducing the amount of fatty, salty and spicy foods;
3. Reduce the use of alcoholic beverages and tobacco;
4. Monitor your body weight.

Survey algorithm

It is possible to diagnose stroke by the characteristic symptoms, but in order to determine the degree of the course of the disease, to which type of stroke it belongs,

It is necessary to undergo a series of diagnostic tests.

Examination by a specialist immediately after the patient is admitted to a medical institution;

Taking blood for laboratory analysis, in order to assess the state of glucose levels, clotting, enzymes;

CT scan in this case, it allows you to obtain more complete information about the disease. In the first 24 hours after the ischemic disorder, it is not possible to find out the localization of the affected area.

This problem can be solved by performing magnetic resonance imaging;

Angiography of cerebral vessels helps to determine with reliable accuracy the area where the lesion has occurred or the level of narrowness of the artery. With this study, you can diagnose aneurysm and pathological connection between the veins and arteries of the brain.

But the results obtained do not allow to correctly estimate the volume of destruction of the nerve tissue. The solution to this problem is to combine vascular angiography with other diagnostic methods;

Cerebrospinal fluid collection for laboratory studies is a threat to the patient's life, but this study allows you to determine what type of stroke belongs to.

This diagnostic method is used mainly in medical institutions that lack more advanced equipment.

Forecast

A favorable outcome after the disease has a category of citizens who have experienced a small form of stroke. With minor restrictions, these patients can normalize their vital functions.

Statistics show that 40% of deaths occur within the first month after illness. 70% show signs of disability in the first month. Over the next 6 months, 40% become disabled. After two years, signs of disability are noticeable in 30% of patients.

Video: ONMK. Signs of a stroke.

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One of the most serious pathologies of the vascular system are acute (ACVA) and chronic processes characterized by cerebral circulation insufficiency. According to statistical data, more than 80% of patients who have suffered an ischemic stroke in the vertebrobasilar system lose their ability to work or remain disabled, unable to self-service, and only about 20% of patients after treatment and recovery return to their professional activities. Among the surviving patients in the next 5-7 years, there is a high risk of recurrent stroke.

Ischemic stroke or cerebral infarction occurs in more than 80% of all cases of stroke. It develops against the background of narrowing or blockage of the arteries that feed the brain. As a result, the supply of a sufficient amount of blood flow decreases and oxygen starvation occurs, after which the symptoms of ischemic brain damage appear within a few minutes.

It was found that about 70% of all transient ischemic attacks occur as a result of stroke in the vertebrobasilar basin.

Development of vertebro-basilar insufficiency

The vertebrobasilar basin is formed by the right and left vertebral arteries, which feed the occipital lobe of the brain, the cerebellum and the trunk. They provide more than 25% of the blood flow to the brain.

Insufficiency of VBP is one of the varieties of cerebrovascular pathology, characterized by circulatory disorders in the vertebral and basilar arteries. It manifests itself in episodes of ischemic damage to the brain tissue with the subsequent development of functional disorders of the central nervous system. Episodes of transient ischemic attacks (TIAs) may recur. Vascular disorders occur in patients of various age categories, in particular in children.

Pathological processes of circulatory disorders in the vertebrobasilar basin are reversible, subject to timely diagnosis and treatment. Without medical care, the likelihood of a cerebral infarction increases.

What leads to ONMK?

Circulatory disorders in the vessels that form VBD have many different causes. The most common are:

• genetic factors;
• congenital anomalies of the vascular system (Kimmerli's anomaly, underdevelopment of the vertebral arteries);
• damage to the cervical spine (with sports injuries, due to car accidents, etc.);
• vasculitis (inflammation of the vascular walls);
• atherosclerosis (damage to the VBD arteries occurs, during which cholesterol deposits form on the vascular walls);
• diabetes;
• persistent increase in blood pressure (hypertension);
• antiphospholipid antibody syndrome (APS): promotes the formation of blood clots;
• dissection (stratification) of arteries: tearing of the vascular wall and the penetration of blood between its membranes, is the cause of acute cerebral infarction;
• compression of the vertebral vessels with intervertebral hernia of the cervical spine, displacement of the vertebrae, degenerative - dystrophic processes of the spinal column.

Symptoms of vertebro - basilar insufficiency

In case of circulatory failure in the vertebral-basilar basin, temporary and permanent signs are distinguished. Temporary symptoms are characteristic of TIA, with the duration of manifestations ranging from several hours to two to three days.

Signs of VBI of a temporary nature are manifested in the form of pressing sensations of pain in the occipital region, uncomfortable and painful manifestations in the cervical spine, as well as severe dizziness.

Symptoms of a permanent nature bother a person all the time, with the progression of pathology, their severity increases. Quite often, an exacerbation occurs, against the background of which transient ischemic attacks occur and the risk of heart attack increases.

Persistent symptoms of circulatory failure VBB:

• constant pain in the back of the head, pulsating in nature or manifested by pressing soreness;
• hearing loss and tinnitus, which in advanced cases is constantly present, at any time of the day;
• decreased memory and attention;
• disorders of visual function: blurring of the contours of objects, diplopia, flies or a veil in front of the eyes, narrowing (loss) of the visual fields;
• violation of balance and coordination of movements;
• rapid fatigue, a constant feeling of weakness and weakness, in the evening patients feel a complete breakdown;
• dizziness, which occurs mainly during an uncomfortable position of the neck, nausea, short-term loss of consciousness;
• increased irritability, sudden mood swings, in childhood - crying for no apparent reason;
• increased sweating, feeling of heat;
• increased heart rate;
• hoarseness, a feeling of perspiration and a lump in the throat appear in the voice.

With the progression of the disease, symptoms manifest themselves in the form of speech disorders, disorders of swallowing function, sudden falls. In the later stages of the disease, cerebral infarction develops.

Diagnostic tests for VBI

Modern diagnostics of VBD blood flow disorders consists in the collection of anamnestic data, physical and instrumental examination. The diagnosis of VBI is made provided that the patient simultaneously exhibits at least three symptoms characteristic of blood flow disturbances, as well as if there are results of studies that confirm the presence of pathological processes in the vessels of the vertebro-basilar system.

Making an accurate diagnosis presents some difficulties, since the symptoms described above can occur in other disorders of cerebral circulation.

For disorders of cerebral circulation, the following are used:

• Doppler ultrasound (ultrasound doppler) - during the study, the patency of the great vessels of the neck and head, hemodynamic parameters (volumetric and linear blood flow velocity), the state of the arterial walls are determined;
• TCDG (transcranial Doppler ultrasound) is one of the methods of ultrasound diagnostics to assess blood flow through the intracerebral vessels;
• MR-angiography and CT in angiography mode - the introduction of a contrast agent followed by visualization of the vessels of the vertebro-basilar basin and the brain, allows you to identify various pathologies, atherosclerotic changes, wall stratification, vascular malformation, their diameter;
• MRI and CT - these methods are not very informative in case of VBD vascular pathologies, however, they can reveal possible etiological factors: structural changes in the spinal cord and spinal column, the presence of herniated intervertebral discs;
• general and biochemical blood test - allows you to determine possible changes in the properties of biological fluid that appear in diabetes, atherosclerosis, inflammatory processes and other pathologies.

Doppler ultrasound

Scheme of therapeutic measures for VBI

The main actions for violations of the blood flow of the vertebro-basilar system are aimed at identifying and eliminating the main causes of the pathological condition, restoring normal blood circulation and blood filling of blood vessels, preventing ischemic attacks of the brain. Treatment consists of the use of drug therapy, massage, gymnastics, physical therapy, and surgery.

Drug treatment

With insufficient blood supply to the brain, the following groups of drugs are prescribed:

• medicines to lower blood lipids - niacin (nicotinic acid, vitamin B3 or PP), fibrates, bile acid sequestrants;
• drugs that prevent thrombus formation (antiplatelet agents) - acetylsalicylic acid;
• vasodilating drugs;
• neurometabolic stimulants (nootropics) - improve the performance of the brain;
• antihypertensive drugs that regulate blood pressure (prescribed, if necessary, on a strictly individual basis);
• symptomatic treatment - drugs for anesthetic, antiemetic and hypnotic effects, antidepressants and sedatives.

Physical treatment

The use of remedial gymnastics is of great importance in violation of the blood flow of the VBB. Exercises should not bring discomfort and painful sensations, movements are performed smoothly and easily. Daily gymnastic exercises eliminate muscle spasms, strengthen the muscles of the back and neck, and contribute to the formation of posture.

An equally important method of treating circulatory disorders of the brain is massage. Massage movements have a positive effect on the vascular system, promoting their expansion, thereby improving blood circulation.

Physiotherapeutic methods are also aimed at improving the blood supply to the great vessels of the neck and head, and eliminating the symptomatic complex. Physiotherapy consists of the use of laser radiation, magnetotherapy and phonophoresis.

Reflexology is prescribed to reduce pain, dizziness and disorders of the visual organ. The method of kinesiological taping is a new direction in the treatment of VBI, aimed at eliminating muscle spasms and vascular infringement.

Surgical intervention

Surgical treatment is prescribed exclusively for severe VBI and an increased risk of development. In the course of surgical intervention, actions are aimed at restoring normal blood circulation in the vertebral arteries by eliminating causes such as narrowing of the vascular lumen due to spasm, compression or stenosis.

Forecast

Timely diagnosis of pathological changes and the implementation of correct therapeutic measures allows you to completely eliminate the lack of blood circulation of blood vessels in the vertebro-basilar system.

In the absence of therapy or improperly selected drugs and physiotherapeutic methods in a particular case, a chronic process may develop, accompanied by a constant deterioration of the condition and an increase in the intensity of symptoms, which leads to frequent TIA and increases the risk of acute and discirculatory encephalopathy.

Treatment of VBI is a rather long and laborious process, which takes from two months to several years. But only with the implementation of all medical recommendations is it possible to protect oneself from serious consequences, often leading to disability or even death.