Catad_theme Chronic ischemia brain - articles

Chronic cerebrovascular accidents

Published in the magazine:
"PHARMATEKA"; Current reviews; No. 15; 2010; pp. 46-50.

O.V. Kotova
Department of Pathology of the Autonomic Nervous System, Research Center of the First Moscow State Medical University named after. THEM. Sechenov, Moscow

Chronic cerebrovascular accidents (CVA) are a progressive form of cerebrovascular pathology with the gradual development of a complex of neurological and neuropsychological disorders. The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension, atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. IN complex treatment For patients with CNM, drugs are used that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. One of these drugs is Vasobral (dihydroergocriptine + caffeine) - an effective and safe treatment for CNM.
Keywords: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular disease (CCVD) is a progressive form of cerebrovascular pathology with gradual development of neurological and neuropsychological disorders. The main causes leading to chronic hypoperfusion of the brain are hypertension, atherosclerosis, and heart disease accompanied by chronic heart failure. In the complex treatment of patients with CCVD, drugs with comprehensive antioxidant, angioprotective, neuroprotective and neurotrophic action are usually used. One these drugs is Vazobral (dihydroergocryptine + coffein), effective and safe preparation for treatment of CCVD.
Key words: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular accidents (CVA) are a progressive form of cerebrovascular pathology, characterized by multifocal or diffuse ischemic brain damage with the gradual development of a complex of neurological and neuropsychological disorders. This is one of the most common forms of cerebrovascular pathology, usually occurring against the background of general cardiovascular diseases.

Etiology of CNMK
There are many extracerebral causes leading to pathology of cerebral circulation. First of all, these are diseases accompanied by a disorder of systemic hemodynamics, leading to a chronic decrease in adequate blood supply - chronic cerebral hypoperfusion. The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension (AH), atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. Other causes include diabetes mellitus, vasculitis in systemic connective tissue diseases, other diseases accompanied by vascular damage, blood diseases leading to changes in its rheology (erythremia, macroglobulinemia, cryoglobulinemia, etc.).

Pathomorphological changes in CNM
For adequate brain function it is necessary high level perfusion. The brain, whose mass is 2.0-2.5% of body weight, consumes 15-20% of the blood circulating in the body. The main indicator of brain perfusion is the level of blood flow per 100 g of brain matter per minute. The average value of hemispheric cerebral blood flow (CBF) is approximately 50 ml/100 g/min, but there are significant differences in the blood supply to individual brain structures. The magnitude of MK in gray matter is 3-4 times higher than in white matter. At the same time, in the anterior parts of the hemispheres, blood flow is higher than in other areas of the brain. With age, the value of MB decreases, and frontal hyperperfusion also disappears, which is explained by diffuse atherosclerotic changes in cerebral vessels. It is known that with CNM, the subcortical white matter and frontal structures are more affected, which may be explained by the indicated characteristics of the blood supply to the brain. Initial manifestations of insufficiency of cerebral blood supply to the brain occur if the blood flow to the brain is less than 30-45 ml/100 g/min. The advanced stage is observed when the blood supply to the brain decreases to a level of 20-35 ml/100 g/min. The threshold of regional blood flow within 19 ml/100 g/min (functional threshold of blood supply to the brain), at which the functions of the corresponding areas of the brain are impaired, is considered critical. The process of death nerve cells occurs when regional arterial cerebral blood flow is reduced to 8-10 ml/100 g/min (infarction threshold of cerebral blood supply).

In conditions of chronic brain hypoperfusion, which is the main pathogenetic link of CNM, compensation mechanisms are depleted, the energy supply of the brain becomes insufficient, as a result, first functional disorders develop, and then irreversible morphological damage. In chronic cerebral hypoperfusion, a slowdown in cerebral blood flow, a decrease in oxygen and glucose levels in the blood, a shift in glucose metabolism towards anaerobic glycolysis, lactic acidosis, hyper-osmolarity, capillary stasis, a tendency to thrombus formation, depolarization of cells and cell membranes, activation of microglia, which begins to produce neurotoxins, which, along with other pathophysiological processes, leads to cell death.

Damage to small penetrating cerebral arteries (cerebral microangiopathy), on which the blood supply to the deep parts of the brain depends, in patients with CNM is accompanied by a variety of morphological changes in the brain, such as:

diffuse damage to the white matter of the brain (leukoencephalopathy);

multiple lacunar infarcts in deep sections brain;

microinfarctions;

microhemorrhages;

atrophy of the cerebral cortex and hippocampus.

To implement autoregulation of cerebral circulation, it is necessary to maintain certain values ​​of blood pressure (BP) in the main arteries of the head. On average, systolic blood pressure (SBP) in the main arteries of the head should range from 60 to 150 mm Hg. Art. With long-term hypertension, these limits shift slightly upward, so autoregulation does not become impaired for a long time and MB remains at a normal level. Adequate brain perfusion is maintained by increasing vascular resistance, which in turn leads to an increase in the load on the heart. Chronic uncontrolled hypertension leads to secondary changes in the vascular wall - lipohyalinosis, which is observed mainly in the vessels of the microvasculature. The resulting arteriolosclerosis leads to changes in the physiological reactivity of blood vessels. Under these conditions, the decrease blood pressure as a result of the addition of heart failure with a decrease in cardiac output or as a result of excessive antihypertensive therapy, or as a result of physiological circadian changes in blood pressure leads to the occurrence of hypoperfusion in areas of the terminal circulation. Acute ischemic episodes in the basin of deep penetrating arteries lead to the occurrence of small-diameter lacunar infarcts in the deep parts of the brain. If the course of hypertension is unfavorable, repeated acute episodes lead to the emergence of the so-called. lacunar state, which is one of the variants of multi-infarct vascular dementia.

In addition to repeated acute disorders, the presence of chronic ischemia in the areas of terminal circulation is also assumed. A marker of the latter is a rarefaction of the periventricular or subcortical white matter (leukoaraiosis), which pathomorphologically represents a zone of demyelination, gliosis and expansion of the perivascular spaces. In some cases of an unfavorable course of hypertension, subacute development of diffuse damage to the white matter of the brain with a clinical picture of rapidly progressing dementia and other manifestations of disconnection is possible, which is sometimes referred to in the literature as “Binswanger’s disease.”

Another significant factor in the development of CNM is atherosclerotic damage to cerebral vessels, which is usually multiple, localized in the extra- and intracranial parts of the carotid and vertebral arteries, as well as in the arteries of the circle of Willis and their branches, forming stenoses. Stenoses are divided into hemodynamically significant and insignificant. If a decrease in perfusion pressure occurs distal to the atherosclerotic process, this indicates a critical or hemodynamically significant narrowing of the vessel.

It has been shown that hemodynamically significant stenoses develop when the vessel lumen narrows by 70-75%. But cerebral blood flow depends not only on the severity of stenosis, but also on the mechanisms that prevent the development of ischemia: the state of collateral circulation, the ability cerebral vessels to expansion. These hemodynamic reserves of the brain allow “asymptomatic” stenoses to exist without complaints and clinical manifestations. However, the obligatory development of chronic cerebral hypoperfusion during stenosis leads to CNM, which is detected by magnetic resonance imaging (MRI). MRI visualizes periventricular leukoaraiosis (reflecting ischemia of the white matter of the brain), internal and external hydrocephalus (caused by atrophy of brain tissue); Cysts may be detected (as a consequence of previous cerebral infarctions, including clinically “silent” ones). It is believed that CNMC is present in 80% of patients with stenotic lesions of the main arteries of the head. Atherosclerotic changes in the vessels of the brain are characterized not only by local changes in the form of plaques, but also by hemodynamic restructuring of the arteries in the area distal to atherosclerotic stenoses and occlusions. All this leads to the fact that “asymptomatic” stenoses become clinically significant.

The structure of the plaques is also of great importance: the so-called. unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents - often of a transient type. When hemorrhaging into such a plaque, its volume quickly increases with an increase in the degree of stenosis and worsening of the signs of CNM. In the presence of such plaques, blocking the lumen of the vessel up to 70% will be hemodynamically significant.

In the presence of damage to the main arteries of the head, cerebral blood flow becomes very dependent on systemic hemodynamic processes. Such patients are especially sensitive to arterial hypotension, which can occur when moving to a vertical position (orthostatic hypotension), with cardiac arrhythmias leading to a short-term decrease in cardiac output.

Clinical manifestations of CNM
The main clinical manifestations of CNM are disturbances in the emotional sphere, balance and gait disorders, pseudobulbar disorders, impairment of memory and learning ability, neurogenic urination disorders, which gradually lead to maladjustment of patients.

During CNM, three stages can be distinguished:

At stage I, the clinical picture is dominated by subjective disorders in the form of general weakness and fatigue, emotional lability, sleep disturbances, decreased memory and attention, and headaches. Neurological symptoms do not form distinct neurological syndromes, but are represented by anisoreflexia, discoordination, and symptoms of oral automatism. Violations of memory, praxis and gnosis can be identified, as a rule, only when special tests are carried out.

At stage II, there are more subjective complaints, and neurological symptoms can already be divided into distinct syndromes (pyramidal, discoordination, amyostatic, dysmnestic), with one neurological syndrome usually dominating. Professional and social adaptation patients is decreasing.

At Stage III neurological symptoms increase, a clear pseudobulbar syndrome, sometimes paroxysmal conditions (including epileptic seizures); severe cognitive impairment leads to disruption of social and everyday adaptation, complete loss performance. Ultimately, CNMK contributes to the formation of vascular dementia.

Cognitive impairment is a key manifestation of CNM, which largely determines the severity of the patient’s condition. They often serve as the most important diagnostic criterion for CNM and are a sensitive marker for assessing the dynamics of the disease. It is worth noting that the localization and degree vascular changes that are detected by MRI or computed tomography are only partially correlated with the presence, type, and severity of neuropsychological findings. In case of CNMC, there is a more pronounced correlation between the severity of cognitive impairment and the degree of brain atrophy. Correcting cognitive impairment is often critical to improving the quality of life of the patient and his relatives.

Methods for diagnosing cognitive impairment
To assess the overall severity of cognitive defect, the Mini-Mental State Examination scale is most widely used. However this method is not an ideal screening tool, since its results are significantly influenced by the patient's premorbid level and type of dementia (the scale is less sensitive to frontal cortex dysfunction and therefore better detects the early stages of Alzheimer's disease than the early stages of vascular dementia). In addition, its implementation requires more than 10-12 minutes, which the doctor does not always have at an outpatient appointment.

Clock drawing test: subjects are asked to draw a clock with its hands pointing to a specific time. Normally, the subject draws a circle and places numbers from 1 to 12 inside it. in the right order at equal intervals, depicts 2 hands (the hour hand is shorter, the minute hand is longer), starting in the center and showing the specified time. Any deviation from correct test performance is a sign of fairly severe cognitive dysfunction.

Speech activity test: subjects are asked to name as many names of plants or animals as possible in a minute (semantically mediated associations) and words starting with a certain letter, for example “l” (phonetically mediated associations). Normally, most elderly people with secondary and higher education name from 15 to 22 plants and from 12 to 16 words starting with “l” per minute. Naming fewer than 12 semantically mediated associations and fewer than 10 phonetically mediated associations usually indicates significant cognitive dysfunction.

Visual memory test: patients are asked to remember 10-12 images of simple, easily recognizable objects presented on one sheet; Subsequently, the following are assessed: 1) immediate reproduction, 2) delayed reproduction after interference (a verbal association test can be used as an interfering effect), 3) recognition (the patient is asked to recognize previously presented objects among other images). Failure to remember more than half of previously presented images may be considered a sign of severe cognitive dysfunction.

Main directions in the treatment of CNM
The main directions in the treatment of CNM stem from the etiopathogenetic mechanisms that led to this process. The main goal is to restore or improve brain perfusion, which is directly related to the treatment of the underlying disease: hypertension, atherosclerosis, heart disease with the elimination of heart failure.

Taking into account the diversity of pathogenetic mechanisms underlying CNM, preference should be given to agents that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. In this regard, the use of drugs that combine several mechanisms of action is justified. Among such drugs, I would like to mention Vasobral, a combined drug that has both nootropic and vasoactive effects. It contains an ergot derivative (dihydroergocryptine) and caffeine. Dihydroergocriptine blocks α1 and α2 adrenergic receptors of vascular smooth muscle cells, platelets, and erythrocytes, and has a stimulating effect on dopaminergic and serotonergic receptors of the central nervous system.

When using the drug, the aggregation of platelets and erythrocytes decreases, the permeability of the vascular wall decreases, blood supply and metabolic processes in the brain improve, and the resistance of brain tissue to hypoxia increases. The presence of caffeine in Vasobral determines the stimulating effect on the central nervous system, mainly on the cerebral cortex, respiratory and vasomotor centers, and increases mental and physical performance. Studies have shown that Vasobral has a vegetative stabilizing effect, which manifests itself in increased pulse blood filling, normalization of vascular tone and venous outflow, which is due to the positive effect of the drug on the sympathetic nervous system while reducing the activity of the parasympathetic system. A course of treatment with Vasobral leads to a decrease or disappearance of symptoms such as dizziness, headache, palpitations, and numbness of the extremities. Positive dynamics of the neuropsychological status of the patient with CNM are noted: increased attention span; improving orientation in time and space, memory for current events, intelligence; increased mood, decreased emotional lability. The use of Vasobral helps reduce fatigue, lethargy, and weakness; there is a feeling of cheerfulness.

The drug is prescribed in a dose of 2-4 ml (1-2 pipettes) or 1/2-1 tablet 2 times a day for 2-3 months. The drug is taken with a small amount of water. Side effects occur rarely and are mildly expressed. It should be noted that due to the presence of liquid and tablet forms, double dosing and good tolerability, Vasobral is convenient for long-term use, which is extremely important in the treatment of chronic diseases.

Non-drug ways to correct the manifestations of CNM should include:

proper organization of work and rest, avoidance of night shifts and long business trips;

moderate physical exercise, therapeutic exercises, dosed walking;

diet therapy: limiting the total calorie content of food and salt consumption (up to 2-4 g per day), animal fats, smoked meats; introduction of fresh vegetables and fruits, fermented milk and fish products into the diet;

climatic treatment at local resorts, in low altitudes and at sea resorts; balneotherapy, which has a positive effect on central hemodynamics, contractile function of the heart, and the state of the autonomic nervous system; the means of choice are radon, carbon dioxide, sulfide, iodine-bromine baths.

In general, an integrated approach to the treatment of CNM and repeated pathogenetically based course treatment can contribute to better adaptation of the patient in society and prolong the period of his active life.

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general information

The left hemisphere controls the functioning of the right half of the body and is responsible for all types of sensitivity, motor activity, vision, and hearing. Approximately 95% of humanity is right-handed, meaning their left hemisphere of the brain is dominant.

It contains centers responsible for the use and perception of different types of speech, mathematical operations, logical, abstract, analytical thinking, the formation of dynamic stereotypes, and the perception of time.

Symptoms

The symptoms that appear depend on the location and size of the lesion. They are divided into general cerebral, vegetative and focal. With cerebral ischemia, general cerebral disorders are less pronounced than with hemorrhagic stroke, and in some cases they may be absent. The most common:

• a sudden attack of severe headache;
• dizziness;
• loss of consciousness, with extensive lesions - coma of varying severity;
• nausea and vomiting;
• convulsions.

Any form of stroke is accompanied by the manifestation of focal symptoms, and their combination and severity are determined by the functional characteristics of the affected area. Left-sided stroke is characterized by:

• paralysis right side bodies of varying degrees of severity;
• sensory disturbances on the right side of the body;
• impairment of vision, hearing, smell, up to complete loss of the ability to perceive relevant stimuli. With severe lesions, the disorder can affect both sides;
• impaired sense of balance and coordination of movements;
• speech disorders.

Suspicion of an attack and first aid

A stroke is an emergency; pathological changes in the lesion develop in a matter of minutes. The faster the patient is provided health care, the greater the chance of a successful outcome.

If your attention is drawn to a person with a strange gait or an unnaturally asymmetrical face, you should:

• Talk to him. With a left-sided stroke, speech is unintelligible, the person is unable to name himself, place, time, does not understand the question or cannot utter a word.
• Ask to smile or stick out your tongue. The asymmetry of the face will increase; with lesions of the left hemisphere, the movements of the facial muscles of the right half of the face are greatly hampered.
• Ask for a show of hands. A stroke is indicated by impaired mobility of the right hand.

Identification of even one of the symptoms is sufficient grounds for an emergency call to the ambulance regarding a suspected stroke. Before the doctors arrive, you must:

• Lay the victim on his side, placing something soft under his head to protect the person in case of possible convulsions;
• Provide air flow;
• Unfasten, loosen, if possible, remove all parts of clothing that impede breathing;
• If it is possible, measure the pressure; an antihypertensive drug can be given only if the victim is conscious and has with him the medicine previously prescribed by the doctor;
• If convulsions develop, open the patient’s mouth;
• If breathing or heart stops, begin resuscitation.

We bring to your attention a video about what a stroke is and how to provide first aid during an attack:

Therapy

Treatment of ischemic stroke begins directly on site. Emergency measures depend on the severity of the patient’s condition and are primarily aimed at stabilizing the condition for transportation to a specialized department.

Immediately after hospitalization, studies are carried out to determine the general physical condition patient, location and size of the lesion. Basic treatment for ischemic strokes is aimed at restoring blood circulation in the affected area, maintaining and restoring vital functions of the body, and preventing possible complications.

Within a few hours of the onset of the attack, the patient is given a thrombolytic drug to dissolve the clot. After this period, thrombosis can only be eliminated surgically. The patient is prescribed drugs that improve blood microcirculation and vascular-strengthening drugs to normalize blood circulation.

For recovery and normalization metabolic processes neurotrophics are prescribed in brain tissue.

As part of the prevention of thrombotic complications, antiplatelet agents, anticoagulants and drugs that improve blood flow are prescribed.

At the same time, treatment of the underlying disease and symptomatic treatment possible complications from vital organs.

The most dangerous early consequences of a stroke are cerebral edema, coma and recurrent stroke, which are the most common cause of death in patients in the acute period.

The severity of residual neurological damage varies greatly, ranging from minor disturbances in speech and motor functions to complete loss of the ability to move and the ability to perform minimal self-care. After a stroke, mental disorders, memory disorders, and speech disorders are observed.

Forecast for life

The prognosis for stroke in general is rather unfavorable; the possible consequences of each specific case are extremely difficult to predict, even after a complete examination of the patient. The prognosis worsens for older people, as well as in the presence of certain chronic diseases.

According to statistics, early complications of ischemic stroke cause death in approximately 25% of patients within a month after a stroke.

Approximately 60% continue to have disabling neurological disorders.

Survival rate within a year approaches 70%, within five years - about 50%, about 25% of surviving patients overcome the ten-year threshold. Recurrent strokes occur in approximately 30% of patients within five years of the first episode.

There are specially developed methods for assessing the risk of a second strike.

Recovery period

The recovery period after a stroke lasts up to three years. Patients are prescribed a diet depending on the condition and the presence of underlying diseases, massage courses, and therapeutic exercises. Spa treatment is indicated. Patients are prescribed maintenance therapy, often lifelong.

There are many useful information about recovery after an illness:

Acute ischemic cerebrovascular accident

Sudden changes in blood flow to the brain are classified as hemorrhagic (bleeding) and ischemic disorders. Such a division is important for the correct choice of therapy method.

The classic abbreviated name for the pathology in acute cerebrovascular accident is “ischemic stroke.” If hemorrhage is confirmed, then it is considered hemorrhagic.

In ICD-10, ACME codes may vary, depending on the type of violation:

• G45 is an established designation for transient cerebral attacks;
• I63 - recommended for statistical registration of cerebral infarction;
• I64 - an option used for unknown differences between cerebral infarction and hemorrhage, used when a patient is admitted in an extremely serious condition, unsuccessful treatment and imminent death.

The frequency of ischemic strokes exceeds hemorrhagic strokes by 4 times and is more associated with general human diseases. The problem of prevention and treatment is considered in programs at the state level, because 1/3 of patients who have suffered the disease die in the first month and 60% remain permanently disabled requiring social assistance.

Why does a lack of blood supply to the brain occur?

Acute ischemic cerebrovascular accident is often a secondary pathology and occurs against the background of existing diseases:

• arterial hypertension;
• widespread atherosclerotic vascular lesions (up to 55% of cases develop due to pronounced atherosclerotic changes or thromboembolism from plaques located in the aortic arch, brachiocephalic trunk or intracranial arteries);
• previous myocardial infarction;
• endocarditis;
• heart rhythm disturbances;
• changes in the valvular apparatus of the heart;
• vasculitis and angiopathy;
• vascular aneurysms and developmental anomalies;
• blood diseases;
• diabetes mellitus.

Up to 90% of patients have changes in the heart and main arteries of the neck. The combination of these reasons sharply increases the risk of ischemia.

Transient attacks are most often caused by:

• spasm of the arterial brain stems or short-term compression of the carotid and vertebral arteries;
• embolization of small branches.

The following risk factors can provoke the disease:

• elderly and senile age;
• excess weight;
• the effect of nicotine on blood vessels (smoking);
• experienced stress.

The basis of the influencing factors is the narrowing of the lumen of the vessels through which blood flows to the brain cells. However, the consequences of such a malnutrition may vary according to:

• stamina,
• localization,
• prevalence,
• severity of vessel stenosis,
• gravity.

A combination of factors determines the form of the disease and clinical symptoms.

Pathogenesis of various forms of acute cerebral ischemia

Transient ischemic attack was previously called transient cerebrovascular accident. It is identified as a separate form because it is characterized by reversible disorders; the heart attack does not have time to form. Usually the diagnosis is made retrospectively (after the disappearance of the main symptoms), within a day. Before this, the patient is treated as if he had a stroke.

The main role in the development of hypertensive cerebral crises belongs to the increased level of venous and intracranial pressure with damage to the walls of blood vessels and the release of fluid and protein into the intercellular space.

The feeding artery is necessarily involved in the development of ischemic stroke. The cessation of blood flow leads to oxygen deficiency in the lesion formed in accordance with the boundaries of the basin of the affected vessel.

Local ischemia causes necrosis of an area of ​​brain tissue.

Depending on the pathogenesis of ischemic changes, types of ischemic strokes are distinguished:

• atherothrombotic - develops when the integrity of an atherosclerotic plaque is disrupted, which causes complete closure of the internal or external feeding arteries of the brain or their sharp narrowing;
• cardioembolic - the source of thrombosis is pathological growths on the endocardium or heart valves, fragments of a blood clot, they are delivered to the brain with the general blood flow (especially when the foramen ovale is not closed) after attacks of atrial fibrillation, tachyarrhythmia, atrial fibrillation in patients in the post-infarction period;
• lacunar - more often occurs when small intracerebral vessels are damaged in arterial hypertension, diabetes mellitus, differs small in size lesion (up to 15 mm) and relatively minor neurological disorders;
• hemodynamic - cerebral ischemia with general decline blood circulation speed and pressure drop against the background of chronic heart diseases, cardiogenic shock.

It is worth explaining the variant of development of strokes of unknown etiology. This often happens when there are two or more reasons. For example, in a patient with carotid artery stenosis and fibrillation after an acute infarction. It should be taken into account that elderly patients already have stenosis of the carotid arteries on the side of the suspected disorder, caused by atherosclerosis, in the amount of up to half the lumen of the vessel.

Stages of cerebral infarction

The stages of pathological changes are distinguished conditionally; they are not necessarily present in every case:

• Stage I - hypoxia (oxygen deficiency) disrupts the permeability of the endothelium of small vessels in the lesion (capillaries and venules). This leads to the transfer of fluid and protein from the blood plasma into the brain tissue and the development of edema.
• Stage II - at the level of capillaries, pressure continues to decrease, which disrupts the functions of the cell membrane, the nerve receptors located on it, and electrolyte channels. It is important that all changes are reversible for now.
• Stage III - cell metabolism is disrupted, lactic acid accumulates, and a transition to energy synthesis occurs without the participation of oxygen molecules (anaerobic). This species does not allow maintaining the necessary level of life of neuronal cells and astrocytes. Therefore, they swell and cause structural damage. Clinically expressed in the manifestation of focal neurological signs.

What is the reversibility of the pathology?

For timely diagnosis, it is important to establish a period of symptom reversibility. Morphologically, this means preserved neuronal functions. Brain cells are in a phase of functional paralysis (parabiosis), but retain their integrity and usefulness.

In the irreversible stage, it is possible to identify a zone of necrosis in which cells are dead and cannot be restored. Around it there is an ischemic zone. Treatment is aimed at supporting adequate nutrition of neurons in this area and at least partially restoring function.

Modern research has shown extensive connections between brain cells. A person does not use all reserves and opportunities in his life. Some cells are able to replace dead ones and provide their functions. This process is slow, so doctors believe that rehabilitation of a patient after an ischemic stroke should continue for at least three years.

Signs of transient cerebral circulatory disorders

Clinicians include the following in the group of transient cerebrovascular accidents:

• transient ischemic attacks (TIA);
• hypertensive cerebral crises.

Features of transient attacks:

• the duration ranges from several minutes to a day;
• every tenth patient after a TIA develops an ischemic stroke within a month;
• neurological manifestations are not grossly severe;
• mild manifestations of bulbar palsy (focus in the brain stem) with oculomotor disorders are possible;
• blurred vision in one eye combined with paresis (loss of sensation and weakness) in the limbs of the opposite side (often accompanied by incomplete narrowing of the internal carotid artery).

Features of hypertensive cerebral crises:

• the main manifestations are cerebral symptoms;
• focal signs occur rarely and are mild.

The patient complains of:

• sharp headache, most often in the back of the head, temples or crown;
• state of stupefaction, noise in the head, dizziness;
• nausea, vomiting.

People around note:

• temporary confusion;
• excited state;
• sometimes - a short-term attack with loss of consciousness, convulsions.

Signs of a cerebral stroke

Ischemic stroke means the occurrence of irreversible changes in brain cells. At the clinic, neurologists distinguish periods of the disease:

• acute - continues from the onset of symptoms for 2–5 days;
• acute - lasts up to 21 days;
• early recovery - up to six months after the elimination of acute symptoms;
• late recovery - takes from six months to two years;
• consequences and residual effects - over two years.

Some doctors continue to distinguish small forms of stroke or focal ones. They develop suddenly, the symptoms do not differ from cerebral crises, but last up to three weeks, then completely disappear. The diagnosis is also retrospective. During the examination, no organic abnormalities were found.

Cerebral ischemia, in addition to general symptoms (headaches, nausea, vomiting, dizziness), manifests itself locally. Their nature depends on the artery that is “turned off” from the blood supply, the state of the collaterals, and the dominant hemisphere of the patient’s brain.

Let's consider the zonal signs of blockage of the cerebral and extracranial arteries.

If the internal carotid artery is damaged:

• vision is impaired on the side of the blocked vessel;
• the sensitivity of the skin on the limbs and face on the opposite side of the body changes;
• paralysis or muscle paresis is observed in the same area;
• possible loss of speech function;
• inability to realize one’s illness (if the focus is in the parietal and occipital lobes of the cortex);
• loss of orientation in parts of one’s own body;
• loss of visual fields.

Narrowing of the vertebral artery at the level of the neck causes:

• hearing loss;
• nystagmus of the pupils (twitching when deviating to the side);
• double vision.

If the narrowing occurs at the confluence with the basilar artery, then the clinical symptoms are more severe, since cerebellar damage predominates:

• inability to move;
• impaired gesticulation;
• chanted speech;
• violation of joint movements of the trunk and limbs.

If there is insufficient blood flow in the basilar artery, manifestations of visual and brain stem disorders (impaired breathing and blood pressure) occur.

If the anterior cerebral artery is damaged:

• hemiparesis of the opposite side of the body (unilateral loss of sensation and movement), often in the leg;
• slowness of movements;
• increased tone of flexor muscles;
• loss of speech;
• inability to stand and walk.

Obstruction of the middle cerebral artery:

• when the main trunk is completely blocked, a deep coma occurs;
• lack of sensitivity and movement in half of the body;
• inability to fix the gaze on an object;
• loss of visual fields;
• loss of speech;
• inability to distinguish left side from the right.

Obstruction of the posterior cerebral artery causes:

• blindness in one or both eyes;
• double vision;
• gaze paresis;
• seizures;
• large tremor;
• impaired swallowing;
• paralysis on one or both sides;
• respiratory and blood pressure disturbances;
• brain coma

When the optic geniculate artery is blocked, the following appears:

• loss of sensation in opposite side body, face;
• severe pain when touching the skin;
• inability to localize the stimulus;
• perverted perceptions of light, knocking;
• “thalamic hand” syndrome - the shoulder and forearm are bent, the fingers are extended at the terminal phalanges and bent at the base.

Impaired blood circulation in the area of ​​the visual thalamus is caused by:

• sweeping movements;
• large tremor;
• loss of coordination;
• impaired sensitivity in half of the body;
• sweating;
• early bedsores.

In what cases can acute stroke be suspected?

The above clinical forms and manifestations require careful examination, sometimes not by one, but by a group of doctors of different specialties.

Cerebrovascular accident is very likely if the patient exhibits the following changes:

• sudden loss of sensation, weakness in the limbs, face, especially one-sided;
• acute loss of vision, the occurrence of blindness (in one eye or both);
• difficulty in pronunciation, understanding words and phrases, composing sentences;
• dizziness, loss of balance, impaired coordination of movements;
• confusion;
• lack of movement in the limbs;
• intense headache.

Additional examination allows us to establish the exact cause of the pathology, the level and location of the vessel lesion.

Purpose of diagnosis

Diagnosis is important for choosing a treatment method. To do this you need:

• confirm the diagnosis of stroke and its form;
• identify structural changes in brain tissue, focal area, affected vessel;
• clearly distinguish between ischemic and hemorrhagic forms of stroke;
• based on pathogenesis, establish the type of ischemia for starting specific therapy in the first 3–6 in order to get into the “therapeutic window”;
• assess indications and contraindications for drug thrombolysis.

It is practically important to use diagnostic methods on an emergency basis. But not all hospitals have enough medical equipment to operate around the clock. The use of echoencephaloscopy and cerebrospinal fluid studies yields up to 20% errors and cannot be used to resolve the issue of thrombolysis. The most reliable methods should be used in diagnosis.

Computed and magnetic resonance imaging allows you to:

• distinguish a stroke from space-occupying processes in the brain (tumors, aneurysms);
• accurately determine the size and location of the pathological focus;
• determine the degree of edema, disturbances in the structure of the ventricles of the brain;
• identify extracranial locations of stenosis;
• diagnose vascular diseases that contribute to stenosis (arteritis, aneurysm, dysplasia, vein thrombosis).

Computed tomography is more accessible and has advantages in research bone structures. And magnetic resonance imaging better diagnoses changes in the parenchyma of brain tissue and the size of edema.

Echoencephaloscopy can only reveal signs of displacement of the median structures with a massive tumor or hemorrhage.

During ischemia, cerebrospinal fluid rarely shows slight lymphocytosis with increased protein. Most often no change. If the patient has a hemorrhage, blood may appear. And with meningitis - inflammatory elements.

Ultrasound examination of blood vessels - Dopplerography method of the arteries of the neck indicates:

• development of early atherosclerosis;
• stenosis of extracranial vessels;
• sufficiency of collateral connections;
• the presence and movement of an embolus.

Duplex sonography can determine the condition of the atherosclerotic plaque and artery walls.

Cerebral angiography is performed if technical capabilities are available. emergency indications. Typically, the method is considered more sensitive in identifying aneurysms and foci of subarachnoid hemorrhage. Allows you to clarify the diagnosis of pathology identified on tomography.

Cardiac ultrasound is performed to detect cardioembolic ischemia in heart disease.

Examination algorithm

The examination algorithm for suspected acute stroke proceeds according to the following plan:

1. examination by a specialist in the first 30-60 minutes after the patient’s admission to the hospital, examination of the neurological status, clarification of the medical history;
2. taking blood and studying its coagulability, glucose, electrolytes, enzymes for myocardial infarction, and the level of hypoxia;
3. if it is not possible to conduct MRI and CT, do an ultrasound of the brain;
4. spinal puncture to exclude hemorrhage.

Treatment

The most important importance in the treatment of cerebral ischemia belongs to the urgency and intensity in the first hours of admission. 6 hours from the onset of clinical manifestations is called the “therapeutic window”. This is the time for the most effective use of the thrombolysis technique to dissolve a blood clot in a vessel and restore impaired functions.

Regardless of the type and form of stroke, the following are carried out in the hospital:

• increased oxygenation (filling with oxygen) of the lungs and normalization of respiratory function (if necessary, through transfer and mechanical ventilation);
• correction of impaired blood circulation (heart rhythm, blood pressure);
• normalization of electrolyte composition, acid-base balance;
• reducing cerebral edema by administering diuretics and magnesium;
• relief of agitation and seizures with special antipsychotic drugs.

A semi-liquid diet is prescribed for the patient's nutrition; if swallowing is impossible, parenteral therapy is prescribed. The patient is provided ongoing care, prevention of bedsores, massage and passive gymnastics.

This allows you to get rid of negative consequences as:

• muscle contractures;
• congestive pneumonia;
• DIC syndrome;
• pulmonary embolism;
• damage to the stomach and intestines.

Thrombolysis is a specific therapy for stroke of ischemic type. The method allows you to preserve the viability of neurons around the necrosis zone, returning all weakened cells to life.

You can read more about the indications and methods of thrombolysis in this article.

The administration of anticoagulants begins with Heparin derivatives (in the first 3–4 days). Drugs of this group are contraindicated for:

• high blood pressure;
• peptic ulcer;
• diabetic retinopathy;
• bleeding;
• impossibility of organizing regular monitoring of blood clotting.

After 10 days they switch to indirect anticoagulants.

Drugs that improve metabolism in neurons include Glycine, Cortexin, Cerebrolysin, Mexidol. Although they are not listed as effective in the evidence-based medicine database, their use leads to improvement in the condition.

Patients may need symptomatic treatment depending on the specific manifestations: anticonvulsants, sedatives, painkillers.

Antibacterial agents are prescribed to prevent kidney infection and pneumonia.

Forecast

Data on prognosis are available only for ischemic infarction; other changes represent precursors indicating an increased risk of stroke.

Atherothrombotic and cardioembolic types of ischemia have the most dangerous mortality rate: during the first month of the disease, from 15 to 25% of patients die. Lacunar stroke is fatal in only 2% of patients. The most common causes of death:

• in the first 7 days - cerebral edema with compression of vital centers;
• up to 40% of all deaths occur in the first month;
• after 2 weeks - pulmonary embolism, congestive pneumonia, cardiac pathology.

Patient survival time:

• 1 year - up to 70%;
• 5 years - 50%;
• 10 years - 25%.

After this period, 16% die per year.

The following have signs of disability:

• after a month - up to 70% of patients;
• six months later - 40%;
• by the second year - 30%.

The rate of recovery is most noticeable in the first three months by an increase in the range of movements, while the functions of the legs return faster than the arms. Remaining immobility in the hands after a month is an unfavorable sign. Speech is restored after years.

The rehabilitation process is most effective with the volitional efforts of the patient and the support of loved ones. Complicating factors include advanced age and heart disease. Seeing a doctor during the phase of reversible changes will help avoid serious consequences.

Instructions for use Indapamide, at what pressure should it be taken?

Indapamide is an antihypertensive drug that is used for hypertension and edema caused by heart failure. But you can take this drug only after consulting a doctor, a full examination and passing the necessary tests, since it has many contraindications. Self-medication is strictly prohibited. You can read a detailed description of Indapamide in our article.

Indapamide: what is the drug prescribed for?

General characteristics of the drug

Indapamide is a white, round, film-coated tablet with convex surfaces. The section clearly shows 2 layers of the drug substance. The inner layer is yellow. This drug belongs to a group related to thiazide diuretics, having moderate hypotensive and diuretic properties. The drug is preferred because it causes fewer side effects and has fewer contraindications. More suitable for long-term treatment than acute conditions. The maximum effect is observed after daily use of Indapamide for at least 8 weeks.

Mechanism of action on the body

The use of 2.5 mg of Indapamide per day leads to a pronounced and prolonged hypotensive effect with a mild diuretic effect. Increasing the dose will not enhance the hypotensive effect, but will enhance the diuretic effect. "Indapamide" leads to a weakening of the muscle layer of blood vessels, which causes blood pressure to decrease. It also inhibits the reabsorption of primary urine, and diuresis increases.

Pharmacological effect on the body

"Indapamide" inhibits ion exchange, as a result of which the level of catecholamines in the blood increases. This leads to a decrease in the force of contraction of the muscle fibers of the medial tunic of the arteries. As vascular tone decreases, blood pressure (BP) decreases. In addition to the pronounced hypotensive effect, there is also a diuretic effect. The drug acts on the proximal and distal tubules of the loop of Henle, where the reabsorption of water, proteins, glucose, sodium, potassium, chlorine and much more occurs, due to which the reabsorption of sodium, chlorine and water is inhibited. Thus, more secondary urine is produced from primary urine.

Indapamide, a drug for high blood pressure

The degree of change in the tubules is directly proportional to the dosage of the medicine, that is, the more you take, the greater the diuretic effect. The drug does not penetrate the blood-brain barrier, resulting in no central effect and fewer side effects. Indapamide can be taken by patients with renal failure, because it does not affect the condition of the glomeruli of the kidneys and does not increase the load on the kidneys.

Why is Indapamide prescribed?

Since the drug has a moderate effect, it is prescribed for continuous use. If an emergency occurs, such as a hypertensive crisis, it is better to use more effective means. This drug is ideal for treating hypertension. The patient himself will be able to regulate the effectiveness: if the diuretic effect is not needed, simply reduce the daily dose to 1.25 mg. It is also good for patients with hypervolemia. Kidney diseases are often complicated by pathologies such as renal arterial hypertension. And here the appointment of "Indapamide" will be very appropriate.

Therapy of arterial hypertension with Indapamide

The method of using Indapamide will depend on the degree of complexity of hypertension. If a hypertensive crisis occurs, you need to take a larger dose, because the diuretic effect in this case will help cope with the preload on the heart and reduce the volume of circulating blood. In addition, it must be combined with other antihypertensive drugs. And if the pressure is moderately increased, then you can limit yourself to one drug and a minimum daily dose of 2.5 mg.

How to take Indapamide

What effect should you expect when combined with other drugs?

• When combined with antiarrhythmic drugs, arrhythmogenicity increases, especially with Quinidine, Disopyramide and Amiodarone.
• Non-steroidal anti-inflammatory drugs, glucocorticoids and sympathomimetics eliminate the hypotensive effect of Indapamide, and Baclofen enhances it.
• Carrying agents, cardiac glycosides and mineralocorticoids increase the likelihood of developing hypokalemia. Therefore, it is necessary to monitor potassium levels.
• X-ray contrast agents containing large amounts of iodine increase the likelihood of dehydration.
• "Indapamide" enhances the effect of muscle relaxants.
• Cyclosporine increases creatinine levels in the blood.

Contraindications:

1. individual hypersensitivity to individual components of the drug;
2. decompensated diabetes mellitus;
3. acute cerebrovascular accident;
4. gout;
5. pregnancy;
6. lactation period;
7. low potassium;
8. liver diseases;
9. use before adulthood.

Instructions for use Indapamide

"Indapamide" during pregnancy

During pregnancy and breastfeeding, taking Indapamide is not recommended, since the effectiveness and safety have not been established. This drug can slow down the growth and development of the fetus in the womb and lead to its malnutrition. And since it is excreted along with milk, use during lactation is not recommended. In cases where treatment is necessary, it is better to refrain from breastfeeding.

Side effect:

1. Immune reactions - urticaria, dermatoses, anaphylactic shock, Quincke's edema.
2. From the central nervous system - dizziness, headaches, weakness, aches throughout the body, paresthesia.
3. The effect on the gastrointestinal tract is manifested by nausea, vomiting, dry mouth, constipation.
4. From the outside of cardio-vascular system– arrhythmia, prolongation of QT waves on the ECG, orthostatic arterial hypotension.
5. From the respiratory system - cough, rhinitis, sinusitis.
6. Changes in tests - decreased platelet count, anemia, leukopenia, agranulocytosis, increased amount of calcium, decreased potassium and sodium, increased urea and creatinine.

Effect of the drug on the ability to work with machinery and drive a car

Indapamide drug for hypertensive patients

The drug lowers blood pressure, which means hypotension is possible. Due to the diuretic effect, long-term use may cause EBV disruption. Both conditions can impair the ability to operate machinery and drive a car.

Analogs of a drug for the treatment of hypertension

If side effects occur, the medicine can be changed. It is best to use another representative of the thiazide-like diuretics. Do not select medications on your own; you need to consult a specialist.

List of drugs:
"Arifon"
"Vazopamide"
"Indapamide Sr",
"Ypres Long"
"Xipogama"
"Ravel Sr",
"Softensif."

"Indapamide" is a mild drug with dual action, due to which it is often used for various pathologies. Mostly patients leave positive reviews. You cannot start treatment on your own, only after consulting a doctor. Before taking the drug, be sure to read the contraindications and if you find at least one point that bothers you, then it is better to abandon this drug. If side effects occur during long-term use, you should stop treatment. Consult a specialist and he may prescribe a similar drug.

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Cerebrovascular accident is one of the most dangerous pathologies. After all, the brain controls all processes in the body: breathing, heartbeat, motor activity, speech, thoughts. If such a misfortune occurs, then social vitality goes downhill, in the worst case, human life fades away.

The symptoms of the pathology will be different for each person, since they completely depend on the severity of the process and the location of the pathological focus.

According to the severity of the process, they are distinguished:

• Acute cerebrovascular accident;
• Chronic circulatory failure.

An acute violation of the blood supply of certain vessels entails a sharp lack of oxygen and nutrients in the tissues, which causes hypoxia of the area, ischemia and further death. Therefore, symptoms will depend on the location of the outbreak.

Acute cerebrovascular accident can cause short-term pathology: transient ischemic attack (TIA) and ischemic and hemorrhagic strokes.

Chronic disruption of the blood supply to blood vessels and the nutrition of certain areas of the cortex and white matter of the brain leads to the development of dyscirculatory encephalopathy.

Blood supply to the brain

Knowing the location of the lesion is very important for an objective choice of further treatment tactics and will help to quickly cope with the disease. To do this, you need to know the anatomy of the location of blood vessels in the brain.

The blood supply to the brain is provided by vessels that originate from two different sources: the carotid arteries and the vertebral arteries. The main arteries in which blockage of a vessel or its rupture most often occur are the cerebral arteries: the anterior, middle, and posterior cerebral arteries.

Depending on the location of the ischemic focus, the pool in which blood circulation is impaired is determined. The anterior and middle cerebral arteries originate from the carotid arteries, which causes a higher incidence of damage than the posterior cerebral artery. This is explained by the fact that the force with which blood flows through the vessels of the brain is greater in the anterior and posterior cerebral arteries, since the carotid artery is in close proximity to the heart in relation to the vertebral vessels.

Causes of blood supply disorders

The reasons for the violation of sufficient blood supply can be various pathologies and processes:

• Vessel aneurysm.
• Thrombosis is the formation of a plaque on the wall of a vessel with an increased content of cholesterol in the blood, high-density lipoproteins at the injured site of the endothelium. The plaque grows, gradually obscuring the lumen of the vessel. In this case, chronic insufficiency of cerebral blood supply occurs, which can turn into acute. This can happen if a blood clot completely blocks the lumen of the artery, and an area of ​​the brain stops receiving oxygen and nutrients.
• Kinks of blood vessels.
• Malformations are a cluster of small vessels that intertwine and form peculiar nodes. They are insolvent and under any stress (physical, emotional) due to increased blood flow they can rupture, which will lead to hemorrhage in the brain.
• Embolism with gas, thrombus, air.
• Hypertension - increases the risk of hemorrhage due to uncontrolled blood pressure. There are two reasons for the manifestations that occur with arterial hypertension: high blood pressure, which exerts a greater force on the vessels and reduces their resistance, and rigidity of the vascular wall (rapid wear of the vessels with increased work in resistance to high blood flow due to hypertension).
• Chronic fatigue - the brain needs to receive more blood and oxygen with increased activity, which quickly depletes the body and brain activity, which can lead to chronic cerebrovascular insufficiency.
• Concussions, head injuries, bruises and hemorrhages.
• Cervical osteochondrosis - vertebrae and hernias put pressure on the vertebral artery, which causes insufficient nutrition of the brain tissue of the posterior cerebral artery basin.

Acute cerebrovascular accident

Acute cerebrovascular accident causes the following diseases:

1. Hemorrhagic stroke;
2. Ischemic stroke;
3. Transient ischemic attack.

Symptoms of acute disorder brain activity vary depending on the location of the lesion and can be observed in the patient to varying degrees and duration:

• General cerebral symptoms - dizziness, nausea, vomiting, depression of consciousness (from stupor to coma) - occur due to swelling of the brain and tissue pressure on the meninges;
• Impaired sensitivity;
• Impaired motor activity - from mild paresis to plegia;
• Violation of the correct full activity of the senses;
• Loss of coordination;
• Brainstem symptoms - disturbance of respiratory activity, cardiac activity, vision, hearing, swallowing (the centers for regulating the listed functions are located in the brainstem);
• Decreased cognitive abilities of a person - impaired mental activity, deterioration of memory, speed of thinking;
• Convulsions, epileptic seizures.

Ischemic stroke is different in that disturbances occur against the background of normal pressure and are caused by blockage of the supply vessel. Fabric does not receive necessary substances, ischemia occurs, against the background of which venous congestion may occur.

This will provide the first symptoms - nausea, vomiting, dizziness, acute headache. Next, the ischemic area ceases to perform its functions, and some of the above symptoms appear. If treatment is ineffective or untimely, the area becomes necrotic, and lost functions cannot be restored.

Hemorrhagic stroke occurs when a blood vessel ruptures as a result of high pressure and vascular tension, aneurysm, cerebral vascular malformation. This type of stroke, unlike ischemic stroke, is often accompanied by clouding of consciousness.

The focus of hemorrhage can be so large that the brain tissue is displaced to the side, which entails dislocation syndrome - deviation along the axis (often with ventricular hemorrhages) and further wedging of the brain stem into the foramen magnum. This is the opening through which the spinal cord connects to the brain. This phenomenon is very dangerous for human life.

Clinically, a transient ischemic attack completely resembles an ischemic stroke, but differs in that the symptoms disappear without a trace within 24 hours. This syndrome is caused by spasm of the vessels that supply the pathological area or by a passing thrombus (embolus that has independently passed beyond the occluded part.

Diagnosis of strokes consists in correctly collecting anamnesis of the disease and life, identifying all clinical manifestations and conducting instrumental methods research.

The most informative method is CT or MRI. Computed tomography is more often used, since its advantage is the rapid determination of fresh blood in soft tissues. The lesion can not be seen immediately, but after a few days. In this case, in order not to waste time, the diagnosis is made at the clinic and the appropriate therapy is selected.

Treatment of acute cerebrovascular accident is basically the same, aimed at restoring damaged cells and reducing the area of ​​necrosis. For this purpose, preparations of B vitamins are used (to restore the myelin sheath), metabolic preparations (to improve nutrition and quick recovery cells; help cells that perform double workload), drugs aimed at eliminating complications (pulmonary edema, brain swelling, cardiac arrest, dislocation syndrome), neuroprotectors (drugs that protect brain cells from harmful influence environment).

One distinctive feature in the treatment of various types of pathology is drugs aimed at eliminating the cause of symptoms. For ischemic stroke, drugs are used that can thin the blood, increase its rheological properties and fluidity. For this purpose, anticoagulants of direct action and then indirect action are used initially. After normalization of blood flow, patients switch to lifelong use of antiplatelet agents.

Hemorrhagic stroke, on the contrary, requires the use of hemostatic agents - prothrombin, aminocaproic acid and other drugs.

Chronic cerebrovascular accident

Discirculatory encephalopathy can develop due to 3 factors.

• Multi-infarction conditions - the reasons for this development of the disease are embolization of small vessels of the brain with blood clots from the heart. They appear due to the development of atrial fibrillation.
• Binswanger's disease provokes thickening of the walls and narrowing of the lumen of the small arteries of the brain, which is why the white matter often suffers. Neuronal death is observed locally, scattered throughout the brain tissue.
• Impairment of the patency of the main arteries supplying the brain - the vertebral and carotid arteries. Blood flow decreases over time, so chronic insufficiency of blood supply to the brain occurs.

These causes cause symptoms such as sleep disturbances, deterioration of cognitive abilities (becomes worse memory, they stop solving complex logical tasks, thinking deteriorates), dementia is observed (memory loss in various manifestations).

Diagnosis of the disease is carried out by collecting anamnesis. At that moment, the doctor must suspect a certain diagnosis, which must be confirmed instrumentally.

The patient should consult with an ophthalmologist to examine the fundus of the eye, since the retina is a mirror of the blood vessels of the brain.

Angiography is performed. It will identify small and large blood clots or spasms that lead to permanent occlusion of small vessels.

Drugs to improve cerebral circulation

Cerebrovascular accident What are the symptoms?

An electroencephalogram will show those small tissue lesions after blockage of blood vessels. Potentials are recorded from healthy living tissue. Changes in the electroencephalogram will show organic changes brain substances.

Treatment of chronic dyscirculatory encephalopathy is carried out with drugs that improve blood rheology and blood flow in the vessels. Essentially, the treatment consists of metabolic drugs that strengthen the vascular wall, reduce blood viscosity, improve its rheological properties, control thrombus formation and the amount of cholesterol and lipoproteins of various groups in the blood.

Proper timely treatment will help protect yourself from complications and death.

Cerebral circulation is the movement of blood through the vessels of the brain and spinal cord. The pathological process that causes cerebrovascular accident is characterized by damage to the cerebral and main arteries, cerebral and jugular veins, as well as venous sinuses. Pathologies of cerebral vessels are different: thrombosis, kinks and looping, embolism, narrowing of the lumen, vascular aneurysms. The concept of cerebrovascular insufficiency can generally be defined as a discrepancy between the amount of blood needed by the brain and the amount of its actual delivery.

Causes

The causes of disorders primarily include atherosclerotic vascular damage. Atherosclerosis is a disease in which a plaque forms in the lumen of a vessel, which interferes with the normal passage of blood through a narrowed area. This plaque can increase in size over time, accumulating platelets. As a result, a blood clot is formed, which either completely closes the lumen of the vessel, or breaks off and is carried away with the blood into the vessels of the brain, clogging them, leading to a stroke, that is, an acute disorder of cerebral circulation.

Another cause of the disease is considered to be hypertension, since many hypertensive patients often do not take their condition seriously when their blood pressure increases and the treatment of this disease.

Like any organ, the brain needs proper rest. If a person overloads it with work, the brain gradually gets tired and exhausts all its resources. Chronic fatigue can also be attributed to the causes of circulatory disorders in the brain. Osteochondrosis of the cervical spine due to compression of the arteries supplying the brain disrupts its blood supply and functionality.

Head injuries such as concussions, bruises and hemorrhages do not go away without leaving a trace. They cause compression of the brain centers, which impairs cerebral circulation, which, in turn, can lead to death.

Types of violations

There are two types of cerebral circulatory disorders: chronic and acute. An acute disorder (ACVA) always develops very quickly - in a matter of hours and even minutes.

ACVA is divided into stroke and transient cerebrovascular accident:

• Hemorrhagic stroke is a condition that occurs due to hemorrhage in tissue when a vessel ruptures under the influence of any factors;
• Ischemic stroke is cerebral hypoxia, which developed after the lumen of the blood vessel supplying this area was closed;
• Transient cerebrovascular accidents are local disturbances in the blood supply to the brain that usually do not affect vital areas and do not cause serious problems.

Chronic cerebral circulatory disorders develop over the years. At the initial stage, symptoms usually do not appear, but as the disease progresses they become pronounced.

Symptoms

The symptoms of the disease will have a different picture in each individual case, but at the same time a similar clinical picture of impaired brain functionality.

Main symptoms:

• subjective: dizziness, headache, tingling sensation and “crawling”;
• violation of the motor function of the body: paresis (partial immobilization of a limb) and paralysis (complete loss of movement of any part of the body);
• decreased functionality of the senses (hearing or vision);
• sensory disturbance (weakening, loss or pain);
• any changes in the cerebral cortex: writing impairment, speech problems, loss of reading ability, etc.;
• epileptic seizures;
• decreased mental abilities, intelligence, memory, absent-mindedness.

Each of the violations has its own characteristics:

• With ischemic stroke, the symptoms of cerebrovascular accident always manifest themselves acutely. With this disease, the patient’s subjective complaints are observed, there may be nausea and vomiting, as well as focal symptoms, which are changes in the system or organ for which the damaged area of ​​the brain is responsible.
• Hemorrhagic stroke occurs when blood from damaged blood vessels enters the brain cavity with further compression and such a dangerous complication as wedging of the brain stem into the foramen magnum. This disease occupies a leading position in the number of deaths among all types of cerebral circulatory disorders.
• Transient ischemic attack (TIA) is a transient cerebrovascular accident that resolves over time. It is accompanied by paresis, impaired speech and visual function, drowsiness and confusion.
• Chronic cerebral circulatory disorders are observed in older people and are characterized by gradual development over many years. Characteristic symptoms: decreased intelligence, mental abilities and memory. Such patients are absent-minded and sometimes aggressive.

Diagnostics

The diagnosis of the disease is made based on the following signs:

• patient complaints characteristic of this disorder;
• the patient has factors that contribute to the development of circulatory disorders: diabetes mellitus, high blood pressure, atherosclerosis;
• duplex scanning – identification of affected vessels;
• Magnetic resonance imaging (MRI) – visualization of the affected area of ​​the brain, the most informative study of the disease.

Treatment

Acute cerebrovascular accidents require emergency assistance from specialists. In case of strokes, assistance should be aimed primarily at maintaining the functionality of vital organs. Basic treatment includes ensuring the patient proper blood circulation and breathing, reducing cerebral edema, correcting water and electrolyte disorders, as well as normalizing blood pressure. Such procedures must be carried out in a hospital.

Subsequent treatment involves eliminating the cause of the disorder, as well as restoring impaired functions and blood flow in the brain.

Chronic circulatory disorders are usually treated with drugs that improve blood flow in the arteries and the rheological properties of the blood. They also normalize blood pressure and blood cholesterol. Normalizing blood circulation in the brain prevents the development of stroke and other serious illnesses of cardio-vascular system. So, along with procedures, doctors often prescribe medications to treat vascular disorders. For example, the combination drug Vasobral improves blood circulation and metabolism in the brain. The components of the drug prevent blood clots, reduce the permeability of vessel walls, increase the resistance of brain tissue to oxygen deficiency, and increase mental and physical performance. The drug's effectiveness in preventing headaches has been clinically proven.

Cerebrovascular accidents are a large group of pathologies (they are also called cerebral cerebrovascular accidents) that affect the cerebral vessels (CB) and are accompanied by hypoxia and ischemia of brain tissue, the development of metabolic disorders and specific neurological symptoms.

At the moment, acute and chronic cerebrovascular accidents are the leading cause of disability among middle-aged and elderly patients, as well as one of the leading causes of death in the world.

At the same time, if recently cerebral blood flow disorders were found mainly in patients over 45 years of age, now they are diagnosed in twenty-year-olds as well.

The leading causes of the appearance of NMC are atherosclerotic damage to the vessels of the brain and neck. Young patients are more likely to experience blood flow disorders such as hemorrhagic stroke or those associated with a hypertensive crisis.

For reference. For elderly patients, the occurrence of ischemic-type cerebrovascular accidents is more typical; the risk of developing severe chronic cerebrovascular accidents also increases with age.

Significantly increases the likelihood of the occurrence of cerebrovascular accidents and the long-term decompensated course of diabetes mellitus. Such patients experience severe vascular damage, microcirculation disorders, ischemic phenomena in organs and tissues, heart rhythm pathologies and a tendency to microthrombosis. In this regard, they often experience ischemic strokes with massive foci of necrosis.

One of the most common causes of development chronic disorder blood flow of the ischemic type, in young patients there is osteochondrosis in the cervicothoracic spine. Office workers who lead a sedentary lifestyle often encounter this problem.

Also, common reasons occurrence of cerebrovascular accidents are:

• CVS pathologies accompanied by cardiogenic thromboembolism;
• rheumatic heart defects and vascular lesions;
• post-infarction cardiosclerotic conditions complicated by cardiac aneurysms or atrial fibrillation;
• various cardiomyopathy ;
• MV (mitral valve) prolapse, accompanied by severe hemodynamic disturbances;
• cerebral amyloid angiopathy;
• systemic autoimmune and post-inflammatory vasculitis;
• blood diseases (various hereditary coagulopathies, etc.);
• aneurysms and malformations of blood vessels of the brain and neck;
• coagulopathies accompanied by increased thrombus formation;
• hemorrhagic diathesis;
• tumors of the brain and neck;
• thyroid diseases;
• metastatic foci in the brain;
• head and spinal injuries in the cervicothoracic region;
• severe intoxication and poisoning;
• neuroinfections.

Predisposing factors that significantly increase the risk of developing acute and chronic cerebrovascular accidents are:

• obesity;
• physical inactivity;
• lipid imbalance;
• smoking;
• frequent physical and emotional stress;
• alcohol abuse;
• neuroses, depression;
• chronic sleep deficiency;
• hypovitaminosis;
• frequent infectious diseases(especially streptococcal tonsillitis).

Types of cerebrovascular accidents

All cerebrovascular accidents are divided into those that arise acutely and those that are chronic. Separately, early manifestations of cerebral ischemia, discirculatory encephalopathies and the consequences of strokes were taken out.

For reference. The group of acute changes in cerebral blood flow includes transient ischemic attacks (TIAs), acute hypertensive encephalopathies and strokes. Strokes, in turn, are divided into brain infarctions and hemorrhages in brain tissue.

Chronic ischemic changes in brain tissue are divided into:

• compensated;
• remitting;
• subcompensated;
• decompensated.

Diagnosis of cerebral blood flow disorders

When symptoms of cerebrovascular accident appear, it is necessary to conduct a thorough examination in order to identify the type of circulatory disorder,
the extent of the lesion, as well as the cause of cervical cerebrovascular accident.

IN mandatory apply:

• neuroimaging methods (computed tomography or magnetic resonance imaging),
• Ultrasound of the vessels of the brain and neck,
• cerebral angiography,
• electroencephalography,
• ECHO-cardiography,
• daily allowance,
• standard ECG.

General and biochemical blood tests, coagulation tests, lipid profile diagnostics, blood glucose determination, etc. are also performed.

Treatment of cerebrovascular accidents

Therapy depends on the type of cerebrovascular accident and the severity of the patient’s condition. All medications should be prescribed only by a neurologist. Self-medication is unacceptable and can lead to a significant deterioration of the condition.

Attention! It is necessary to understand that acute transient blood flow disorders in the absence of treatment always end in the development of ischemic strokes. Therefore, even if the symptoms of a TIA disappear a few minutes after the attack began, you should still call an ambulance.

Symptoms in initial NMC are also reversible, but only in the initial stages. Without timely treatment, the development of progressive dyscirculatory encephalopathy with irreversible damage to brain tissue is possible.

Treatment of NMC includes normalization of blood pressure and lipid profile, control of glucose levels, and prevention of thrombus formation. Neuroprotectors, drugs that improve cerebral circulation, antioxidant and antiplatelet agents, as well as anticoagulants are also prescribed.

Additionally, vitamins, omega-3 preparations, and metabolic agents are prescribed. In the presence of neuroses or increased emotional lability, the patient may be prescribed sedatives or tranquilizers.

When strokes develop, treatment is aimed at:

• prevention of cerebral edema,
• elimination of the source of ischemia or cessation of bleeding,
• reduction in the severity of neurological symptoms,
• stopping a convulsive attack,
• normalization of cardiovascular activity,
• elimination of respiratory disorders.

For reference. It is also mandatory to begin early prevention of complications and rehabilitation treatment aimed at restoring lost functions.

Prevention of stroke

Prevention of cerebrovascular accidents includes following a lipid-lowering diet, monitoring blood sugar levels, regularly monitoring blood pressure, and stopping smoking and drinking alcohol.

It is necessary to increase the consumption of fresh vegetables and fruits, nuts, juices, bran, etc.

It is also recommended to normalize body weight and increase physical activity. However, excessive physical activity is strictly contraindicated. Walking in the fresh air, swimming, slow cycling, moderate orbital exercise, etc. are effective.

For reference. Overwork, stress and emotional overstrain are contraindicated. Strong tea and coffee should be replaced with herbal teas (mint, linden, chamomile, sage, thyme, yarrow, lemon balm, immortelle, etc.).

However, it must be taken into account that all herbs have different indications and contraindications. Before use, you must study the list of contraindications - allergic reactions, hormonal disorders, pregnancy, etc.

A course of taking multivitamin preparations and supplements containing magnesium and potassium is also effective.

How to recognize NMC in yourself and your loved ones

NMCs in the initial stage often occur in young patients with osteochondrosis in the cervicothoracic spine. Additional risk factors are smoking a large number of cigarettes, alcohol abuse, metabolic syndrome, lack of normal physical activity, frequent stress and overwork, chronic lack of sleep, and migraine attacks.

The initial symptoms of NMC may be:

• increased fatigue and decreased performance;
• noise and ringing in the ears;
• decreased visual acuity;
• decreased learning ability and memory impairment;
• constant drowsiness and muscle weakness;
• irritability, nervousness or depression.

Encephalopathy

Chronic cerebrovascular disease of the discirculatory encephalopathy type most often occurs in elderly patients. Additional risk factors are smoking, obesity, a sedentary lifestyle, severe vascular atherosclerosis, pathologies of lipid metabolism, coagulopathies accompanied by increased thrombus formation, the patient having diabetes mellitus, arterial hypertension, a history of heart attack or stroke.

Symptoms of chronic disorders of cerebral blood flow appear:

• progressive memory loss,
• decreased intelligence (up to mental retardation),
• decreased vision and hearing,
• the appearance of tinnitus,
• constant dizziness,
• dysfunctions of the pelvic organs (urinary and fecal incontinence).

Severe emotional lability is also noted. Patients are prone to rapid mood swings, depressive states, mania, psychosis, attacks of irritability and aggression, and “silly” moods.

Speech disorders may occur. The patients' speech becomes slurred and muttering. They answer questions inappropriately and often talk to themselves.

For reference. The progression of symptoms of cerebrovascular accident can lead to a complete loss of the ability to self-care due to the development of senile dementia (the third stage of dyscirculatory encephalopathy).

Transient cerebrovascular accident (TIA)

The term is used to designate acute disorders of blood flow in the brain, accompanied by the occurrence of a limited area of ​​ischemia of brain tissue, but not leading to necrosis of brain tissue (that is, not accompanied by the development of a stroke).

The clinical picture of transient cerebrovascular accidents is unstable (the duration of the developed disorders should not exceed 24 hours).

In most cases, TIA symptoms last a few minutes, rarely more than an hour. After the end of the attack there is full recovery changed functions.

For reference. Transient disorders of cerebral circulation in adults develop against the background of the appearance of a local ischemic focus in the brain tissue, which developed due to a reversible decrease in cerebral perfusion (blood flow). Symptoms of TIA disappear immediately after full blood flow is restored.

The causes of TIA can be;

• microemboli of a cardiogenic nature;
• atherosclerotic lesions of cerebral vessels, leading to their narrowing;
• microthrombi associated with the separation of part of an ulcerated atherosclerotic plaque.

The cause of hemodynamic disorders of blood flow is a sharp decline blood pressure due to:

• stenosis of the great vessels;
• hypovolemia;
• blood loss;
• shock states;
• severe anemia;
• orthostatic hypotension;
• overdose of alcoholic beverages, medicinal or narcotic substances;
• infectious intoxication;
• hyperventilation;
• severe and prolonged cough.

Less commonly, transient cerebrovascular accidents can occur against the background of prolonged arterial hypertension or a hypertensive crisis.

The clinical picture depends on in which vascular basin the blood flow is impaired. Carotid TIAs are accompanied by the occurrence of motor disturbances, changes in sensitivity, numbness of the limb, a feeling of tingling and crawling all over the body, speech and visual disorders, convulsions of the type of focal epileptic Jacksonian seizures (convulsions begin in the fingers and then spread to the entire affected half of the body).

Visual pathologies may manifest as dark spots before the eyes, decreased visual acuity, the appearance of fog before the eyes, double vision.

Lethargy, inappropriate or aggressive behavior, and disorientation in time and space may also be observed.

Vertebrobasilar transient cerebrovascular accidents manifest themselves:

• severe dizziness,
• nausea and vomiting,
• increased sweating,
• flashing of colored spots before the eyes,
• double vision,
• transient blindness,
• nystagmus,
• swallowing disorder
• transient attacks of amnesia,
• loss or confusion of consciousness.

There may be numbness of the face or unilateral paralysis of the facial muscles, as well as severe coordination disorders.

Hypertensive cerebral crises

For reference. Acute cerebrovascular accidents associated with a sharp increase in blood pressure are called hypertensive cerebral crises.

The main manifestations of the crisis are severe headaches, vomiting, tachycardia, tinnitus and visual disturbances. Increased sweating, a feeling of fear, anxiety or severe lethargy and drowsiness of the patient, redness or paleness of the face, and a feeling of heat may also be noted. In some cases, severe muscle weakness may occur.

In severe cases, meningeal symptoms and seizures may occur.

Such symptoms of cerebrovascular accident are more often observed against the background of uncontrolled hypertension of the second and third stages. Predisposing factors may include severe overwork and stress, excessive salt consumption, alcohol abuse, as well as the patient having diabetes mellitus or dyscirculatory encephalopathy of the second or third stage.

Symptoms of strokes

Hemorrhagic strokes (bleeding in the brain) most often develop in young people against the background of hypertensive crises. Clinical symptoms occur acutely. As a rule, the patient feels a severe and acute headache, after which he loses consciousness. Depending on the severity of the hemorrhage, after some time either consciousness is restored or the patient falls into a coma.

Also characteristic are vomiting, temporal and spatial disorientation, visual and speech disorders, nystagmus, lack of reaction of the pupil (on one side) to light, paralysis of the facial muscles (due to unilateral paralysis, the impression of a distorted face is created), unilateral paresis of the limbs, sensory disturbances, convulsions and etc.

For reference. Often, signs of cerebrovascular accident may be accompanied by the appearance of meningeal symptoms (vomiting, photophobia, stiff neck). Involuntary urination or bowel movements may occur.

Ischemic strokes occur more often in older patients. Symptoms can occur either acutely or gradually. The patient is noted to be lethargic, drowsy, unilateral paresis and paralysis, facial distortion, lack of pupillary response to light, decreased visual acuity, fog in front of the eyes, and nystagmus.

Patients often do not understand speech addressed to them or cannot answer the question asked of them. As a rule, speech disorders are noted.

Consciousness during ischemic strokes is usually not impaired. Convulsions are observed rarely, more often with massive ischemic foci.