MRI in the diagnosis of cerebrovascular disorders. Treatment of ischemic stroke in the acute period of acute stroke according to the ischemic type in the left basin

Acute cerebrovascular accident (ACVA) of the ischemic type in the middle cerebral artery basin (I65) is a sharply occurring focal neurological and/or cerebral symptomatology caused by focal ischemic disorders in the brain, lasting longer than 24 hours.

Prevalence of strokes: 1-4 cases per 1000 people per year. Ischemic stroke accounts for 70-85% of cases.

Risk factors: hypertension, lipid metabolism disorders, smoking, increased body weight, diabetes mellitus, alcohol abuse, sedentary lifestyle.

Acute cerebrovascular accident occurs as a result of atherosclerotic damage to the vessels of the head, cardiogenic embolism in heart disease, increased blood clotting, etc.

Symptoms of acute cerebrovascular accident

Before the onset of stroke, precursors may appear in the form of short-term neurological disorders. In 75% of cases, an ischemic episode occurs during sleep. Symptoms appear over several minutes or hours and may gradually increase. An increase in blood pressure is typical on the first day of the disease. Patients are concerned about the following complaints: headache (90%), weakness (75%) and/or numbness (70%) in one half of the body/limbs, decreased vision (30%), speech impairment (45%). 15% of patients may deny the presence of weakness/numbness in the limbs.

A neurological examination reveals a general cerebral syndrome, contralateral hemiplegia, hemianesthesia, homonymous hemianopsia, adversion of the head and concomitant deviation of the eyes, central paralysis of the face, tongue on the contralateral half of the lesion, motor-sensory aphasia, alexia, acalculia. Anosognosia, a disorder of the body diagram, is determined by damage to the non-dominant hemisphere.

Diagnosis of acute cerebrovascular accident

To identify the etiology of stroke of ischemic type, the following diagnostic methods are necessary:

• Blood tests (electrolytes, hemostasis indicators, glucose, lipid spectrum, antiphospholipid antibodies).
• Electrocardiography, blood pressure measurement.
• Auscultation of vessels on the extremities, duplex scanning, transcranial Dopplerography of precerebral arteries.

• Computed tomography (CT) of the brain shows a hypodense zone 12-24 hours after the development of an ischemic stroke. SPECT (in earlier stages of cerebral ischemia).

• Cerebral angiography (stenosis, occlusion, ulceration, aneurysm).

Differential diagnosis:

• Acute hypertensive encephalopathy.
• Dysmetabolic or toxic encephalopathy.
• Migraine stroke.
• Traumatic brain injury.
• The debut of multiple sclerosis.

Treatment of acute cerebrovascular accident

• Maintaining vital functions of the body, antihypertensive drugs (at blood pressure 200/120 mm Hg), anticoagulants (the appropriateness of prescription is determined by the duration of the disease and concomitant pathology), antiplatelet agents, vasoactive drugs (Cavinton, Actovegin, Cinnarizine) , "Instenon"), neuroprotectors ("Cerebrolysin", "Ceraxon", "Piracetam", "Gliatilin", "Semax"), "Reopoliglyukin", "Trental", decongestants ("Lasix", "Mannitol").
• Passive exercise therapy, breathing exercises, speech therapy classes.
• Consider thrombolysis upon admission within 3-6 hours of illness.
• Rehabilitation activities.
• Secondary prevention.

Treatment is prescribed only after confirmation of the diagnosis by a medical specialist.

Essential drugs

There are contraindications. Specialist consultation is required.

• (anticoagulant). Dosage regimen: IV or SC in the initial dose - IV (injection) 5000 IU, maintenance: continuous IV infusion - 1000-2000 IU/h (20000-40000 IU/day), pre-diluted in 1000 ml of isotonic NaCl solution; regular IV injections - 5000-10000 IU every 4-6 hours; s/c (deep) - 15,000-20,000 IU every 12 hours or 8,000-10,000 IU every 8 hours.
• (diuretic). Dosage regimen: intramuscularly or intravenously (slow stream) 20-60 mg 1-2 times a day, if necessary, the dose can be increased to 120 mg. The drug is administered for 7-10 days or more, and then the drug is taken orally.
• (nootropic drug). Dosage regimen: administered intramuscularly or intravenously, starting from 2.0-4.0 g/day, quickly increasing the dose to 4-6 g/day. After the condition improves, the dose is reduced and switched to oral administration - 1.2-1.6 g / day. (0.4 g 3-4 times a day).
• (a drug that improves cerebral circulation). Dosage regimen: intravenously 20-25 mg in 500 ml infusion solution. Within 2-3 days, the dose can be increased to no more than 1 mg/kg/day. The average course duration is 10-14 days. After completing the course of intravenous therapy, it is recommended to continue treatment with Cavinton tablets, 2 tablets 3 times a day.
• (vasodilator, improves microcirculation). Dosage regimen: two intravenous infusions per day (morning and afternoon), at a dose of 200 mg (2 amps of 5 ml) or 300 mg (3 amps of 5 ml) in 250 ml or 500 ml of 0.9% solution sodium chloride or Ringer's solution.

One of the main problems in neurology and neurosurgery today is considered to be a violation of the blood supply to the brain of both acute and chronic origin, leading to temporary or persistent negative consequences for the patient. This is due to damage to various brain structures (neurons of the cortex, subcortical and stem formations) due to a deficiency of nutrients and oxygen, which cannot be fully and sufficiently delivered to the area through pathologically altered vessels. One of the most difficult in terms of prognosis for the health and life, treatment and rehabilitation of the patient is acute cerebrovascular accident (usually abbreviated as stroke in medical documentation), in which transient (transient) ischemic attacks develop, and there is also a high risk of ischemic stroke ( heart attack) or hemorrhagic type (hemorrhage).

Causes of stroke

For the development of this pathology, reasons are needed that change the structure and tone of the capillaries, interfering with the full delivery of blood rich in oxygen and nutrients to the brain.
The main risk factors are vascular pathologies (aneurysms, vasculitis, atherosclerosis) or arterial hypertension, especially with a crisis course.

Even before serious problems develop, it is possible to identify minimal manifestations typical of atherosclerotic lesions of veins and arteries. These include sleep disorders and headaches, decreased performance, especially in the evening, periodic dizziness and a feeling of noise in the head. Irritability and nervousness may occur; strong emotionality with sharp transitions from joy to tears; decreased hearing and memory; absent-mindedness; decreased concentration; periodically occurring unpleasant sensations on the skin in the form of tingling, crawling.

Symptoms of neuroses - asthenic, hypochondriacal or depressive - are common.

Dangerous in terms of strokes or transient ischemic attacks are becoming more frequent hypertensive crises, leading to a sharp spasm of blood vessels, a disorder of the water-electrolyte balance and rheological properties of the blood (it thickens, becomes viscous, and flows worse through the capillaries). The listed pathological changes lead to stimulation of the adrenal glands, which increases the release of vasopressor (constricting) factors, which, in turn, contributes to the development of temporary or permanent vascular spasm.

The presence of vascular pathology, disturbing symptoms, and poor health is a serious reason for starting preventive treatment in order to prevent the acute form of the disease.

Acute cerebrovascular accident: development of pathology

To understand what stroke in medicine is, it is important to determine how the brain is supplied with blood and which failures of the circulatory system are the most dangerous. The cervical arteries supply oxygenated and nutrient-rich blood through the foramen magnum into the cranial cavity. The entire organ is densely intertwined with a network of arteries and veins with capillaries extending from them, which allows the neurons to be fully supplied with blood. Each branch of the artery has its own area of ​​responsibility, and through the veins the blood flows from the head, gradually collecting into large vessels.

Both interruptions in the flow of blood through the arteries and failure of the outflow of blood through the veins (so-called stagnation) are dangerous. Typically, acute cerebral circulatory failure occurs in cases where the arteries are damaged and rupture with bleeding or blockage with severe spasm and ischemia of a certain area. Venous problems are more typical for the chronic course of pathological processes due to stagnation of blood in the arteries and veins and a slowdown in the outflow rate.

What is acute stroke with persistent impairments?

At its core, an acute cerebrovascular accident is a sharp discrepancy between the volumes of incoming blood, bringing oxygen and nutrients to the tissues, with the existing needs. Such a dangerous situation arises as a result of persistent ischemia of a certain area of ​​tissue as a result of severe spasm or blockage of the lumen by a thrombus or embolus. Ischemic stroke develops through this mechanism. Another option for interruption of blood circulation, which may result in damage to the brain, is rupture of capillaries with leakage of blood into the tissue, hemorrhage with the formation of a hematoma or an area of ​​hemorrhagic impregnation. Both options refer to persistent circulatory problems.

What is a transient stroke?

As a result of sudden and relatively short-term effects, transient disorders associated with temporary but pronounced vasospasm can develop. If we talk about transient circulatory disorders, what they are can be understood by knowing the basic mechanisms of their formation. This is a temporary spasm of the capillaries in the head, caused by various unfavorable external factors or internal pathological processes, leading to the formation of a certain set of negative symptoms. Neurological manifestations of spasm persist for several minutes or hours to a day, followed by complete restoration of all impaired functions.

Such conditions are classified as pre-stroke; they require special attention from doctors and patients themselves, since without adequate treatment and elimination of all the causes leading to this anomaly, such failures threaten the development of a stroke in the future.

The most common causes of TIA (transient ischemic attack) are the following:

• arterial hypertension with a crisis course, against the background of which sharp spasms occur;
• atherosclerotic damage to the walls of capillaries, leading to a narrowing of their lumen, due to which blood flow to the gray matter of the brain decreases;
• cardiac arrhythmias that impair blood circulation, including the head area;
• heart failure or acute vascular collapse.

It is not difficult to describe transient acute disorders of cerebral circulation and what they are in terms of manifestations. All symptoms can be divided into:

• general cerebral;
• focal.

General cerebral symptoms:

• the appearance of a sharp and severe, painful headache with dizziness, attacks of nausea and vomiting;
• short-term loss of consciousness or a feeling of stupor, disorientation of the patient in space and time are possible.

Focal symptoms:

• the occurrence of temporary paralysis and paresis (partial paralysis of a separate zone), as well as a feeling of crawling (paresthesia);
• visual disturbances with flickering dots, flashes of light or spots;
• various speech disorders;
• problems coordinating when walking or moving limbs;
• non-compliance with the functions of individual nuclei of the cranial nerves (problems with opening the mouth, blinking the eyes, swallowing).

If the diagnosis of a transient circulatory disorder is made immediately, and active professional treatment measures begin to eliminate the spasm, restore normal blood flow, and a competent fight against arrhythmias and hypertension is carried out, then the blood supply is restored, and all negative symptoms disappear within 24 hours without consequences. If such manifestations are ignored or self-medicated, more serious pathological conditions - strokes - can occur.

ACVA, cerebral stroke: what is this diagnosis?

In the presence of persistent circulatory disorders of the brain, long periods of bleeding of certain areas are formed with progressive death of neurons and the formation of an area of ​​tissue necrosis, which forms a cerebral stroke.

If we are talking about a diagnosis of a persistent disorder, what does this mean from a clinical point of view? This is the formation of severe disorders and severe symptoms, up to a coma and death of the patient from increasing respiratory and vascular disorders.

Thus, patients with stroke are people who have experienced a hemorrhagic stroke (hemorrhage due to capillary rupture) or ischemic stroke (irreversible blockage by a thrombus or embolus, persistent irreversible spasm of an atherosclerotic vessel).

Signs

With a hemorrhagic stroke, the symptoms develop acutely, the signs are usually detected against the background of physical or emotional stress in the morning or daytime, loss of consciousness occurs, and the patient may become comatose.

External signs of stroke: the patient’s face turns red, strabismus or eye deviation to the side develops, the face and head turn towards the site of hemorrhage. On the side of the body opposite the hematoma, paralysis of the limb is noted - upper and lower, and pathological reflexes of the tendons and muscles are determined. If the hemorrhage is localized in the area of ​​the stem formations, progressive vascular, cardiac and respiratory disorders and increased blood pressure occur.

Against the background of ischemic stroke, the symptoms develop less acutely, but last longer, gradually the manifestations of the disease increase in strength and severity. Neurological symptoms in this type depend on the location of the feeding artery, the extent of the ischemic zone and the duration of exposure. When a large artery is blocked, a coma is possible with irreversible changes in speech, motor sphere and persistent disorders of the functions of the patient’s internal organs.

Consequences of this pathology

If transient ischemic attacks become more frequent, their duration becomes longer and longer and the causes leading to such cases are not eliminated, strokes and patient disability become the main consequences of stroke. Conditions with deep lesions of consciousness with the early development of cerebral coma have especially unfavorable prognoses. In this case, a real threat to the patient’s life is created, especially against the background of lysis of the blood clot and re-bleeding with worsening harmful consequences.

If the condition after an acute cerebrovascular accident leads to the development of paralysis of the limbs with impairment of the motor sphere, or visual impairments, speech defects, orientation and memory disorders are formed, the patient will need constant medical care and medical assistance.

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Definition of the concept

Vascular diseases of the brain attract the attention of scientists around the world. This is due to their widespread, high mortality, disability of tens of thousands of young and middle-aged people, which makes this problem not only medical, but also social.

In Ukraine, a classification of ONMC has been adopted, according to which the following are distinguished:

1) transient cerebrovascular accident (TCI), transient ischemic attack (TIA);

2) meningeal hemorrhages;

3) stroke (hemorrhagic and ischemic - non-embolic and embolic cerebral infarction);

4) acute hypertensive encephalopathy (AHE).

PNMK- acutely occurring cerebral vascular insufficiency, which is manifested by rapidly passing (according to WHO, within 24 hours) focal or cerebral symptoms or a combination thereof.

PNMK, according to this classification, is divided into transient ischemic attacks (TIA) and PNMK according to the type of hypertensive cerebral crisis. Additionally, PNMK is distinguished according to the type of hypertensive crisis (HC with focal neurological symptoms. PNMK is usually the first acute manifestation of vascular pathology of the brain, and in some cases it is a harbinger of a stroke.

Hypertensive crisis- characterized by a sharp rise in blood pressure, which is observed diffusely throughout the brain tissue, and therefore is often accompanied by general cerebral symptoms (headache, nausea, vomiting of central origin, i.e., not bringing relief).

Stroke also called acute cerebrovascular accident, which is accompanied by focal and or cerebral symptoms and lastsmore than 24 hours. As a result of a stroke, symptoms of persistent organic damage to the nervous system appear. There are two main forms of stroke: and.

Causes of the disease

In the etiology of stroke, the leading role belongs to hypertension, symptomatic arterial hypertension, atherosclerosis, or a combination thereof. Less commonly, the cause of stroke is cerebral vasculitis as a manifestation of collagenosis (rheumatism, periarteritis nodosa, systemic lupus erythematosus), specific arteritis, blood diseases, myocardial infarction, congenital heart defects, mitral valve prolapse, etc.

The etiology of ischemic stroke is atherosclerosis, its combination with hypertension, hypertension, cerebral vasculitis with collagenosis, blood diseases (leukemia, erythremia), myocardial infarction, congenital heart defects, etc.

Mechanisms of occurrence and development of the disease (Pathogenesis)

In hypertensive cerebral crises, apparently, the leading role is the disruption of autoregulation of cerebral vessels with the phenomena of excessive cerebral hyperemia, vasodilation, slowing of blood flow, increased permeability of the vascular wall with the development of perivasal edema, and in severe cases, microhemorrhage. The mechanism of vasospasm cannot be excluded. In TIA, one of the important mechanisms is transient ischemia in the area of ​​the atherosclerotic vessel, which occurs during atherosclerotic occlusion or congenital anomaly, as well as in the presence of extracerebral factors (decreased systemic blood pressure, decreased pulse, decreased cardiac output), which occur more often in acute cardiac arrest. vascular insufficiency. Often, PNMK develops as a result of arterio-arterial microembolism, mainly from the main arteries of the head (fragments of a thrombus of an ulcerated atheromatous plaque). As a result of the introduction of computed tomography into the diagnosis of PNMC, it has been established that in a number of cases the development of PNMC is associated with microhemorrhages and microinfarctions.

Clinical picture of the disease (symptoms and syndromes)

PNMK of the HA type develops against a background of high blood pressure, significantly exceeding its normal level in the patient, most often in the daytime and against the background of stressful situations. It is characterized by increasing general cerebral symptoms: headache, which at first can be local in nature (usually in the back of the head), and then becomes diffuse, bursting, pulsating, accompanied by nausea, vomiting, non-systemic dizziness, noise and ringing in the ears, occasionally - disturbances of consciousness (its short-term loss, stunning). In severe cases of PNMK, due to the development of cerebral edema, longer periods of loss of consciousness are possible, up to the development of stupor and superficial coma, convulsive syndrome (usually generalized seizures), and meningeal symptoms. This condition is regarded as OGE. Consequently, PNMK of the HA type is mainly characterized by general cerebral symptoms, and in addition to autonomic symptoms and disorders - hyperemia of the skin of the face, neck, upper chest, hyperhidrosis, tachycardia, etc. Transient neurological deficits are possible: nystagmus, revival and asymmetry of tendon reflexes, inconsistent pathological signs. If PNMK is accompanied by more persistent neurological symptoms - transient dysfunction of the cranial nerves (oculomotor, facial, hypoglossal, etc.), short-term speech disorders, paresis, sensitivity disorders - this indicates in favor of PNMK of the GC type with focal manifestations.

With TIA, the clinical picture of the disease is usually dominated by focal symptoms of damage to the nervous system, which are very diverse and depend on the vascular system. With TIA in the carotid artery, most often there is paresthesia in half of the tongue, in the area of ​​the lips, face, arms, less often in the legs, mono- or hemiparesis, speech impairment in case of damage to the left carotid artery in right-handed people. Less commonly observed are attacks such as Jacksonian epilepsy of the motor or sensory type, and sometimes oculo-pyramidal syndrome (decreased vision on the side of the pathology with contralateral hemiparesis and hemihypesthesia). With TIA in the vertebrobasilar region, systemic dizziness, nystagmus, loss of visual field, diplopia, photopsia and darkening of the eyes, ataxia, dysarthria, weakness in the limbs. TIA in the vertebral-basilar region is observed 2 times more often than in the carotid. In cases where the neurological symptoms of PNMC do not completely regress within 24 hours, the pathology is classified as a “minor stroke”.

The most severe stroke occurs in cases of severe cerebral edema, acute obstructive hydrocephalus, blood breakthrough into the ventricles and subarachnoid space, and secondary hemorrhage into ischemic tissue. As a consequence of these processes, an increase in intracranial pressure develops with brain dislocation and compression of vital formations of the brainstem or compressive ischemia of the cerebral cortex, a sharp decrease in the level of wakefulness and a deepening of neurological deficit with sometimes a prognostically unfavorable outcome, including the development of a persistent vegetative state and brain death.

Cerebral edema is defined as excess accumulation of fluid in the brain tissue, resulting in an increase in brain volume. The more pronounced the cerebral edema, the more severe the stroke. There are three types of cerebral edema: cytotoxic, vasogenic and interstitial (hydrostatic). Cytotoxic edema is caused by a violation of the active transport of sodium ions across the cell membrane, as a result of which sodium freely enters the cell and retains water. This type of edema is characteristic of the early (minutes) stage of cerebral ischemia and is more pronounced in the gray matter than in the white matter. Vasogenic edema is caused by increased permeability of the blood-brain barrier and increased entry of protein macromolecules into the intracellular space. This type of edema is characteristic of the subacute (hours) stage of cerebral catastrophe and can be observed both with heart attacks and with cerebral hemorrhages. Interstitial edema is often caused by acute obstructive hydrocephalus and is usually seen on CT as a “periventricular glow” (see below).

Cerebral edema reaches its peak on the 2-5th day, and then, from the 7th-8th day, if the patient survives this period, it begins to slowly regress. As a rule, the larger the size of the lesion, the more pronounced the edema, although to a certain extent this depends on its location.

Diagnosis of the disease

The diagnosis of stroke is methodologically made in three stages. Initially, stroke is distinguished from other acute conditions associated with brain damage. At the second stage, the nature of the stroke itself is determined - ischemic or hemorrhagic. In conclusion, the localization of hemorrhage and its possible mechanisms of development in hemorrhagic stroke or the basin of the affected vessel and the pathogenesis of cerebral infarction in ischemic stroke are clarified.

Stage I

Diagnosing a stroke as such rarely causes significant difficulties for doctors. The main role in this case is played by the anamnesis collected from the words of relatives, others or the patient himself. Sudden and acute, within a few seconds or minutes, development of persistent neurological deficit in the form of motor, sensory and often speech disorders in persons, usually over 45 years of age, against the background of significant emotional, physical stress, immediately after sleep or taking a hot bath, with high or low blood pressure allows you to accurately diagnose acute cerebrovascular accident. Additional information about the presence of any vascular diseases in the patient (recent myocardial infarction, atrial fibrillation, atherosclerosis of the lower extremity vessels, etc.) or risk factors makes the initial diagnosis more reliable.

The most common misdiagnosis of stroke is made during epileptic seizures (correct diagnosis is helped by a thorough history, EEG, and CT scan of the brain); brain tumors (a gradual increase in the clinical picture after the appearance of the first neurological symptoms, CT scan with contrast; it should be borne in mind that the development of hemorrhage into the tumor or infarction in the tumor area is often possible - conditions that can only be confidently diagnosed using X-ray and radiological methods); arteriovenous malformations (sometimes a history of epileptic seizures, cranial noise, hemorrhagic telangiectasia, CT or MRI, cerebral angiography); chronic subdural hematomas (head injury in recent weeks, severe constant headache, progressive increase in symptoms, use of anticoagulants, hemorrhagic diathesis, alcohol abuse), as well as in hypoglycemic conditions, hepatic encephalopathy, etc.

Stage II

The most difficult and responsible task is to accurately and quickly diagnose the nature of a stroke, since in the acute period of the disease it is these moments that largely determine further treatment tactics, including surgical ones, and, consequently, the prognosis for the patient. It should be emphasized that an absolutely accurate diagnosis of the nature of a stroke - hemorrhage or cerebral infarction - only on the basis of clinical data is hardly possible. On average, in every 4-5th patient, the clinical diagnosis of stroke, made even by an experienced doctor, turns out to be erroneous, which is equally true for both hemorrhage and cerebral infarction. Therefore, along with clinical data, it is highly desirable to carry out a priority CT scan of the brain, since the timeliness and effectiveness of the assistance provided largely depends on this. In general, CT scans of the brain are the international standard for diagnosing stroke.

The accuracy of diagnosing hemorrhages with CT reaches almost 100%. In the absence of evidence of hemorrhage on CT and the presence of appropriate clinical and anamnestic data indicating an acute ischemic cerebrovascular accident, the diagnosis of cerebral infarction can be made with great accuracy even in the absence of any changes in the density of the brain substance on tomograms, which is often observed in the first hours after the development of a stroke. In approximately 80% of cases, a brain CT scan detects an area of ​​low density, clinically corresponding to a cerebral infarction, within the first day after the onset of the disease.

Magnetic resonance imaging is more sensitive than CT in the early hours of cerebral infarction and almost always detects changes in brain matter not visible on conventional CT, as well as changes in the brain stem. However, MRI is less informative for cerebral hemorrhages. Therefore, CT is still widely used even in the most well-equipped neurological clinics in the world dealing with acute cerebrovascular pathology.

Stage III

The localization of hemorrhage or infarction in the brain is important in terms of both emergency medical and surgical procedures, and is also important for predicting the further course of the disease. The role of CT here is also difficult to overestimate. As for the mechanisms of development of acute cerebrovascular accidents, they are, of course, of great importance for the correct choice of treatment tactics for a patient from the very first days of a stroke, but in approximately 40% of cases it is not possible to accurately establish the pathogenesis of a stroke, despite a carefully worked out history and clinical picture development of the disease and the full power of modern instrumental and biochemical research methods. First of all, this concerns cerebral infarction, where the desire to determine its subtype (atherothrombotic, cardioembolic, lacunar, etc.) already in the acute period is necessary, since the choice of therapy depends on this (thrombolysis, regulation of general hemodynamics, treatment of atrial fibrillation, etc.). d.). This is also important for preventing early recurrent episodes of heart attacks.

Treatment of the disease

Approach to patients with acute stroke. Organizational matters

Patients with acute stroke should be hospitalized as quickly as possible. The direct dependence of the prognosis of stroke on the time of initiation of its treatment has been clearly proven. The timing of hospitalization in the first 1-3 hours after the onset of the disease is optimal, although reasonable treatment is also effective in a later period. The optimal option is to hospitalize patients in a multidisciplinary hospital with modern diagnostic equipment, including computed tomography or MRI scanners and angiography, which also has an angioneurological department with an intensive care unit and an intensive care unit with a specially designated unit (beds) and trained personnel to manage these patients. An indispensable condition is also the presence of a neurosurgical department or a team of neurosurgeons in the hospital, since about a third of patients need consultation or provision of this type of specialized care. Staying in such clinics significantly improves the outcomes of acute cerebrovascular accidents and the effectiveness of subsequent rehabilitation.

An altered level of wakefulness (from stupor to coma), increasing symptoms indicating signs of brainstem herniation, as well as severe disturbances in vital functions require hospitalization of the patient in the intensive care unit (ICU). It is advisable to stay in the same departments for stroke patients with severe disturbances of homeostasis, decompensated cardiopulmonary, renal and endocrine pathologies.

Emergency measures upon admission

The examination of the patient upon admission to the emergency room should begin with an assessment of the adequacy of oxygenation, blood pressure levels, and the presence or absence of seizures. Providing oxygenation, if necessary, is carried out by installing an airway and clearing the respiratory tract, and, if indicated, by transferring the patient to mechanical ventilation. Indications for starting mechanical ventilation are: PaO2 - 55 mm Hg. and lower, vital capacity less than 12 ml/kg body weight, as well as clinical criteria - tachypnea 35-40 per minute, increasing cyanosis, arterial dystonia. It is not customary to reduce blood pressure if it does not exceed 180-190 mm Hg. for systolic and 100-110 mm Hg. for diastolic pressure, since in stroke autoregulation of cerebral blood flow is disrupted and cerebral perfusion pressure often directly depends on the level of systemic blood pressure. Antihypertensive therapy is carried out with caution with small doses of beta-blockers (obzidan, atenolol, etc.) or angiotensin-converting enzyme blockers (Renitec, etc.), which do not cause significant changes in the autoregulation of cerebral blood flow. In this case, blood pressure is reduced by approximately 15-20% of the initial values.

With cortical-subcortical lesions and blood breakthrough into the ventricular system, seizures are often observed. Stopping them is also necessary before the start of a neurological examination, since they severely deplete the neurons of the brain. For this purpose, Relanium is used, administered intravenously. In severe cases, sodium thiopental is used. Further, in such patients it is necessary to immediately begin prophylactic administration of long-acting anticonvulsants (finlepsin, etc.).

A neurological examination of the patient upon admission should be brief and include an assessment of the level of wakefulness (Glasgow Coma Scale), the condition of the pupils and oculomotor nerves, motor and, if possible, sensitive areas, speech. Immediately after the examination, a CT scan of the brain is performed. Due to the fact that determining the nature of a stroke is often crucial for further differentiated treatment, including surgery, patients with stroke are recommended to be hospitalized in clinics that have the necessary diagnostic equipment.

After the CT scan, the required minimum of diagnostic tests is performed: ECG, blood glucose level, plasma electrolytes (K, Na, etc.), blood gases, osmolarity, hematocrit level, fibrinogen, activated partial thromboplastin time, urea and creatinine levels, general blood test with platelet count, chest x-ray.

If signs of hemorrhage in the brain are detected on CT and an assessment of its volume and localization is carried out, the question of the advisability of surgical intervention is discussed together with neurosurgeons. For ischemic strokes, it is recommended to perform panarteriography of the main arteries of the head or arteriography on the side of the brain lesion (if blockage of the vessel is suspected). Detection of occlusion of the arteries supplying the brain requires resolving the issue of thrombolytic therapy. Detection of blood in the subarachnoid space on CT often indicates the possibility of subarachnoid hemorrhage. In these cases, the possibility of angiography should be discussed to determine the location and size of the aneurysm and decide on surgery. In doubtful cases, a lumbar puncture may be performed. It is optimal to carry out all of these activities immediately in the emergency room and X-ray department of the clinic.

Conservative treatment

Treatment of patients in the acute period of stroke (approximately the first three weeks) consists of general measures for the treatment and prevention of various types of somatic complications, usually developing against the background of acute cerebrovascular accidents (ACVA), as well as specific methods of treating the stroke itself, depending on its nature .

General measures: maintaining an optimal level of oxygenation, blood pressure, monitoring and correction of cardiac activity, constant monitoring of the main parameters of homeostasis, swallowing (in the presence of dysphagia, a nasogastric tube is placed to prevent aspiration bronchopneumonia and ensure adequate nutrition of the patient), monitoring the condition of the bladder, intestines, skin care. From the very first hours, passive gymnastics and massage of the arms and legs are necessary as an indispensable and most effective condition for the prevention of one of the main causes of mortality in strokes - pulmonary embolism (PE), as well as bedsores and early post-stroke contractures.

Daily care for seriously ill patients should include: turning from side to side every 2 hours; every 8 hours, wiping the patient’s body with camphor alcohol; enemas (at least every other day); administering fluid to the patient at the rate of 30-35 ml per kg of body weight per day; every 4-6 hours, toilet the oropharynx and nasopharynx using suction, followed by rinsing with a warm infusion of 5% chamomile solution or its substitutes. Antibacterial therapy, if necessary, with mandatory intake of adequate doses of antifungal drugs. If signs of disseminated intravascular coagulation appear, administer low molecular weight heparin in doses of 7500 units 2-3 times a day subcutaneously. When transferring a patient to mechanical ventilation, carry out in full the measures described in detail in the manuals on resuscitation and neuroreanimatology.

Currently, hyperventilation and osmotic diuretics are most widely used to treat cerebral edema. Hyperventilation (reducing PaCO2 to a level of 26-27 mm Hg) is the fastest and most effective method of reducing intracranial pressure, but its effect is short-lived and lasts about 2-3 hours. Among the osmotic diuretics, mannitol is most often used. The drug is recommended to be administered intravenously at an initial dose of 0.5-1.5 g/kg body weight over 20 minutes, and then at a dose of half the original every 4-5 hours at the same rate depending on the clinical situation and with taking into account the level of plasma osmolarity. It should be taken into account that exceeding the level of osmolarity above 320 mOsm/L, as well as long-term use of mannitol, is dangerous, since this leads to electrolyte changes, renal pathology and other disorders, which is extremely unfavorable prognostically for the patient. The administration of mannitol in this mode can last no more than 3-4 days. In the absence of mannitol, it is possible to use glycerin in the same dosages orally every 4-6 hours. Corticosteroids and barbiturates have not been shown to be effective in the treatment of cerebral edema in stroke, although their cytoprotective effect is debated.

Acute obstructive hydrocephalus (AOH) is based on severe extraventricular compression of the cerebrospinal fluid ducts or their blockage by blood clots (intraventricular occlusion). This condition, which can be diagnosed only by CT data, develops most often in the first two days with subtentorial and almost one third of supratentorial hemorrhages, as well as with cerebellar infarctions exceeding a third of its hemisphere. With subtentorial lesions, tomography reveals compression of the IV ventricle, a sharp increase in the III and lateral ventricles, with supratentorial lesions - compression of the III and homolateral lateral ventricle or filling them with blood clots with a significant increase in the contralateral lateral ventricle. An increase in OG leads to an increase in brain volume, an increase in intracranial pressure and a deepening of the dislocation of brain structures, including its stem. This, in turn, causes a sharp disruption of liquor outflow and an increase in the difference in pressure between the supra- and subtentorial space, which further increases the displacement and deformation of the trunk. The brain substance is saturated with cerebrospinal fluid from the dilated ventricles. A CT scan reveals the already mentioned x-ray phenomenon - “periventricular glow” - a zone of reduced density in the white matter of the brain around the expanded part of the ventricular system.

The optimal methods for treating AOG are drainage of the lateral ventricles, decompression of the posterior cranial fossa, removal of the hematoma (for hemorrhagic stroke) or necrotic cerebellar tissue (for ischemic stroke). All of them are essentially life-saving operations. The use of decongestant therapy alone in these situations does not have the desired effect.

Blood breakthrough into the ventricular system and subarachnoid space has previously always been considered a poor prognostic, often fatal sign of hemorrhagic stroke. It has now been shown that in more than a third of cases of cerebral hemorrhages, the breakthrough of blood into the ventricles does not lead to death, even if it occurs in the third and fourth ventricles. Blood enters the ventricles from a certain “threshold” volume of the hematoma, characteristic of its particular location. The closer to the midline of the hemispheres the hemorrhage is located, the higher the risk of blood entering the ventricles of the brain and vice versa. The combination of blood breakthrough into the ventricular system and subarachnoid space is observed very often in patients with hemorrhagic stroke. This is usually observed when hematoma volumes exceed 30-40 cm3. There are no reliably proven effective treatments for this complication yet.

Secondary hemorrhage into necrotic tissue is usually observed on days 1-10 with extensive, large and medium-sized cerebral infarctions. Like the previous two complications, it is reliably established based on CT data. Detection of hemorrhagic transformation is possible only with repeated x-ray examinations. This is often a consequence of uncontrolled blood pressure and reperfusion (mainly thrombolytic) therapy, sometimes carried out without taking into account contraindications to it.

Specific treatments for stroke

Hemorrhagic stroke

In every second case, the cause of intracerebral non-traumatic hemorrhage is arterial hypertension, about 10-12% are due to cerebral amyloid angiopathy, about 10% are due to the use of anticoagulants, 8% are due to tumors, and all other causes account for about 20%. Pathogenetically, intracerebral hemorrhages can develop either as a result of vessel rupture or through diapedesis, usually against the background of previous arterial hypertension.

There are currently no specific drug treatments for hemorrhagic stroke; antihypoxants and antioxidants are used. The basis of treatment is general measures to maintain homeostasis and correct major complications (see above). Epsilon-aminocaproic acid is not indicated, since its hemostatic effect does not reach its target, while the risk of pulmonary embolism increases. An important and often decisive method of treating hemorrhagic stroke is surgical intervention - removal of the hematoma using an open or stereotactic method, taking into account its volume, location and impact on brain structures.

Ischemic stroke

Treatment of ischemic stroke is much more difficult than hemorrhagic stroke. First of all, this is due to the diversity (heterogeneity) of the pathogenetic mechanisms underlying it. Based on the mechanism of their development, cerebral infarctions are divided into atherothrombotic, cardioembolic, hemodynamic, lacunar, hemorheological and others. Different subtypes of ischemic strokes differ from each other in frequency, causes, clinical picture of development, prognosis and, of course, treatment.

The basis of cerebral infarctions is developing ischemia associated with complex cascades of interaction between blood components, endothelium, neurons, glia and extracellular spaces of the brain. The depth of such interactions gives rise to varying degrees of trauma to brain structures and, accordingly, the degree of neurological deficit, and their duration determines the time limits for adequate therapy, that is, the “window of therapeutic opportunity.” It follows from this that drugs that differ in their mechanisms and points of application also have different time limits for their effect on the affected areas of the brain.

The basis of specific therapy for ischemic stroke is two strategic directions: reperfusion and neuronal protection, aimed at protecting poorly functioning or almost non-functioning, but still viable neurons located around the infarction site (the “ischemic penumbra” zone).

Reperfusion is possible through thrombolysis, vasodilation, increasing perfusion pressure and improving the rheological properties of blood.

Thrombolytic therapy

The main cerebral thrombolytics are urokinase, streptokinase and their derivatives, as well as tissue plasminogen activator (tPA). All of them act directly or indirectly as plasminogen activators. Currently, the effectiveness of the use of thrombolytics, in particular tPA, has been reliably proven, but it is recommended only after CT and angiography, no later than the first 3 hours (!) from the onset of stroke at a dose of 0.9 mg/kg body weight intravenously, for small lesions on CT and blood pressure not higher than 190/100 mm Hg, no history of strokes, peptic ulcers, etc. Thrombolytic therapy, as a rule, does not eliminate the original causes that caused blockage of blood vessels, since residual atherostenosis remains, but restores blood flow. Hemorrhagic complications when using various thrombolytics, according to various sources, range from 0.7 to 56% (!), which depends on the time of administration and properties of the drug, the size of the infarction, and compliance with the entire range of contraindications to this type of drug therapy.

Vasodilators

The clinical use of vasodilators usually does not give positive results, perhaps because these drugs increase intracranial pressure, reduce mean blood pressure and have a shunting effect, diverting blood from the ischemic zone. Their real role in the development of collateral blood supply to the ischemic focus is still being studied (this applies primarily to aminophylline, the positive effect of which is often noted in clinical practice).

Increasing cerebral perfusion pressure and improving the rheological properties of blood

One of the most well-known methods used for this purpose is hemodilution. It is based on two principles of influencing the microcirculation of the ischemic brain: reducing blood viscosity and optimizing circulatory volume. It is advisable to carry out hypervolemic hemodilution with low molecular weight dextrans (reopolyglucin, rheomacrodex, etc.) only if the patient’s hematocrit level exceeds 40 units, in volumes that ensure its reduction to 33-35 units. In this case, in persons with severe cardiac and/or renal pathology, the state of central hemodynamics should be monitored to prevent the development of pulmonary edema, as well as the level of creatinine, urea and glucose in the blood. The administration of rheopolyglucin for the purpose of correcting hematocrit for more than 7-8 days starting from the moment of stroke development, except in special cases, is not justified. If the effectiveness of the hemodilution method has been proven in approximately half of the international multicenter controlled studies, then the feasibility of other drugs used for these purposes is still the subject of intensive research.

Antiplatelet agents

Aspirin is an effective proven treatment during the acute period of cerebral infarction. It can be used in two modes - 150-300 mg or in small doses of 1 mg/kg body weight daily. There is virtually no risk of hemorrhage. However, very often aspirin cannot be used in patients with gastrointestinal problems. In these cases, its special dosage forms are used (thrombotic ACC, etc.). The feasibility of using antiplatelet agents of other effects, including ticlopidine and dipyridamole (Curantyl), in the acute period, is still being studied, as is the effect of pentoxifylline (Trental).

Direct anticoagulants

There is still no clear evidence for the widespread use of anticoagulants in acute stroke, even in patients with atrial fibrillation. Anticoagulant therapy does not have a direct connection with a reduction in mortality and disability in patients. At the same time, there is strong evidence that heparin (low molecular weight heparin) does prevent deep venous thrombosis and, therefore, the risk of pulmonary embolism (see above).

Neuroprotection

This is the second strategic direction in the treatment of ischemic strokes. Severe metabolic disorders, rapid depolarization of membranes, uncontrolled release of excitatory amino acids and neurotransmitters, free radicals, development of acidosis, sudden entry of calcium into cells, changes in gene expression - this is not a complete list of points of application for neuroprotective drugs in conditions of cerebral ischemia.

Currently, there is a whole range of drugs that have neuroprotective properties: postsynaptic glutamate antagonists; presynaptic glutamate inhibitors (lubeluzole); calcium channel blockers, antioxidants (emoxypine, L-tocopherol); nootropics (piracetam, cerebrolyzin) and others. The feasibility of their use has been proven under experimental conditions. There is still no clear clinical evidence of effectiveness for the vast majority of neuroprotective drugs. In cases where some authors do manage to obtain positive results from their studies, they are almost always questioned by others who conduct their clinical trials to approximately the same standards. In this regard, the validity of their use in patients is not entirely clear. In general, the high promise of neuroprotection as a treatment method is beyond doubt. Its widespread implementation is certainly a matter of the near future.

Prevention of recurrent cerebrovascular accidents

Due to the wide variety of causes underlying strokes, it is necessary, already in the first days of the disease, along with the mentioned treatment methods, to take measures aimed at preventing relapses of stroke.

For cardioembolic strokes due to atrial fibrillation, indirect anticoagulants are recommended. If there are contraindications to their use, it is recommended to use aspirin. The optimal timing for initiating anticoagulant therapy after an acute episode is still unclear. It is believed that to reduce the risk of cerebral hemorrhage, initial treatment should begin with aspirin and continue until the underlying deficit caused by the stroke has resolved, or, if it is a severe stroke, approximately two weeks after the onset of the stroke. Indirect anticoagulants and aspirin are rarely used together. Of course, selection of cardiac therapy itself is also necessary.

For arterio-arterial embolisms and occlusive pathology of the main arteries of the head, taking aspirin, ticlopidine, and dipyridamole is effective. The most optimal is individual testing of the patient’s blood reaction to a particular prescribed drug. This method has been successfully used in our clinic for several years. Treatment and prevention of recurrent cerebral hemorrhages are based primarily on carefully selected antihypertensive therapy, and the prevention of recurrent ischemic strokes is based on ECG and blood pressure monitoring.

In conclusion, it should be emphasized once again that for strokes there is not and cannot be a single universal remedy or treatment method that radically changes the course of the disease. The prognosis for life and recovery is determined by a combination of timely and comprehensive general and specific measures in the first days of the disease, including, among others, constant correction of homeostasis - a determining factor, without normalization of which all subsequent treatment becomes ineffective, as well as active neurosurgical manipulations along with early physical and psychological rehabilitation . First of all, this applies to strokes of moderate and severe severity. A clear understanding of the pathogenetic mechanisms underlying strokes is precisely the key with which it is possible to select reasonable and effective treatment within the first hours of the onset of development of vascular brain damage and ensure a favorable prognosis.

Surgery

Surgical methods occupy a certain place in the prevention of ischemic strokes, especially in cases of severe stenosis or occlusion of the carotid and vertebral arteries, embologenic, heterogeneous atherosclerotic plaques (endarteriectomy, revascularization - see Medical Newspaper No. 21 of 03/19/99).

Surgical methods of treatment for cerebellar infarctions against the background of acute obstructive hydrocephalus, as well as drainage of the cerebral ventricles, are currently used with high efficiency. The feasibility of other surgical interventions in the acute period of ischemic stroke requires additional evidence.

CRITERIA FOR DIAGNOSTICS OF SPECIFIC FORMS of stroke

Stroke includes acute disorders of cerebral circulation, characterized by the sudden (within minutes, less often - hours) appearance of focal neurological symptoms (motor, speech, sensory, coordination, visual and other disorders) and/or general cerebral disorders (changes in consciousness, headache, vomiting, etc.), which persist for more than 24 hours or lead to the death of the patient in a shorter period of time due to a cause of cerebrovascular origin.

Stroke is divided into hemorrhagic and ischemic (cerebral infarction). A minor stroke is distinguished, in which impaired functions are completely restored during the first 3 weeks of the disease. However, such relatively mild cases occur in only 10-15% of stroke patients.

Transient cerebrovascular accidents (TCI) are characterized by the sudden onset of focal neurological symptoms that develop in a patient with vascular disease (arterial hypertension, ischemic heart disease, rheumatism, etc.) and last several minutes, less often - hours, but no more than a day and end with complete restoration of the impaired functions. Transient neurological disorders with focal symptoms that develop as a result of short-term local cerebral ischemia are also referred to as transient ischemic attacks (TIA). A special form of PNMK is acute hypertensive encephalopathy. More often, acute hypertensive encephalopathy develops in patients with malignant arterial hypertension and is clinically manifested by severe headache, nausea, vomiting, impaired consciousness, convulsive syndrome, and in some cases is accompanied by focal neurological symptoms.

The appearance of a TIA or minor stroke indicates a high risk of repeated and, as a rule, more severe strokes (since the pathogenetic mechanisms of these conditions are largely similar) and requires the prevention of repeated strokes.

II. STAGED MANAGEMENT OF PATIENTS WITH cerebrovascular accident

Basic principles of organizing medical care for stroke.

I. Diagnosis of stroke at the prehospital stage.

II. The earliest possible hospitalization of all patients with stroke.

III. Diagnosis of the nature of the stroke.

IV. Clarification of the pathogenetic subtype of stroke.

V. Selection of optimal treatment tactics.

VI. Rehabilitation and measures for secondary prevention of stroke.

III. EVENTS AT THE PREHOSPITAL STAGE

Main goals:

1. Diagnosis of stroke.

2. Carrying out a set of emergency treatment measures.

3. Carrying out emergency hospitalization of the patient.

Assistance is provided by linear or specialized neurological emergency medical teams.

1. ACVA is diagnosed with the sudden appearance of focal and/or cerebral neurological symptoms in a patient with general vascular disease and in the absence of other causes (trauma, infection, etc.)

2. Emergency treatment measures are determined by the need to ensure sufficient ventilation and oxygenation, maintain stability of systemic hemodynamics, and relieve convulsive syndrome.

Assessment: number and rhythm of respiratory movements, condition of visible mucous membranes and nail beds, participation of auxiliary muscles in the act of breathing, swelling of the neck veins.

Measures: if necessary - cleansing the upper respiratory tract, placing an air duct, and if indicated (tachypnea 35-40 per minute, increasing cyanosis, arterial dystonia) - transferring the patient to artificial ventilation (ALV). Manual breathing devices (ADR-2, Ambu type) and automatic devices are used.

2.2. Maintaining an optimal level of systemic blood pressure.

Emergency parenteral administration of antihypertensive drugs should be avoided if systolic blood pressure does not exceed 200 mmHg, diastolic blood pressure does not exceed 120 mmHg, and the calculated mean blood pressure does not exceed 130 mmHg. (mean BP = (systolic BP - diastolic BP): 3 + diastolic BP). Blood pressure should not be reduced by more than 15-20% of the initial values. It is preferable to use drugs that do not affect the autoregulation of cerebral vessels - alpha - beta - blockers, beta - blockers, angiotensin-converting enzyme (ACE) inhibitors.

For arterial hypotension, it is recommended to use drugs that have a vasopressor effect (alpha adrenergic agonists), drugs that improve myocardial contractility (cardiac glycosides), and volume-replacing agents (dextrans, plasma, saline solutions).

2.3. Relief of convulsive syndrome (anticonvulsants - tranquilizers, antipsychotics; if necessary - muscle relaxants, inhalation anesthesia).

3. Stroke is a medical emergency, so all patients with stroke must be hospitalized.

Hospitalization time should be minimal from the onset of focal neurological symptoms, preferably within the first 3 hours from the onset of the disease.

A contraindication for hospitalization of a patient with stroke is only an agonal state.

IV. EVENTS AT THE HOSPITAL STAGE

IV.1. Organizational events

Hospitalization of patients with stroke is carried out in a multidisciplinary hospital that has the necessary X-ray and radiological equipment (including computed tomography (CT), magnetic resonance imaging (MRI), angiography) and ultrasound equipment, as well as:

a) a department for patients with cerebrovascular accidents with an intensive care unit;

b) a neurointensive care unit or intensive care unit with specially designated beds and trained personnel for the management of patients with stroke;

c) department of neurosurgery.

Patients who have:

Altered level of wakefulness (from mild stupor to coma);

Breathing and swallowing disorders;

Severe disturbances of homeostasis;

Decompensation of cardiac, renal, hepatic, endocrine and other functions against the background of stroke.

Patients with acute stroke who do not require emergency resuscitation and neurosurgical care are hospitalized in the department for patients with cerebrovascular accidents. At the same time, patients are admitted to the intensive care ward:

With unstable (progressive) neurological symptoms (“developmental stroke”);

With severe neurological deficits, requiring intensive individual care;

With additional somatic disorders.

IV.2. Diagnostic measures

IV.2.1. HOSPITAL DIAGNOSTICS STAGE

The goal is to confirm the diagnosis of stroke and determine its nature (ischemic, hemorrhagic).

Requirements:

1. Help for patients with stroke is provided by a neurologist, resuscitator, therapist and neurosurgeon.

2. Patients with acute stroke should have the right to priority instrumental and laboratory examination so that the diagnostic process is as complete and fast as possible (within an hour from the moment of hospitalization).

3. For patients with TIA, diagnostic examinations are also carried out in the hospital and to the same extent as for patients with stroke.

All patients with a presumptive diagnosis of stroke are advised to undergo a computed tomography (CT) scan of the head, which in most cases allows one to distinguish a hemorrhagic stroke from an ischemic one and exclude other diseases (tumors, inflammatory diseases, CNS injuries). Magnetic resonance imaging (MRI) of the head is a more sensitive method for diagnosing cerebral infarction at an early stage. However, it is inferior to CT in detecting acute hemorrhages, and therefore is less suitable for emergency diagnosis.

In cases where CT or MRI are not available, echoencephaloscopy (M-ECHO) is mandatory; in the absence of contraindications, lumbar puncture and cerebrospinal fluid examination.

Lumbar puncture is contraindicated in case of inflammatory changes in the lumbar region and if an intracranial space-occupying process is suspected (danger of dislocation disorders).

BASIC DIAGNOSTIC MEASURES FOR PATIENTS WITH cerebrovascular accident

(regardless of the nature of the stroke)

1. Clinical blood test with platelet count, hematocrit.

2. Blood type, Rh factor.

3. Blood test for HIV.

4. Blood test for HBs antigen.

5. Wasserman reaction.

6. Biochemical blood test: sugar, urea, creatinine, bilirubin, AST, ALT, cholesterol, triglycerides, high and low density lipoproteins.

7. Electrolytes (potassium, sodium), plasma osmolality.

8. Blood gas composition, acid-base balance.

9. Screening - study of the hemostasis system: fibrinogen, fibrinolytic activity (lysis of euglobulins), thrombin time, activated partial thrombin time (APTT), prothrombin test with calculation of the international normalized ratio (MHO), blood clotting time, bleeding time, D - dimer, platelet aggregability (adrenaline-, ADP-, collagen-induced), blood viscosity.

10. Clinical urine analysis.

12. X-ray of the chest organs.

13. X-ray of the skull.

14. Consultation with a therapist.

15. Consultation with an ophthalmologist.

Additional diagnostic measures (according to indications)

1. Glycemic profile.

2. Glucosuric profile.

3. Consultation with an endocrinologist.

4. EEG (in the presence of convulsive syndrome).

5. Study of markers of intravascular activation of the hemostatic system: prothrombin fragments I+II, thrombin-antithrombin complex (TAT) and protein C system, fibrin - peptide A, soluble fibrin-monomer complexes, D-dimer, plasmin-antiplasmin complex (PAP).

6. Assessment of intravascular platelet aggregation: platelet factor 4, thromboxane B2, beta thrombomodulin.

Result: verification of the diagnosis of stroke and the nature of the stroke (ischemic, hemorrhagic).

IV.2.2. THE STAGE OF "IN-DEPTH" HOSPITALIZATION DIAGNOSTICS is a direct continuation of the previous stage.

PURPOSE: to clarify the pathogenetic subtype of stroke:

A. Ischemic stroke:

Atherothrombotic (includes stroke due to arterio-arterial embolism);

Cardioembolic;

Hemodynamic;

Lacunar;

Stroke type of hemorheological microocclusion.

B. Hemorrhagic stroke:

Non-traumatic subarachnoid hemorrhage (hypertensive, aneurysm rupture);

Parenchymal hemorrhage;

Hemorrhage into the cerebellum;

Subarachnoid - parenchymal;

Ventricular hemorrhage;

Parenchymatous - ventricular.

A. ISCHEMIC STROKE.

Mandatory studies (conducted within an hour from the moment of hospitalization):

1. Ultrasound examination of extra- and intracranial vessels, including duplex scanning.

2. Emergency cerebral angiography - performed only in cases where it is necessary to make a decision on drug thrombolysis.

3. Echocardiography.

Additional studies (conducted during the first 1 - 3 days):

1. Planned cerebral angiography:

Carried out to clarify the cause of ischemic stroke,

The scope of the study includes angiography of the branches of the aortic arch, the main arteries of the head, and intracranial vessels.

2. Holter ECG monitoring.

3. Daily blood pressure monitoring.

Special studies are carried out if indicated during the acute period of the disease, their types and volume are determined by a council with the participation of relevant specialists - hematologist, cardiologist - rheumatologist, etc.

Result: clarification of the leading mechanism of development of stroke and the pathogenetic subtype of ischemic stroke, choice of patient management tactics, including resolving the issue of the need for surgical correction.

B. HEMORRHAGIC STROKE.

Purpose: to clarify the pathogenetic basis of hemorrhage (hypertensive, due to rupture of an aneurysm or arteriovenous malformation)

Diagnostic measures:

1. Cerebral angiography:

1.1 Indications:

Subarachnoid hemorrhage;

Atypical localization of intracerebral hematoma (according to CT, MRI);

Ventricular hemorrhage.

1.2 Scope of the study: bilateral carotid and vertebral angography.

2. Transcranial Dopplerography - to identify and assess the severity of cerebral vasospasm, its dynamics during treatment.

An emergency consultation with a neurosurgeon is indicated:

1. Hemorrhagic stroke:

a) supra- and subtentorial hematoma;

b) subarachnoid hemorrhage.

2. Cerebellar infarction.

3. Presence of acute obstructive hydrocephalus.

A planned consultation with a neurosurgeon and/or vascular surgeon is indicated for ischemic stroke, PNMK in the presence of hemodynamically significant stenoses, occlusion of the main arteries of the head, tortuosity of the neck arteries, stenosis/occlusion of the cerebral arteries.

Indications for surgical treatment of patients with stroke.

A. Hemorrhagic stroke.

1. Intracerebral hemispheric hemorrhages with a volume of more than 40 ml (according to CT scan of the head).

2. Hemorrhage into the cerebellum.

3. Obstructive hydrocephalus.

B. Aneurysms, arterio-venous malformations, arterio-sinus fistulas, accompanied by various forms of intracranial hemorrhage and/or cerebral ischemia.

B. Ischemic stroke.

1. Cerebellar infarction with severe secondary brainstem syndrome, brainstem deformation (according to CT/MRI of the head), obstructive hydrocephalus.

IV.3. Management of patients with different forms of stroke (see Appendix III)

General principles of treatment of patients with stroke include basic therapy (regardless of the nature of stroke) and differentiated therapy, taking into account the nature and pathogenetic subtype of stroke.

IV.3.1. Basic therapy measures for stroke

1. Measures aimed at normalizing the function of external respiration and oxygenation (sanitation of the respiratory tract, installation of an air duct, tracheal intubation, and, if necessary, mechanical ventilation).

2. Regulation of the function of the cardiovascular system:

a) maintaining blood pressure 10% higher than the numbers to which the patient is adapted (when carrying out antihypertensive therapy, beta blockers, ACE inhibitors, calcium channel blockers are preferred; for arterial hypotension, drugs that have a vasopressor effect (dopamine, alpha adrenergic agonists) and volume replacement therapy (dextrans, single-group fresh frozen plasma);

b) antiarrhythmic therapy for cardiac arrhythmias;

c) for ischemic heart disease (post-infarction cardiosclerosis, angina) - antianginal drugs (nitrates);

d) drugs that improve the pumping function of the myocardium - cardiac glycosides, antioxidants, optimizers of tissue energy metabolism.

3. Control and regulation of homeostasis, including biochemical constants (sugar, urea, creatinine, etc.), water-salt and acid-base balance.

4. Neuroprotection - a set of universal methods for protecting the brain from structural damage - begins at the prehospital stage (may have some features for different subtypes of stroke).

5. Measures aimed at reducing cerebral edema (have features depending on the nature of the stroke).

6. Measures for the prevention and treatment of somatic complications: pneumonia, bedsores, urinary infection, disseminated intravascular coagulation syndrome, phlebothrombosis and pulmonary embolism, contractures, etc.

7. Symptomatic therapy, including anticonvulsant, psychotropic (for psychomotor agitation), muscle relaxants, analgesics, etc.

IV.3.2. General principles of pathogenetic treatment for ischemic stroke

The modern strategy for treating patients with ischemic strokes is based on early diagnosis of the pathogenetic subtype of stroke.

The basic principles of pathogenetic treatment of ischemic stroke include:

1) restoration of blood flow in the ischemic zone (recirculation, reperfusion).

2) maintaining the metabolism of brain tissue and protecting it from structural damage (neuroprotection).

Basic recycling methods

1. Restoration and maintenance of systemic hemodynamics.

2. Drug thrombolysis (recombinant tissue plasminogen activator, alteplase, urokinase).

3. Hemangiocorrection - normalization of the rheological properties of blood and the functionality of the vascular wall:

a) antiplatelet agents, anticoagulants, vasoactive agents, angioprotectors;

b) extracorporeal methods (hemosorption, ultrahemofiltration, laser irradiation of blood);

c) gravitational methods (cyt-, plasmapheresis).

4. Surgical methods of recirculation: extra-intracranial microanastomosis, thrombectomy, reconstructive surgery on arteries.

Basic methods of neuroprotection

1. Restoration and maintenance of homeostasis.

2. Drug protection of the brain.

3. Non-drug methods: hyperbaric oxygenation, cerebral hypothermia.

Decongestant therapy for ischemic stroke

1. Osmotic diuretics (under the control of plasma osmolality).

2. Hyperventilation.

3. An additional anti-edematous effect is provided by the use of neuroprotectors and the maintenance of homeostasis.

4. If occlusive hydrocephalus develops due to cerebellar infarction, surgical treatment is performed according to indications (decompression of the posterior cranial fossa, ventricular drainage).

IV.3.2.1. Features of treatment of various pathogenetic subtypes of ischemic stroke

When verifying a stroke due to obstruction of the afferent artery (atherothrombotic, including due to arterio-arterial embolism, cardioembolic infarction) upon admission of the patient in the first 3-6 hours from the onset of the disease and the absence of changes in a CT examination of the head (hemorrhagic changes, mass effect) , with stable blood pressure not higher than 185/100 mm Hg. it is possible to carry out drug thrombolysis: recombinant tissue plasminogen activator (rt-PA) at a dose of 0.9-1.1 mg/kg of patient weight, 10% of the drug is administered as an intravenous bolus (with the intra-arterial catheter in place - i.a.), the remaining dose - IV drip for 60 minutes). However, the need for highly specialized preliminary examination of a possible recipient, including CT scan of the head, angiography, and the significant risk of hemorrhagic complications of thrombolytic therapy currently do not allow us to recommend this method of treatment for widespread use and force it to be limited to specialized angioneurological centers.

1. CARDIOEMBOLIC STROKE:

a) anticoagulants - direct action in the acute period, followed by transition to long-term maintenance therapy with indirect anticoagulants;

b) antiplatelet agents;

c) neuroprotectors;

d) vasoactive drugs;

e) adequate treatment of cardiac pathology (antiarrhythmic drugs, antianginal drugs, cardiac glycosides, etc.).

2. ATHEROTHROMBOTIC STROKE:

a) antiplatelet agents (platelet, erythrocyte);

b) with a progressive course of the disease (increasing thrombosis), direct-acting anticoagulants are indicated with a transition to indirect ones;

c) hemodilution (low molecular dextrans, single-group fresh frozen plasma);

d) angioprotectors;

e) neuroprotectors.

3. HEMODYNAMIC STROKE:

a) restoration and maintenance of systemic hemodynamics:

Drugs with vasopressor action, as well as those that improve the pumping function of the myocardium;

Volume-substituting agents, mainly biorheological preparations (plasma), low-molecular dextrans;

For myocardial ischemia - antianginal drugs (nitrates);

For dysrhythmia - antiarrhythmics, for conduction disorders (bradyarrhythmia) - implantation of an electrical pacemaker (temporary or permanent);

b) antiplatelet agents;

c) vasoactive drugs (taking into account the state of systemic hemodynamics, blood pressure, cardiac output, the presence of dysrhythmias);

d) neuroprotectors.

4. LACUNARY STROKE:

a) basis - optimization of blood pressure (ACE inhibitors, angiotensin II receptor antagonists, beta blockers, calcium channel blockers);

b) antiplatelet agents (platelet, erythrocyte);

c) vasoactive agents;

d) antioxidants.

5. STROKE BY TYPE OF HEMORHEOLOGICAL MICROOCLUSION:

a) hemangiocorrectors of various groups (antiplatelet agents, angioprotectors, vasoactive drugs, low molecular weight dextrans);

b) in case of insufficient effectiveness, development of disseminated intravascular coagulation syndrome - the use of direct and then indirect anticoagulants;

c) vasoactive drugs;

d) antioxidants.

6. ACUTE HYPERTENSIVE ENCEPHALOPATHY:

a) a gradual decrease in blood pressure by 10-15% from the initial level (the use of easily dosed ACE inhibitors, alpha-beta adrenergic blockers, beta-adrenergic blockers is preferable; the use of vasodilating drugs is contraindicated);

b) dehydration therapy (saluretics, osmotic diuretics);

c) hyperventilation;

d) neuroprotectors;

e) angioprotectors;

f) hemangiocorrectors (mainly biorheological preparations - plasma, low molecular weight dextrans);

g) symptomatic treatment (anticonvulsants, antiemetics, analgesics, etc.).

IV.3.3. General principles of treatment of hemorrhagic stroke

The basics of basic therapy for hemorrhagic stroke have some features.

1. Regulation of the function of the cardiovascular system:

a) in case of hypertensive hemorrhages, optimization of blood pressure has pathogenetic significance;

b) in some cases, patients require long-term controlled arterial hypotension. The drug of choice for this treatment method is sodium nitroprusside, which is administered through an infusion pump with continuous blood pressure monitoring.

2. Measures aimed at reducing cerebral edema:

a) the use of membrane stabilizers (dexazone 4-8 mg IM 4 times a day);

b) hyperventilation;

c) use of neuroprotectors;

d) restoration and maintenance of homeostasis;

e) surgical methods - hematoma removal, ventricular drainage, decompression.

3. Neuroprotection (see Ischemic stroke).

4. Measures for the prevention and treatment of somatic complications: DIC - syndrome, phlebothrombosis and pulmonary embolism (use of hemangiocorrectors - antiplatelet agents, anticoagulants, low molecular weight dextrans). The decision to prescribe them must be made by a council with the participation of a hematologist.

Pathogenetic treatment of hemorrhagic stroke (conservative)

1. The use of angioprotective agents that help strengthen the vascular wall.

2. For subarachnoid hemorrhage and intracerebral hematomas with blood breakthrough into the cerebrospinal fluid system - prevention of vascular spasm (vasoselective calcium channel blockers - nimodipine up to 25 mg/day IV drip or 0.3-0.6 every 4 hours orally; vasoactive drugs).

3. To improve microcirculation and prevent secondary ischemic lesions of brain tissue, low-molecular dextrans and antiplatelet agents are used under conditions of continuous monitoring of blood pressure and parameters of the hemostatic system.

V. Rehabilitation of patients with stroke

V.1. Main tasks of rehabilitation.

1. Restoration (improvement) of impaired functions.

2. Mental and social readaptation.

3. Prevention of post-stroke complications (spasticity, contractures, etc.).

V.2. Indications and contraindications for rehabilitation.

All patients with stroke need rehabilitation measures.

Contraindications to active rehabilitation are:

1. severe somatic pathology in the stage of decompensation;

2. mental disorders.

V.3. Basic principles of rehabilitation.

The main principles of rehabilitation are: early start, duration and systematicity, stages, complexity, active participation of the patient.

The duration of rehabilitation is determined by the timing of restoration of impaired functions: maximum improvement in motor functions is observed in the first 6 months, everyday skills and ability to work - within 1 year, speech functions - within 2-3 years from the moment of development of stroke.

V.4. Organization of stage-by-stage care for patients who have suffered a stroke.

1. Angioneurological department of a multidisciplinary hospital.

2. Early rehabilitation department of a multidisciplinary hospital:

Patients are transferred, as a rule, 1 month after the onset of stroke,

A full course of rehabilitation treatment is carried out,

The duration of the course is 1 month.

3. Further treatment is determined by the severity of the neurological defect:

A) if there are motor, speech or other disorders, the patient is sent to a rehabilitation center or rehabilitation sanatorium;

B) in the absence of pronounced neurological disorders, the patient is sent to a local sanatorium with a neurological or cardiovascular profile;

B) patients with severe residual neurological impairment or who have contraindications to active rehabilitation are discharged home or transferred to a specialized care hospital.

4. Patients with moderate severity of residual neurological disorders continue rehabilitation on an outpatient basis (rehabilitation departments or clinics).

5. Repeated courses of inpatient rehabilitation are indicated for continued restoration of impaired functions and the prospect of restoration of working capacity.

VI. Prevention of recurrent strokes

The risk of stroke in reversible forms of cerebrovascular pathology (TIA, minor stroke) is high and is at least 5% per year. Prevention of recurrent strokes should be carried out taking into account the pathogenetic mechanisms of their development.

If the cause of a TIA or minor stroke turns out to be a cardiogenic embolism, in addition to the correction (medical, surgical) of cardiac pathology, the use of indirect anticoagulants or antiplatelet agents is indicated. In case of detection of a small deep (lacunar) infarction, pathogenetically associated with hypertension, the main direction of preventing recurrent strokes becomes adequate antihypertensive therapy.

Stroke prevention is more difficult in patients with atherosclerotic changes in the carotid arteries (atherothrombotic, hemodynamic stroke, and also due to arterio-arterial embolism). The significance of the pathology of the carotid artery for a particular patient is determined by the individual characteristics of the structure of the vascular system of the brain, the severity and prevalence of its damage, as well as the structure of atherosclerotic plaques.

Currently, in patients with TIA and minor stroke due to pathology of the carotid arteries, two areas of stroke prevention are generally recognized:

1. use of antiplatelet agents;

2. Angiosurgery: elimination of carotid artery stenosis; if there are contraindications, cranio-cerebral bypass can be performed.

Prescribing antiplatelet drugs to patients who have suffered a TIA or minor stroke reduces their risk of developing a recurrent stroke by 20-25%. In the case of significant stenosis of the carotid artery (more than 70% of the lumen of the vessel) on the side of the affected cerebral hemisphere, carotid endarterectomy as a means of preventing recurrent stroke is significantly more effective than the use of antiplatelet agents. A prerequisite is to perform the operation in a specialized clinic, in which the level of complications associated with the operation does not exceed 3-5%. For carotid artery stenosis up to 30%, preference is given to drug prevention. Surgery may become necessary if a medium-sized complicated plaque becomes the source of recurrent cerebral embolism.

Prevention of recurrent stroke in patients who have experienced hemorrhagic stroke is:

1. in patients with arterial hypertension - in carrying out adequate antihypertensive therapy;

2. in patients with hemorrhage due to rupture of an arterial aneurysm or arteriovenous malformation - during angiosurgery.

Passport details:

FULL NAME. Kriksina Alexandra Dmitrievna

Female gender

Age: 60 years old (02/21/41)

Permanent place of residence: Moscow, st. Leskova, 9-179

Profession: Pensioner

Date of admission: 10/29/01

Supervision date: 11/22/01

Complaints of sudden speech disturbances, weakness in the right leg and right arm.

History of the present disease. (Anamnesis morbi.)

According to her son-in-law: she became acutely ill on November 29, 2001, when the patient suddenly lost her speech, weakness appeared in her right limbs, the patient fell to the floor and did not lose consciousness. The patient has been suffering from hypertension (stage III) for a long time. In September 2001, the patient suffered an acute cerebrovascular accident with speech disorders without paresis. However, within a month, speech was almost completely restored.

Life story. (Anamnesis vitae).

Born in 1941 on February 21 in Moscow. The birth proceeded normally, without pathology. The patient is the second child in the family; she did not lag behind her peers in mental and physical development. Education: Secondary.

Family and sexual history:

Married, 2 children.

Nutrition: excess, varied, high in calories.

Past illnesses:

childhood infections (whooping cough, chickenpox, scarlet fever). The patient has tuberculosis. The patient denies having jaundice or sexually transmitted diseases.

Allergy history:

There are no allergic reactions to foods, serums or vaccines.

Heredity:

Not burdened.

The present condition of the patient. (Status praesents).

General examination.

Upon general examination of the patient, the condition is satisfactory, the position is active. The physique is correct, the constitutional type is normosthenic. Posture is slouchy. Body temperature 36.4 degrees Celsius.

The skin is pale, the face is hyperemic, dry over the entire surface of the body, without pigment spots. Visible mucous membranes are pale pink in color, without any pigment spots.

Subcutaneous fatty tissue is moderately developed, there is no pain or crepitus on palpation. There is no swelling.

Lymph nodes: inguinal, axillary, cervical are non-palpable and painless. Pharynx: the root of the tongue and the soft palate are not hyperemic, there is no plaque or swelling. The tonsils are not enlarged, not hyperemic, without plaque.

There is no pain on palpation of the skeletal system, no deformation is noted.

Respiratory system.

When examining the respiratory organs, no cough is observed. There is no shortness of breath in the active or passive position. There is no chest pain.

When auscultating breathing in symmetrical areas of both lungs, vesicular. Bronchophony in symmetrical areas of the chest is the same.

The cardiovascular system.

At the time of monitoring the complaints, there was no pain in the heart area, shortness of breath, suffocation, palpitations, or swelling. The arteries and veins are not enlarged, there is no visible pulsation (there is no positive venous pulse). The heart area is without visible changes.

There is an expansion of the left border of the heart to the left.

On auscultation of the heart, the sounds are muffled. The rhythm is correct.

There is no aortic pulsation in the jugular fossa.

The arterial pulse is the same in both arms, 92 beats per minute, of average value, tension and filling. Blood pressure 180/100 mmHg.

Upon examination and palpation of the neck veins, no swelling or pulsation was detected. There is no dilatation of the veins of the chest, abdominal wall, or limbs.

Digestive system.

Gastrointestinal tract.

Vomiting, dyspepsia, flatulence, and stool disorders are absent. When examining the oral cavity, the tongue is moist, pink, without plaque, cracks, or ulcers. The gums, hard and soft palate are pink, without visible damage. Appetite is reduced.

On examination, the abdomen is of regular shape, symmetrically participates in the act of breathing, there is no bulging or retraction of the abdominal wall, there is no visible peristalsis.

Upon percussion of the abdomen, free and encysted fluid is absent. Mendel's sign is negative.

On superficial palpation there is no pain or tension in the abdominal muscles.

On auscultation: peristalsis of normal strength, duration, periodic. Abdominal friction and vascular sounds are not heard.

Liver and gall bladder.

At the time of supervision, there were no complaints of pain in the right hypochondrium and dyspeptic symptoms.

Upon examination, there are no protrusions or retractions in the area of ​​the right hypochondrium.

The gallbladder is not palpable.

Spleen.

At the time of supervision, there were no complaints of pain in the left hypochondrium.

When examining a limited protrusion in the area of ​​the left hypochondrium and breathing restrictions in this area were not revealed.

The spleen is not palpable.

Peritoneal friction noise is not heard.

Pancreas.

Pain in the upper abdomen, no dyspeptic symptoms.

On palpation, enlargement and thickening of the pancreas were not detected.

Urinary system.

Upon examination of the genitourinary system, there was no pain in the lumbar region. There is no pain in the bladder area, urination is not impaired and painless. Urine: straw-yellow, transparent, no blood impurities.

Examination of the lumbar and suprapubic region revealed no pathological changes.

The kidneys are non-palpable in a horizontal and vertical position, the bladder is not palpable. Pain at the costovertebral point and along the ureters is not detected.

Endocrine system.

No growth or physique abnormalities were identified, the physique is proportional. There is no obesity. The skin is dry, thinned, without roughness. There is no increase in the size of the nose, jaws, ears, hands, or feet.

The thyroid gland is not enlarged and painless.

Neurological status.

In consciousness, contact is difficult due to speech disorders. There are no cerebral or meningeal symptoms.

Cranial nerves.

I. Olfactory nerve. The sense of smell is preserved. There are no distortions of smell or olfactory hallucinations.

II. Optic nerve. Vision is reduced. Loss of the right fields of vision in both eyes. Color perception is preserved.

III Oculomotor, IV trochlear, VI abducens nerves. The right palpebral fissure is widened D>S. The range of eye movements in all directions is completely preserved. There are no floating eye movements. Paresis of gaze to the right. Setting the gaze to the left. The pupils are of medium size, D=S. The photoreaction (direct and friendly) is preserved. There is no strabismus, diplopia, or exophthalmos.

V. Trigeminal nerve. There is no pain in the area where the nerve branches exit. There are no paresthesias. Peripheral and segmental sensory impairment was detected. The sensitivity of the mucous membranes of the mouth, tongue, nose and eyes is unimpaired. When opening the mouth, the lower jaw does not deviate to the side. The trophication muscles are not impaired. Corneal and conjunctival reflexes (V-VII) are positive.

VII. Facial nerve. There is no immobility or mask-like appearance of the face. The right nasolabial fold is smoothed. The right palpebral fissure is widened. Asymmetry is observed with wrinkling of the forehead, frowning of the eyebrows, and baring of the teeth. Positive “sail” symptom.

VIII. Auditory nerve. Hearing is preserved on both sides. There is no ringing or noise in the ears. There is no nystagmus or systemic vertigo.

IX. Glossopharyngeal, Xvagus nerves. Mild dysphagia, pharyngeal reflexes high D=S. Sensation in the upper part of the pharynx is preserved. The voice is quiet, hoarse.

XI. Accessory nerve. Raising the shoulders and turning the head, raising the left arm above the horizontal, bringing the shoulder blades closer together are preserved. On the right side, these voluntary movements are limited. Head position without tilting to the side. The trophism of the sternocleidomastoid muscles is not impaired.

XII.Hypoglossal nerve. When protruding, the tongue deviates to the right without atrophy or fibrillary twitching. Dysarthria.

Propulsion system.

Upon examination and palpation of the muscular system, atrophy, pseudohypertrophy, fibrillar and fascicular twitching are absent. Passive movements of the upper and lower extremities are fully preserved. Lack of active movements in the right limbs. There is a weakening of muscle strength, revealed in the Barre test, up to 2-3 points in the right extremities with an increase in muscle tone (in the upper extremities the flexor tone is increased, in the lower extremities the extensor tone is increased) of a spastic type. Akinesis, bradykinesia, hyperkinesis (tremor, chorea, athetosis, choreoathetosis, hemiballismus, myoclonus, torsion dystonia, tics) are absent. Automated gesture syndrome was not identified.

There are no seizures or convulsive twitches.

Coordination of movements.

The finger-nose test is carried out confidently. There was no intention tremor, adiadochokinesis, hypermetry, or scanned speech.

Reflexes.

Tendon and periosteal reflexes are animated: from the upper extremities D>S, from the lower extremities: knee (L2-L4, femoral nerve), Achilles (S 1

S2, tibial nerve) - D>S.

Skin reflexes: upper (Th7 - Th8), middle (Th9 - Th10), lower (Th11 - Th12), abdominal, plantar (tibial nerve, L5-S2) reduced D>S.

The joint reflexes of Mayer (ulnar and median nerves, C7-Th1) and Lehry (ulnar and median nerves, C6-Th1) are reduced.

Pathological reflexes:

pyramidal: the Babinsky reflex on the right is detected, the Oppenheim, Gordon, and Schaeffer reflexes are negative;

reflexes of the Rossolimo group (Bekhterev 1, 2, Zhukovsky) are negative.

Defensive reflexes:

positive on the right.

Raymist synkinesis is revealed.

Pseudobulbar reflexes:

Positive reflexes of oral automatism were identified: naso-labial, labial, proboscis, palmar-mental.

Sensitivity.

Superficial sensitivity (pain, temperature, tactile, hair) is absent on the right, preserved on the left. Deep sensitivity (muscular-articular feeling, vibration, feeling of pressure and weight) is absent on the right, preserved on the left. Complex sensitivity (kinesthetic, discriminative, two-dimensional, stereognosis) is absent on the right, defined on the left. Pain points along the peripheral nerves and roots are not identified.

Autonomic nervous system.

Hyperthermia and hyperemia of the face are determined symmetrically on both sides. Persistent white dermographism. There is no acrocyanosis. The function of the pelvic organs, as well as the patient’s control over them, is not impaired.

Higher cortical functions.

Results of instrumental methods and laboratory studies.

General blood test dated November 20, 2001:

Hemoglobin 128g/l

Hematocrit 0.5

Leukocytes 6.5

Band 13

Segmented 61

Eosinophils5

Basophils 0

Lymphocytes 20

Monocytes 4.2

General urine analysis:

Color straw yellow

Full transparency

Density 1018

The reaction is acidic

Glucose absent

Leukocytes absent

Protein absent.

Syndromic diagnosis.

During the examination, the patient is diagnosed with:

Movement disorders in the form of:

A) Central right-sided hemiparesis:

-

-

hyperreflexia, decreased skin reflexes D>S,

-

-

-

synkinesis Rainest,

-

B) Central paresis of the 7th and 12th nerves on the right:

-

smoothness of the right nasolabial fold,

-

asymmetry with wrinkling of the forehead, frowning of the eyebrows, baring of teeth,

-

Positive "sail" symptom

-

when protruding, it deviates to the right side without atrophy and fibrillary twitching,

-

B) Pseudobulbar palsy:

-

dysphagia,

-

dysphonia,

-

-

-

Sensory impairment in the form of:

A) Right-sided hemianesthesia: violation of all types of sensitivity on the right side according to the hemitype.

B) Right-sided homonymous hemianopsia.

B) Paresis to the right.

Violation of higher cortical functions:

A) Sensomotor aphasia, agraphia, alexia.

Thus, the patient has a syndrome of three “hemi” (hemiparesis, hemianesthesia, hemianopsia).

Topical diagnosis.

1. Motor disorders in the form of central right-sided hemipares indicate damage to the pyramidal tract, which begins in the right hemisphere in the neurons of the precentral gyrus, then it goes to the internal capsule (anterior two-thirds of the posterior thigh), then it passes in the middle part of the cerebral peduncles, descends through the base of the pons and into the lower part of the medulla oblongata moves to the opposite side and approaches the anterior horns.

Central paresis of the VII and XII nerves indicates a unilateral lesion of the corticonuclear pathway passing in the knee of the internal capsule, in the middle part of the cerebral peduncles. When approaching the nuclei, this path also crosses. This pathology is due to the fact that only the nucleus XII and the lower pole of the nucleus VII of the cranial nerve have unilateral connections with the cortex.

Pseudobulbar syndrome indicates bilateral damage to the corticonuclear pathway (its supranuclear portion).

2. Sensitive disorders in the form of:

A) right-sided hemianesthesia indicates damage to the fibers passing in the posterior third of the posterior thigh and internal capsule.

Surface sensitivity:

The first neuron is located in the spinal ganglion, the second neuron (spino-thalamic) begins at the cells of the dorsal horn, its fibers pass through the anterior commissure to the opposite side, entering the white matter. They rise up the brain stem and end in the ventral part of the optic thalamus. The third neuron begins at the outer part of the optic thalamus, goes through the posterior third of the posterior thigh of the left internal capsule to the superior parietal lobule (thalamo-cortical tract).

Deep Sensitivity:

The central process of the first neuron participates in the formation of the dorsal root and, without entering the dorsal horn of the segment, is directed to the dorsal columns. As part of the Gaulle and Burdach bundles, the pathways rise, without interruption, to the nuclei of the same name in the lower part of the medulla oblongata. They are the beginning of the second neuron (bulbo-thalamic tract), which immediately passes to the opposite side of the medulla oblongata and, after decussation, forms a medial loop, to which the spinothalamic tract approaches in the area of ​​the pons. The third neuron is formed from the cells of the outer nucleus of the visual thalamus and their fibers, which through the posterior part of the posterior thigh of the internal capsule to the cortex of the posterior central gyrus and the superior parietal lobe.

B) right-sided homonymous hemianopsia with preservation of the pupil’s reaction to light indicates damage to the Graziole radiance, because it contains non-pupillary fibers.

C) gaze palsy to the right indicates damage to the left frontal oculomotor pathway.

Violation of higher cortical functions in the form of sensorimotor aphasia, agraphia, alexia with damage to the posterior part of the inferior frontal gyrus - Broca's area (field 44), the superior temporal gyrus - Wernicke's area (field 22) of the left hemisphere.

The syndrome of three “hemi” indicates damage to the entire posterior part of the posterior thigh of the left internal capsule. This area is vascularized by the middle cerebral artery, which is a branch of the left internal carotid artery. This patient also had lesions in the Graziole radiator, 44 and 22 cortical fields of the left hemisphere.

Clinical diagnosis.

The underlying disease: repeated acute ischemic cerebral disorder in the left internal carotid artery system. Atherosclerosis of cerebral vessels. Dyscirculatory encephalopathy grade III.

Concomitant diseases: stage III hypertension, circulatory failure 1.

Clinical diagnosis was made based on:

Complaint: according to her son-in-law (due to the patient’s speech impairment), the patient fell due to sudden weakness in her right limbs. However, without loss of consciousness or vomiting. Also complaints of speech impairment. History of the development of the present disease: a patient with a vascular history has been suffering from hypertension for a long time (20 years), and overnutrition. The patient has cerebral atherosclerosis. Also in September 2001, the patient suffered an ischemic stroke in the left internal carotid artery. Examination data: absence of cerebral and meningeal symptoms, left hemisphere focal symptoms in the form of right-sided hemiparesis, right-sided hemianopsia and hemianesthesia. The presence of pseudobulbar palsy, as well as sensorimotor aphasia, alexia, agraphia.

Thus, taking into account the patient’s age, long-term vascular history, and a history of ischemic stroke in the past, we can talk about damage to the left internal capsule (her posterior thigh), as well as damage to the cerebral cortex due to an ischemic stroke of the artery feeding the etizone. The presumed mechanism of damage is non-thrombotic, occurring more often due to vascular occlusion by an atherosclerotic plaque and vascular tortuosity.

Treatment plan.

Stationary mode. Table 10 Sol.Rheopholyglucini 400 IV drip. Tab.Glicini up to 1 g per day under the tongue. Tab.Aspirini ¼ at night. Exercise therapy. Massage. Barotherapy. Consultations with specialists.

11/22/01 Condition is satisfactory. The patient makes no complaints due to speech impairment. Right-sided hemiparesis and hemianesthesia are preserved. Pseudobulbar symptoms are pronounced. Muscle tone is increased in the right extremities of the post-spastic type.

Heart rate 80 beats/min, respiratory rate 18/min. BP 150/100.

26.11.01 Condition is satisfactory. He makes no complaints due to the persistence of speech impairments. Neurological and somatic status unchanged. There is an increase in muscle strength in the right limbs up to 3.5 points.

Exercise therapy, massage, and barotherapy are provided.

Heart rate 75 beats/min, respiratory rate 19/min, blood pressure 140/100.

The greatest severity of the condition in patients with ischemic stroke is observed in the first 10 days of the disease, then a period of improvement is noted when the patient’s severity of symptoms begins to decrease. However, the pace of recovery may vary. With good and rapid development of collateral circulation, it is possible to restore function on the first day of a stroke, but more often after a few days. Mortality reaches 20-25%. However, in the case of this patient, a poor prognosis is possible due to the fact that she recently suffered a stroke and the risk of another stroke increases significantly.

Stage epicrisis.

21st day of stay.

Prevention.

Primary prevention of cerebral stroke consists of eliminating possible risk factors (overeating, smoking, stress, etc.), organizing the patient’s work and rest regime, nutrition, and health improvement. Secondary prevention includes measures aimed at systematic monitoring of the condition of patients with cardiovascular diseases, their treatment, and antiplatelet therapy.

Rationale

In a patient with a burdened vascular history who has been suffering for a long time……. Against this background, the limbs suddenly weakened without general cerebral and meningeal symptoms.

Examination by a speech therapist dated 11/22/01.

The patient is generally active, responds adequately to speech addressed to her, performs simple tasks, and when speech instructions become more complex, partial sensory aphasia is revealed. Expressive speech is poor, monosyllabic, with large lateral paraphasias, which are noted both in spontaneous and repeated speech. Automated speech sequences are relatively preserved (their detached repetition is possible). Alexia, agraphia.

Stage epicrisis.

21st day of stay.

Dynamics of complaints: does not present clear complaints in connection with aphasic disorders.

Dynamics of condition: relatively satisfactory condition, conscious, in contact. Against the background of vascular-metabolic therapy, hemodynamic parameters normalized - blood pressure 150-180/100. Neurological status without negative dynamics. She sits, is active, tries to restrain herself. Speech disturbances persist. Right-sided central hemiparesis with spastic muscle tone.

ECG from November 16, 2001 in dynamics from November 6, 2001: blood supply to the anterior wall of the left ventricle is improving.

Ds: Repeated acute ischemic cerebrovascular accident in the system of the left internal carotid artery.

Results of instrumental methods and laboratory studies.

General blood test dated 02/26/01:

Hemoglobin 128 g/l

Hematocrit 0.5

Leukocytes 6.5

Band 13

Segmented 61

Eosinophils 5

Basophils 0

Lymphocytes 20

Monocytes 4.2

General urine analysis:

Color straw yellow

Full transparency

Density 1018

The reaction is acidic

Glucose absent

Leukocytes absent

Protein absent.

Treatment plan.

Stationary mode. Table 10 Sol.Rheopholyglucini 400 IV drip. Tab.Glicini up to 1 g per day under the tongue. Tab.Aspirini ¼ at night.