Ischemic stroke is a pathological condition that is not a separate or independent disease, but an episode that develops as part of a progressive general or local vascular lesion in various diseases of the cardiovascular system. Often, ischemic stroke accompanies the following diseases: arterial hypertension, atherosclerosis, rheumatic heart disease, coronary heart disease, diabetes mellitus and other forms of pathology with vascular damage. The clinic of ischemic stroke consists of cerebral and focal symptoms, depending on the localization of vascular disorders. The most important method of instrumental diagnosis of ischemic stroke, as well as its differentiation from hemorrhagic stroke, is CT and MRI of the brain.
I63 Brain infarction
Ischemic stroke is called cerebral circulatory disorders characterized by the sudden appearance of focal neurological or cerebral symptoms that persist for more than 24 hours or cause the death of the patient in a shorter period.
Since ischemic stroke is not considered as a separate disease, it is impossible to determine a single etiological factor for it. However, there are risk factors associated with an increased incidence of ischemic stroke, which can be divided into two groups:
- myocardial infarction
- arterial hypertension
- atrial fibrillation
- diabetes mellitus
- asymptomatic lesion of the carotid arteries.
- hereditary predisposition
In addition, there are risk factors associated with lifestyle: low level of physical activity, acute stress or prolonged psychoemotional stress, overweight, smoking.
A certain sequence of molecular and biochemical changes in the brain substance caused by acute focal ischemia of the brain can lead to tissue disorders, as a result of which cell death occurs (brain infarction). The nature of the changes depends on the level of decrease in cerebral blood flow, the duration of such a decrease and the sensitivity of the brain substance to ischemia. The degree of reversibility of tissue changes at each stage of the pathological process is determined by the level of decrease in cerebral blood flow and its duration in combination with factors determining the sensitivity of the brain to hypoxic damage.
The term “infarct nucleus” denotes the zone of irreversible damage, the term “ischemic penumbra” (penumbra) — the zone of ischemic damage of a reversible nature. The duration of the penumbra’s existence is the most important moment, since over time reversible changes take on an irreversible character. The oligemia zone is a zone in which a balance is maintained between tissue needs and the processes that provide these needs, despite a decrease in cerebral blood flow. It is able to exist indefinitely for a long time without passing into the nucleus of a heart attack, so it is not referred to as penumbra.
Ischemic stroke can be a consequence of a disease of the cardiovascular system. There are several pathogenetic variants of ischemic stroke. In the TOAST classification (Trial of Org 10172 in Acute Stroke Treatment), which has received the most widespread, the following variants of ischemic stroke are distinguished:
- cardioembolic — ischemic stroke that occurred due to arrhythmia, valvular heart disease, myocardial infarction;
- atherothrombotic is an ischemic stroke that occurred due to atherosclerosis of large arteries, which resulted in an arterio-arterial embolism;
- lacunar — ischemic stroke that occurred due to occlusion of small-caliber arteries;
- ischemic stroke associated with other, rarer causes: blood hypercoagulation, arterial wall dissection, non-atherosclerotic vasculopathies;
- ischemic stroke of unknown origin is a stroke with an unknown cause or with the presence of two or more possible causes, when it is not possible to establish an accurate diagnosis.
In addition, a small stroke is isolated when the existing symptoms regress during the first three weeks of the disease.
There are also several periods of ischemic stroke:
- the most acute period is the first 3 days. Of these, the first three hours received the definition of a “therapeutic window” when it is possible to use thrombolytic drugs for systemic administration. In case of regression of symptoms, a transient ischemic attack is diagnosed during the first day;
- acute period — up to 4 weeks;
- early recovery period — up to six months;
- late recovery period — up to 2 years;
- the period of residual phenomena is after 2 years.
The clinical symptom complex in ischemic stroke is diverse and depends on the localization and volume of the lesion of the brain. Localization of the lesion in the carotid basin is more common than others (up to 85%), less often — in the vertebral-basilar.
Brain infarction in the MCA
A feature of a heart attack in the blood supply pool of the middle cerebral artery is the presence of a pronounced system of collateral blood supply. Occlusion of the proximal part of the middle cerebral artery can cause subcortical infarction, while the cortical area of blood supply remains unaffected. In the absence of these collaterals, it is possible to develop a massive infarction in the area of blood supply to the middle cerebral artery.
For a heart attack in the area of blood supply to the superficial branches of the middle cerebral artery, the occurrence of deviation of the eyeballs and head towards the affected hemisphere is typical. At the same time, in the case of a lesion of the dominant hemisphere, ipsilateral ideomotor apraxia and total aphasia develop, and in the case of a lesion of the subdominant hemisphere, anosognosia, dysarthria, aprosody and contralateral ignoring of space.
The main clinical manifestation of cerebral infarction in the area of the branches of the middle cerebral artery is contralateral hemiparesis and contralateral hemianesthesia. In the case of extensive lesions, the appearance of friendly withdrawal of the eyeballs and fixation of the gaze towards the affected hemisphere is possible. With subdominant hemisphere infarcts, emotional disturbances and spatial neglect develop.
The spread of paresis in infarction in the blood supply basin of the striatocapsular arteries depends on the localization and size of the lesion (upper limb, face or the entire contralateral part of the body). In the case of extensive striatocapsular infarction, as a rule, typical manifestations of occlusion of the middle cerebral artery (aphasia, homonymous lateral hemianopia) develop. Lacunar infarction is clinically manifested by the development of lacunar syndromes (isolated hemiparesis and hemihypesthesia or their combination).
Brain infarction in the ACA
The most frequent clinical manifestation of a heart attack in the blood supply pool of the anterior cerebral artery is motor disorders. In most cases of occlusion of the cortical branches, motor deficiency develops in the foot and the entire lower limb, as well as mild paresis of the upper limb with extensive damage to the tongue and face.
Brain infarction in the PCA
As a result of occlusion of the posterior cerebral artery, infarcts of the occipital temporal lobe, as well as the mediobasal parts of the temporal lobe, develop. In such cases, the clinical manifestations are visual field defects (contralateral homonymous hemianopia). It is also possible to combine them with visual hallucinations and photopsias.
Brain infarction in the vertebrobasilar pool
Stroke in the vertebrobasilar blood supply basin occurs as a result of occlusion of the only perforating branch of the basilar artery and is accompanied, as a rule, by symptoms of cranial nerve damage on the ipsilateral side. Occlusion of the vertebral artery or its main penetrating branches extending from the distal sections leads to the development of Wallenberg syndrome (lateral medullary syndrome).
When collecting anamnesis, it is necessary to determine the beginning of cerebral circulation disorders, to establish the sequence and rate of progression of certain symptoms. For ischemic stroke, the sudden onset of neurological symptoms is typical. In addition, attention should be paid to possible risk factors for ischemic stroke (diabetes mellitus, hypertension, atrial fibrillation, atherosclerosis, hypercholesterolemia, etc.).
Physical examination of a patient with a possible diagnosis of “ischemic stroke” is carried out according to generally accepted rules for organ systems. Assessing the neurological status, pay attention to the presence and severity of cerebral symptoms (headache, impaired consciousness, generalized seizures, etc.), focal neurological symptoms and meningeal symptoms. Laboratory tests should include general and biochemical blood tests, coagulogram, general urine analysis.
Instrumental diagnosis of ischemic stroke:
- MRI of the brain. The effectiveness of a new mode of MRI examination, with the help of which diffusion-weighted images are obtained, has been proved. As a result of cytotoxic edema in ischemic stroke, water molecules move from the extracellular space to the intracellular space, which leads to a decrease in their diffusion rate. These changes are manifested on diffusely weighted MRI images in the form of an increase in the signal, which indicates the development of irreversible structural damage to the brain substance.
- CT scan of the brain. One of the early CT signs of ischemic damage in the SMA system is the lack of visualization of the lenticular nucleus or the islet cortex (due to cytotoxic edema developing in the affected area). In some cases, with ischemic stroke, the hyperdensity of the middle and, much less often, the posterior cerebral artery on the affected side is determined as early changes (a sign of thrombosis or embolism of these vessels). Already at the end of the first week in the zone of ischemic lesion in the gray matter, an increase in density to an isodensive and even slightly hyperdensive state is observed, which indicates the development of neovasogenesis and restoration of blood flow. This phenomenon has a “blurring effect”, because there are difficulties in identifying the boundaries of the ischemic lesion zone in the subacute period of a brain infarction.
MRI and CT scans of the brain are also used to differentiate ischemic stroke from other forms of intracranial pathology and dynamic control over tissue changes during the treatment of ischemic stroke. First of all, ischemic stroke must be differentiated from hemorrhagic stroke. Neuroimaging research methods will play a decisive role in this issue. In addition, in some cases, there is a need to differentiate ischemic stroke from acute hypertensive encephalopathy, metabolic or toxic encephalopathy, brain tumors, as well as infectious brain lesions (abscess, encephalitis).
If an ischemic stroke is suspected, the patient should be hospitalized in specialized departments. In the event that the duration of the disease is less than 6 hours — to the intensive care unit of the same departments. Transportation should be carried out only when the patient’s head is raised to 30 degrees. The relative limitations to hospitalization are considered terminal coma, terminal stage of cancer, as well as the presence of a history of dementia with severe disability.
Non-drug treatment of ischemic stroke should include patient care measures, correction of swallowing function, prevention and therapy of infectious complications (pneumonia, urinary tract infections, etc.). A coordinated multidisciplinary approach to it should be applied in a specialized vascular department with an intensive care unit (ward) with the possibility of round-the-clock ECG, CT, clinical and biochemical blood tests, as well as ultrasound examinations.
Therapy in the acute period
Drug treatment of ischemic stroke is most effective at the very beginning of the disease (3-6 hours after the first signs of the disease). With thrombotic etiology of stroke, selective or systemic thrombolysis is performed, with cardioembolic genesis – anticoagulant therapy.
In the first 48 hours of the disease, it is necessary to periodically determine the saturation of hemoglobin with arterial blood oxygen. If this indicator reaches 92%, oxygen therapy should be performed, starting from 2-4 liters per minute. A decrease in the patient’s level of consciousness to 8 points or less (Glasgow coma scale) is an absolute indicator for tracheal incubation. The decision of the issue in favor of the ventilator or against it is made based on the basic general resuscitation provisions.
With a reduced level of wakefulness, in the presence of clinical or neuroimaging signs of cerebral edema or increased intracranial pressure, it is necessary to maintain the patient’s head elevated by 30 degrees (without bending the neck!). It is necessary to minimize (and, if possible, exclude) cough, epileptic seizures and motor arousal. Infusions of hypoosmolar solutions are contraindicated.
An important component of ischemic stroke therapy is the correction of vital functions and maintenance of homeostasis. This requires constant monitoring of basic physiological parameters, correction and maintenance of hemodynamic parameters, water-electrolyte balance, respiration, correction of increased intracranial pressure and cerebral edema, prevention and control of complications.
- Infusion therapy. Routine use of glucose-containing solutions is impractical due to the risk of hyperglycemia, so the main infusion solution in the treatment of ischemic stroke is sodium chloride solution (0.9%). With concomitant diabetes mellitus, patients are transferred to subcutaneous injections of short-acting insulins, except in cases when adequate glycemic control is carried out, and the patient is in clear consciousness and without impaired swallowing function.
- Provision of food. Regardless of the location of the patient (intensive care unit, intensive care unit or neurological department), the daily task of basic therapy of ischemic stroke is adequate nutrition of the patient, as well as control and replenishment of water-elictrolytic losses. The progression of certain swallowing disorders is considered an indicator for the conduct of enteral probe nutrition. At the same time, the calculation of nutrient doses should be carried out taking into account the metabolic needs and physiological losses of the body. When food is administered orally or through a probe, the patient should be in a semi-sitting position for 30 minutes after feeding.
- Prevention of thrombosis. In order to prevent deep vein thrombosis in ischemic stroke, wearing compression stockings or appropriate bandaging is indicated. For those purposes, as well as to prevent pulmonary embolism, direct anticoagulants (low molecular weight heparins) are used.
- Neuroprotection. Its main direction is the use of drugs with neuromodulatory and neurotrophic effects. Currently, the most well—known neurotrophic drug is a hydralizate from the brain of pigs. The brain and spinal cord have no depositing properties, and the cessation of blood flow for 5-8 minutes causes the death of neurons. Therefore, the introduction of neuroprotective drugs should be carried out already in the first minutes of an ischemic stroke.
Thus, early rehabilitation against the background of basic therapy, as well as a combination of reperfusion and neuroprotection, make it possible to achieve certain success in the drug treatment of ischemic stroke.
Surgical treatment of ischemic stroke involves surgical decompression — a decrease in intracranial pressure, an increase in perfusion pressure, as well as preservation of cerebral blood flow. Statistics indicate a decrease in the mortality rate in ischemic stroke from 80 to 30%.
In the rehabilitation period after an ischemic stroke, all efforts of neurologists are aimed at restoring the lost motor and speech functions of the patient. Electromyostimulation and massage of paretic limbs, physical therapy, mechanotherapy are performed. To correct speech disorders (aphasia, dysarthria), as well as swallowing disorders, a speech therapist consultation is necessary.
Prognosis and prevention
The prognosis for ischemic stroke depends primarily on the localization and volume of brain damage, the age of the patient, as well as the severity of concomitant diseases. The most severe condition of the patient falls on the first 3-5 days of the disease, when swelling of the brain increases in the area of the lesion. Then comes a period of stabilization or improvement with the possible restoration of impaired functions. Currently, the percentage of deaths in ischemic stroke is 15-20%.
The basis for the prevention of ischemic stroke is the prevention of blood vessel thrombosis, which occurs when “cholesterol plaques” form in the blood. To do this, it is necessary to maintain a healthy lifestyle, adequate body weight, abstinence from smoking and other bad habits. Patients suffering from various diseases of the cardiovascular system, arterial hypertension, hypercholesterolemia and diabetes mellitus are also at risk.
Secondary prevention of ischemic stroke is a comprehensive program that includes four directions: hypotensive therapy (angiotensin-converting enzyme inhibitors and diuretics); antithrombotic therapy (indirect anticoagulants and antiplatelet agents); hypolipidemic therapy (statins); surgical treatment of carotid arteries (carotid endaterectomy).