For normal functioning of the brain, a large amount of blood is required, which is a natural transporter of oxygen. Damage to the main arteries, venous and jugular veins, due to the development of thrombosis, embolism, aneurysms, etc. leads to serious oxygen deficiency, tissue death and the loss of certain vital functions for the body. Impaired blood circulation in the brain is a serious pathology that requires urgent treatment.
Features of the blood supply to the brain
According to the most rough estimates, the human brain contains about 25 billion nerve cells. There is a hard and soft shell, gray and white matter.The brain consists of five main divisions: terminal, posterior, intermediate, middle and oblong, each of which performs its own required function... The obstructed blood supply to the brain leads to disruptions in the coordinated work of departments, the death of nerve cells. As a result, the brain loses certain functions.
Signs of poor circulation to the head
Initially, the symptoms of poor circulation are of little or no intensity. But as the disorders develop, clinical manifestations are becoming more evident.Symptoms of the disease include:
If blood circulation in the brain is impaired, oxygen starvation occurs, provoking a gradual increase in the intensity of symptoms. Each of the manifestations can indicate a number of other diseases and require compulsory treatment to a neurologist.
Causes of obstructed blood supply to the brain
The anatomy of the blood supply is complex. Oxygen and other nutrients are transported through four arteries: vertebral and internal.For normal functioning, the brain needs to receive about 25-30% of the oxygen that has entered the body. The supply system includes about 15% of the total blood volume in the human body.
Insufficient blood circulation has symptoms that indicate the presence of certain disorders.
The reason for the development of pathology is: 
Whatever the cause of circulatory failure, the consequences of violations are reflected not only in the activity of the brain itself, but also in the work of internal organs. The result of therapy is influenced by the accuracy of the established cause - the catalyst and the timely elimination of violations.
Why are the problems of poor blood flow in the brain dangerous?
A sharp violation of the blood circulation in the brain leads to serious complications. The consequences of an attack can be:- Ischemic stroke - accompanied by nausea and vomiting. With focal lesions, it affects the work of individual internal organs. Affects motor and speech function.
- Hemorrhagic stroke - disorders are provoked by blood that has entered the brain area. As a result of the increased pressure, the brain is compressed, tissue wedging into the occipital foramen occurs. The high speed of blood flow in the vessels of the brain leads to a rapid deterioration in the patient's condition. Hemorrhagic stroke leads in the number of deaths.
- Transient ischemic attack is a temporary lesion. Blood circulation can be restored with the help of medications that improve brain activity and stimulate blood formation.
Transient attack occurs mainly in elderly patients. The attack is accompanied by impaired motor and visual function, numbness and paralysis of the limbs, drowsiness and other symptoms.
Impaired cerebral blood flow in children
For children, the minimum indicators of blood flow in the arteries, sufficient for normal brain function, are 50% higher than in adults. For every 100 gr. brain tissue requires about 75 ml. blood per minute.The change in the total index of cerebral blood flow over 10% is critical. In this case, a change in the tension of oxygen and carbon dioxide is observed, which leads to serious disturbances in brain activity.
In both adults and children, several major arteries and vessels supply the brain with blood:
- The middle cerebral artery supplies blood to the deep parts of the brain and the eyeball. The internal one is responsible for nutrition of the cervical region, scalp and face.
- The posterior cerebral artery supplies blood occipital lobes hemispheres. The task is helped by small blood vessels that feed directly to the deepest parts of the brain: gray and white matter.
- Peripheral circulation - controls the collection of venous blood from the gray and white matter sections.
Control over the operation of the system is carried out thanks to a complex regulation mechanism. Since the brain tissue continues to develop after the birth of a child, new synapses and neural connections constantly appear, any disturbances in the blood circulation of the brain in a newborn affect his mental and physical development. Hypoxia is fraught with complications at a later age.
When solving a mathematical problem or any other mental load, an increase in the speed parameters of blood flow through the cerebral arteries is observed. So, the regulation process is triggered by the emerging need for more glucose and oxygen.
Why newborns have problems with the blood supply to the brain
Among the many reasons due to which disorders of the blood supply to the brain develop, only two main ones can be distinguished:
What is dangerous for a baby with a disturbed blood supply to the head
For the normal development of a child, it is required that the volume of incoming blood in relation to the brain tissue is 50% more than that of an adult. Deviations from the norm are reflected in mental development.The complexity of therapy lies in the fact that when prescribing drugs that improve blood circulation in the vessels of the brain, the doctor must take into account the effect of drugs on the still fragile structures of the child's life: the gastrointestinal tract, the nervous system, etc.
The consequence of a lack of blood supply is:
- Poor concentration of attention.
- Learning problems.
- Borderline intellectual disability.
- The development of hydrocephalus and cerebral edema.
- Epilepsy.
How to check the blood supply to the brain
Insufficient blood supply to the brain tissue is suspected in the presence of neurological symptoms and disorders. To determine the factors of damage and prescribe the necessary therapy, an additional examination is carried out using instrumental methods for studying blood circulation:
Any drugs, tablets, injections and other medicines are prescribed only after full examination the patient and determine the problem that affected the deterioration of the blood supply to the brain.
How and how to improve cerebral circulation
According to the results diagnostic research medications are selected that make cerebral circulation better. Since the cause of violations is the most different factors, the course of therapy for one patient may not coincide with that prescribed for another patient.What improves blood circulation, what drugs
There is no single medicine to improve blood circulation in the brain that can eliminate the disturbance. In case of any deviation, a course of therapy is prescribed, which includes one or more drugs of the following groups:
Some drugs have a special purpose. So, cortexin, in the form of intramuscular injections, is recommended for use during pregnancy and after childbirth with pronounced encephalopathy. Emoxipin is used for internal bleeding... Available as intravenous injections.
New generation drugs are constantly emerging with fewer negative side effects. Prescribes drug therapy exclusively by the attending physician. Self-medication is strictly prohibited!
How to improve blood flow without medication
At the initial stage, it is possible to improve the blood supply to the brain without the help of drugs. There are several ways to influence a person's well-being:
It would be useful to include in the therapy the intake of vitamins E and C, which increase blood flow, and also visit a nutritionist in order to select an effective therapeutic diet.
Folk remedies for improving blood supply to the brain
Treatment of circulatory disorders of the brain with folk remedies does not eliminate the need for professional medical care. Unconventional methods therapies relieve symptoms of disorders well:
Herbs that improve blood flow can cause bleeding. Before taking herbal tinctures, it is recommended to consult with your doctor.
Respiratory gymnastics to improve blood circulation
The set of exercises is aimed at enriching the blood with oxygen. There are several types of breathing exercises.As with any effective remedy, exercise without proper supervision and preparation can be dangerous. The first lessons should be done in conjunction with an instructor.
Breathing exercises are present in yoga and other oriental gymnastics. Compatriots also developed effective methods. So, the Streltsova method deserves special mention, which allows you to quickly restore the lost functions of the brain.
Exercise and gymnastics
Exercise therapy to improve the patient's well-being is aimed at the source-catalyst of the problem. During classes, the pressure and the work of the cardiovascular system are normalized.Optimal fit the following types gymnastics:
- Yoga.
- Qigong.
- Pilates.
- Pool activities, swimming.
Diet with poor cerebral circulation
We are what we eat! Life itself proves the truth of this statement. A person's diet, eating habits have a negative or positive effect on the blood supply to the brain.What foods improve blood flow
Foods that improve blood counts include:- Fatty fish.
- Seafood.
- Dairy products.
- Vegetables and fruits, especially rich in iron vitamins.
Food that is harmful to the supply of blood to the brain
At poor circulation blood flow should be discarded from rich in and saturated fatty acids products.The ban includes:
- Sugar.
- Sweets and flour products.
- Smoked and fatty foods.
- Flavors and synthetic condiments.
- Carbonated and alcoholic drinks.
Alcohol and cerebral circulation
Moderate doses of alcohol have a beneficial effect on the blood supply to the brain by preventing blockage of blood vessels. These are small to moderate portions.Alcohol abuse is fatal to humans. With prolonged abuse, the likelihood of developing a fatal hemorrhagic stroke is high.
According to a recent study published in the Stroke: Journal of the American Heart Association, moderate consumption improves blood flow, while excessive consumption leads to atrophy of brain cells.
Chronic disorder cerebral circulation(HNMK) is a syndrome of chronic progressive brain damage of vascular etiology, which develops as a result of repeated acute cerebrovascular accidents (clinically obvious or asymptomatic) and / or chronic hypoperfusion of the brain.
In Russia, most experts consider KhNMK as a holistic state without highlighting individual clinical syndromes... This view also forms a holistic approach to the selection of therapy. Various diagnoses are used to designate HNMK: "slowly progressive cerebrovascular insufficiency", "dyscirculatory encephalopathy", "cerebrovascular insufficiency", "chronic cerebral dysfunction of vascular etiology", "chronic cerebral ischemia", etc.
In Europe and North America, it is customary to associate certain symptoms with risk factors and highlight the features of the damaging effect of a vascular factor on brain function. This is how the terms "moderate vascular cognitive impairment - CI" (vascular mild cognitive impairment), "post stroke depression", "CI in stenosis of the carotid arteries" (cognitive impairment in patient with carotid stenosis), etc.
WITH clinical point both approaches are correct. Generalization of world experience and national traditions will increase the effectiveness of therapy. All patients with brain damage due to the action of vascular risk factors should be included in the HNMK group.
This is a group of patients with heterogeneous causes of CCI: patients with arterial hypertension (AH), atrial fibrillation, chronic heart failure (CHF), stenosis of the brachiocephalic arteries, patients who have had an ischemic stroke (IS) or transient ischemic attack (TIA) or hemorrhage, patients with metabolic disorders and multiple "silent" strokes.
Modern concepts of the pathogenesis of cerebrovascular diseases reveal a number of features of the metabolism of nervous tissue against the background of risk factors and under conditions of altered perfusion. This determines the tactics of patient management and influences the choice of drug therapy.
Firstly, the increase in blood pressure(BP), cardiogenic or arterial embolism, hypoperfusion associated with damage to small (microangiopathy, hyalinosis) or large (atherosclerosis, fibromuscular dysplasia, pathological tortuosity) vessels. Also, the reason for the progression of cerebrovascular accident can be a sharp decrease in blood pressure, for example, with aggressive antihypertensive therapy.
Secondly, the processes of brain damage have two vectors of development. On the one hand, damage can be caused by acute or chronic impairment of cerebral perfusion, on the other hand, vascular damage leads to the activation of degenerative processes in the brain. Degeneration is based on the processes of programmed cell death - apoptosis, and such apoptosis is pathological: not only neurons suffering from insufficient perfusion are damaged, but also healthy nerve cells.
Degeneration is often the cause of CN. Degenerative processes do not always develop at the time of cerebrovascular accident or immediately after it. In some cases, degeneration can be delayed and manifests itself a month after exposure to the trigger factor. The reason for these phenomena remains unclear.
The involvement of cerebral ischemia in the activation of degenerative processes plays an important role in patients with a predisposition to such common diseases as Alzheimer's disease and Parkinson's disease. Very often progression vascular disorders and impaired perfusion of the brain become a triggering factor for the manifestation of these diseases.
Thirdly, impaired cerebral circulation is accompanied by macroscopic changes in the brain tissue. The manifestation of such a lesion can be a clinically obvious stroke or TIA or "silent" stroke. Magnetic resonance imaging (MRI) allows you to determine the changes in the brain in such patients, however, the main method is clinical assessment existing violations.
MRI in patients with chronic cerebrovascular accident can reveal the following syndromes, the knowledge of which makes it possible to objectify some of the neurological disorders:
- multifocal brain damage - the consequences of multiple lacunar infarctions in the deep parts of the brain;
- diffuse lesion of the white matter of the brain (leukoencephalopathy, leukoaraiosis);
- replacement hydrocephalus - expansion of the Virchow-Robin space, an increase in the size of the ventricles of the brain, subarachnoid space;
- hippocampal atrophy;
- stroke in strategic areas;
- multiple microhemorrhages.
Fourth, modern data from basic research reveal previously unknown features of the pathogenesis of brain damage in CIU. The brain has a high potential for regeneration and compensation.
Factors that determine the likelihood of brain damage:
- duration of ischemia - short-term ischemia with early spontaneous restoration of blood flow contributes to the development of TIA or "silent" stroke, and not the stroke itself;
- the activity of compensation mechanisms - many neurological disorders are easily compensated for due to preserved functions;
- the activity of the mechanisms of autoregulation of cerebral blood flow allows you to quickly restore perfusion due to the opening of collateral blood flow;
- neuroprotective phenotype - many pathological conditions can promote the activation of endogenous defense mechanisms (for example, diabetes mellitus - diabetes mellitus - is an example of metabolic preconditioning), which can increase the resistance of brain tissue to ischemia.
Thus, the peculiarities of the metabolism of brain tissue make it possible to compensate for many, including severe, cerebral perfusion disorders in patients with a long history of vascular risk factors. CI and focal symptoms do not always correlate with the severity of morphological brain damage.
Having multiple risk factors does not necessarily result in significant brain damage. The mechanisms of endogenous protection of the nervous tissue play a great role in the development of damage, some of which are congenital, and some are acquired.
Clinical manifestations of HNMK
As noted, CNMC is a syndrome of brain damage in patients with a variety of cardiovascular disorders, combined by common features of blood flow and degenerative processes. This makes it possible to distinguish three groups of symptoms in such patients: CN syndrome; affective (emotional) disorders; focal neurological disorders (consequences of clinically obvious or "silent" strokes). This separation is essential for patient management.
Affective (emotional) disorders
The development of emotional disorders is associated with the death of monoaminergic neurons in the brain, in which serotonin, norepinephrine and dopamine act as the main neurotransmitters. The opinion is expressed that their deficiency or imbalance in the central nervous system leads to the appearance of emotional disorders.
Clinical manifestations of affective disorders associated with deficiency of serotonin, dopamine and norepinephrine:
- symptoms associated with serotonin deficiency: anxiety, panic attacks, tachycardia, sweating, tachypnea, dry mucous membranes, indigestion, pain;
- symptoms associated with dopamine deficiency: anhedonia, indigestion, impaired smoothness and meaningfulness of thinking;
- symptoms associated with a deficiency of norepinephrine: fatigue, impaired attention, difficulty concentrating, slowing down thought processes, motor retardation, pain.
The doctor can group the patient's complaints according to belonging to the group of symptoms of monoamine deficiency and, based on this, select drug therapy... Thus, many drugs belonging to the group of neuroprotectors affect monoamine systems and, in some situations, can affect the emotional sphere. However, there is little research on this topic.
Thus, behind all complaints, emotional disorders and diagnoses are hidden: a syndrome of decreased activity in the central nervous system of GABA neurons, serotonin neurons, dopamine neurons; syndrome of increased activity in the central nervous system and autonomic nervous system: histamine neurons, glutamate neurons, norepinephrine neurons, P.
The defeat of monoaminergic neurons leads to the formation of various groups of syndromes: depression, anxiety, asthenia, apathy, "a decrease in the threshold of perception from intero- and exteroreceptors", etc. "A decrease in the threshold of perception from intero- and exteroreceptors" in combination with somatic diseases and age characteristics of the patient contributes to the formation of the following syndromes and complaints: polymyalgic syndrome, numbness in the extremities, palpitations, lack of air, noise in the head, "flies in front of the eyes", irritable bowel syndrome, etc.
Affective disorders in patients with cerebrovascular disorders differ from those in patients with normal cerebral blood flow:
- the severity of depression, as a rule, does not reach the degree of major depressive episode according to the criteria of DSM-IV;
- depression is often combined with anxiety;
- in the early stages of the disease, emotional disorders are hidden under the "mask" of hypochondria and somatic symptoms (sleep disturbances, appetite disorders, headache, etc.);
- the leading symptoms are anhedonia and psychomotor retardation;
- there is a large number of cognitive complaints (decreased concentration of attention, slowness of thinking);
- severity depressive symptoms with chronic cerebrovascular accident, it depends on the stage of the disease and the severity of neurological disorders;
- neuroimaging reveals damage primarily to the subcortical parts of the frontal lobes. The presence and severity of symptoms of depression depend on the severity of focal changes in the white matter of the frontal lobes of the brain and neuroimaging signs of ischemic damage to the basal ganglia;
- there is a paradoxical response to drugs;
- there is a high response to placebo;
- a high frequency of undesirable effects of antidepressants is characteristic (it is recommended to use their small doses and selective drugs with a favorable tolerance profile);
- there is mimicry under somatic diseases.
Depression requires compulsory treatment, since it not only affects the quality of life of patients with chronic cerebrovascular accident, but is also a risk factor for stroke. Depression can lead to cognitive decline and make it difficult to communicate with the patient. Long-term depression causes degenerative processes in the form of a deterioration in metabolism and structural changes in the brain.
Against the background of prolonged depression and cognitive deficit, there may be a violation of the ability to be aware of one's feelings and formulate complaints: coenesthesia (a feeling of indefinite total physical distress) and alexithymia (the patient's inability to formulate his complaints), which is an unfavorable prognostic sign.
Depression in CNI is closely related to CN. Patients are aware of the growing intellectual and movement disorders. This makes a significant contribution to the formation depressive disorders(provided there is no pronounced decrease in criticism in the early stages of the disease).
Affective disorders and CI can result from dysfunctions of the frontal regions of the brain. Thus, normally, the connections between the dorsolateral frontal cortex and the striatal complex are involved in the formation of positive emotional reinforcement in achieving the goal of the activity. As a result of the phenomenon of disconnection in chronic cerebral ischemia, there is a lack of positive reinforcement, which is a prerequisite for the development of depression.
The emotional state of patients can also deteriorate as a result of therapy with somatotropic drugs. Cases of drug-induced anxiety and depression have been reported. Some somatotropic drugs contribute to the development of anxiety and depressive disorders in patients with CNI: anticholinergics, beta-blockers, cardiac glycosides, bronchodilators (salbutamol, theophylline), nonsteroidal anti-inflammatory drugs, etc.
Features of cognitive impairment
The most common syndrome in CNI is impairment of cognitive (cognitive) functions. In the group of vascular CNs, there are:
- moderate KN;
- vascular dementia;
- mixed (vascular-degenerative) type - a combination of KN of the Alzheimer's type with cerebrovascular disease.
The urgency of the problem of diagnosis and treatment of CI is beyond doubt, it acquires particular importance for doctors who, in everyday clinical practice, have to meet with a heterogeneous group of patients with cardiovascular pathology and impaired cognitive functions.
A higher incidence of hospitalizations, disability and mortality in patients with CI compared with patients without these disorders has been proven. This is largely due to a decrease in cooperation in this group of patients and a violation of the ability to adequately assess the symptoms of the underlying disease.
CI often precede the development of other neurological disorders, such as gait disturbance, pyramidal and extrapyramidal movement disorders, and cerebellar disorders. It is believed that vascular CIs are a predictor of stroke and vascular dementia... Thus, early diagnosis, prevention and effective therapy of CI are an important aspect of the management of patients with CI.
Various diseases of the cardiovascular system, which lead to acute disorders of cerebral circulation or chronic cerebral ischemia, are the causes of vascular CI. The most important of them are hypertension, cerebral atherosclerosis, heart disease, diabetes mellitus. More rare reasons there may be vasculitis, hereditary pathology (for example, CADASIL syndrome), senile amyloid angiopathy.
The concept of the pathogenesis of CD in CI is constantly improving, but the opinion remains unchanged for decades that their development is based on a long-term pathological process leading to significant violation blood supply to the brain.
Clinical and pathogenetic variants of vascular CI described by V.V. Zakharov and N.N. Clearly, they allow you to clearly understand the mechanism of their development and choose what is needed in each clinical case direction of diagnosis and treatment.
There are the following options for CN:
- CI due to a single cerebral infarction, which developed as a result of lesions of the so-called strategic zones (thalamus, striated bodies, hippocampus, prefrontal frontal cortex, parieto-temporal-occipital junction zone). CIs arise acutely, and then completely or partially regress, as happens with focal neurological symptoms in stroke;
- CI due to repeated large-focal cerebral infarctions of a thrombotic or thromboembolic nature. There is an alternation of stepwise intensification of disorders associated with repeated cerebral infarctions and episodes of stability;
- subcortical vascular CI due to chronic uncontrolled hypertension, when high blood pressure leads to changes in small-caliber vessels with damage primarily to the deep structures of the cerebral hemispheres and basal ganglia with the formation of multiple lacunar infarctions and leukoaraiosis zones in this group of patients. There is a steady progression of symptoms with episodes of their intensification;
- CI due to hemorrhagic stroke. A picture is revealed that resembles that of repeated cerebral infarctions.
The clinical picture of vascular CN is heterogeneous. However, their subcortical variant has characteristic clinical manifestations. The defeat of the deep parts of the brain leads to dissociation of the frontal lobes and subcortical structures and the formation of secondary frontal dysfunction. This is primarily manifested by neurodynamic disorders (a decrease in the speed of information processing, deterioration in switching attention, a decrease in working memory), impaired executive functions.
Decrease short-term memory is of a secondary nature and is due to neurodynamic disorders existing in such patients. Often these patients have emotional affective disorders in the form of depression and emotional lability.
The clinical features of other variants of vascular CI are determined by both their pathogenesis and the localization of the pathological focus. Deterioration of short-term memory with signs of primary inadequacy of memorizing information is rare in chronic cerebrovascular accident. The development of the "hippocampal" type of mnestic disorders (there is a significant difference between immediate and delayed reproduction of information) in this group of patients is prognostically unfavorable in relation to the development of dementia. In this case, further dementia is mixed (vascular-degenerative nature).
A thorough study of cognitive functions and their impairments in various groups of patients with chronic cerebrovascular accidents makes it possible to distinguish the features of these disorders depending on the leading etiological factor. Thus, it was found that patients with systolic CHF are characterized by a fronto-subcortical type of cognitive disorders (CI of a dysregulatory nature) and signs of impairment of short-term memory.
Disorders of the fronto-subcortical type include violations of executive functions and neurodynamic changes: a slowdown in the speed of information processing, impairment in switching attention and working memory. At the same time, an increase in the severity of CHF to III functional class is accompanied by an increase in the degree of dysfunction of the parietotemporal-occipital region of the brain and visual-spatial disorders.
Knowledge of the features of CI in patients with CIU will allow not only to determine the causes of their development, but also to formulate recommendations for conducting schools for such patients. For example, patients with fronto-subcortical type of CI should be taught algorithms of behavior when the state of health changes, and for patients with dysfunction of the parietotemporal-occipital region, it is advisable to repeat the necessary information many times, while the visually perceived information should be as simple as possible for memorization.
In the case of dementia of the vascular type in the clinical picture, in addition to signs of professional, everyday, social maladjustment, there are gross behavioral disorders - irritability, decreased criticism, pathological eating and sexual behavior (hypersexuality, bulimia).
Features of focal symptoms
Focal symptoms are an integral part of HNMC, they appear in the advanced stage of the disease. Focal symptoms also impair quality of life and can lead to frequent falls.
To the most typical focal symptoms gait disturbance (slowing down, stiffness, shuffling, staggering and difficulties in spatial organization of movements). Also, many patients have mild bilateral pyramidal insufficiency and frontal symptoms. Thus, early markers of movement disorders in chronic cerebrovascular accident are impaired gait initiation, "freezing", and pathological asymmetry of the step.
The leading cause of impaired walking and posture may be amiostatic syndrome. With the development of parkinson's syndrome, it is advisable to prescribe drugs from the group of dopamine receptor agonists (piribedil) and amantadines. The use of these antiparkinsonian drugs can positively affect the patient's walking, as well as improve cognitive function.
Modern therapy of KhNMK
Impossible to create universal medicine, which could affect the vascular damaging factors of the brain, CI, affective disorders and at the same time be a neuroprotective agent. Therefore, all qualitative studies were carried out for individual clinical situations: vascular CI, depression in stroke, prevention of stroke and CI, etc. Therefore, one cannot speak of universal drugs for the treatment of CIU.
The main principle of CIH therapy is an integrated approach, since it is necessary not only to influence symptoms and complaints, but also to prevent the progression of CI and emotional disorders by reducing cardiovascular risk.
The second principle of CNMC therapy is patient adherence to treatment and feedback. Each patient should have a dialogue with his doctor and regularly follow his instructions, and the doctor should listen to the patient's complaints and explain the need to take medications.
Complex effective therapy of HNMC should include:
- secondary prevention of stroke and CI;
- CN treatment;
- treatment of depression and other mood disorders;
- neuroprotective therapy.
Secondary prevention of ischemic stroke
With chronic cerebrovascular accident, the principles of secondary prevention of stroke are applicable. The goal of secondary prevention is to reduce the risk of stroke, brain damage, and progression of CI. Prevention should be aimed at preventing not only stroke, but also myocardial infarction, TIA and sudden cardiac death. In such patients, the problem of comorbidity and the need to combine several drugs comes to the fore.
Secondary prevention is a key link in the treatment of chronic cerebrovascular accidents. First, it allows you to stop or slow down the progression of the disease. Secondly, the absence of secondary prophylaxis prevents effective therapy for CI, affective disorders, and neuroprotection.
Thus, it has been shown that the effectiveness of neuroprotection is significantly reduced in patients with stenoses and occlusions of the cerebral arteries. This means that without ensuring adequate cerebral blood flow and metabolism, efficiency drugs will be low.
Basic therapy of CNMC includes modification of risk factors, antihypertensive, lipid-lowering and antithrombotic therapy.
For a successful selection of the basic therapy, it is necessary to determine the underlying disease that caused the cerebrovascular accident. This is especially important in the initial stages of the disease, when one factor is the cause of the development of brain damage. However, in the advanced stage of the disease, one of the factors can also prevail and cause the progression of all the corresponding syndromes.
The patient needs to explain what drugs are prescribed to him and what is the mechanism of their action. It should be pointed out that the effect of some drugs cannot be felt immediately, since it manifests itself in restraining the progression of depression and CI.
When prescribing antithrombotic therapy, it is necessary to separately draw the attention of patients to the importance of regular medication. Skipping medications can lead to ineffective therapy and the development of a new stroke. “Medicinal holidays” and missed medication are an independent risk factor for stroke.
Cognitive impairment treatment
At the stage of vascular and mixed dementia, central acetylcholinesterase inhibitors (galantamine, rivastigmine, donepizil) and the reversible blocker of NMDA receptors memantine have been successfully used for symptomatic purposes.
There are no unequivocal recommendations for the treatment of vascular non-demented (mild and moderate) CI. Various therapeutic approaches are proposed. From our point of view, the use of drugs is justified, proceeding from the neurochemical mechanisms underlying the development of vascular CI.
It is known that acetylcholine is one of the most important mediators for cognitive processes. It has been shown that acetylcholinergic insufficiency largely correlates with the overall severity of CI. The role of acetylcholine is to maintain the sustainability of attention, which is necessary for memorization new information... Thus, the deficiency of acetylcholine, the main source of which is the mediobasal parts of the frontal lobes (their structures are projected into the hippocampus and parietotemporal regions of the brain), leads to increased distraction and poor memorization of new information.
The mediator dopamine (produced in the ventral tectum of the brainstem, whose structures are projected into the limbic system and the prefrontal cortex of the frontal lobes) plays an important role in ensuring the speed of cognitive processes, switching attention, and implementing executive functions. Its deficiency leads primarily to neurodynamic disorders and disorders of executive functions. Both mechanisms of development of impairments in cognitive functions are realized in vascular CI.
Treatment of depression and other mood disorders
Treatment of depression in HNMC - serious problem, which cannot be detailed within the framework of this article. However, it should be noted that the selection of psychotropic drugs should take into account the causes and clinical manifestations of neurotransmitter deficiency. The selection of drugs should be based on an assessment of the neurochemical pathogenesis of brain damage and the characteristics of drug action.
Antidepressants are used as primary drugs. With syndromes of a complex structure, for example, when depression is combined with severe anxiety, antipsychotics and tranquilizers are additionally used.
In patients with chronic cerebrovascular accident, it is important to remember about the safety of therapy. Therefore, it is undesirable to use drugs that increase the level of systemic blood pressure, affect urination and reduce the threshold of epileptic activity. When conducting complex therapy it is necessary to take into account the problem of the interaction of various drugs.
Neuroprotective therapy
Despite the large number of studies devoted to this problem, there are currently very few drugs with proven neuroprotective action that have been shown to be effective in large studies. In Russia, a special situation has developed in which drugs belonging to the group of neuroprotectors are widely used for various clinical syndromes.
Most of these drugs have not been tested according to Good Clinical Practice. Many doctors prescribe multiple neuroprotective agents, although there are no studies showing the use of multiple drugs. Very often, these drugs are prescribed to the detriment of secondary prevention... Unreasonable and incorrect use of drugs can lead to polypharmacy and is dangerous for elderly patients. With weighted and rational approach the appointment of neuroprotective agents can be effective both in acute disorders of cerebral circulation and in chronic cerebrovascular accident.
A feature of the action of neuroprotectors is the dependence of their effect on brain perfusion. If the perfusion of the brain is reduced, the drug may not enter the ischemic zone and have no effect. Therefore, the primary task of the treatment of CNMC is to identify the causes of perfusion disorders and their elimination.
The second feature of the action of neuroprotective agents is the dependence of the effect on the damaging factor. These drugs are most effective during the action of the damaging factor, that is, in clinical practice, risk situations should be identified and neuroprotective agents should be prescribed to reduce the damage.
One of the most studied drugs of the neuroprotective group is citicoline (ceraxon), which is involved in the synthesis of structural phospholipids of cellular, including neuronal, membranes, ensuring the repair of the latter. In addition, citicoline, as a precursor of acetylcholine, ensures its synthesis, increasing the activity of the cholinergic system, and modulates dopamine and glutamatergic neurotransmission. The drug does not interfere with the mechanisms of endogenous neuroprotection.
There have been many clinical trials of citicoline in patients with CI, including tests according to the rules of good clinical practice with an assessment of its effect on vascular CI. varying degrees severity - from mild to severe. Citicoline is the only drug that is rated as a promising agent in the European guidelines for the treatment of the acute period of ischemic stroke.
For the treatment of CNI and the prevention of CN, it is advisable to use Ceraxon in the form of a solution for oral administration, 2 ml (200 mg) 3 times a day. For the formation of a persistent neuroprotective response, the course of therapy should be at least 1 month. The drug can be used for a long time, for several months.
Citicoline has a stimulating effect, therefore it is preferable to enter it no later than 18 hours. In acute conditions, therapy should be started as early as possible, 0.5-1 g 2 times a day intravenously, for 14 days, and then 0.5-1 g 2 times a day intramuscularly. After that, it is possible to switch to oral administration drug. The maximum daily dose should not exceed 2 g.
The effectiveness of neuroprotection will be higher if its goals are clearly defined. First, it is advisable to use neuroprotectors in CI to inhibit their progression. V this case the cause of CN, as mentioned above, can be various somatic factors, for example, drops in blood pressure, decompensation renal failure or CHF, infection, etc. These factors can disrupt brain perfusion. This ischemic process can continue for a long time and subsequently lead to degeneration.
Therefore, with the progression of CI, long-term courses of neuroprotective therapy are required. It is preferable to use drugs in oral form for several weeks or months. It is also reasonable to prescribe at the beginning of therapy an infusion course of a neuroprotective drug for 10–20 days, followed by its long-term oral administration.
Secondly, the use of neuroprotective agents is advisable for the prevention of brain damage in patients with CNI. As our experimental studies show, prophylactic neuroprotective agents are more effective. Since cerebral circulation can be impaired in a number of clinical situations (atrial fibrillation, pneumonia, hypertensive crisis, myocardial infarction, diabetes mellitus decompensation, etc.), it is advisable to use neuroprotective agents prophylactically until symptoms appear.
Third, neuroprotective agents must be used to prevent stroke in patients who are to undergo surgery. Surgical intervention is a significant risk factor for stroke and postoperative CI. This is especially true for patients with CI, in whom the likelihood of developing CI is higher than in healthy people.
The high risk of perioperative stroke is caused by hypoperfusion associated with the stages of surgery. One of the stages of the operation for carotid atherosclerosis is the occlusion of the carotid artery for a few minutes, and during stenting and angioplasty cerebral vessels a large number of arterioarterial athero- and thromboembolisms can occur.
During heart surgery with the use of heart-lung machines, the average systemic blood pressure decreases to 60–90 mm Hg. Art., with stenosis of cerebral vessels or impaired autoregulation of cerebral blood flow, one of the forms of brain damage may develop.
Thus, patients undergoing surgery are at risk for ischemic brain damage and may be candidates for neuroprotective prophylaxis. The use of neuroprotective agents can reduce the number of complications after surgery.
Fourth, neuroprotective agents can be used to prevent stroke in patients at high vascular risk, either in the presence of TIA or in the presence of cerebral arterial stenosis. As long as there is a quota system in Russia, patients with carotid artery stenosis will have to wait for surgery for several weeks. During this period, the patient should be prescribed neuroprotective agents. Patients with TIA and atherosclerosis may be advised to carry neuroprotective agents such as ceraxon with them.
Fifth, neuroprotectors can be prescribed during rehabilitation to stimulate reparative processes and speedy functional recovery.
Thus, CNMC is a syndrome of brain damage caused by vascular risk factors, in which both ischemic damage and degenerative processes act as damage. Among the manifestations of HNMK are CI, affective disorders and focal syndromes that require integrated approach in the selection of preventive, psychotropic and neuroprotective therapy.
Thus, CNMC syndrome is a collective concept and cannot be considered as a separate nosological unit. Further studies of CI and the isolation of certain syndromes associated with risk factors and clinical manifestations are needed (for example, CI in patients with essential hypertension, depressive syndrome in patients with atrial fibrillation, etc.).
In each such clinical situation, the pathogenesis should be studied and effective therapy and methods of prevention, based on the mechanisms underlying the violations detected. The first steps in this direction have already been taken, both abroad and in Russia.
Shmonin A.A., Krasnov V.S., Shmonina I.A., Melnikova E.V.
It is customary to distinguish the initial manifestations of cerebrovascular accidents as an early stage of CCI and DE (discirculatory encephalopathy) - multifocal brain damage caused by chronic insufficiency blood circulation.
In turn, the following forms of DE are distinguished:
- atherosclerotic;
- hypertensive;
- venous;
- mixed.
Causes and pathogenesis of HNMC
As a rule, chronic cerebrovascular accident - consequences cardiovascular disease... Usually KhNMK develops against the background of:
- vegetative-vascular dystonia;
- atherosclerosis, hypertension;
- diabetes;
- heart diseases of various etiologies;
- vasculitis;
- diseases of the blood, accompanied by a violation of its rheological properties.
These pathologies change the general and cerebral hemodynamics and lead to a decrease in cerebral perfusion (less than 45-30 ml / 100 g per minute). The most important factors involved in the pathogenesis of CCI include:
- changes in the extra-, intracranial parts of the vessels of the head;
- lack of collateral circulation capabilities;
- violation of autoregulation of blood circulation;
- violation of rheology.
Obesity, physical inactivity, alcohol abuse and smoking play a significant role in the progression of CNI.
Symptoms of chronic cerebrovascular accident
In the early stages of CCI, the picture is characterized by patients' complaints of a feeling of heaviness in the head, mild dizziness, unsteadiness when walking, noise in the head, rapid fatigue, decreased attention and memory, as well as sleep disturbance. The initial manifestations of circulatory failure occur after psychoemotional and / or physical overstrain, against the background of alcohol consumption, under unfavorable meteorological conditions. Patients have signs of vegetative-vascular and emotional lability, a certain slowdown in thinking processes, and a lack of convergence is possible. The progression of the initial manifestations of circulatory failure leads to the formation of the next stage - DE.
Depending on the severity of manifestations, there are three stages of chronic cerebrovascular accident. In stage I, the symptoms are insignificant, patients usually remain functional; in stage II, the symptoms are moderately expressed, and in stage III, patients become disabled.
With atherosclerotic encephalopathy, that is, with DE caused by atherosclerotic lesions of the vessels that provide blood supply to the brain, in stage I, a decrease in attention and memory is noted, especially for current events, it is difficult to memorize new information, it is difficult for the patient to switch from one activity to another. At the same time, mild cognitive impairments, as a rule, are compensated for by the preserved everyday and professional skills, as well as intellectual capabilities. Often, patients complain of increased fatigue and decreased performance, often there is emotional lability with a decrease in the psycho-emotional background. Diffuse, noise in the head is noted. Complaints of patients about instability when walking are characteristic. In the neurological status, insignificant disseminated symptoms are revealed in the form of moderate signs pseudobulbar syndrome, tendon hyperreflexia and anisoreflexia, as well as postural instability.
In stage II, clinical manifestations progress, cognitive impairment increases, performance decreases, patients become touchy and irritable. Narrowing of interests is noted, memory disorders are increasing. Dull headaches, dizziness, and unsteadiness when walking are often present. In the neurological status, anisoreflexia, pseudobulbar symptoms, vestibulo-cerebellar disorders, and subcortical symptoms are revealed.
In stage III, there is a further aggravation of neurological manifestations. Patients have significant diffuse neurological symptoms in the form of an increase pyramidal insufficiency, pseudobulbar disorders, cerebellar and extrapyramidal symptoms, and control disorders pelvic organs... Possible epileptic seizures... Stage III is characterized by severe violations higher mental functions: significant cognitive disorders before dementia, development of apatoabulic syndrome is likely, pronounced emotional and personal changes. In the later stages, patients lose self-care skills. For atherosclerotic encephalopathy, sleepiness after eating, the Windsheid triad, is typical. In stage III, Hackebusch's disease, or pseudo-Alzheimer's form of atherosclerosis, is a symptom complex, the main manifestation of which is dementia. At the same time, a decrease in memory, confabulations, a pronounced narrowing of the range of interests, uncriticality, speech disorders, gnosis and praxis are noted. In addition, in the late stage of atherosclerotic encephalopathy, the formation of the Demage-Oppenheim syndrome is possible, which is characterized by gradually developing central tetraparesis.
Chronic hypertensive encephalopathy is a form of DE caused by arterial hypertension. Arterial hypertension leads to diffuse damage to the brain tissue, the disease progresses rather quickly with significant fluctuations in blood pressure, repeated hypertensive crises... The disease can manifest itself in enough young age, on average 30-50 years old. In the initial stages clinical picture hypertensive encephalopathy is characterized by sufficient dynamism and reversibility of symptoms. Characterized by a neurosis-like syndrome, frequent headaches, mainly occipital localization, noise in the head. In the future, signs of bilateral pyramidal insufficiency, elements of akinetic-rigid syndrome, tremors, emotional and volitional disorders, decreased attention and memory, slowness of mental reactions may appear. As the progression progresses, personality disorders occur, the range of interests narrows, speech intelligibility is impaired, anxiety increases, and weakness is noted. Patients are characterized by disinhibition.
In the III stage of hypertensive encephalopathy in patients, as a rule, severe atherosclerosis occurs, the condition is characterized by features typical for atherosclerotic encephalopathy - developing dementia. In an advanced stage, patients lose the ability to self-care, control of pelvic functions, signs of apatho-abulic or paranoid syndromes may appear.
A variant of hypertensive encephalopathy in combination with atherosclerotic brain damage is Binswanger's encephalopathy (progressive vascular leukoencephalopathy). It usually manifests itself at the age of 50 and is characterized by memory impairment, cognitive impairment, motor impairment in chronic subcortical cerebrovascular accident. Sometimes there are epileptic seizures. As a rule, encephalopathy in chronic cerebrovascular accident develops gradually, although stepwise progression associated with vascular crises, fluctuations in blood pressure and heart disorders is possible.
Venous DE is different venous congestion in the skull, chronic hypoxia and intracranial hypertension. Venous DE more often develops in patients with cardiopulmonary diseases, as well as with arterial hypotension.
Diagnostic procedures for chronic cerebrovascular accident include the collection of anamnesis, taking into account information about somatic pathology (especially about cardiovascular diseases), analysis of patient complaints, neurological, neuropsychological examination. Instrumental examination suggests Doppler ultrasound (USDG), rheoencephalography, CT) or MRI, ophthalmoscopy and angiography. As a rule, an examination of the heart (electrocardiography - ECG, echocardiography) is necessary, as well as a study of the rheological properties of blood.
Treatment of chronic cerebrovascular accident
Arterial hypertension is one of the most important risk factors for CVI, however, episodes of hypotension are also unfavorable for patients with DE. In the process of correction, it is advisable to maintain blood pressure at a stable level slightly exceeding the "optimal" indicators: 140-150 mm Hg. It is necessary to select medications for chronic disorders of cerebral circulation, taking into account the characteristics of the patient, his reaction to the prescribed medications. For the treatment of arterial hypertension, angiotensin-converting enzyme inhibitors are used - ACE (captopril, perindopril, enalapril, enalaprilat), angiotensin II receptor antagonists (candesartan, eprosartan), β-blockers (in particular, atenistolol, labetolol, metolopetol central α-adrenergic receptors (clonidine), slow calcium channel blockers (nifedipine). Diuretics as antihypertensive therapy are used only according to indications (for example, heart failure, ineffectiveness of other antihypertensive drugs) due to a possible deterioration in blood rheology.
Forecast
Usually, chronic cerebrovascular accident is characterized by a slowly progressive course, although a stepwise progression is possible (usually after vascular crises). In stage I, the ability to work and household adaptation of patients in most cases is preserved, in stage II there is a slight or moderate decrease in working capacity, in stage III patients are disabled, often unable to self-service.
The article was prepared and edited by: surgeonCerebral circulation disorders are an extensive group of pathologies (also called NMC) that affect the vessels of the brain (GM) and are accompanied by hypoxia and ischemia of brain tissues, the development of metabolic disorders and specific neurological symptoms.
On this moment, acute and chronic cerebrovascular accidents are the leading cause of disability among middle-aged and elderly patients, as well as one of the leading causes of death in the world.
At the same time, if not long ago disorders of cerebral blood flow occurred mainly in patients over 45 years old, now they are also diagnosed in twenty-year-olds.
Atherosclerotic lesions of the GM vessels and the neck are also the leading causes of the appearance of CMC. In young patients, blood flow disorders such as hemorrhagic stroke or associated with a hypertensive crisis are more often observed.
For reference. For elderly patients, the onset of ischemic CCD is more typical, and the risk of developing severe chronic cerebrovascular accidents also increases with age.
Significantly increases the likelihood of CCD and prolonged decompensated diabetes mellitus. In such patients, severe vascular lesions, microcirculation disorders, ischemic phenomena in organs and tissues, heart rhythm pathology and a tendency to microthrombosis are observed. In this regard, they often have ischemic strokes with massive foci of necrosis.
One of the most common reasons for the development of chronic ischemic blood flow disorder in young patients is osteochondrosis in cervicothoracic spine spinal column. This problem is often encountered by office workers leading a sedentary lifestyle.
Also, frequent reasons the occurrence of cerebrovascular accidents are:
- CVS pathologies accompanied by cardiogenic thromboembolism;
- rheumatic heart defects and vascular lesions;
- postinfarction cardiosclerotic conditions complicated by cardiac aneurysms or atrial fibrillation;
- various cardiomyopathy ;
- prolapse MK ( mitral valve), accompanied by severe hemodynamic disturbances;
- cerebral amyloid angiopathy;
- systemic autoimmune and post-inflammatory vasculitis;
- blood diseases (various, hereditary coagulopathies, etc.);
- aneurysms and malformations of the GM vessels and neck;
- coagulopathy, accompanied by increased thrombus formation;
- hemorrhagic diathesis;
- GM and neck tumors;
- diseases of the thyroid gland;
- metastatic foci in the brain;
- head injuries, as well as the spine in the cervicothoracic region;
- severe intoxication and poisoning;
- neuroinfection.
The predisposing factors that significantly increase the risk of developing acute and chronic disorders of cerebral circulation are:
- obesity;
- hypodynamia;
- violation of lipid balance;
- smoking;
- frequent physical and emotional stress;
- alcohol abuse;
- neuroses, depression;
- chronic sleep deficiency;
- hypovitaminosis;
- frequent infectious diseases(especially streptococcal tonsillitis).
Types of cerebrovascular accident
All IMCs are divided into acute and chronic ones. The early manifestations of GM ischemia, discirculatory encephalopathy and the consequences of strokes are separately taken out.
For reference. Group acute changes cerebral blood flow includes transient CMC (transient ischemic attacks - TIA), acute encephalopathy of a hypertensive nature and strokes. Strokes, in turn, are divided into GM infarctions and hemorrhages in the brain tissue.
Chronic ischemic changes in brain tissues are divided into:
- compensated;
- remitting;
- subcompensated;
- decompensated.
Diagnosis of cerebral blood flow disorders
When symptoms of CCD appear, it is necessary to carry out thorough examination, in order to identify the type of circulatory disorder, 
the vastness of the lesion, as well as the causes of IMC.
It is mandatory to apply:
- neuroimaging methods (computed tomography or magnetic resonance imaging),
- Ultrasound of the vessels of the brain and neck,
- cerebral angiography,
- electroencephalography,
- ECHO cardiography,
- daily,
- standard ECG.
General and biochemical blood tests, a study of coagulogram indicators, diagnostics are also performed lipid profile, determination of blood glucose, etc.
Treatment of cerebrovascular accident
Therapy depends on the type of IUD and the severity of the patient's condition. All medications should only be prescribed by a neurologist. Self-medication is unacceptable and can lead to a significant deterioration in the condition.
Attention! It must be understood that acute transient blood flow disorders in the absence of treatment always end in the development of ischemic strokes. Therefore, even if the symptoms of TIA have disappeared within a few minutes after the onset of the attack, you still need to call an ambulance.
Symptoms in the initial CCD are also reversible, but only in the initial stages. Without timely treatment, it is possible to develop progressive discirculatory encephalopathy with irreversible damage to brain tissue.
Treatment of CCD includes normalization of blood pressure and lipid profile, control of glucose levels, prevention of thrombus formation. Also prescribed are neuroprotectors, drugs that improve cerebral circulation, antioxidant and antiplatelet agents, as well as anticoagulants.
Additionally, vitamins, omega-3 preparations, metabolic agents are prescribed. In the presence of neuroses or increased emotional lability, sedatives or tranquilizers may be prescribed to the patient.
With the development of strokes, treatment is aimed at:
- prevention of cerebral edema,
- elimination of the focus of ischemia or cessation of bleeding,
- decrease in the severity of neurological symptoms,
- relief of a convulsive attack,
- normalization of cardiovascular activity,
- elimination of respiratory disorders.
For reference. Also compulsorily begin early prevention complications and rehabilitation treatment aimed at restoring lost functions.
Prevention of CMD
Prevention of cerebrovascular accident includes adherence to a lipid-lowering diet, control of blood sugar levels, regular monitoring of blood pressure, quitting smoking and drinking alcohol.
It is necessary to increase the consumption of fresh vegetables and fruits, nuts, juices, bran, etc.
It is also recommended to normalize body weight and increase physical activity... At the same time, excessive physical activity is strictly contraindicated. Walking in the fresh air, swimming, slow cycling, moderate exercise in the orbit track, etc. are effective.
For reference. Overwork, stress and emotional stress are contraindicated. Strong tea and coffee should be replaced with herbal teas (mint, linden, chamomile, sage, thyme, yarrow, lemon balm, immortelle, etc.).
However, it must be borne in mind that for all herbs there are different indications and contraindications. Before use, it is necessary to study the list of contraindications - allergic reactions, hormonal disorders, pregnancy, etc.
Also effective is the course of taking multivitamin preparations and supplements containing magnesium and potassium.
How to recognize NMK in yourself and your loved ones
CCD in the initial stage is often found in young patients with osteochondrosis in the cervicothoracic spine. Smoking is an additional risk factor. a large number cigarettes, alcohol abuse, metabolic syndrome, lack of normalized physical activity, frequent stress and overwork, chronic lack of sleep, migraine attacks.
The initial symptoms of CCD may include:
- increased fatigue and decreased performance;
- noise and ringing in the ears;
- decreased visual acuity;
- decreased learning ability and memory impairment;
- persistent drowsiness and muscle weakness;
- irritability, nervousness, or depression.
Encephalopathy
Chronic IUD of the type of discirculatory encephalopathy most often occurs in elderly patients. Additional risk factors are smoking, obesity, a sedentary lifestyle, severe vascular atherosclerosis, lipid metabolism pathologies, coagulopathy accompanied by increased thrombus formation, the patient has diabetes mellitus, arterial hypertension, heart attack or stroke in history.
Symptoms of chronic disturbance of cerebral blood flow are manifested:
- progressive memory impairment,
- a decrease in intelligence (up to mental retardation),
- decreased vision and hearing,
- the appearance of noise in the ears,
- constant dizziness
- dysfunction of the pelvic organs (urinary and fecal incontinence).
There is also marked emotional lability. Patients are prone to rapid mood swings, depression, mania, psychosis, bouts of irritability and aggression, "silly" moods.
Speech disorders may occur. Patient speech becomes slurred, muttering. They answer questions out of place, often talk to themselves.
For reference. The progression of symptoms of cerebrovascular accident can lead to a complete loss of the ability to self-care due to the development of senile dementia (the third stage of discirculatory encephalopathy).
Transient cerebrovascular accident (TIA)
The term is used to denote acutely occurring disorders of blood flow in the brain, accompanied by the occurrence of a limited area of brain tissue ischemia, but not leading to necrosis of brain tissue (that is, not accompanied by the development of a stroke).
The clinical picture with transient disorders of cerebral circulation is unstable (the duration of the developed disorders should not exceed 24 hours).
In most cases, TIA symptoms last several minutes, rarely more than an hour. After the end of the attack, a complete restoration of the altered functions is observed.
For reference. Transient disorders of cerebral circulation in adults develop against the background of the appearance of a local ischemic focus in the brain tissue, which has developed due to a reversible decrease in cerebral perfusion (blood flow). TIA symptoms disappear immediately after full blood flow resumes.
The causes of TIA can be;
- microemboli of a cardiogenic nature;
- atherosclerotic lesions of the cerebral vessels, leading to their narrowing;
- microthrombi associated with the detachment of a part of the ulcerated atherosclerotic plaque.
The cause of hemodynamic disorders of blood flow is a sharp decrease in blood pressure due to:
- stenosis of the great vessels;
- hypovolemia;
- blood loss;
- shock conditions;
- severe anemia;
- orthostatic hypotension;
- overdose of alcoholic beverages, medicinal or narcotic substances;
- infectious intoxication;
- hyperventilation;
- strong and prolonged cough.
Less commonly, transient disorders of cerebral circulation can occur against the background of prolonged arterial hypertension or hypertensive crisis.
The clinical picture depends on which vascular basin the blood flow is disturbed in. Carotid TIAs are accompanied by the onset of movement disorders, changes in sensitivity, numbness of the limb, tingling and creeping sensations on the body, speech and visual disturbances, seizures of the type of focal epileptic Jacksonian seizures (seizures begin in the fingers and then spread to the entire affected half of the body).
Visual pathologies can be manifested by the appearance dark spots before the eyes, decreased visual acuity, the appearance of fog before the eyes, double vision.
There may also be lethargy, inadequate or aggressive behavior, disorientation in time and space.
Vertebrobasilar transient disorders of cerebral circulation are manifested:
- severe dizziness
- nausea and vomiting
- increased sweating,
- the flickering of colored spots in front of the eyes,
- double vision
- transient blindness
- nystagmus,
- swallowing disorder,
- transient attacks of amnesia,
- loss or blurred consciousness.
There may be numbness of the face or unilateral paralysis of facial muscles, as well as severe coordination disorders.
Hypertensive cerebral crises
For reference. Acute disorders of cerebral circulation associated with a sharp increase in blood pressure are called hypertensive cerebral crises.
The main manifestations of a crisis are severe headaches, vomiting, tachycardia, tinnitus and visual disturbances. There may also be increased sweating, a feeling of fear, anxiety or severe lethargy and drowsiness of the patient, redness or paleness of the face, a feeling of heat. In some cases, there may be severe muscle weakness.
In severe cases, meningeal symptoms and seizures may appear.
Such symptoms of cerebrovascular accident are more often observed against the background of uncontrolled hypertension of the second and third stages. Predisposing factors can be severe fatigue and stress, excessive salt intake, alcohol abuse, as well as the presence of diabetes mellitus or discirculatory encephalopathy of the second - third stage.
Stroke symptoms
Hemorrhagic strokes (cerebral hemorrhage) most often develop in young people against a background of hypertensive crises. Clinical symptoms are acute. As a rule, the patient feels a severe and acute headache, after which he loses consciousness. Depending on the severity of the hemorrhage, after a while either consciousness is restored, or the patient falls into a coma.
Also characteristic are vomiting, temporary and spatial disorientation, visual and speech disorders, nystagmus, lack of pupil response (on the one hand) to light, paralysis of the facial muscles (due to unilateral paralysis, the impression of a twisted face is created), unilateral paresis of the limbs, impaired sensitivity, convulsions, etc. etc.
For reference. Often, signs of impaired cerebral circulation may be accompanied by the appearance of meningeal symptoms (vomiting, photophobia, stiff neck). Involuntary urination or defecation may occur.
Ischemic strokes are more common in older patients. Symptoms can occur both acutely and gradually. Lethargy, drowsiness of the patient, unilateral paresis and paralysis, face distortion, lack of reaction of pupils to light, decreased visual acuity, the appearance of fog before the eyes, nystagmus are noted.
Patients often do not understand the speech addressed to them or cannot answer the question asked to them. As a rule, speech disorders are noted.
Consciousness in ischemic strokes, as a rule, is not impaired. Convulsions are rare, more often with massive ischemic foci.
The brain is a "mystical" organ that can fill us with incredible sensations, show its own "movie", a dream, accumulate experience and wisdom that allows us to think. This is the body that controls and regulates the work of the whole organism as a whole and of each organ and system separately; providing the balance, protection, and compensatory reactions to disturbances necessary for our body. This small organ, weighing about 1400-1500 grams (2% of body weight), has incredible abilities that are not yet fully understood.
What does the brain need? Working without rest day and night, he is in dire need of oxygen (the brain consumes 20% of all oxygen entering the body) and nutrients, without which he cannot do even for a few minutes. It is a known fact that oxygen reserves are not created in the brain, and there are no substances capable of supplying it under anaerobic (in the absence of oxygen) conditions. That is, the nerve cells of the brain are constantly in need of oxygen, glucose and "cleaning" (cleansing of waste products of cells).
Excursion into physiology
The uninterrupted supply of substances necessary for the nerve cells of the brain and the purification of waste is carried out by the cerebral circulation system, where arterial blood carries oxygen and nutrition to the brain, and venous blood removes toxins and metabolic products.
The cerebral vessels have a peculiar, perfect structure that perfectly regulates blood flow, ensuring its stability. They are designed in such a way that with an increased flow of blood into large vessels, a strong pulse of blood coming from the heart is weakened due to the numerous bends (siphons) of the vessels along the vascular bed, which contribute to the pressure drop and smoothing of the pulsating blood flow. Due to the complex mechanisms of regulation with an increase in total blood pressure, the pressure in the brain remains stable for a long time. Regulatory systems make it possible to redistribute blood flow from parts of the brain with less stress to areas with enhanced brain activity.
The brain has an autonomous system of regulation, which allows it to be in a healthy functional state and to control the processes of continuous adaptation of the body to constantly changing external and internal environment... In a state of functional rest, the brain receives 750 ml of blood per minute, which is 15% of the cardiac output. In children, the activity of blood flow is 50-55% higher, and in the elderly it is 20% lower than in a person in adulthood.
It should be noted that the gray matter of the brain (cellular bodies of neurons) is provided with blood more intensively than the white matter (pathways), which is due to the greater activity of the cells. So with intense mental work, local blood flow in the cerebral cortex can increase by 2-3 times compared with the state of rest.
The brain has the richest capillary network. Nerve cells are not only entwined, but also penetrated by capillaries. The vessels of the brain are interconnected by collaterals ("bridges"). Arterial collateral circulation of the brain, which is important for maintaining normal blood flow, plays an especially significant role in compensating for circulatory disorders in the event of blockage of one of the cerebral arteries.
With a high intensity of blood flow in the vessels of the brain, the blood pressure in them is kept relatively constant. A complex chain of regulatory mechanisms protects the brain from a drop in blood pressure and hypoxia (a decrease in oxygen). On the path of blood flow to the brain, there are many sensitive cells (pressoreceptors, chemoreceptors) that can respond to blood pressure and regulate the heart rhythm and vascular tone.
The activity of the vasomotor centers of the brain is associated not only with the nervous and humoral mechanisms of regulation, but also with the system of autonomous regulation, which allows, despite significant fluctuations in total blood pressure, to maintain cerebral blood flow at a constant level.
Thus, cerebral circulation is provided with complex regulatory mechanisms that allow maintaining a constant supply of the substances it needs.
With an excessive blood supply to the brain, excessive hydration (accumulation of fluid) can occur with the subsequent development of edema and damage to vital centers that are incompatible with life. The reason for the excess blood supply may be, for example, an increase in systemic arterial pressure to 160-170 mm Hg. Art. and higher.
In the problem of impaired blood supply to the brain, much attention is paid to the arteries. But venous circulation is no less significant. Through the veins, waste substances (toxins) are removed with the blood - that is, cleansing the brain. Thanks to these vessels, constant intracranial pressure is maintained.
Violation of venous outflow leads to stagnation of blood and accumulation of fluid in the brain, causes hydrocephalus with compression of the brain centers, contributes to the occurrence of phlebitis and thrombophlebitis.
There is one more feature of cerebral veins that needs to be considered. The wall of a venous vessel in the brain does not have a valve apparatus, unlike, for example, the veins of the extremities (valves help withstand the load, moving the blood up and not allowing it to move in the opposite direction). Therefore, venous blood in the vessels of the brain is freely passed in both directions, depending on the pressure that has arisen. This creates the danger of a rapid spread of infection from the sinuses of the nose and eye sockets, which is also facilitated by the atomic features of the structure of the nose and its paranasal sinuses, which are in the immediate vicinity of the brain. When coughing, venous pressure increases, reverse venous flow, congestion, and hypoxia of the brain become possible. There are known cases of loss of consciousness during a coughing attack in the presence of a chronic respiratory disease and in young children, when they "go" in a cough during illness and cry with a cry before coughing.
It becomes clear why long-term respiratory disorders, accompanied by constant swelling and coughing, can cause cerebrovascular accidents. Because they not only cause brain hypoxia, but also disrupt the venous outflow and, being a constant focus of infection, promote its penetration into the brain.
For example, an ophthalmologist can observe manifestations of congestion in the brain (dilated, blood-filled vessels of the fundus). But this can also be seen with the naked eye: red, puffy eyes after sleep (due to alcohol intake the day before, overeating at night, lack of sleep) are a symptom of congestion in the brain.
After a short excursion into physiology, it becomes clear that the reasons for the deterioration of cerebral circulation can be associated with impaired blood flow to the brain and blood outflow from the brain.
What happens when blood pressure rises?
At first, the vascular tone is slowly disrupted. Over time, while high blood pressure (BP) persists, minor cerebral hemorrhages and strokes can occur.
As a result of a constant increase in blood pressure in hypertension, plasma is released (part of the blood without shaped elements), which ultimately leads to the destruction of the vessel walls.
How does this happen? A specific protein (a hyaline-like substance resembling cartilage in structure) is deposited on the walls of the vessels, which leads to the development of hyalinosis. The vessels become like glass tubes, losing their elasticity and ability to hold blood pressure. In addition, the permeability of the vascular wall increases, and blood can freely pass through it, soaking the nerve fibers (diapedetic bleeding). The result of such transformations can be the formation of microaneurysms and rupture of the vessel with hemorrhage and blood entering the white medulla. The resulting edema and hematomas lead to the following hemorrhages (hemorrhagic stroke).
Atherosclerosis accompanying hypertension, or existing without it (which is rare) contributes to brain ischemia - insufficient supply of nutrients and oxygen to the tissues (except for atherosclerotic plaques that narrow the lumen of the arteries, the blood itself is thick and viscous).
Acute circulatory disorders are strokes (hemorrhagic and ischemic). But it all starts with transient disorders of cerebral circulation against the background of hypertension and atherosclerosis, as well as obesity, diabetes mellitus, and respiratory tract diseases often accompanying them.
Symptoms of cerebrovascular accident
With the formation of a focus in the brain with impaired blood supply, the patient may become numb in half of the body (from the side opposite to the lesion site) and part of the face around the lips, short-term paresis of the limbs or other parts of the body and face is possible. Speech is impaired, an epileptic seizure may occur.
In case of impaired blood circulation, depending on the location of the lesion, legs and arms may weaken, dizzy, the patient may find it difficult to swallow and pronounce sounds, photopsia occurs (the appearance of luminous dots, sparks, etc. in the eyes) or diplopia (bifurcation of visible objects) ... A person loses orientation, he has memory lapses.
Signs of impaired cerebral circulation against a background of hypertension are manifested in the following: the head begins to hurt badly and eyeballs, a person experiences drowsiness, ear congestion (like on an airplane during takeoff or landing) and bouts of nausea. The face turns red, sweating intensifies.
Unlike strokes, all these symptoms, which are called "transient attacks", disappear within 24 hours.
Chronic disturbance of cerebral circulation (CCI), in contrast to acute forms, develops gradually. In this case, there are three stages of the disease:
- In the first stage, symptoms are vague. They look more like a syndrome chronic fatigue... A person quickly gets tired, becomes hot-tempered and absent-minded, forgets some insignificant moments. His sleep is disturbed, his mood often changes, his head hurts and is dizzy.
- At the second stage, chronic cerebrovascular accident is accompanied by a significant memory impairment, small motor dysfunctions develop, causing unsteadiness of gait. There is a constant noise in the head. A person does not perceive information well, with difficulty concentrating his attention on it. Becomes irritable and insecure, loses intelligence, responds inadequately to criticism, often becomes depressed. He gradually degrades as a person and does not adapt well socially. He is constantly dizzy and has a headache. He always wants to sleep. The performance is significantly reduced.
- In the third stage, all symptoms are worse. Degradation of personality turns into dementia, memory suffers. Leaving the house alone, such a person will never find his way back. Motor functions are impaired, which manifests itself in hand tremors, stiffness of movements. A noticeable violation of speech, uncoordinated movements.
Consequences of cerebrovascular accidents
Disability is a sad outcome of acute and, in many cases, chronic cerebrovascular accident.
Acute cerebrovascular accident has dire consequences. In most cases, a person who has suffered a stroke becomes completely helpless. He cannot eat on his own, perform hygiene procedures, dress, etc. Such people have a completely impaired ability to think. They lose track of time and are completely disoriented in space.
Some have the ability to move. But many people after a cerebrovascular accident remain bedridden forever. Many of them retain a clear mind, understand what is happening around them, but are speechless and cannot express their desires and feelings in words.
How to prevent cerebrovascular accident
The ability to protect yourself from this serious illness, regardless of what category it belongs to, exists. Only many people neglect it.
This is an attentive attitude to one's health and all changes in the body.
Agree that healthy person there should be no headaches. And if you suddenly feel dizzy, it means that there is some kind of deviation in the work of the systems responsible for this organ.
An elevated temperature is evidence of a malfunction in the body. But many go to work with a temperature of 37 ° C, considering it normal (explaining that the tests did not reveal anything).
There is a short-term numbness of the limbs? Most people rub them without wondering: why is this happening?
It is not normal to live on constant medication when chronic diseases nose and respiratory tract, do not associate them with existing internal violations and not think about the consequences (because there is no time, because the ENT doctor will carry out the procedure and it will become easier for a while).
It's not okay to live with obesity and diabetes mellitus without thinking about the consequences, indulging their eating habits.
After all, all these are satellites of the first minor changes in the cerebral blood flow system.
Often, an acute disturbance of cerebral circulation is preceded by a transient one. But since his symptoms disappear within a day, not every person rushes to see a doctor in order to be examined and receive the necessary medication.
Today, doctors are armed with effective drugs - thrombolytics. They literally work wonders by dissolving blood clots and restoring cerebral circulation. However, there is one "but". To achieve maximum effect, they should be administered to the patient within three hours after the onset of the first symptoms of a stroke. Unfortunately, in most cases, seeking medical help is carried out too late, when the disease has turned into difficult stage and the use of thrombolytics is already useless. In the case of chronic disorders, taking only thrombolytics and blood thinners does not give the desired result, since it is necessary to determine and eliminate true reasons leading to these violations.
And here again the instructions of the great Avicenna are recalled: "Set up food, sleep, wakefulness ... and the disease will recede."
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