Vascular dementia: variety of causes, forms, symptoms

Dementia is colloquially referred to as acquired dementia acquired during life rather than at birth. It more often affects people of mature age and is associated with damage to the brain structure.
The disease usually develops in one of two directions: atrophic or vascular. There are also mixed forms that combine both options.

Atrophic dementia is associated with the destruction of brain tissue and accounts for the largest percentage of cases. This includes the well-known Alzheimer's disease, as well as Pick's disease, Huntington's chorea, etc.

Vascular dementia develops against the background of “spoiled” cerebral circulation and accounts for approximately 15% of all dementors. It occurs with a variety of symptoms, which depends on the location of the pathological process, the area of the lesion and the caliber of the affected line.

Causes and essence of the disease

Vascular dementia develops due to disruption or cessation of blood circulation in one of the brain areas, as a result of which some brain cells die. The rate of progression of the process and the severity of symptoms will depend on how quickly the provoking factor acts.

Acute development of pathology is observed with stroke, ischemic or hemorrhagic. In the case of an ischemic stroke, a blood line is blocked by a thrombus. Its hemorrhagic form is characterized by rupture of the vessel. Both phenomena interfere with blood supply, which leads to irreversible death of cells in the brain area.

Typically, vascular dementia occurs in 25% of stroke patients. This happens if 50 ml of brain tissue is affected. The area and affected area play a big role. However, there are particularly sensitive areas of the brain, where even the slightest destruction entails disastrous consequences. These are, for example, the frontal lobes, visual hillocks.

For patients with vascular dementia, there is such a pattern: the first symptoms can appear either immediately after a stroke, or delayed, within six months. A period of 6 months is an indicative sign of vascular dementia. Typically, a stroke, especially a hemorrhagic one, leads to a rapid development of events, the appearance and increase of symptoms.

In a chronic destructive process, when small vessels are damaged, brain cell atrophy occurs gradually. Its compensatory mechanisms are activated, and symptoms increase gradually. The first signs are difficult to identify. Sometimes they hide not only from others, but also from the patient himself.

The main provoking factor that causes disruption of the patency and integrity of the blood network in the brain is atherosclerosis, that is, the deposition of sclerotic plaques on the vascular walls. Other reasons include:

heart disease, cardiovascular failure;
arterial hypertension;
arterial hypotension;
vasculitis – inflammation of the vessel wall;
diabetes;
hyperlipidemia;
lack of estrogen;
bad habits;
excess body weight.

Clinical course and prognosis

The clinical course and prognosis of the disease is influenced by the cause that caused pathological changes in the central nervous system. For example, in post-traumatic dementia, when the underlying disease is not prone to development, with adequate treatment, significant improvements are possible as a result of developing compensatory reactions. When other, unaffected areas of the cerebral cortex will be able to take over some of the functions. Alzheimer's disease and vascular dementia are among the most common types of steadily progressive dementia. Treatment of these diseases is only the removal of unpleasant symptoms, slowing down the disease process, social and personal adaptation of patients, and prolonging their life. With a rapidly progressing disease that causes dementia, the prognosis is unfavorable. The patient dies several years, sometimes months, after the first symptoms of the disease appear. Death is usually caused by concomitant diseases, such as pneumonia, sepsis, which develop against the background of damage to the central regulation of human systems and organs.

General groups of symptoms

The disease distinguishes two groups of disorders: cognitive and neurological.

Cognitive disorders come to the fore, that is, regression of cognitive and thinking functions.

At the initial stage of the disease, memory is primarily affected. At first these are subtle changes. A person forgets some events, individual names and dates, and cannot find the right word to express a thought. The process of assimilation of new knowledge worsens, and it becomes increasingly difficult for the patient to remember and analyze new information.

Gradually, amnestic symptoms increase. The person does not grasp the meaning of what was said, and it becomes more and more difficult to find words. Because of this, his speech becomes meager, his sentences are short and monosyllabic. If talkativeness manifests itself, then it is incoherent; letters in words can be rearranged, words can be replaced. The person himself does not understand the meaning of what he said. Speech impairment leads to difficulties with writing and reading.

Amnesia occurs in the following forms:

progressive - the patient begins to forget what happened to him recently, and then earlier events;
fixation – inability to perceive, analyze, store new material, current events. Consciousness in such patients is preserved; they remember well the events of the past, but cannot remember what they talked about with the person 5 minutes ago. Having bought milk, brought it home and put it in the refrigerator, a few minutes later they are going to the store again to buy it, since they have already forgotten that they purchased it;
Paramnesia is false memories when the patient supplements reality with unreal events. For example, he may pass off as reality events read in a book or seen in a film, and believe that this actually happened to him. Or he simply fantasizes, passing off as reality what did not happen. It is possible that events may shift in time, that is, what happened many years ago is perceived by a person as having happened yesterday.

In addition to memory, other cognitive functions are affected in vascular dementia. Attention is scattered, it is impossible to fix it for a long time. Perception is disrupted. Thinking becomes inflexible. It is difficult to switch from one activity to another.

Often, as the process progresses, patients develop a symptom such as Korsakoff's syndrome, named after the doctor who first described it. It combines several symptoms. First of all, this is fixation amnesia. As already mentioned, the patient does not remember current events, but retains memory of the past. In this regard, he loses orientation in time and space. So-called amnestic disorientation develops.

There are also various variations of paramnesia: doubts about the occurrence of a particular event, their displacement in time, a mixture of fictional and true events.

Against this background, a person gets lost in an unfamiliar environment. He doesn't understand where he is. While in the hospital, he cannot find his bed, but in a familiar environment, at home, he finds his way around perfectly.

Classification by localization

Cortical dementia - formation occurs with predominant damage to the cerebral cortex. Examples are Alzheimer's disease and alcoholic encephalopathy. This type is characterized by amnesia, significant cognitive disorders, such as impairment of abstract thinking and calculation, speech disorders, even absence, and inability to recognize faces. The patient does not remember his name and does not recognize his relatives. Movement disorders are not typical.
Subcortical dementia is a disease that affects subcortical structures. Examples are: dementia in Parkinson's disease, Huntington's disease, toxic dementia, as well as dementia in diseases such as normal pressure hydrocephalus, metabolic encephalopathy, corticobasal degeneration. The disease is characterized by slow thinking, nasal or muffled speech, mild memory impairment - forgetfulness, severe motor impairment, and tremor.
Cortical-subcortical dementia is formed when the cortex and subcortical structures are damaged, with the presence of two types of symptoms. Typical representatives are: vascular dementia, dementia with Lewy bodies, corticobasal degeneration.
Multifocal dementia is a rapidly progressing type; the disease is characterized by multiple focal lesions in all parts of the brain. An example is Creutzfeldt-Jakob disease. Characterized by amnesia, perceptual disturbances, speech impairment and loss of practical skills.

Neurological disorders

In the initial stage of the disease, neurological dysfunctions manifest themselves as general symptoms. Weakness and fatigue, absent-mindedness, and irritability appear. I am bothered by systematic headaches and sleep is disturbed. There is an unstable emotional background. Depressive states are possible. The person is unrestrained, hot-tempered, and embittered. Emotional incontinence usually manifests itself in violent crying or laughter, weakness.

Among other neurological indicators, cerebellar syndrome occurs, characterized by uncoordinated movements. It seems that the arms and legs are moving chaotically. Because of this, the gait changes: it becomes shaky, slack. The person appears to be drunk. Instability of the step provokes falls.

The disease causes accentuation of personality traits. For example, if previously a person was scrupulous and meticulous, then pathology turns him into a picky grumbler.

Pseudobulbar syndrome is expressed by a triad of signs:

dysarthria - pronunciation disorder;
dysphonia – loss of voice sonority;
dysphagia – problems with swallowing.

There are cases of paralysis and paresis, but quite rarely. Muscle tone and reflexes are increased.

Quite often, malfunctions in the functioning of the pelvic organs occur, and epileptic seizures occur.

In general, dementia of vascular origin is characterized by narrowness and fixation of mental processes, loss of flexibility of thinking, fading of cognitive abilities, and a narrow range of interests.

Environmental

There are several reasons, we list them:

Advanced age. After 60–65 years, the risk of the disease increases significantly, this is due to the fact that older people, due to their age, are more susceptible to external factors.
Diabetes. This disease often affects blood vessels, including the brain, and in the absence of adequate treatment can lead to dementia.
Stroke. When a stroke occurs, certain blood vessels are damaged and there is bleeding in the brain, which can contribute to the onset of dementia.
High pressure. Hypertension also negatively affects the health of blood vessels and can lead to dementia.
Any brain injuries, as well as tumors, hematomas, large abscesses.
Smoking and alcohol have a huge negative impact on the brain. The result is senile dementia.
Level of education and professional activity. Highly educated people who engage in mental work all their lives are less susceptible to senile dementia, and vice versa: people who do not have an education and do not train their brains get sick more often, and their disease progresses faster.\
Violation of immunity and metabolism in the body.

Hereditary

If a blood relative of an older person has had Alzheimer's disease or other similar diseases, the likelihood of developing dementia increases.

Cases of vascular dementia

Scientists have established for certain that the Russian writer, imperial maid of honor Smirnova Alexandra Osipovna, whom A.S. once admired. Pushkin, suffered from vascular dementia.

From her youth, she was distinguished by her gloomy mood or its swings, insomnia. At the age of 40, she suddenly lost weight and became haggard. I didn’t want to see doctors. She was treated on her own: sermons, rituals. Her heredity was burdened with mental disorders.

At the age of 69, her condition worsened further. Her speech became incoherent, she rearranged syllables in words and distorted them. Memory suffered and behavior was disrupted. The mental state deteriorated sharply, reaching the level of mental disorder.

According to data collected from eyewitnesses, Alexandra Osipovna was diagnosed with “atherosclerotic dementia.”

Another famous writer, the author of Uncle Tom's Cabin, Harriet Beecher Stowe, was also diagnosed with vascular dementia. She devoted her entire life to caring for her large family, fighting poverty and disease. In the last years of her life, after the death of her husband, Harriet lived completely alone. She exhibited strange behavior. Sometimes she came to Twain’s house and wandered around the rooms there. She didn’t pay attention to anyone, she was aloof. After walking around a bit among the people, she returned home. Her mental abilities had completely deteriorated, she practically could not take care of herself. The patient's memory underwent special destructive changes.

Living with someone with dementia

People with dementia behave like little children. At the same time, they gradually lose skills without acquiring new ones. Relatives should take this fact for granted and not blame themselves for anything. If you detect the first signs of memory impairment, you should convince your loved one to contact a neurologist. Typically, at the onset of dementia, patients agree to this proposal. Neurologists at the Yusupov Hospital advise people who live next to a person with dementia to adhere to the following rules:

1. Don't be left alone with your problems. Caring for a loved one should not destroy connections with the outside world. You should ask relatives to call and come more often. You need to find people who were in a similar situation and communicate with them; 2. Do not refuse the help of your family and friends. You need to make others feel that their participation is extremely important to you; 3. Do not wait for negative emotions to spill out in the presence of the patient. Take your anger out somewhere else; 4. If you are tired or experiencing emotional exhaustion, contact a psychologist at the Yusupov Hospital. It will help prevent depression; 5. Pay proper attention to yourself, visit beauty salons, dress well.

If a loved one has memory impairment, you should not leave him alone with the problem. By contacting the specialists at the Yusupov Hospital, the patient’s relatives will receive recommendations that will allow them to live more comfortably. Our experts will tell you how to care for it, organize your life, and ensure safety.

Organization of patients' everyday life

If doctors have diagnosed a patient with dementia, his relatives should specially arrange rooms for the patient to live. You need to put locks in them, leave a minimum number of things and furniture, and remove sharp and cutting objects. Most people with dementia exhibit aggression and a tendency to vandalism. They can harm themselves and others. To prevent the patient from throwing away or destroying money and documents, they should be removed from the room and hidden.

A patient suffering from dementia will never be able to appreciate the actions of a caregiver or show gratitude. There is no need to be offended by him about this, just as we are not offended by small children. Dementia does not necessarily progress to the third stage of the disease. In many cases, severe memory impairment can be prevented with adequate therapy.

Some memory disorders are reversible. Sometimes, through the joint efforts of doctors and people caring for a patient, it is possible to partially restore impaired functions and improve the quality of life. Neurologists, psychotherapists and rehabilitation specialists at the Yusupov Hospital together create an individual treatment program for each patient. This guarantees the maximum effect of the therapy. Doctors at the neurology clinic constantly monitor patients and, if indicated, change medications, their doses, and the regimen of use.

To provide your loved one with adequate medical care and professional care if dementia develops, call the contact center at any time of the day, regardless of the day of the week. Our specialists will select a convenient time for consultation with a neurologist who specializes in the diagnosis and treatment of memory disorders.

Forms of vascular dementia

The brain provides us with conscious existence, being responsible for mental, emotional, and adaptive processes. Its substance is strictly structured. Each of its departments is responsible for its functions.

However, any part of the brain can undergo destructive changes, as a result of which a certain type of activity is disrupted. Based on this, several forms of the disease are distinguished, differing not only in location, but also in the caliber of the affected vessels.

Dysmnestic or lacunar dementia occurs against the background of destruction of small-diameter vessels. As a result, multiple infarct foci appear in the thickness of the white and gray matter. This is the most classic variant of the course of the disease, in which all pathological manifestations are not clearly expressed. There is a measured decrease in intellectual abilities, mild memory impairment, and slight slowness of psychomotor skills.

The multi-infarction form is accompanied by damage to vessels of medium diameter, and usually develops in non-acute pathological processes. Its manifestations are insignificant and go unnoticed for a long time even by the patient himself. Its course is gradual. The disorders first progress and then freeze at a certain stage until the next micro-stroke. Among the symptoms of this type of disease, cognitive impairment comes to the fore. Neurological and emotional disorders gradually develop.

Subcortical vascular dementia is a disease of small vessels, against which atrophy of white matter cells occurs with the formation of ischemic areas. Scientists see the reason for this process in the accumulation of amyloid in the walls of the arteries, followed by its inflammation. The clinical picture of the disease is somewhat atypical. It can occur as Alzheimer's disease or as isolated dementia.

Autoimmune vasculitis, such as systemic lupus erythematosus and panarteritis, cause another form of the disease - cerebral vasculitis. It is expressed by dementia and confusion. As a rule, it affects patients over 50.

Mixed dementia combines two forms: vascular and atrophic, that is, Alzheimer's type. Therefore, in the picture of the disease one can observe symptoms of both vascular dementia and Alzheimer's disease, but the latter prevail over the former.

Dementia atherosclerotic, senile

Dementia

- translated from Lat. dementia means insanity - a serious disease caused by organic damage to the brain, expressed in a sharp decrease in mental abilities, collapse of mental functions, irreversible loss of acquired knowledge and skills, decreased ability to self-care, persistent decrease in the speed of mental reactions, impoverishment of emotions, impaired emotional control, motivation and social behavior.

The clinical picture of dementia is characterized by the causes that caused organic brain damage, the localization and extent of the defect, and the initial state of the body. But in all cases of the disease, memory impairment, attention disorders, decreased thinking and learning abilities, and loss of basic skills are characteristic. Dementia is an irreversible degenerative disease, and at a young age its development occurs as a result of addictive behavior from addictions - alcohol addiction. Senile dementia - translated from Latin. senilis means senile - is colloquially called senile marasmus and develops in people after 65 years of age.

According to WHO, there are more than 47 million people with dementia in the world and more than 7 million new cases of the disease are registered annually.

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Binswanger's disease

The pathology is named after its discoverer and is subcortical atherosclerotic encephalopathy. Develops as a result of damage to small cerebral vessels and is a fairly common form of dementia: about 1/3 of all dementors.

It has been established that arterial hypertension plays a major role in the development of pathology. It was observed in 80% of patients with this form. Most often, the disease starts after 50 years and begins suddenly. The first signs of it may be a transient disturbance of cerebral circulation, accompanied by sudden paralysis, which, however, also suddenly disappears. Other signs include small strokes and parkinsonism. A magnetic gait is observed when the legs seem to stick to the floor.

Emotional incontinence appears in the form of sudden laughter or crying, speech is impaired, and control over vital functions (for example, urination) is lost. Problems with memory and thinking appear already at the beginning of the disease.

The symptoms of the pathology are quite varied. After all, the process causes extensive damage to brain tissue with ischemia, destruction of nerve cell processes, and demyelination of nerve fibers. The process is accompanied by steady progression, although cases of persistent remission are possible.

Cerebrovascular insufficiency: clinical picture, diagnosis and therapy

Stroke and chronic forms of cerebrovascular insufficiency represent one of the most pressing problems of modern neurology. According to epidemiological data, the incidence of stroke in the world is 150 cases per 100 thousand population per year. Chronic insufficiency of blood supply to the brain is also very widespread.

In the domestic literature, the term “dyscirculatory encephalopathy” (DE) is usually used to denote the clinical syndrome of brain damage resulting from insufficient blood supply to the brain. According to the classification of vascular diseases of the brain proposed by E.V. Schmidt (1985), dyscirculatory encephalopathy refers to chronic disorders of cerebral circulation.

Vascular diseases of the brain (E.V. Schmidt et al., 1985)

Acute cerebrovascular accidents
*Stroke
– Ischemic stroke (thrombotic, embolic, hemodynamic, lacunar)
– Hemorrhagic stroke (parenchymal hemorrhage, subarachnoid hemorrhage)
*Transient cerebrovascular accidents
– Transient ischemic attacks
– Hypertensive cerebral crises
Chronic cerebrovascular accidents
*Initial manifestations of insufficient blood supply to the brain
*Encephalopathy

However, as modern research shows, various cardiovascular diseases, as a rule, lead simultaneously to chronic cerebral ischemia and repeated acute cerebrovascular accidents. Therefore, it would be more correct to define discirculatory encephalopathy as a syndrome of chronic progressive brain damage, which is based on repeated strokes and/or chronic insufficiency of blood supply to the brain (N. N. Yakhno, I. V. Damulin, 2001).

Etiology and pathogenesis of DE

The most common causes of impaired blood supply to the brain are atherosclerosis of the main arteries of the head, heart disease with a high risk of thromboembolism in the brain, and hypertension. Less commonly, cerebrovascular accidents develop as a result of inflammatory changes in blood vessels (vasculitis), disorders of the blood coagulation system, abnormalities in vascular development, etc. In the vast majority of cases, cerebral vascular insufficiency develops in elderly people suffering from the above cardiovascular diseases.

As follows from the definition of DE, 2 main pathogenetic mechanisms play a role in the formation of this syndrome: stroke and chronic cerebral ischemia. Ischemic strokes of the brain develop as a result of thrombosis of cerebral arteries, thromboembolism in the brain, arteriolosclerosis, rheological and hemodynamic disorders.

Chronic cerebral ischemia is based on structural changes in the vascular wall, which arise as a consequence of prolonged arterial hypertension or an atherosclerotic process. It has been established that lipohyalinosis of small-caliber vessels penetrating the brain substance can lead to chronic ischemia of the deep white matter. A reflection of this process are changes in the white matter (leukoaraiosis), which are defined as focal or diffuse changes in signal intensity from deep cerebral structures on T2-weighted images of magnetic resonance imaging of the brain. These abnormalities are considered to be typical neuroimaging symptoms that develop in patients with long-term uncontrolled arterial hypertension.

Clinical manifestations of DE

The clinical picture of DE is highly variable. As mentioned above, most patients with chronic vascular diseases of the brain have a history of strokes, often repeated. The localization of strokes undoubtedly largely determines the characteristics of the clinic. However, in the overwhelming majority of cases with cerebrovascular pathology, along with the consequences of strokes, there are also neurological, emotional and cognitive symptoms of dysfunction of the frontal lobes of the brain. This symptomatology develops as a result of disruption of connections between the frontal cortex and the subcortical basal ganglia (the “disconnection” phenomenon). The reason for the “disconnection” lies in diffuse changes in the white matter of the brain, which, as mentioned above, are a consequence of the pathology of small-caliber cerebral vessels.

Depending on the severity of the disorders, it is customary to distinguish 3 stages of dyscirculatory encephalopathy. The first stage is characterized mainly by subjective neurological symptoms. Patients complain of headache, dizziness, heaviness or noise in the head, sleep disorders, increased fatigue during physical and mental stress. These symptoms are based on a mild to moderate decrease in mood associated with dysfunction of the frontal lobes of the brain. Objectively, mild impairments of memory and attention, as well as possibly other cognitive functions, are detected. There may be an asymmetrical increase in tendon reflexes, uncertainty when performing coordination tests, and slight changes in gait. Instrumental research methods that make it possible to detect the pathology of cerebral vessels are important in the diagnosis of cerebral vascular insufficiency at this stage of the pathological process.

The second stage of discirculatory encephalopathy is spoken of in cases where neurological or mental disorders form a clinically defined syndrome. For example, we may be talking about mild cognitive impairment syndrome. This diagnosis is legitimate in cases where impairments in memory and other cognitive functions clearly go beyond the age norm, but do not reach the severity of dementia. At the second stage of DE, neurological disorders such as pseudobulbar syndrome, central tetraparesis, usually asymmetrical, extrapyramidal disorders in the form of hypokinesia, mild or moderate increase in muscle tone of the plastic type, ataxic syndrome, neurological disorders of urination, etc. can also develop.

At the third stage of dyscirculatory encephalopathy, a combination of several of the above neurological syndromes is noted and, as a rule, vascular dementia is present. Vascular dementia is one of the most severe complications that develops with the unfavorable course of cerebrovascular insufficiency. According to statistics, vascular etiology underlies at least 10–15% of dementia in old age.

Vascular dementia, like DE in general, is a pathogenetically heterogeneous condition. Vascular dementia is possible after a single stroke in a strategic area of the brain for cognitive activity. For example, dementia can develop acutely as a result of a heart attack or hemorrhage in the thalamus. However, much more often vascular dementia is caused by repeated strokes (so-called multi-infarct dementia). Another pathogenetic mechanism of vascular dementia is chronic cerebral ischemia, reflected by changes in the white matter of the brain. Finally, in addition to cerebral ischemia and hypoxia, secondary neurodegenerative changes play an important role in the pathogenesis of dementia in cerebrovascular insufficiency, at least in some patients with DE. Modern research has convincingly proven that insufficient blood supply to the brain is a significant risk factor for the development of degenerative diseases of the central nervous system, in particular Alzheimer's disease. The addition of secondary neurodegenerative changes undoubtedly aggravates and modifies cognitive disorders in cerebrovascular insufficiency. In such cases, the diagnosis of mixed (vascular-degenerative) dementia is legitimate.

Clinical manifestations of vascular dementia in each specific case depend on the pathogenetic mechanisms determining the disease. In post-stroke and multi-infarction dementia, clinical features depend on the location of the strokes. Changes in the white matter of the deep lobes of the brain as a result of chronic ischemia lead to cognitive impairment of the “frontal” type. These disorders are characterized by emotional disorders in the form of decreased mood, depression or apathy, and loss of interest in the environment. Emotional lability, which is a rapid, sometimes causeless change of mood, tearfulness or increased irritability, is also very characteristic. In the cognitive sphere, memory and attention impairments, slowness of thinking, decreased intellectual flexibility, and difficulties associated with switching from one type of activity to another are determined. The behavior of patients changes: the ability for self-criticism and the sense of distance are reduced, increased impulsiveness and distractibility are noted, symptoms such as disregard for socially accepted rules of behavior, asociality, foolishness, flat and inappropriate humor, etc. may be present.

The presence of secondary neurodegenerative changes in vascular dementia is manifested primarily by progressive memory impairment. At the same time, to a greater extent, the patient forgets what happened recently, while memories of distant events are retained for quite a long time. The neurodegenerative process is also characterized by disturbances in spatial orientation and speech.

Diagnosis of dyscirculatory encephalopathy

To diagnose dyscirculatory encephalopathy syndrome, it is necessary to carefully study the medical history, assess the neurological status, and use neuropsychological and instrumental research methods. It is important to emphasize that the presence of cardiovascular diseases in an elderly person does not in itself serve as evidence of the presence of cerebral vascular insufficiency. A necessary condition for correct diagnosis is to obtain convincing evidence of a cause-and-effect relationship between neurological and cognitive symptoms and cerebrovascular pathology, which is reflected in the currently accepted diagnostic criteria for DE.

Diagnostic criteria for DE (N. N. Yakhno, I. V. Damulin, 2001)

Presence of signs (clinical, anamnestic, instrumental) of brain damage.
Presence of signs of acute or chronic cerebral dyscirculation (clinical, anamnestic, instrumental).
The presence of a cause-and-effect relationship between hemodynamic disorders and the development of clinical, neuropsychological, and psychiatric symptoms.
Clinical and paraclinical signs of progression of cerebrovascular insufficiency.

Evidence of a vascular etiology for symptoms would include the presence of focal neurological symptoms, a history of stroke, characteristic neuroimaging changes such as post-ischemic cysts or marked white matter changes.

Treatment of cerebrovascular insufficiency

Cerebrovascular insufficiency is a complication of various cardiovascular diseases. Therefore, etiotropic therapy for DE should be, first of all, aimed at the underlying pathological processes of cerebrovascular insufficiency, such as arterial hypertension, atherosclerosis of the main arteries of the head, heart disease, etc.

Antihypertensive therapy is an essential factor in the secondary prevention of the increase in mental and motor symptoms of cerebrovascular insufficiency. To date, however, the question of what blood pressure levels should be achieved in the treatment of hypertension has not been resolved. Most neurologists believe that complete normalization of blood pressure in elderly patients with a long history of hypertension, while reducing the risk of acute vascular episodes, can simultaneously contribute to the aggravation of chronic cerebral ischemia and an increase in the severity of cognitive dysfunction of the “frontal” type.

The presence of hemodynamically significant atherosclerosis of the main arteries of the head requires the prescription of antiplatelet agents. Drugs with proven antiplatelet activity include acetylsalicylic acid at doses of 75-300 mg per day and clopidogrel (Plavix) at a dose of 75 mg per day. The study showed that the use of these drugs reduces the risk of ischemic events (myocardial infarction, ischemic stroke, peripheral thrombosis) by 20-25%. The possibility of simultaneous use of these drugs has now been proven. Medicines with antiplatelet properties also include dipyridamole (chimes), which is used in doses of 25 mg three times a day. Monotherapy with this drug does not provide prevention of cerebral or other ischemia, however, with combined use, dipyridamole significantly increases the preventive effect of acetylsalicylic acid. In addition to the prescription of antiplatelet agents, the presence of atherosclerotic stenosis of the main arteries of the head requires referral of the patient for consultation with a vascular surgeon to decide on the advisability of surgical intervention.

If there is a high risk of thromboembolism in the brain, for example in cases of atrial fibrillation and valvular disease, antiplatelet agents may be ineffective. The listed conditions serve as an indication for the prescription of indirect anticoagulants. The drug of choice is warfarin. Therapy with indirect anticoagulants should be carried out under strict monitoring of coagulogram parameters.

The presence of hyperlipidemia that cannot be corrected by diet requires the prescription of lipid-lowering drugs. The most promising drugs are from the statin group (Zocor, Simvor, Simgal, Rovacor, Medostatin, Mevacor, etc.). According to some data, therapy with these drugs not only normalizes lipid metabolism, but also may have a preventive effect against the development of a secondary neurodegenerative process against the background of cerebrovascular insufficiency.

An important pathogenetic event is also the impact on other known risk factors for cerebral ischemia. These include smoking, diabetes, obesity, physical inactivity, etc.

In the presence of cerebrovascular insufficiency, the prescription of drugs that act primarily on the microvasculature is pathogenetically justified. These include:

phosphodiesterase inhibitors: aminophylline, pentoxifylline, vinpocetine, tanakan, etc. The vasodilating effect of these drugs is associated with an increase in the cAMP content in the smooth muscle cells of the vascular wall, which leads to their relaxation and an increase in the lumen of blood vessels;
calcium channel blockers: cinnarizine, flunarizine, nimodipine. They have a vasodilating effect due to a decrease in the intracellular calcium content in the smooth muscle cells of the vascular wall. Clinical experience suggests that calcium channel blockers, such as cinnarizine and flunarizine, may be more effective for vertebrobasilar circulatory failure; this is manifested by symptoms such as dizziness and unsteadiness when walking;
α2-adrenergic receptor blockers: nicergoline. This drug eliminates the vasoconstrictor effect of the mediators of the sympathetic nervous system: adrenaline and norepinephrine.

Vasoactive drugs are among the most commonly prescribed drugs in neurological practice. In addition to the vasodilatory effect, many of them also have positive metabolic effects, which allows these drugs to be used as symptomatic nootropic therapy. Experimental data indicate that the vasoactive drug tanakan has the ability to deactivate free radicals, thereby reducing the processes of lipid peroxidation. The antioxidant properties of this drug also allow it to be used for secondary prevention of the increase in memory impairment and other cognitive functions in cases of secondary neurodegenerative changes.

In domestic practice, vasoactive drugs are usually prescribed in courses of 2-3 months, 1-2 times a year.

Metabolic therapy is widely used for cerebrovascular insufficiency, the purpose of which is to stimulate the reparative processes of the brain associated with neuronal plasticity. In addition, metabolic drugs have a symptomatic nootropic effect.

Piracetam was the first drug specifically synthesized to affect memory and other higher brain functions. In recent years, however, it has been possible to prove that in previously taken doses this drug has a relatively small clinical effect. Therefore, the use of piracetam in dosages of at least 4–12 g/day is currently recommended. Intravenous administration of this drug in saline solution is more appropriate: 20–60 ml of piracetam per 200 ml of saline solution intravenously, 10–20 infusions per course.

The peptidergic drug Cerebrolysin is no less successfully used for cerebrovascular insufficiency, as well as vascular and degenerative dementia. As in the case of piracetam, views on the dosage regimen of this drug have changed significantly in recent years. According to modern concepts, the clinical effect occurs in the case of intravenous administration of Cerebrolysin in doses of 30–60 ml intravenously in 200 ml of saline, 10–20 infusions per course.

Peptidergic drugs that have a beneficial effect on cerebral metabolism also include Actovegin. Actovegin is used in the form of intravenous infusions (250–500 ml per infusion, 10–20 infusions per course), or in the form of intravenous or intramuscular injections of 2–5 ml 10–20 injections, or orally 200–400 mg 3 times a day within 2-3 months.

Like vasoactive drugs, metabolic therapy is carried out in courses 1-2 times a year. Pathogenetically justified and appropriate is the combined implementation of vasoactive and metabolic therapy. Currently, the doctor has several combined dosage forms at his disposal, which include active substances with vasoactive and metabolic effects. These drugs include instenon, vinpotropil, fezam and some others.

The development of vascular dementia syndrome requires more intensive nootropic therapy. Among modern nootropic drugs, acetylcholinesterase inhibitors have the most powerful clinical effect on cognitive functions. Initially, drugs in this group were used in the treatment of mild and moderate dementia due to Alzheimer's disease. Today it has been proven that acetylcholinergic deficiency plays an important pathogenetic role not only in this disease, but also in vascular and mixed dementia. Therefore, cognitive disorders of vascular and mixed etiology are increasingly appearing among the indications for the prescription of acetylcholinesterase inhibitors.

In Russia, two drugs from the group of latest generation acetylcholinesterase inhibitors are currently available: Exelon and Reminyl. Exelon is prescribed at an initial dose of 1.5 mg 2 times a day, then the single dose is increased by 1.5 mg every 2 weeks. up to 6.0 mg 2 times daily or until side effects occur. Common side effects when using Exelon are nausea and vomiting. These phenomena do not pose a threat to the life or health of the patient, but may interfere with the achievement of a therapeutic effect. Reminyl is prescribed at 4 mg 2 times a day for the first 4 weeks, and then 8 mg 2 times a day. This drug is less likely to cause adverse events.

First generation acetylcholinesterase inhibitors include neuromidin. According to some data, this drug has a positive nootropic effect in both vascular and primary degenerative and mixed dementia. It is prescribed in a dose of 20–40 mg 2 times a day.

Therapy with acetylcholinesterase inhibitors should be carried out continuously. In this case, it is necessary to monitor the level of liver enzymes in the blood once every 3–6 months.

The use of akatinol memantine is also pathogenetically justified for vascular dementia. This drug is an inhibitor of NMDA glutamate receptors. Chronic intake of akatinol memantine has a symptomatic nootropic effect, and may also slow down the rate of increase in cognitive disorders. The effect of the drug was manifested in both mild and moderate and severe dementia. It should be noted that akatinol memantine is the only drug effective at the stage of severe dementia. It is prescribed during the first week 5 mg 1 time per day, during the second week - 5 mg 2 times a day, starting from the third week and then continuously - 10 mg 2 times a day.

In conclusion, it should be emphasized that a comprehensive assessment of the state of the cardiovascular system of patients with cerebrovascular insufficiency, as well as the impact on both the cause of the disorders and the main symptoms of DE, undoubtedly contribute to improving the quality of life of patients and preventing severe complications of cerebrovascular insufficiency, such as , such as vascular dementia and movement disorders.

V.V. Zakharov, Doctor of Medical Sciences Clinic of Nervous Diseases named after. A. Ya. Kozhevnikova, Moscow

Diagnostics

First of all, the diagnosis of the disease is carried out on the basis of the clinical picture, or, more precisely, the presence of cognitive and neurological defects in it. They significantly poison the patient’s life and do not disappear even with clear consciousness.

Correctly identifying symptoms, and subsequently prescribing effective treatment, allows timely diagnosis. Thanks to visual research methods, it has become very simplified, and this makes it possible to recognize the pathology in a timely manner without delaying treatment.

Among these methods are prescribed:

MRI, CT;
angiography, which allows you to assess the condition of blood vessels;
rheoencephalography, which determines blood filling of blood vessels;
EEG, which records the bioelectric signals of brain cells;
nuclear resonance imaging, visualizing white matter, etc.

Consultations with related specialists are required: neurologist, cardiologist, psychiatrist. Blood pressure is systematically monitored.

Benefits of treating dementia at the Yusupov Hospital

The Yusupov Hospital has created all the conditions for the treatment of patients suffering from dementia:

Comfortable rooms equipped with forced-air ventilation and air conditioning;
Complete high-quality nutrition;
Competent medical staff;
Highly qualified doctors;
Modern equipment from leading global manufacturers;
Individual approach to choosing a treatment method for each patient.

The neurologists at the clinic have extensive experience in treating patients with various types of dementia. If relatives do not have the opportunity to provide care for the patient at home, comfortable conditions for the patient’s stay have been created in the hospice at the Yusupov Hospital.

To make an appointment with a neurologist, you should call. Contact center specialists will offer a convenient time for consultation with a doctor who specializes in the diagnosis and treatment of memory disorders.

Disease statistics

World statistics provide disappointing information: the number of people suffering from dementia is steadily growing. In 2009, the number of people with dementia was estimated to be about 35 million, and the number was projected to be 115 million by 2050. But the forecast has now been increased by 15 million. That is, the rate of increase in the incidence of dementia is steadily increasing, this is an alarming sign.

Currently, the morbidity statistics in Russia are not encouraging either. We are in seventh place in the world in terms of incidence of this serious disease. According to the most optimistic estimates, about two million elderly people in Russia are currently diagnosed with dementia, and this figure is growing.

Diagnosis

An accurate diagnosis, determining the type of dementia and the degree of development of the probable causes of the disease, can only be made by a doctor (neurologist or psychiatrist). To do this, data is collected on the signs and course of the disease, the patient himself, close friends and relatives living with him are interviewed. Various medical examinations are carried out: cerebral vascular examination, blood tests, MRI... The patient is tested using neuropsychological screening scales.

Causes of dementia

What are the causes of the death of nerve cells in the brain and the development of acquired dementia? Doctors agree that brain disorders can be caused by many different diseases and negative factors that can destroy brain vessels:

Diseases of the vascular system Disturbances in the functioning of blood vessels lead to a lack of blood and oxygen supply to brain tissue with all the ensuing consequences;
Infectious diseases Damage to brain tissue by various viruses, bacteria or toxins due to encephalitis, meningitis, AIDS and other viral diseases often leads to disruption of brain activity;
Oncological diseases Various tumors, hemorrhages and inflammatory processes affecting the cerebral cortex often cause various disorders with signs of dementia...
Traumatic brain injuries Physical destruction of brain tissue naturally leads to the death of nerve cells.
Alcohol and drug abuse Long-term destructive effects of various toxins on nerve cells cannot but affect brain activity.
Metabolic disorders A whole bunch of hormonal diseases, kidney and liver diseases lead to the accumulation of harmful substances in the blood that adversely affect brain activity.

There is no point in listing all the “risk factors” that, according to modern medicine, can lead a person to dementia. In such a situation, it would seem like a miracle for any person to live to be 80 years old and retain his sanity.

On the other hand, it is never possible to say exactly what exactly was the impetus for the development of senile dementia. If this misfortune happens to a loved one, be patient and contact a specialist...