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Encephalopathy

Dyscirculatory encephalopathy is a chronic disease of the brain, manifested by a progressive multifocal disorder of its functions, due to insufficiency of cerebral circulation. Synonyms of dyscirculatory encephalopathy are cerebral atherosclerosis, hypertensive encephalopathy, chronic cerebral ischemia, cerebrovascular disease. Various conditions lead to the development of dyscirculatory encephalopathy - atherosclerosis, arterial hypertension, heart disease (atrial fibrillation, coronary artery disease, etc.), diabetes mellitus. Dyscirculatory encephalopathy is conditionally divided into hypertensive, atherosclerotic, mixed and venous. As a rule, in practice there is a combination of several pathogenetic factors, primarily atherosclerosis and arterial hypertension. Chronic cerebral ischemia leads to the following pathomorphological changes in the area of ​​hypoperfusion:
- microgliosis;
- astrogliosis;
- loss of myelin;
- capillary remodeling;
- rarefaction of white matter;
- cell death.

Morphological markers of chronic cerebral ischemia (Fig. 2):

Legend:
1 - increase in the size of the ventricles of the brain
2 - increase in the size of subarachnoid spaces and cortical atrophy
3 - leukareosis
4 - focal changes

Rice. 2. Morphological markers of chronic cerebral ischemia

The first clinical manifestations of dyscirculatory encephalopathy are memory and attention disorders, as well as emotional disorders (anxiety, depression), usually somatized. In the future, as the disease progresses, multiple, polymorphic subjective complaints are replaced by gross neurological disorders, leading to significant social maladaptation. Conventionally, 3 stages are distinguished in the development of dyscirculatory encephalopathy (Table 2).

Table 2.

Stages of dyscirculatory encephalopathy

It is important to note that the rate of the course of the disease, social and professional maladjustment, the onset of disability in patients with dyscirculatory encephalopathy is determined mainly by a psychopathological defect.

Do you know that...

... the great composer Georg Friedrich Handel suffered three right-sided lacunar strokes in 1737, 1743 and 1745. According to the descriptions of contemporaries, the clinical picture of strokes corresponded to the "dysarthria - awkward hand" syndrome, which, unfortunately, made it difficult for the composer to play the piano.

In 1751, Handel developed acute blindness in his left eye. It can be assumed that the composer had a significant stenosis of the left carotid artery with recurring arterio-arterial embolisms in smaller branches of the middle cerebral artery and the retinal artery. Risk factors could be arterial hypertension, smoking and, most likely, hyperlipidemia.

Cognitive impairment in dyscirculatory encephalopathy

Cognitive impairment in dyscirculatory encephalopathy debuts with neurodynamic disorders: slowness of mental processes, memory loss for recent events and attention deficit, while primary cortical functions rarely suffer - speech, praxis, gnosis, counting. A characteristic feature is the fluctuation of the cognitive defect, including during the day, while in the evening, when the patient is tired, the defect grows. Vascular cognitive impairment is characterized by sudden onset of impairments in one or more cognitive areas, stepwise progression, and the presence of focal neurological symptoms. A cognitive defect is often combined with emotional-affective and behavioral disorders. As the disease progresses, the cognitive defect increases, leading to the development of vascular dementia. The diagnosis of vascular dementia is established using the following criteria:

For patients with dyscirculatory encephalopathy, it is extremely important to diagnose cognitive impairment at the pre-dementia stage, at the stage of mild and moderate cognitive impairment (the criteria are presented in Table 3), then the effect of therapy is much higher.

Table 3

Criteria for mild and moderate cognitive impairment

Neurologists, as well as general practitioners, should focus on early detection of cognitive impairment in older patients. In practice, neurologists widely use such screening neuropsychological tests as a brief scale for assessing mental status, a battery of frontal tests. Nevertheless, to date, cognitive impairments at the level of primary health care are not diagnosed successfully enough. Among the main reasons for the insufficient diagnosis of cognitive impairment, general practitioners themselves name the lack of time at the reception, the absence of active patient complaints about memory impairment, as well as obvious signs of dementia in the patient and confidence in the incurability of cognitive impairment. Many doctors, when suggesting a patient to take a test for cognitive impairment, are afraid of a conflict situation. Some doctors do not have enough experience to conduct cognitive tests. At the same time, among patients over 65 years of age, dementia syndrome is detected in 8.8%, in 65% for the first time, while 67% do not present any cognitive complaints to doctors.

For the diagnosis of cognitive impairment in primary health care settings, the Mini-Cog test, which includes three tasks, can become the optimal screening tool.

Mini-cog test (Borson S., 2000)
1. Repeat after the doctor and remember three unrelated words (for example, chair, square, apple).
2. Draw a dial with arrows and set the time (for example, fifteen minutes to an hour).
3. Name three words that were remembered at the beginning of the test.

The test is interpreted as follows: if the patient remembered all three words, then there are no gross cognitive impairments; if he did not remember any, then there are cognitive impairments. If the patient remembered two or one word, then the clock pattern is analyzed at the next stage. If the drawing is correct, then there are no gross cognitive impairments; if it is incorrect, then there are cognitive disorders. The sensitivity of the test is 99%, the specificity is 93% (for comparison, the sensitivity of the Mini-Mental Status Assessment Scale (SMSS) is 91%, the specificity is 92%). The Mini-Cog test can be used in individuals with speech disorders, a language barrier. Another advantage of the test is its low time consumption: the KShOPS takes an average of 8 minutes for the doctor, while the Mini-Cog test takes only 3 minutes and can be used at the appointment of a general practitioner.

Cognitive impairment in dyscirculatory encephalopathy should be differentiated from cognitive impairment associated with other causes. In the first place, the causes of potentially reversible cognitive impairment should be excluded, which include:

Therefore, the examination of patients with cognitive impairment should include not only a physical and neurological examination, tests that assess the state of the cardiovascular system (glucose, cholesterol, lipid profile, ECG, blood pressure monitoring, ultrasound duplex scanning), but also the following additional research methods, to identify diseases that cause cognitive impairment:

It is also important to assess the emotional state of patients, in particular, to identify possible depression, which can mask cognitive disorders. Other causes of secondary cognitive impairment in the elderly are normotensive hydrocephalus, post-traumatic encephalopathy, intracranial masses (tumor, subdural hematoma), infectious diseases (Creutzfeldt-Jakob disease, HIV, neurosyphilis). Patients with suspected secondary cognitive impairment require neuroimaging.

Differential diagnosis of the syndrome of cognitive impairment in dyscirculatory encephalopathy is also carried out with Alzheimer's disease and other neurodegenerative diseases. It should be noted that chronic cerebral ischemia is directly a risk factor for the development of Alzheimer's disease. Unlike dyscirculatory encephalopathy, which is characterized by a stepwise development of symptoms, Alzheimer's disease develops gradually and steadily. If neurodynamic functions (attention, speed of thought processes) primarily suffer in dyscirculatory encephalopathy, then Alzheimer's disease is characterized primarily by a decrease in memory, to a greater extent for recent events. As Alzheimer's disease progresses, a decrease in memory for distant events develops, as well as a violation of other cortical functions: visual-spatial orientation (the patient notes that it is difficult for him to navigate in an unfamiliar area), speech (difficulties arise in choosing words, the patient becomes depleted), accounts (it is difficult for the patient to shop in the store), praxis (the patient cannot perform his usual activities). However, unlike patients with dyscirculatory encephalopathy, those suffering from Alzheimer's disease do not have focal neurological symptoms. In the differential diagnosis of dyscirculatory encephalopathy and Alzheimer's disease, the Khachinsky scale can also help (Table 4).

Table 4

Khachinski scale (Hachinski V. et al., 1974)

A score of 7 or more is considered vascular dementia, and a score of 4 or less is considered neurodegenerative.

Movement disorders in dyscirculatory encephalopathy

The development of motor disorders in dyscirculatory encephalopathy has common features with the course of cognitive impairment. The disease debuts with movement disorders, while at the onset of the disease they are manifested by general slowness, impaired standing and walking, which patients often interpret as dizziness. Early markers of movement disorders in dyscirculatory encephalopathy are:
- violations of the initiation of walking;
- "freezing";
- pathological asymmetry of the step.

Do you know that...

...according to biographers, the great composer Franz Joseph Haydn suffered from a progressive disease for the last 10 years of his life, manifested by emotional-affective, cognitive and motor disorders. The disease began when the composer was 67 years old. The composer's contemporaries said that at the age of 67, Haydn lost interest in life and work. At the age of 70, the composer began to develop movement disorders - balance and walking disorders, and on December 26, 1803, he gave his last concert in Vienna. The apraxia that appeared at that time did not allow the composer to play the piano. At the same time, in letters Haydn mentions memory disorders. In 1801, 1803, 1805 and 1806 the composer suffered lacunar strokes. These data suggest that the composer suffered from subcortical vascular encephalopathy (Binswanger's disease).

Pyramidal and pseudobulbar syndromes develop in the later stages of the disease. Like vascular cognitive impairment, movement disorders in dyscirculatory encephalopathy are characterized by a sudden acute onset and a stepwise progression. As a rule, mild or moderate paresis develops, which first regress completely, and then, in later stages, leave behind pyramidal symptoms. Pyramidal syndrome is often asymmetric, predominantly reflex, more pronounced in the legs. Despite the frequent development of pyramidal symptoms, the cause of movement disorders in patients with dyscirculatory encephalopathy is primarily an amyostatic syndrome, clinically resembling Parkinson's syndrome. Amyostatic syndrome is manifested by hypokinesia, difficulty initiating movements, mild muscle rigidity, more pronounced in the legs. The phenomenon of resistance is characteristic. Unlike Parkinson's disease, the administration of levodopa may not improve or even worsen the condition. Amyostatic syndrome occurs as a result of diffuse damage to the brain, primarily corticostriatal and corticospinal connections on both sides.

Another violation of the motor sphere in patients with dyscirculatory encephalopathy, leading to significant maladaptation, are postural disorders. Particular attention should be paid to complaints of elderly patients about falls. In more than 50% of cases, falls are accompanied by injuries, and in 10% of cases these injuries are severe (fractures, subdural hematoma, severe soft tissue or head injuries). Falls account for 16.8% of all causes of death. Falls in the elderly can be caused not only by postural disorders, but also by acute cerebrovascular accident, acute heart failure, cardiac arrhythmias, epileptic seizures, orthostatic hypotension, drop attacks, dizziness, and the use of certain drugs, in particular antihypertensive and psychotropic drugs.

Emotional and affective disorders in patients with dyscirculatory encephalopathy

Along with cognitive impairment, depression is the main maladjusting factor in patients with cerebrovascular pathology. When managing an elderly patient with depression, it must be remembered that depressive disorders can be a direct manifestation of various somatic diseases. "Myxedema dementia" was described as early as the 19th century, making depression the most typical psychiatric symptom of hypothyroidism. Depressive disorders can occur with long-term anemia, rheumatoid arthritis. Depression can be caused by taking certain drugs, primarily interferon-alpha, glucocorticoids, reserpine, non-steroidal anti-inflammatory drugs, cardiac glycosides, tranquilizers, antiepileptic drugs, antiparkinsonian drugs.

Vascular depression was first described by G.S. Alexopoulos et al. The criteria for vascular depression are presented in Table. 5.

Table 5

Criteria for vascular depression

Symptoms of vascular depression appear after 65 years of age, are often the first sign of discirculatory encephalopathy and include:

Many practitioners mistakenly view depression in patients with cerebrovascular disease as a reaction to the presence of a chronic disease. This leads to underdiagnosis and undertreatment of depression in older patients. There are other reasons for the underdiagnosis of depressive disorders in general practice: the predominance of many somatic symptoms and the absence of complaints of mental distress. It is an organic defect that leads to the development of vascular depression, since among the relatives of patients with vascular depression, depressive disorders occur with the same frequency as in the population. Vascular depression can also develop against the background of an already existing primary depressive disorder, while the course of the disease may change.

Unlike patients with post-stroke depression, patients with vascular depression may not have a clinically defined stroke, sometimes in the anamnesis, information can only be obtained about a transient ischemic attack. One study compared the clinical characteristics of post-stroke and vascular depression in 670 patients in a geriatric rehabilitation center who were divided into groups with apparent stroke, those with cerebrovascular risk factors but no stroke, and a group without stroke and no cerebrovascular risk factors. There were no significant differences in the prevalence of depression between the stroke group (36.4%) and the group of patients with cerebrovascular risk factors (35.2%), but the frequency of depression increased significantly in the presence of cerebrovascular risk factors. Another study showed that the more vascular risk factors in older patients, the higher their risk of developing depression (Fig. 3).

Rice. 3. 2-year incidence of depression in older adults with one or more vascular risk factors and no vascular risk factors

From fig. Table 3 shows that the combination of three or more vascular risk factors significantly increases the risk of developing vascular depression.

The clinical picture of vascular depression has a number of features.
1. The severity of depressive disorders, as a rule, does not reach the degree of a major depressive episode according to the DSMIV criteria.
2. In the early stages of the disease, depression in DE has hypochondriacal features and is mainly represented by somatic symptoms (sleep disturbance, appetite disturbance, headaches).
3. The leading symptoms are anhedonia and psychomotor retardation.
4. A large number of cognitive complaints (decreased concentration, slow thinking).
5. The severity of depressive symptoms in DE depends on the stage of the disease and the severity of neurological disorders.
6. 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. These observations also confirm the organic nature of depression in dyscirculatory encephalopathy, probably associated mainly with the phenomenon of fronto-subcortical uncoupling.
7. Often associated with anxiety symptoms.

Depression in dyscirculatory encephalopathy has a close relationship with cognitive disorders. Psychogenic factors play a certain role: the experience of one's growing intellectual and, as a rule, motor incapacity contributes to the formation of depressive disorders, at least in the early stages of dementia, in the absence of a pronounced decrease in criticism. Emotional-affective and cognitive disorders can be the result of dysfunction of the frontal parts of the brain. Thus, in the norm, the connections of the dorsolateral frontal cortex and the striatal complex are involved in the formation of positive emotional reinforcement when the goal of the activity is achieved. As a result of the phenomenon of uncoupling in chronic cerebral ischemia, there is a lack of positive reinforcement, which is a prerequisite for the onset of depression.

Anxiety disorders are also extremely common among older patients, are closely associated with depression and cognitive impairment, and are organic in nature. The high prevalence of anxiety disorders among the elderly is largely due to a wide range of drug-induced anxiety conditions, which increases significantly in the elderly and senile age due to an increase in the consumption of somatotropic drugs, which include:

Anxiety disorders are very common in patients with dyscirculatory encephalopathy. So, if anxiety disorders occur in 38% of patients with Alzheimer's disease, then in 72% of patients with dyscirculatory encephalopathy. Anxiety disorders are observed in 94% of patients with vascular dementia, i.e., they are practically its obligate syndrome. However, like depression and cognitive impairment, anxiety disorders are not always sufficiently diagnosed.

Objective difficulties in detecting and identifying an anxiety disorder and its individual subtypes are associated with the multiplicity and inconsistency of patient complaints. Patient anxiety is unreasonably interpreted as a natural response to a serious illness or as a natural emotional reaction to a physical illness.

Anxiety disorders include two blocks of clinical manifestations: mental and somatic symptoms of anxiety (Table 6).

Table 6

Mental and somatic symptoms of anxiety

A feature of the course of anxiety and depressive disorders in elderly patients with dyscirculatory encephalopathy is the predominance of somatic symptoms over mental ones, which makes it difficult to differentiate between anxiety and depressive disorder and somatic pathology. Often, dizziness, headache, sleep disturbances, fatigue, decreased performance, an indefinite feeling of discomfort are mistakenly interpreted as a manifestation of dyscirculatory encephalopathy directly. However, these symptoms may hide emotional and affective disorders that require correction. The key differential diagnostic criterion for anxiety disorders is the polysystem nature of somatovegetative manifestations. In other words, one patient may simultaneously have complaints from the cardiovascular system (tachycardia, hyper- and hypotension, extrasystole), respiratory system (lack of air, shortness of breath, suffocation, yawning, respiratory rhythm disturbances, intermittent shallow breathing), digestive system (nausea, dry mouth, belching, flatulence, abdominal pain), thermoregulatory systems (chills, hyperthermia, hyperhidrosis), nervous system (paresthesia, dizziness, headache), etc. One study showed that the most common symptoms of anxiety in patients with dyscirculatory encephalopathy are:

For screening diagnosis of anxiety and depression, it is recommended to use the Hospital Anxiety and Depression Scale.

Hospital Anxiety and Depression Scale

For each of the scales of anxiety (T) and depression (D), the sum of points is calculated. A total score above 7 indicates that the patient may have a syndrome of depression and/or anxiety.

Stroke patients may experience post-stroke asthenia - a decrease in internal energy in the absence of other symptoms of anxiety and depression. A number of authors emphasize the organic, vascular genesis of post-stroke asthenia. Thus, asthenia occurs in patients after a stroke more often than in the general population, and in 39% is not associated with depression and other disorders. The significance of post-stroke asthenia is underestimated, however, asthenia is an independent risk factor for both mortality after stroke and disability. Asthenia is equally common among patients with ischemic and hemorrhagic stroke, is significantly more common in minor stroke compared to transient ischemic attack, and significantly increases in recurrent strokes. Asthenia occurs when the structures shown in Fig. 1 are involved in the stroke zone. four.

Rice. four. The alleged topic of post-stroke asthenia. right insula; anterior cingular cortex on the right; frontal lobes

»

Patients with such syndromes complain of fatigue and general weakness, irritability and tearfulness, sleep disturbance. They have apathy and daytime sleepiness, verbosity and difficulty in pronunciation, as well as other visible signs of encephalopathy.

Stages of development of encephalopathy of the brain

In the development of encephalopathy of the brain, 3 stages are divided
I stage of encephalopathy - moderately expressed or compensated, is characterized by cerebrosthenic syndrome. What is manifested by forgetfulness, frequent short-term headaches, emotional status disorders, dizziness. As well as dystonic vegetovascular reactions and various psychopathic reactions. For example, asthenodepressive and hypochondriacal, paranoid and affective type. At this stage, the dominance of cerebrosthenia is noted, which is manifested by some disinhibition, incontinence and slight excitability, as well as a quick change of mood and a very disturbing dream.

II stage of encephalopathy - subcompensation. Where do the first organic changes in the structural units of the brain occur? Outwardly, we see not an increase, but an increase in the stability of the external signs of the first stage. The same headaches with the appearance of persistent tinnitus intensify and psychopathic symptoms become more obvious. Cerebrasthenia changes into its hypodynamic form. In other words, lethargy and depression now prevail, memory loss and loss of sleep. This is because reduced cerebrovascular activity causes small-focal lesions of the brain of all structures and levels of its organization. Hence, signs of a stable neurological syndrome are formed. That is, there are pseudobulbar and amyostatic symptom complexes. And pyramidal insufficiency, namely dysphonia (hearing impairment), dysarthria (malnutrition), reflexes of oral automatism, deviation (violation of the combined work of the lower part of the face and tongue) are fixed. What is manifested by hypomimism and slowness of their actions. In the fingers, there is a slight but steady tremor, discoordination, awkwardness of the simplest movements. Head tremor and photopsia (visual impairment). There are epileptic seizures (called Jacksonian) and anisoreflexia. As well as atypical pathological flexion reflexes.

III stage of encephalopathy - decompensatory. In the morphology of brain tissues, there are severe diffuse changes, there is the formation of perivascular lacunae and granular atrophy of the cortex of both hemispheres. MRI and CG reveal a decrease in the density of individual areas of the white matter of the brain around the lateral ventricles and in the cerebral hemispheres, namely in their subcortical regions, which is called leukoariosis.
Of the visual symptoms, there are worsening of the existing symptoms with a predominance of disturbances in the functioning of one of the areas of the brain. For example, cerebellar disorders or the development of vascular parkinsonism, paresis, or a sharp deterioration in memory. Epileptic seizures become more frequent and lengthen in time. Frequent mental disorders, expressed in the consolidation of signs of deep dementia. The general somatic state is also disturbed. Develop disorders in the blood supply to the brain.

About discirculatory encephalopathy

Dyscirculatory encephalopathy of the hypertensive type most often occurs at a younger age than its atherosclerotic counterpart. And it proceeds more rapidly, especially in those cases when cerebral hypertensive crises are connected to it. Outwardly, we will see an increase in agitation and disinhibition, the presence of euphoria and emotional instability.

Dyscirculatory encephalopathy of the mixed type is characterized by a mixture of symptom complexes of the hypertensive and atherosclerotic types. Another type of dyscirculatory encephalopathy is the venous variety. This is a consequence of a violation of the outflow of venous blood from the cranial cavity. That is, the result of primary disorders in the form of cerebral venous dystonia, craniostasis, pulmonary heart failure and compression of the internal and external cranial veins. What happens due to the development of various local pathological processes. As a result, venous congestion and edema develop in the medulla. Clinically, this is manifested by a relapsing hypertensive syndrome of a chronic type. Namely, the presence of mild, but constant headaches of a pressing type, aggravated by sneezing and coughing, and dizziness, general apathy and lethargy. There are signs of small-focal lesions of the brain as a whole. In severe cases, nausea and vomiting, meningeal signs and congestion in the fundus are noted.

The effectiveness of the treatment of encephalopathy of any origin depends on the speed of initiation of high-quality therapy, the qualifications of the doctor and the patience of the patient, since the treatment of this disease takes a long time, when a person must strictly follow all the recommendations of the attending physician.

The Brain Clinic uses only proven and effective methods for the treatment of cerebral encephalopathy of any origin.

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A patient

How do my and not my genes affect my post-stroke encephalopathy

Doctor

Genes provide individual parameters for the formation of an organism. Both the possibility of recovery and the further prognosis depend on this.

A patient

According to the results of MRI and examination by a neurologist, I was diagnosed with DEP of the II degree. Can you help me?

Doctor

Must watch. Situations with this diagnosis can be different. Everything is very individual.

A patient

Hello, I have a baby, we are a month old. The pregnancy went well and so did the delivery. After the birth, we were taken to the intensive care unit with suspected hypoxia. The doctors explained that the child had deformed in utero and swallowed water, the water turned out to be green. We were in three hospitals, underwent a complete examination of everything, and now we are taking tests for gynecology. Initially, we did not have a sucking swallowing reflex, in one of the hospitals we tried to eat through silicone nozzles, and slowly sucked the bottle. Didn't take the chest. They fed on breast milk. About something went wrong, regurgitation became more frequent. We thundered into intensive care, at first we breathed on our own and stood on a ventilator, and after 3 hours I stopped breathing. Stayed in a coma for 3 weeks. We got out of a coma, began to react to the examination, removed the ventilator, now partially under oxygen. She was transferred to another intensive care unit and treated. Help us please, I'm a mother in despair. We live in Volgograd, our medical history was sent to Moscow. The exact diagnosis was not established.

Doctor

We are sorry, but we do not cater for children under 14 years of age.

A patient

Hello, I am 45 years old, doing an examination, they found on K.T-Moderate phenomena of vascular encephalopathy. I'm getting ready for IVF. Can I carry out this procedure. Thank you. The cost can only be determined after assessing your health status. The therapeutic program is calculated individually and depends on the volume of necessary procedures.
In most cases, several rounds of active therapy are required, which are combined with home treatment. After assessing your health status by our specialist, you will be offered an individual therapeutic program.

A patient

Hello. My friend has been diagnosed with neuroencephalopathy. Has accompanying chronic diseases, HIV, hepatitis C. A friend cannot take care of himself. What to do? How to treat encephalopathy? The doctor said there was no cure for it. What to do, how to be treated? Can it be cured? And the most important thing. How many people live with this disease. Doctor, help. What to do?

Doctor

There is no cure, but the condition can be maintained for a long time. The prognosis can only be given by his attending physician.

Encephalopathy of the brain is a pathological condition in which, due to insufficient supply of oxygen and blood to the brain tissue, the death of its nerve cells occurs. As a result, areas of decay appear, blood stagnation occurs, small local areas of hemorrhages form, and edema of the meninges forms. The disease mainly affects the white and gray matter of the brain.

Encephalopathy is not an independent disease, but occurs against the background of other diseases. She finds herself in different age groups: both in adults and in children. Its course is undulating, chronic. Sometimes the deterioration phase is replaced by a temporary improvement in the condition, but the prognosis of the disease is disappointing: such a disease is incurable, although many people live quite a long life, observing the medication regimen, systematically monitoring pressure indicators and using folk remedies for prevention, which significantly reduces the negative consequences of the disease.

Causes of encephalopathy

The development of the disease is unhurried, however, there are exceptions. For example, with severe damage to the liver and kidneys, as well as with malignant hypertension, the disease progresses suddenly and rapidly. Currently, encephalopathies are classified based on the reasons for their formation:

1. congenital (perinatal) encephalopathy. The causes of its occurrence are genetic metabolic disorders, entanglement of the umbilical cord, infectious diseases suffered during gestation, birth trauma;
2. acquired:

• discirculatory. It occurs with a non-inflammatory lesion of the meninges, causing insufficiency of cerebral blood supply, as well as in the presence of pathologies of the cerebral vessels. It is subdivided into atherosclerotic, venous, hypertensive and mixed encephalopathy;
• progressive vascular leukoencephalopathy. The reason for its appearance is the damage to the vessels of the brain and the violation of their microcirculation, as well as the presence of arterial hypertension;
• toxic encephalopathy. Occurs when the body is exposed to toxic substances. It happens alcoholic, narcotic, "Wernicke" and medication. So, alcoholic - develops with toxic damage to the meninges, the cause of which is the abuse of alcoholic beverages. Wernicke's encephalopathy manifests itself with a deficiency of vitamin B1;
• post-traumatic or "Missed Impact Syndrome" (SPU). The cause of her appearance is a traumatic brain injury. Often found in athletes involved in boxing, karate, football, etc.;
• radial. Occurs when the human brain is exposed to radioactive irradiation;
• progressive multifocal leukoencephalopathy. Occurs with the progression of the JC virus (lymphoma, AIDS, leukemia);
• metabolic. Its appearance is associated with metabolic disorders in the body. There are hyperosmolar, hypoglycemic, hyperglycemic (or diabetic), pancreatic, hepatic, uremic, etc.

Unlike congenital, acquired encephalopathy appears already during a person's lifetime.

Symptoms of encephalopathy

Recognizing the appearance of encephalopathy is problematic. After all, the condition that precedes its development can be characterized by symptoms common to a person, which are of a temporary nature, such as headache, dizziness, tinnitus. At first, this can be mistakenly associated with a change in the weather, excessive physical or mental stress, or severe stress. But, if you do not pay attention to them, you can allow the progression of the disease, since even such symptoms can indicate a deterioration in cerebral circulation.

By its nature, the symptoms of encephalopathy are very diverse. But the most common of its signs, with the exception of the above three, are:

• general weakness;
• increased fatigue;
• tearfulness;
• lack of initiative;
• sudden mood changes;
• depressive state;
• irascibility;
• clouding of consciousness, destruction of memory;
• deterioration of the functions of vision and hearing;
• bad sleep;
• obsessive desire to die.

At a doctor's appointment, such patients often have difficulty pronouncing some words, their speech is verbose, their range of interests is narrowed, and there is a desire to sleep in the daytime. These are the common and most common symptoms of encephalopathy. You should also know that each type of disease has its own symptomatic set.

So, for the development of dyscirculatory encephalopathy, 3 stages are characteristic, characterized by a certain set of signs:

1. compensated stage. Here, the appearance of general symptoms, such as dizziness, memory impairment, headaches, is observed.
2. subcompensated stage. Symptoms are more pronounced and clear:

• persistent headache;
• persistent tinnitus;
• worsening sleep;
• tearfulness;
• a state of depression;
• lethargy;

Progressive vascular leukoencephalopathy can lead to dementia. Symptoms of this encephalopathy:

• headache;
• nausea, vomiting;
• memory impairment;
• dizziness;
• the appearance of phobias;
• psychopathy;
• the occurrence of hallucinations;
• asthenia.

Toxic and, above all, alcoholic encephalopathy is dangerous, the destructive effect of toxic substances on the vessels of the human brain, manifested by the following symptoms:

• prolonged, acutely ongoing neuropsychiatric personality disorder;
• an increase in the volume of the ventricles of the brain;
• overcrowding of the meninges with blood;
• swelling of the brain.

Post-traumatic encephalopathy is dangerous because of the latent course of symptoms that appear long after the injury:

• behavioral disorders;
• disturbed thinking;
• distraction;
• memory loss.

It should be noted that the severity of these symptoms will be the stronger, the more severe and dangerous the injury. Radiation encephalopathy is characterized by 2 types of disorders: asthenic and psychological. Symptoms that characterize progressive multifocal leukoencephalopathy:

• violation of the higher functions of the brain;
• a disorder of consciousness that can lead to dementia;
• epileptic seizures and ataxia are rare.

This leukoencephalopathy is the most "aggressive" of a large number of encephalopathies, its prognosis is disappointing - a fatal outcome.

Symptoms of metabolic encephalopathy:

• confusion;
• distraction;
• drowsiness;
• lethargy;
• speech disorder;
• the occurrence of hallucinations;
• violation of the worldview;
• coma - with the progression of the disease.

Diagnosis of the disease

The successful detection of encephalopathy is facilitated by a comprehensive diagnosis. For this, it is necessary, firstly, to study the data of the patient's anamnesis. And secondly, to test the patient for:

• coordination of movements;
• memory state;
• psychological condition.

These studies can show the presence of changes in the patient's psyche, and if third-party diseases are detected, the doctor will most likely be able to make a preliminary diagnosis.

In parallel with the above studies, the patient is assigned the following tests:

• general blood analysis. The key here will be the indicator of blood lipids. If its value exceeds the norm, then it can be judged that the dyscirculatory encephalopathy of the brain in the patient begins to progress;
• metabolic tests illustrating the numerical indicators of glucose, electrolytes, ammonia, oxygen and lactic acid contained in the blood. Also included in this testing is the numerical measurement of liver enzymes;
• an autoantibody test showing the presence of neuron-destroying antibodies that contribute to the development of dementia;
• blood pressure monitoring;
• a test for the detection of drugs and toxins in the body (with a toxic form);
• measurement of creatinine level - allows you to identify abnormalities in the functioning of the kidneys.

For a more accurate picture of the disease, studies are also carried out using methods such as:

• ultrasound dopplerography of the vessels of the brain and neck. Shows the presence of pathological circulation, helps to identify abscesses;
• ultrasound scanning - to detect plaques or spasms in the walls of blood vessels;
• ultrasound monitoring allows you to identify the cause of the formation of blood clots and the location of emboli;
• computed tomography, MRI - to find tumors and brain anomalies;
• electroencephalography - to detect brain dysfunctions;
• rheoencephalography - to assess the state of blood vessels and cerebral blood flow;
• radiography of the spine (cervical) with functional tests.

To make a diagnosis, not all of the above studies are prescribed by a doctor. Indications for a specific study are dictated by the severity of the disease and certain difficulties in making a diagnosis.

Treatment of encephalopathy

Treatment of encephalopathy is quite long. Its duration depends on the duration and severity of the disease, on the age and presence of parallel current diseases in the patient. During the year, the patient is required to carry out treatment in the amount of 2-3 courses (inpatient and outpatient). Its main areas will be:

• medical treatment. Includes in the appointment of drugs that optimize cerebral circulation and neuroprotectors. This treatment is a course (1–3 months each);
• physiotherapy treatment. Includes acupuncture, ozone therapy, electrophoresis, blood irradiation, treatment with magnetic therapy techniques;
• surgical treatment - is designed to improve the blood flow of the brain, through the implementation of endovascular surgery to expand the affected vessels.

Correction of the standard of living contributes to the successful treatment of the disease, which includes:

• refusal of alcohol (in the alcoholic form), drugs, smoking;
• fat-free and salt-free diet;
• body weight adjustment;
• motor mode.

Treatment of encephalopathy can also be carried out with folk remedies:

• 1 st. l. green onion juice mixed with 2 tbsp. l. honey, taken before meals, minimizes the effects of the disease;
• 1.5 st. l. clover flowers brew 300 ml of boiling water, leave for 2 hours. Consume 3 times a day (30 minutes before meals). This folk remedy is for noise in the head;
• 2 tbsp. l. rosehip per 500 ml of boiling water - aged for several hours. It is an excellent folk remedy in the treatment of encephalopathy.

And although such a powerful disease as encephalopathy is a shock to a person, if you follow the doctor's recommendations in combination with treatment with folk remedies, you can not only minimize the consequences of the disease, reduce the number of side effects, but also improve the prognosis of the disease, as well as quality of life.

Is everything correct in the article from a medical point of view?

Answer only if you have proven medical knowledge

Encephalopathy is a whole group of brain diseases that are non-inflammatory in nature. The disease can manifest itself in children and adults, but at different ages it has its own characteristics. Treatment of encephalopathy includes complex diagnostics, identification of the causes of the disease, courses of drug and manual therapy, and physiotherapy. The general classification divides the pathology into perinatal and acquired.

Symptoms of encephalopathy

Among the main causes of non-inflammatory diseases of the brain are injuries, pathologies of pregnancy and childbirth, atherosclerosis, some diseases of the liver and kidneys, diabetes, ischemia, radiation sickness, changes in the walls of inflammatory vessels, severe intoxication with various substances.

Symptoms characteristic of encephalopathy:

• memory impairment;
• clouding of consciousness;
• pain and noises in the head;
• dizziness;
• depressive state;
• desire to die;
• increased fatigue;
• distraction and irritability;
• physical weakness even after a long rest.

During a medical examination, the patient behaves apathetically, there is confusion in thoughts, difficulty with pronunciation of certain words. Patients may have severe daytime sleepiness and a significant decrease in the range of interests in daily activities.

In the diagnosis of encephalopathy, MRI, radiography (a snapshot of the spine in the cervical region is taken), ultrasound and REG are used. When making a diagnosis, the neurological and psychological status of the patient, the results of his tests, including studies of the cerebrospinal fluid, are necessarily taken into account.

Methods for the treatment of encephalopathy of the brain

Treatment of brain encephalopathy involves symptomatic therapy, exercise therapy, massages, dietary nutrition, and the use of pharmacological drugs. In the treatment of encephalopathy, timely therapy can completely get rid of the disease in 20-30% of cases, which is a very good indicator.

Medical centers and specialized clinics, in addition to the methods listed above, practice the treatment of cerebral encephalopathy with acupuncture, manual therapy, osteopathy, blockade and surgery.

The program and duration of the course is determined by the severity of the manifestations of the disease and the causes that caused it. Also, the set of methods and drugs used is influenced by the prevailing symptoms. The total duration of therapy is 2-3 years, while the patient can take a course on an outpatient basis or in a hospital.