Discirculatory encephalopathy (DEP) is a common disease in neurology. According to statistics, about 5-6% of the Russian population suffer from dyscirculatory encephalopathy. Together with acute strokes, malformations and aneurysms of cerebral vessels, DEP belongs to vascular neurological pathology, in the structure of which it takes first place in the frequency of occurrence.
Traditionally, discirculatory encephalopathy is considered a disease mainly of the elderly. However, the general tendency to “rejuvenate” cardiovascular diseases is also observed in relation to DEP. Along with angina pectoris, myocardial infarction, cerebral stroke, discirculatory encephalopathy is increasingly observed in people under the age of 40 years.
Reasons for DEP
Encephalopathy is a disease that develops as a result of dystrophic processes in the brain. Similar phenomena are observed with insufficient nutrition of brain cells, and this applies both to nutrients and oxygen, which is delivered due to the processes of blood circulation and blood supply in the body.
Many diseases, including the chronic course, often cause some barriers that interfere with the normal blood supply to the brain, thereby reducing trophism. Thus, foci with dystrophic lesions are gradually formed, which leads to the development of a severe brain disease.
How to prevent the occurrence of encephalopathy?
This question is of interest to many people, but especially for those who already have a history of diseases that are the cause of cerebral dystrophy. They are at risk, but with all the medical recommendations and regular examination, they have every chance of preventing severe brain damage.
- The causes of brain encephalopathy include the following conditions:
- Hypoxia of any genesis.
- Infectious diseases.
- Chronic alcoholism.
- Metabolic problems.
- Renal and hepatic failure.
- Tumors of the brain.
- Instability of intracranial pressure.
- Vascular pathology
- Acute poisoning and prolonged intake of small doses of toxic substances.
- Ionizing radiation.
- Inadequate, poor nutrition.
All these reasons are basic, but far from the only ones, which once again confirms the wide possibilities of encephalopathy.
Most often, the symptoms of encephalopathy in adults are based on neurological disorders of a different nature, motor disorders are possible, but they are recorded much less often. The main indicators of encephalopathy include the following indicators:
- General malaise, weakness, disability.
- Impaired memory, decreased erudition, belated reactivity to events, lethargy.
- Changing mood, from visible overexcitation, a person can plunge into the deepest depression. More often, patients experience negative emotions – danger, anxiety, suspiciousness, manic symptoms, etc.
- Headaches, dizziness, cramping.
- Over time, tremor or a change in gait, movements may appear.
Severe cases are characterized by serious mental disorders, paralysis, and even coma. Often patients say that they are worried about fever with encephalopathy, others say they have high blood pressure or complain of thirst, frequent urination, etc.
However, these clinical signs do not occur as a result of encephalopathy, they are symptoms of the underlying disease that caused the damage to brain cells.
The result of successful treatment of encephalopathy is timely medical assistance to the patient, and for this it is necessary to conduct a diagnostic examination at the first sign of the disease and report all complaints to the attending physician.
Patients who have a history of chronic diseases, such as hypertension, diabetes mellitus, atherosclerosis, liver problems, should monitor their lifestyle and follow all the doctor’s instructions. Do not expect an intense manifestation of encephalopathy when nothing can be done. You need to visit a doctor regularly and not let the disease prevail over you.
In our multidisciplinary medical center, all the necessary diagnostics are carried out, with the help of which we manage to make the correct diagnosis, differentiating it from all other neurological diseases.
Remember that the first signs of encephalopathy in most cases are blurry and difficult to diagnose, so only a professional can help you. Come, we are waiting for you!
The development of DEP is based on chronic cerebral ischemia that occurs as a result of various vascular pathologies. In about 60% of cases, dyscirculatory encephalopathy is caused by atherosclerosis, namely, atherosclerotic changes in the walls of the cerebral vessels. The second place among the causes of DEP is occupied by chronic arterial hypertension, which is observed with hypertension, chronic glomerulonephritis, polycystic kidney disease, pheochromocytoma, Itsenko-Cushing’s disease, etc. With hypertension, circulatory encephalopathy develops as a result of spastic state of cerebral vessels leading to depletion of the brain.
Among the reasons for which discirculatory encephalopathy appears, the pathology of the vertebral arteries, which provide up to 30% of cerebral circulation, is distinguished. The clinic of the vertebral artery syndrome includes manifestations of discirculatory encephalopathy in the vertebro-basilar brain pool. The causes of insufficient blood flow through the vertebral arteries, leading to DEP, may be: osteochondrosis of the spine, instability of the cervical dysplastic character or after suffering a vertebral injury, Kimmerly anomaly, malformations of the vertebral artery.
Often, discirculatory encephalopathy occurs against the background of diabetes mellitus, especially in cases where it is not possible to maintain blood sugar levels at the level of the upper limit of normal. In such cases, diabetic macroangiopathy leads to the appearance of symptoms of DEP. Other causative factors of discirculatory encephalopathy include traumatic brain injuries, systemic vasculitis, hereditary angiopathies, arrhythmias, persistent or frequent arterial hypotension.
The hypertensive form of encephalopathy is a consequence of advanced hypertension. The reasons may be:
- Sharp hypertension;
- Jade in the acute stage;
- Hypertensive crisis.
The last reason is the most dangerous, since the consequence of a hypertensive crisis can be a violation of the functions of many organs.
2 groups of causes can lead to increased pressure: congenital and acquired. Congenital – vascular structure features available since birth. These may include an aneurysm or a decreased tone of the vascular wall.
Possible acquired causes include:
- Acute jade;
- Hypertensive crisis;
- Excessive alcohol consumption;
- Narcotic intoxication;
- Certain medications;
- Brain disease.
Symptoms of DEP II-III stage
Characteristic is a subtle and gradual onset of discirculatory encephalopathy. In the initial stage of DEP, disorders of the emotional sphere can come to the fore. In approximately 65% of patients with discirculatory encephalopathy, this is depression. A distinctive feature of vascular depression is that patients are not inclined to complain about low mood and depression. More often, like patients with hypochondriac neurosis, patients with DEP are fixed on various uncomfortable somatic sensations. Discirculatory encephalopathy in such cases occurs with complaints of back pain, arthralgia, headaches, ringing or noise in the head, pain in various organs and other manifestations that do not quite fit into the clinic of the patient’s somatic pathology. Unlike depressive neurosis, depression with discirculatory encephalopathy occurs against the background of an insignificant traumatic situation or for no reason at all, it is difficult to drug treatment with antidepressants and psychotherapy.
Initial stage dyscirculatory encephalopathy can be expressed in increased emotional lability: irritability, sudden mood swings, cases of uncontrollable crying for an insignificant reason, attacks of aggressive attitude towards others. Similar manifestations, along with the patient’s complaints of fatigue, sleep disturbances, headaches, distraction, and initial discirculatory encephalopathy are similar to neurasthenia. However, for discirculatory encephalopathy, a combination of these symptoms with signs of impaired cognitive function is typical.
In 90% of cases, cognitive impairment is manifested in the very initial stages of the development of discirculatory encephalopathy. These include: impaired ability to concentrate, memory impairment, difficulties in organizing or planning any activity, slowing the rate of thinking, fatigue after mental stress. Typical for DEP is a violation of the reproduction of the received information while maintaining the memory of life events.
Movement disorders accompanying the initial stage of discirculatory encephalopathy mainly include complaints of dizziness and some instability when walking. Nausea and vomiting may occur, but unlike true vestibular ataxia, they, like dizziness, appear only when walking.
Stage II-III dyscirculatory encephalopathy is characterized by an increase in cognitive and motor impairment. Significant memory impairment, lack of attentiveness, intellectual decline, marked difficulties, if necessary, to perform feasible earlier mental work, are noted. Moreover, patients with DEP themselves are not able to adequately assess their condition, overestimate their performance and intellectual capabilities. Over time, patients with discirculatory encephalopathy lose the ability to generalize and develop a program of action, begin to poorly navigate in time and place. In the third stage of discirculatory encephalopathy, pronounced disturbances in thinking and praxis, personality disorders and behavior are noted. Dementia develops. Patients lose their ability to work, and with deeper violations they lose their self-care skills.
Of the disorders of the emotional sphere, dyscirculatory encephalopathy of later stages is most often accompanied by apathy. There is a loss of interest in previous hobbies, lack of motivation for any occupation. With stage III dyscirculatory encephalopathy, patients may be engaged in some unproductive activity, and more often do nothing at all. They are indifferent to themselves and the events taking place around them.
Movement imperceptible in stage I of discirculatory encephalopathy, subsequently become apparent to others. Slow walking with small steps, accompanied by shuffling due to the fact that the patient is unable to tear off the foot from the floor, is typical for DEP. Such a shuffling gait with discirculatory encephalopathy was called the “skier’s gait.” It is characteristic that when walking, it is difficult for a patient with DEP to start moving forward and also difficult to stop. These manifestations, as well as the gait of the patient with DEP, have a significant similarity with the clinic of Parkinson’s disease, however, in contrast to it, they are not accompanied by motor disorders in the hands. In this regard, clinical manifestations of discirculatory encephalopathy similar to Parkinson’s disease are called by clinicians “lower body parkinsonism” or “vascular parkinsonism”.
In stage III of DEP, symptoms of oral automatism, severe speech disorders, tremors, paresis, pseudobulbar syndrome, urinary incontinence are observed. The appearance of epileptic seizures is possible. Often, stage II-III discirculatory encephalopathy is accompanied by falls when walking, especially when stopping or turning. Such falls can result in fractures of the limbs, especially with a combination of DEP with osteoporosis.
Discirculatory encephalopathy develops in several stages, which have various symptoms:
- At the first stage of the disease, patients are characterized by symptoms of fatigue, weak memory, decreased concentration, lethargy, or irritability. There is asthenic syndrome and neurological symptoms. Treatment of the disease at this stage is most favorable for the patient;
- At the second stage of the disease, there are symptoms of a violation of the first stage, only in a more aggravated form. In addition, there are disorders of the vestibular apparatus, coordination of movements. Patients begin to show mental abnormalities, memory, emotional sphere suffer more;
- Discirculatory encephalopathy of the third stage is characterized by severe neurological dysfunctions, as a rule, patients can not do without outside help, poorly adapt in everyday life, are unable to work. Treatment helps to eliminate only some signs of the disease, but does not eliminate the disease as a whole.
The brain regulates the activity of all organs of the human body: this is the work of muscles, and sensory organs, and thinking, etc. Accordingly, signs of pathology vary depending on the damaged area of the brain.
Acute hypertonic encephalopathy is characterized by symptoms that are usually reversible. Signs of damage will disappear as the swelling passes and patency on the vascular bed is restored.
At the initial stage, the pathological process may not manifest itself in any way – this is typical for cases when a small number of lesions are observed, because they are localized in places that are not strategically important. However, as the foci of necrosis grows, symptoms will persist even after the attack is stopped.
Acute encephalopathy develops at the time of a hypertensive crisis. There is no single level of pressure that could be called critical. For those whose blood pressure rises regularly, an increase in systolic pressure up to 180-190 mm Hg can also be such a level. In patients who are characterized by hypotension, a hypertensive crisis can also occur at a pressure of 140/90. The symptoms of acute hypertensive encephalopathy are as follows:
- Headaches of increasing intensity, which are first localized in the occipital region, then spread throughout the head. Pain is usually bursting.
- Nausea and vomiting.
- Visual impairment, which is associated with edema of the optic disc.
- Increased severity of symptoms when sneezing, coughing.
- Sensory Disorders.
- Hearing loss.
Vegetative-vascular reactions can also be observed: heart pain, tachycardia, redness, or, conversely, pallor of the skin on the face.
If such symptoms occur, a person needs emergency medical intervention. If you do not provide assistance at this stage, then the spread of foci of ischemia will lead to further deterioration.
Acute hypertensive encephalopathy may indicate a stroke.
The clinical picture of the chronic form involves the passage of three stages. For 1 patient complains of distracted attention, impossibility of concentration, rapid fatigability, decreased short-term memory, headaches and dizziness. However, a physical examination does not reveal any changes.
Pronounced neurological symptoms are already observed in the second stage. The patient’s complaints are growing, however, he is not always able to really assess their severity. As a result of this, patients often refuse to follow the recommendations given by the doctor and do not start treatment. As a result, further deterioration and the development of the disease are observed.
Possible manifestations of encephalopathy are a violation of the motivational sphere, initiative, as well as the functions of planning and forecasting. It is impossible not to notice changes in human behavior: there are emotional changes, touchiness, tearfulness.
The help of a psychiatrist may also be required. Existing symptoms may indicate organic brain damage.
At stage 3, new ones may join existing violations. Probably the development of lacunar infarction. Epileptiform seizures, signs of parkinsonism may occur. The cognitive sphere suffers so much that there are signs of dementia.
The etiological factors of DEP in one way or another lead to a deterioration of cerebral circulation, and hence to hypoxia and impaired trophism of brain cells. As a result, brain cells die with the formation of areas of rarefaction of brain tissue (leukoaraiosis) or multiple small foci of the so-called “silent heart attacks”.
The most vulnerable to chronic cerebrovascular accident are the white matter of the deep parts of the brain and subcortical structures. This is due to their location on the border of the vertebro-basilar and carotid basins. Chronic ischemia of the deep parts of the brain leads to a disruption in the connections between the subcortical ganglia and the cerebral cortex, which is called the “disconnect phenomenon”. According to modern concepts, it is the “uncoupling phenomenon” that is the main pathogenetic mechanism for the development of discirculatory encephalopathy and causes its main clinical symptoms: cognitive disorders, disorders of the emotional sphere and motor function. It is characteristic that dyscirculatory encephalopathy at the beginning of its course is manifested by functional disorders, which, if properly treated, can be reversible, and then a persistent neurological defect, which often leads to patient disability, is gradually formed.
It was noted that in about half of cases, dyscirculatory encephalopathy occurs in combination with neurodegenerative processes in the brain. This is due to the commonality of factors leading to the development of both vascular diseases of the brain and degenerative changes in brain tissue.
Methods of diagnosis
The diagnosis of hypertensive encephalopathy requires several steps. Firstly, it is necessary to confirm the presence of hypertension and that it leads to disturbances in the brain.
Then, a neurologist is examined, which identifies the existing symptoms, and if necessary, conducts special tests.
Since some complaints may coincide with signs of other mental illness, a psychiatrist consultation may be required.
In order to exclude diabetes mellitus, renal failure and other diseases that can provoke cerebral disorders, laboratory tests are performed: a general blood test and biochemistry.
To assess the state of the brain, research methods such as MRI and CT can be used. However, these studies are not relevant for the first stage of the disease – at this stage they will not reflect any changes. However, from the second stage, one can observe ischemic lesions with cavities – gaps.
In order to determine the level of cerebrospinal fluid pressure, a spinal puncture is taken from the patient.
By etiology, discirculatory encephalopathy is divided into hypertonic, atherosclerotic, venous and mixed. By the nature of the course, slowly progressing (classical), remitting and rapidly progressing (galloping) discirculatory encephalopathy is distinguished.
Depending on the severity of the clinical manifestations, dyscirculatory encephalopathy is classified into stages. Stage I dyscirculatory encephalopathy is characterized by the subjectivity of most manifestations, mild cognitive impairment, and the absence of changes in neurological status. Stage II dyscirculatory encephalopathy is characterized by clear cognitive and motor impairments, aggravation of disorders of the emotional sphere. Stage III dyscirculatory encephalopathy is essentially vascular dementia of varying severity, accompanied by various motor and mental disorders.
Methods of treatment
Treatment is primarily aimed at lowering the pressure. At the same time, drugs are selected that gradually lower the pressure level, leading it to normal. It should be noted that the opinion that the pressure indicators are at the level of 150/90 mm Hg for older patients are normal – wrong. Even provided that people feel good, such pressure becomes the cause of the development of pathological changes in the body.
Pressure-lowering drugs are selected taking into account individual characteristics. As a rule, specialists opt for long-acting drugs that allow you to maintain normal blood pressure throughout the day. Treatment involves a combination of drugs. ACE inhibitors, diuretics, beta-blockers, calcium antagonists are used. Diuretics remove excess fluid from the body, remove puffiness, and allow you to adjust the salt balance in the body.
In parallel with the need to lower blood pressure, specialists also set a goal to improve blood circulation in the vessels. For this, drugs of disaggregating and thrombolytic action, vitamin complexes are prescribed. For changes affecting the cognitive sphere, neurometabolic stimulants are used – drugs that activate higher brain functions.
Of the drugs, trental, mexidol, aspirin, clopidogrel are usually used. In severe depressive states, emotional and behavioral disorders, sedatives are prescribed.
Often, sodium nitroprusside is used to treat hypertensive encephalopathy, a fast-acting drug that is quickly eliminated from the body. Use this medication is possible only with constant monitoring of the patient’s condition. Cases in which it is not possible to lower the pressure are dangerous and can result in the development of complications and death.
- intracranial bleeding;
- heart attack.
Prognosis and prevention
In most cases, timely, adequate and regular treatment can slow the progression of encephalopathy I and even stage II. In some cases, rapid progression is observed, in which each subsequent stage develops after 2 years from the previous one. An unfavorable prognostic sign is a combination of dyscirculatory encephalopathy with degenerative changes in the brain, as well as hypertensive crises, acute cerebrovascular accidents (TIA, ischemic or hemorrhagic strokes) and poorly controlled hyperglycemia that occur against the background of DEP.
The best prevention of the development of discirculatory encephalopathy is the correction of existing lipid metabolism disorders, the fight against atherosclerosis, effective antihypertensive therapy, an adequate selection of hypoglycemic treatment for diabetics.
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