Dyscirculatory encephalopathy is a brain lesion that occurs as a result of a chronic slowly progressive violation of cerebral circulation of various etiologies. Disease is manifested by a combination of cognitive impairment with disorders of the motor and emotional spheres. Depending on the severity of these manifestations, pathology is divided into 3 stages. The list of examinations conducted for dyscirculatory encephalopathy includes ophthalmoscopy, EEG, REG, Echo-EG, ultrasound and duplex scanning of cerebral vessels, MRI of the brain. Dyscirculatory encephalopathy is treated with an individually selected combination of hypotensive, vascular, antiplatelet, neuroprotective and other drugs.
ICD 10
I65 I66 I67.4
General information
Dyscirculatory encephalopathy (DEP) is a widespread disease in neurology. According to statistics, approximately 5-6% of the world’s 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 occupies the first place in frequency of occurrence.
Traditionally, dyscirculatory encephalopathy is considered a disease mainly of the elderly. However, the general trend towards “rejuvenation” of cardiovascular diseases is also noted in relation to DEP. Along with angina pectoris, myocardial infarction, cerebral stroke, disease is increasingly observed in people under the age of 40.
Causes
The development of DEP is based on chronic cerebral ischemia resulting from various vascular pathologies. Approximately 60% of cases of dyscirculatory encephalopathy are caused by atherosclerosis, namely atherosclerotic changes in the walls of cerebral vessels. The second place among the causes of DEP is occupied by chronic arterial hypertension, which is observed in hypertension, chronic glomerulonephritis, polycystic kidney disease, pheochromocytoma, Itsenko-Cushing’s disease, etc. In hypertension, dyscirculatory encephalopathy develops as a result of a spastic state of the cerebral vessels, leading to depletion of cerebral blood flow.
Among the reasons why dyscirculatory encephalopathy appears, there is a pathology of the vertebral arteries that provide up to 30% of cerebral circulation. The clinic of vertebral artery syndrome also includes manifestations in the vertebral-basilar basin of the brain. The causes of insufficient blood flow through the vertebral arteries leading to DEP may be: osteochondrosis of the spine, instability of the cervical spine of a dysplastic nature or after a spinal injury, Kimberly anomaly, malformations of the vertebral artery.
Often, disease occurs against the background of diabetes mellitus, especially in cases when it is not possible to keep blood sugar levels at the upper limit of the norm. Diabetic macroangiopathy leads to the appearance of symptoms of DEP in such cases. Other causal factors include traumatic brain injuries, systemic vasculitis, hereditary angiopathies, arrhythmias, persistent or frequent arterial hypotension.
Pathogenesis
Etiological factors of DEP in one way or another lead to deterioration of cerebral circulation, which means hypoxia and violation of trophic brain cells. As a result, the death of brain cells occurs with the formation of areas of rarefaction of brain tissue (leukoareosis) or multiple small foci of so-called “mute infarcts”.
The most vulnerable in chronic violation of cerebral circulation 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 violation of the connections between the subcortical ganglia and the cerebral cortex, called the “phenomenon of disconnection”. According to modern concepts, it is the “phenomenon of disconnection” that is the main pathogenetic mechanism of the development 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, with correct treatment, can be reversible, and then a persistent neurological defect is gradually formed, often leading to disability of the patient.
It is 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.
Classification
According to the etiology, dyscirculatory encephalopathy is divided into hypertensive, atherosclerotic, venous and mixed. According to the nature of the course, slowly progressive (classical), remitting and rapidly progressive (galloping) dyscirculatory encephalopathy is distinguished.
Depending on the severity of clinical manifestations, dyscirculatory encephalopathy is classified into stages. Stage I dyscirculatory encephalopathy is characterized by subjectivity of most manifestations, mild cognitive impairment and no changes in neurological status. Dyscirculatory encephalopathy of stage II is characterized by obvious cognitive and motor disorders, aggravation of disorders of the emotional sphere. Dyscirculatory encephalopathy of stage III is essentially vascular dementia of varying severity, accompanied by various motor and mental disorders.
Initial symptoms
Characteristic is the subtle and gradual onset of dyscirculatory encephalopathy. In the initial stage of DEP, emotional disorders may come to the fore. Approximately 65% of patients with dyscirculatory encephalopathy have depression. A distinctive feature of vascular depression is that patients are not inclined to complain of low mood and depression. More often, like patients with hypochondriac neurosis, patients with DEP are fixed on various uncomfortable sensations of a somatic nature. Dyscirculatory encephalopathy in such cases proceeds with complaints of back pain, arthralgia, headache, 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 existing somatic pathology. Unlike depressive neurosis, depression with dyscirculatory encephalopathy occurs against the background of a minor traumatic situation or for no reason at all, it does not respond well to medication with antidepressants and psychotherapy.
Dyscirculatory encephalopathy of the initial stage 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 disorders, headaches, absent-mindedness, initial dyscirculatory encephalopathy are similar to neurasthenia. However, for dyscirculatory encephalopathy, a combination of these symptoms with signs of impaired cognitive functions is typical.
In 90% of cases, cognitive impairment is manifested at the very initial stages of the development of this disease. These include: impaired ability to concentrate attention, memory impairment, difficulties in organizing or planning any activity, a decrease in the pace of thinking, fatigue after mental exertion. Typical for DEP is a violation of the reproduction of the received information while preserving the memory of life events.
Motor disorders accompanying the initial stage include mainly 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.
Symptoms
Dyscirculatory encephalopathy of stage II-III is characterized by an increase in cognitive and motor disorders. There is a significant deterioration in memory, lack of attentiveness, intellectual decline, pronounced difficulties if necessary to perform previously feasible mental work. At the same time, patients with DEP themselves are not able to adequately assess their condition, overestimate their performance and intellectual capabilities. Over time, patients with dyscirculatory encephalopathy lose the ability to generalize and develop a program of action, begin to orient themselves poorly in time and place. In the third stage, there are marked disorders of thinking and praxis, personality and behavior disorders. Dementia develops. Patients lose the ability to work, and with deeper violations they lose self-service 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 they do nothing at all. They are indifferent to themselves and the events happening around them.
Motor disorders that are hardly noticeable in the first stage, subsequently become obvious to others. Typical for DEP are slow walking with small steps, accompanied by shuffling due to the fact that the patient cannot lift his foot off the floor. Such a shuffling gait with dyscirculatory encephalopathy is called the “skier’s gait”. It is characteristic that when walking, it is difficult for a patient with DEP to start moving forward and it is also difficult to stop. These manifestations, as well as the gait of a DEP patient itself, have significant similarities with the clinic of Parkinson’s disease, but unlike it are not accompanied by motor disorders in the hands. In this regard, clinical manifestations of dyscirculatory encephalopathy similar to parkinsonism are called by clinicians “parkinsonism of the lower body” or “vascular parkinsonism”.
In stage III of DEP, symptoms of oral automatism, severe speech disorders, tremor, paresis, pseudobulbar syndrome, urinary incontinence are observed. Epileptic seizures may occur. Often, dyscirculatory encephalopathy of stage II-III is accompanied by falls when walking, especially when stopping or turning. Such falls can result in limb fractures, especially when combined with DEP and osteoporosis.
Diagnostics
Of indisputable importance is the early detection of symptoms, which allows timely initiation of vascular therapy of existing disorders of cerebral circulation. For this purpose, a periodic examination by a neurologist is recommended for all patients at risk of developing DEP: hypertensive patients, diabetics and persons with atherosclerotic changes. Moreover, all elderly patients can be attributed to the latter group. Since cognitive disorders, which are accompanied by dyscirculatory encephalopathy of the initial stages, may remain unnoticed by the patient and his family, special diagnostic tests are necessary to detect them. For example, the patient is asked to repeat the words spoken by the doctor, draw a dial with arrows indicating a given time, and then recall the words that he repeated after the doctor.
As part of the diagnosis of dyscirculatory encephalopathy, an ophthalmologist is consulted with ophthalmoscopy and determination of visual fields, EEG, Echo-EG and REG. Ultrasound of the vessels of the head and neck, duplex scanning and MRA of cerebral vessels are important in detecting vascular disorders in DEP. MRI of the brain helps to differentiate dyscirculatory encephalopathy with cerebral pathology of a different genesis: Alzheimer’s disease, multiple encephalomyelitis, Creutzfeldt-Jakob disease. The most reliable sign of dyscirculatory encephalopathy is the detection of foci of “mute” heart attacks, while signs of cerebral atrophy and areas of leukoareosis can also be observed in neurodegenerative diseases.
Diagnostic search for etiological factors that caused the development of dyscirculatory encephalopathy includes consultation with a cardiologist, blood pressure measurement, coagulogram, determination of cholesterol and blood lipoproteins, blood sugar analysis. If necessary, patients with DEP are prescribed an endocrinologist’s consultation, daily blood pressure monitoring, a nephrologist’s consultation, an ECG and daily ECG monitoring for the diagnosis of arrhythmia.
Treatment
Complex etiopathogenetic treatment is the most effective against dyscirculatory encephalopathy. It should be aimed at compensating for the existing causal disease, improving microcirculation and cerebral circulation, as well as protecting nerve cells from hypoxia and ischemia.
Etiotropic therapy of dyscirculatory encephalopathy may include an individual selection of hypotensive and hypoglycemic agents, an antisclerotic diet, etc. If dyscirculatory encephalopathy occurs against the background of high blood cholesterol levels that do not decrease with a diet, then cholesterol-lowering drugs (lovastatin, gemfibrozil, probukol) are included in the treatment of DEP.
The basis of pathogenetic treatment of dyscirculatory encephalopathy consists of medications that improve cerebral hemodynamics and do not lead to the effect of “stealing”. These include calcium channel blockers (nifedipine, flunarizine, nimodipine), phosphodiesterase inhibitors (pentoxifylline, ginkgo biloba), a2–adrenergic receptor antagonists (piribedil, nicergoline). Since dyscirculatory encephalopathy is often accompanied by increased platelet aggregation, patients with DEP are recommended to take antiplatelet agents for almost a lifetime: acetylsalicylic acid or ticlopidine, and if there are contraindications to them (stomach ulcer, LC bleeding, etc.) — dipyridamole.
An important part of the therapy of dyscirculatory encephalopathy consists of drugs with neuroprotective effect that increase the ability of neurons to function in conditions of chronic hypoxia. Of such drugs, patients with dyscirculatory encephalopathy are prescribed pyrrolidone derivatives (piracetam, etc.), GABA derivatives (N-nicotinoyl-gamma-aminobutyric acid, gamma-aminobutyric acid, aminophenyl butyric acid), animal medicines (hemodialysate from the blood of dairy calves, cerebral hydrolysate of pigs, cortexin), membrane stabilizing drugs (choline alfoscerate), cofactors and vitamins.
In cases where dyscirculatory encephalopathy is caused by a narrowing of the lumen of the internal carotid artery, reaching 70%, and is characterized by rapid progression, episodes of PNMC or minor stroke, surgical treatment of DEP is indicated. With stenosis, the operation consists in a carotid endarterectomy, with complete occlusion — in the formation of an extra-intracranial anastomosis. If dyscirculatory encephalopathy is caused by an anomaly of the vertebral artery, then its reconstruction is carried out.
Prognosis and prevention
In most cases, timely adequate and regular treatment can slow the progression of encephalopathy of stage I and even stage II. In some cases, rapid progression is observed, in which each subsequent stage develops 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 occurring against the background of DEP, acute disorders of cerebral circulation (TIA, ischemic or hemorrhagic strokes), poorly controlled hyperglycemia.
The best prevention of the development of dyscirculatory encephalopathy is the correction of existing lipid metabolism disorders, the fight against atherosclerosis, effective hypotensive therapy, adequate selection of hypoglycemic treatment for diabetics.
