Chronic cerebrovascular insufficiency (CVI) is the most common manifestation of cerebrovascular pathology. Usually occurs against the background of vegetative-vascular dystonia, atherosclerosis, arterial hypertension and their combination. CSMN can be a consequence of cardiac pathology, vasculitis, blood diseases and other conditions leading to disorders of systemic hemodynamics and microcirculation and, against this background, to periodic and subsequently permanent manifestations of cerebrovascular pathology.

In the pathogenesis of CSMN, morphological changes in the extra- and intracranial sections of the great vessels of the head, a decrease in the compensatory capabilities of collateral circulation, and a breakdown in autoregulation are important. cerebral circulation; disorders of central hemodynamics, changes in the rheological and coagulation properties of blood, disorders of brain metabolism.

Initial manifestations of cerebrovascular insufficiency

Initial manifestations of cerebrovascular insufficiency (CBF) are an early stage of CHF. They are characterized by a predominance of subjective disorders: episodic headaches, a feeling of heaviness, noise in the head, “flickering dots” before the eyes, mild short-term dizziness. There are sleep disturbances, increased fatigue, decreased memory and mental performance. These disorders usually occur after physical or emotional stress, alcohol consumption, or under the influence of adverse meteorological factors. A neurological examination reveals elements of emotional lability, a decrease in the pace and quality of mental activity, signs of vegetative-vascular dysfunction, and sometimes mild symptoms of oral automatism.

Encephalopathy

Clinical manifestations. In contrast to NPCI, dyscirculatory encephalopathy (DE) is characterized by small-focal diffuse changes in the brain caused by cerebral circulatory insufficiency. Clinical manifestations similar to those observed with NPNMK are more persistent. Intellectual and mnestic disorders are more significant (attention decreases, assimilation of new material becomes difficult, the range of interests gradually narrows, memory loss progresses), changes in the emotional-volitional sphere are expressed. Focal neurological symptoms gradually appear in the form of signs of pyramidal insufficiency, pseudobulbar syndrome, parkinsonism syndrome, and coordination disorders.

As the disease progresses, there is a decrease in performance; patients can still perform their usual duties, but a new stereotype is difficult to develop. It becomes difficult to switch from one type of activity to another, mistakes are made more and more often during mental work, thinking slows down, activity and initiative decrease. Patients become faint-hearted, and the lack of criticism of their condition is increasingly noticeable. There is a decrease in the volume of perception, pronounced difficulties in the formation of associative connections, processing new information, and the ability and quality of memorizing and retaining information decreases. Elements of aphasia, agnosia, and apraxia arise. There is a persistent neurological deficit with impaired motor and sensory functions. Subsequently, dementia develops. Against this background, episodes of acute cerebrovascular accidents are possible.

Diagnostics. For the diagnosis of CHMS, it is important to establish the nature of the main pathological process affecting the cardiovascular system (atherosclerosis, arterial hypertension, etc.). In this regard, it is valuable to study the lipid spectrum, blood glucose levels, its coagulation and rheological properties. Important information is provided by data on the condition of the myocardium, aorta and large vessels obtained from ultrasound and echocardiography. ECG, ophthalmoscopy, biomicroscopic examination of the vessels of the conjunctiva are of some importance; if necessary, computer or magnetic resonance imaging, psychological studies, and electroencephalography are used.

Treatment and prevention of chronic cerebrovascular insufficiency

Conservative treatment. In case of CHMS, the organization of a work and rest regime, limitation of psycho-emotional overload, correction of blood pressure, rational nutrition, dosed physical exercise. It is advisable to use angioprotectors (Prodectin, Doxium), antiplatelet agents (aspirin, trental, stugeron, ticlid, etc.), nootropic drugs (piracetam, Semax, Instenon, glycine, Cerebrolysin). According to indications, correction of lipid metabolism (including the use of statins) and antihypertensive therapy (diuretics, calcium channel blockers, ACE inhibitors, and combinations thereof) are carried out. In the presence of psycho-emotional disorders, sedatives, tranquilizers, and in some cases antidepressants are used. The progression of the disease with increasing severity of neurological deficit requires a medical and social examination and the establishment of a disability group.

Surgery. Indications are disturbances in the patency of the extracranial sections of the arteries supplying blood to the brain (aorta, subclavian and innominate, carotid and vertebral arteries).

The most common type of operation is endarterectomy - excision of the atherosclerotic plaque along with the affected intima. At the site where the artery is opened, a suture is placed on its wall. If there is an extensive wall defect, as well as if there is extensive damage to the arterial wall or there is a risk of postoperative stenosis, a wall patch is used superficial vein legs. When the artery is completely occluded, the affected area is resected and replaced with a vein graft or a special prosthesis. When looping, an elongated part of the artery is excised and its ends are sutured. In addition to open operations, to eliminate stenosis, endovasal dilatation of the affected artery is used using special balloon catheters and the introduction of internal prostheses - stents - into the narrowed area of ​​the artery.

To prevent ischemic brain damage due to “switching off” blood flow through the artery during surgery, the functional activity of the brain is monitored (EEG, somatosensory evoked potentials are recorded), and an optimal level of blood pressure is maintained; It is advisable to use barbiturates that protect the brain from hypoxia. If there are signs of cerebral circulatory failure due to compression of the artery during surgery, bypass surgery is used.

NEUROLOGY

NATIONAL GUIDELINES

This brochure contains a section on chnonic cerebrovascular insufficiency (authors V.I. Skvortsova, L.V. Stakhovskaya, V.V. Gudkova, A.V. Alekhin) from the book “Neurology. National leadership" ed. E.I. Guseva, A.N. Konovalova, V.I. Skvortsova, A.B. Gekht (M.: GEOTAR-Media, 2010)

Chronic cerebral circulatory insufficiency is a slowly progressive brain dysfunction resulting from diffuse and/or small-focal damage to brain tissue in conditions of long-term insufficiency of cerebral blood supply.

Synonyms: discirculatory encephalopathy, chronic cerebral ischemia, slowly progressive cerebrovascular accident, chronic ischemic brain disease, cerebrovascular insufficiency, vascular encephalopathy, atherosclerotic encephalopathy, hypertensive encephalopathy, atherosclerotic angioencephalopathy, vascular (atherosclerotic) parkin sonism, vascular (late) epilepsy , vascular dementia.

The most widely used of the above synonyms in domestic neurological practice is the term “dyscirculatory encephalopathy,” which retains its meaning to this day.

Codes according to ICD-10. Cerebrovascular diseases are coded according to ICD-10 in categories I60-I69. The concept of “chronic cerebrovascular insufficiency” is absent in ICD-10. Discirculatory encephalopathy (chronic cerebral circulatory failure) can be coded in rubric I67. Other cerebrovascular diseases: I67.3. Progressive vascular leukoencephalopathy (Binswanger's disease) and I67.8. Other specified cerebrovascular diseases, subsection “Cerebral ischemia (chronic)”. The remaining codes from this section reflect either only the presence of vascular pathology without clinical manifestations(vessel aneurysm without rupture, cerebral atherosclerosis, Moyamoya disease, etc.), or the development acute pathology(hypertensive encephalopathy).

An additional code (F01*) can also be used to indicate the presence of vascular dementia.

Rubrics I65-I66 (according to ICD-10) “Occlusions or stenosis of precerebral (cerebral) arteries that do not lead to cerebral infarction” are used to code patients with an asymptomatic course of this pathology.

EPIDEMIOLOGY

Due to the noted difficulties and discrepancies in the definition of chronic cerebral ischemia, the ambiguity in the interpretation of complaints, the nonspecificity of both clinical manifestations and changes detected by MRI, there are no adequate data on the prevalence of chronic cerebral circulatory failure.

To some extent, it is possible to judge the frequency of chronic forms of cerebrovascular diseases based on epidemiological indicators of the prevalence of stroke, since acute cerebrovascular accident, as a rule, develops against a background prepared by chronic ischemia, and this process continues to increase in the post-stroke period. In Russia, 400,000-450,000 strokes are recorded annually, in Moscow - more than 40,000 (Boiko A.N. et al., 2004). At the same time, O.S. Levin (2006), emphasizing the special significance of cognitive disorders in the diagnosis of discirculatory encephalopathy, suggests focusing on the prevalence of cognitive dysfunctions, assessing the frequency of chronic cerebral circulatory failure. However, these data do not reveal the true picture, since only vascular dementia is recorded (5-22% among the elderly population), without taking into account pre-dementia conditions.

PREVENTION

Due to common risk factors for the development of acute and chronic cerebral ischemia, preventive recommendations and measures do not differ from those reflected in the section “Ischemic stroke” (see above).

SCREENING

To identify chronic cerebrovascular insufficiency, it is advisable to carry out, if not a mass screening examination, then at least an examination of persons with major risk factors (arterial hypertension, atherosclerosis, diabetes mellitus, heart and peripheral vascular diseases). Screening examination should include auscultation of the carotid arteries, ultrasound examination of the great arteries of the head, neuroimaging (MRI) and neuropsychological testing. It is believed that chronic cerebral circulatory failure is present in 80% of patients with stenotic lesions of the main arteries of the head, and stenoses are often asymptomatic up to a certain point, but they are capable of causing hemodynamic restructuring of the arteries in the area located distal to the atherosclerotic stenoses (echeloned atherosclerotic brain damage), leading to the progression of cerebrovascular pathology.

ETIOLOGY

The causes of both acute and chronic cerebrovascular accidents are the same. Among the main etiological factors, atherosclerosis and arterial hypertension are considered; a combination of these 2 conditions is often identified. Other diseases of the cardiovascular system can also lead to chronic cerebrovascular insufficiency, especially those accompanied by signs of chronic heart failure, heart rhythm disturbances (both permanent and paroxysmal forms of arrhythmia), often leading to a drop in systemic hemodynamics. Anomalies in the vessels of the brain, neck, shoulder girdle, and aorta, especially its arch, are also important, which may not appear until an atherosclerotic, hypertensive, or other acquired process develops in these vessels. A major role in the development of chronic cerebrovascular insufficiency in Lately attributed to venous pathology, not only intra-, but also extracranial. Compression of blood vessels, both arterial and venous, can play a certain role in the formation of chronic cerebral ischemia. One should take into account not only the spondylogenic effect, but also compression by altered neighboring structures (muscles, fascia, tumors, aneurysms). Low blood pressure has an adverse effect on cerebral blood flow, especially in older people. This group of patients may develop damage to the small arteries of the head associated with senile arteriosclerosis.

Another cause of chronic cerebral circulatory failure in elderly patients is cerebral amyloidosis - deposition of amyloid in the vessels of the brain, leading to degenerative changes in the walls of blood vessels with possible rupture.

Very often, chronic cerebral circulatory failure is detected in patients with diabetes mellitus; they develop not only micro-, but macroangiopathies various localizations. Other pathological processes can also lead to chronic cerebral vascular insufficiency: rheumatism and other diseases from the group of collagenoses, specific and nonspecific vasculitis, blood diseases, etc. However, in ICD-10 these conditions are quite rightly classified under the headings of the specified nosological forms, which determines the correct treatment tactics.

As a rule, clinically detectable encephalopathy is of mixed etiology. In the presence of the main factors for the development of chronic cerebrovascular insufficiency, the rest of the variety of causes of this pathology can be interpreted as additional causes. Identification of additional factors that significantly aggravate the course of chronic cerebral ischemia is necessary to develop the correct concept of etiopathogenetic and symptomatic treatment.

Causes of chronic cerebrovascular insufficiency

Basic:

Atherosclerosis;

Arterial hypertension. Additional:

Heart disease with signs of chronic circulatory failure;

Heart rhythm disturbances;

Vascular anomalies, hereditary angiopathy;

Venous pathology;

Vascular compression;

Arterial hypotension;

Cerebral amyloidosis;

Diabetes;

Vasculitis;

Blood diseases.

PATHOGENESIS

The above diseases and pathological conditions lead to the development of chronic brain hypoperfusion, that is, to a long-term lack of supply by the brain of the main metabolic substrates (oxygen and glucose) delivered by the blood flow. With the slow progression of brain dysfunction developing in patients with chronic cerebrovascular insufficiency, pathological processes unfold primarily at the level of small cerebral arteries (cerebral microangiopathy). Extensive small artery disease causes diffuse bilateral ischemic damage, mainly in the white matter, and multiple lacunar infarcts in the deep parts of the brain. This leads to disruption normal operation brain and the development of nonspecific clinical manifestations - encephalopathy.

For adequate brain function, a high level of blood supply is required. The brain, whose mass is 2.0-2.5% of body weight, consumes 20% of the blood circulating in the body. The amount of cerebral blood flow in the hemispheres averages 50 ml per 100 g/min, but in the gray matter it is 3-4 times higher than in the white matter, and there is also relative physiological hyperperfusion in the anterior parts of the brain. With age, the amount of cerebral blood flow decreases, and frontal hyperperfusion also disappears, which plays a role in the development and increase of chronic cerebral circulatory failure. Under resting conditions, the brain's oxygen consumption is 4 ml per 100 g/min, which corresponds to 20% of the total oxygen entering the body. Glucose consumption is 30 µmol per 100 g/min.

In the vascular system of the brain there are 3 structural and functional levels:

The main arteries of the head are carotid and vertebral, carrying blood to the brain and regulating the volume of cerebral blood flow;

Superficial and perforating arteries of the brain, which distribute blood to various regions of the brain;

Vessels of the microcirculatory bed, providing metabolic processes.

In atherosclerosis, changes initially develop mainly in the main arteries of the head and arteries of the surface of the brain. In arterial hypertension, the perforating intracerebral arteries that supply the deep parts of the brain are primarily affected. Over time, in both diseases the process spreads to the distal parts arterial system and secondary restructuring of the microvasculature occurs. Clinical manifestations of chronic cerebral circulatory failure, reflecting angioencephalopathy, develop when the process is localized mainly at the level of the microvasculature and in small perforating arteries. In this regard, a measure to prevent the development of chronic cerebrovascular insufficiency and its progression is adequate treatment of the underlying underlying disease or diseases.

Cerebral blood flow depends on perfusion pressure (the difference between systemic blood pressure and venous pressure at the level of the subarachnoid space) and cerebral vascular resistance. Normally, thanks to the autoregulation mechanism, cerebral blood flow remains stable, despite blood pressure fluctuations from 60 to 160 mmHg. In case of damage to cerebral vessels (lipohyalinosis with the development of areactivity vascular wall) cerebral blood flow becomes more dependent on systemic hemodynamics.

With long-term arterial hypertension, a shift in the upper limit of systolic pressure is noted, at which cerebral blood flow still remains stable and autoregulation disorders do not occur for quite a long time. Adequate brain perfusion is maintained by an increase in vascular resistance, which in turn leads to an increase in the load on the heart. It is assumed that an adequate level of cerebral blood flow is possible until pronounced changes in small intracerebral vessels occur with the formation of a lacunar state characteristic of arterial hypertension. Consequently, there is a certain margin of time when timely treatment of arterial hypertension can prevent the formation of irreversible changes in the blood vessels and brain or reduce their severity. If the basis of chronic cerebrovascular insufficiency is only arterial hypertension, then the use of the term “hypertensive encephalopathy” is legitimate. Severe hypertensive crises are always a breakdown of autoregulation with the development of acute hypertensive encephalopathy, which each time aggravates the phenomena of chronic cerebral circulatory failure.

A certain sequence of atherosclerotic vascular lesions is known: first the process is localized in the aorta, then in the coronary vessels of the heart, then in the vessels of the brain and later in the extremities. Atherosclerotic lesions of cerebral vessels are, as a rule, multiple, localized in the extra- and intracranial sections of the carotid and vertebral arteries, as well as in the arteries that form the circle of Willis and its branches.

Numerous studies have shown that hemodynamically significant stenoses develop when the lumen of the main arteries of the head narrows by 70-75%. But cerebral blood flow depends not only on the severity of stenosis, but also on the state of collateral circulation and the ability of cerebral vessels to change their diameter. These hemodynamic reserves of the brain allow asymptomatic stenoses to exist without clinical manifestations. However, even with hemodynamically insignificant stenosis, chronic cerebral circulatory failure will almost certainly develop. The atherosclerotic process in the vessels of the brain is characterized not only by local changes in the form of plaques, but also by hemodynamic restructuring of the arteries in an area localized distal to the stenosis or occlusion.

The structure of the plaques is also of great importance. So-called unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents, most often in the form of transient ischemic attacks. Hemorrhage into such a plaque is accompanied by a rapid increase in its volume with an increase in the degree of stenosis and worsening signs of chronic cerebral circulatory failure.

When the main arteries of the head are damaged, cerebral blood flow becomes very dependent on systemic hemodynamic processes. Such patients are especially sensitive to arterial hypotension, which can lead to a drop in perfusion pressure and an increase in ischemic disorders in the brain.

In recent years, 2 main pathogenetic variants of chronic cerebrovascular insufficiency have been considered. They are based on morphological characteristics- nature of damage and preferential localization. With diffuse bilateral damage to the white matter, leukoencephalopathic, or subcortical Biswanger, variant of discirculatory encephalopathy is distinguished. The second is the lacunar variant with the presence of multiple lacunar foci. However, in practice, mixed options are often encountered. Against the background of diffuse damage to the white matter, multiple small infarcts and cysts are found, in the development of which, in addition to ischemia, repeated episodes of cerebral hypertensive crises can play an important role. In hypertensive angioencephalopathy, lacunae are located in the white matter of the frontal and parietal lobes, putamen, pons, thalamus, and caudate nucleus.

The lacunar variant is most often caused by direct occlusion of small vessels. In the pathogenesis of diffuse damage to the white matter, the leading role is played by repeated episodes of a drop in systemic hemodynamics - arterial hypotension. The cause of a drop in blood pressure may be inadequate antihypertensive therapy, a decrease in cardiac output, for example, with paroxysmal cardiac arrhythmias. Persistent cough, surgical interventions, and orthostatic arterial hypotension due to autonomic-vascular insufficiency are also important. Moreover, even a slight decrease in blood pressure can lead to ischemia in the end zones of the adjacent blood supply. These zones are often clinically “silent” even with the development of infarctions, which leads to the formation of a multi-infarction state.

Under conditions of chronic hypoperfusion - the main pathogenetic link of chronic cerebral circulatory failure - compensation mechanisms can be depleted, the energy supply to the brain becomes insufficient, as a result, functional disorders first develop, and then irreversible morphological damage. In chronic cerebral hypoperfusion, a slowdown in cerebral blood flow, a decrease in oxygen and glucose levels in the blood (energy hunger), oxidative stress, a shift in glucose metabolism towards anaerobic glycolysis, lactic acidosis, hyperosmolarity, capillary stasis, a tendency to thrombus formation, depolarization of cell membranes are detected. , activation of microglia, which begins to synthesize neurotoxins, which, along with other pathophysiological processes, leads to cell death. In patients with cerebral microangiopathy, granular atrophy of the cortical parts is often detected.

A multifocal pathological state of the brain with predominant damage to the deep parts leads to disruption of connections between cortical and subcortical structures and the formation of so-called disconnection syndromes.

A decrease in cerebral blood flow is obligately combined with hypoxia and leads to the development of energy deficiency and oxidative stress - a universal pathological process, one of the main mechanisms of cell damage during cerebral ischemia. The development of oxidative stress is possible under conditions of both oxygen deficiency and excess. Ischemia has a damaging effect on the antioxidant system, leading to a pathological pathway of oxygen utilization - the formation of its active forms as a result of the development of cytotoxic (bioenergetic) hypoxia. The free radicals released mediate cell membrane damage and mitochondrial dysfunction.

Spicy and chronic forms ischemic cerebrovascular accidents can transform into one another. Ischemic stroke, as a rule, develops against an already changed background. Patients are diagnosed with morphofunctional, histochemical, and immunological changes caused by a previous discirculatory process (mainly atherosclerotic or hypertensive angioencephalopathy), the symptoms of which increase significantly in the post-stroke period. The acute ischemic process, in turn, triggers a cascade of reactions, some of which are completed in the acute period, and some persist for an indefinite period and contribute to the emergence of new ones. pathological conditions, leading to an increase in signs of chronic cerebral circulatory failure.

Pathophysiological processes in the post-stroke period are manifested by further damage to the blood-brain barrier, microcirculatory disorders, changes in immunoreactivity, depletion of the antioxidant defense system, progression of endothelial dysfunction, depletion of anticoagulant reserves of the vascular wall, secondary metabolic disorders, and disruption of compensatory mechanisms. Cystic and cystic-gliotic transformation of damaged areas of the brain occurs, separating them from morphologically undamaged tissues. However, at the ultrastructural level, cells with apoptosis-like reactions initiated in the acute period of stroke may persist around necrotic cells. All this leads to worsening chronic cerebral ischemia that occurs before a stroke. The progression of cerebrovascular insufficiency becomes a risk factor for the development of recurrent stroke and vascular cognitive disorders, including dementia.

The post-stroke period is characterized by an increase in the pathology of the cardiovascular system and disturbances not only of cerebral, but also of general hemodynamics.

In the residual period of ischemic stroke, depletion of the anti-aggregation potential of the vascular wall is noted, leading to thrombus formation, an increase in the severity of atherosclerosis and the progression of insufficiency of blood supply to the brain. This process is of particular importance in elderly patients. In this age group, regardless of previous stroke, activation of the blood coagulation system, functional insufficiency of anticoagulant mechanisms, deterioration of the rheological properties of blood, and disorders of systemic and local hemodynamics are noted. The aging process of the nervous, respiratory, and cardiovascular systems leads to disruption of autoregulation of cerebral circulation, as well as to the development or increase of brain hypoxia, which in turn contributes to further damage to the mechanisms of autoregulation.

However, improving cerebral blood flow, eliminating hypoxia, and optimizing metabolism can reduce the severity of dysfunction and help preserve brain tissue. In this regard, timely diagnosis of chronic cerebrovascular insufficiency and adequate treatment are very relevant.

CLINICAL PICTURE

The main clinical manifestations of chronic cerebrovascular insufficiency are disorders in emotional sphere, polymorphic movement disorders, deterioration of memory and learning ability, gradually leading to maladjustment of patients. Clinical features chronic cerebral ischemia - progressive course, stages, syndromicity.

In domestic neurology, for quite a long time, the initial manifestations of cerebral circulatory failure were classified as chronic cerebrovascular insufficiency along with dyscirculatory encephalopathy. Currently, it is considered unfounded to identify such a syndrome as “initial manifestations of insufficiency of blood supply to the brain,” given the non-specificity of the complaints of an asthenic nature and the frequent overdiagnosis of the vascular origin of these manifestations. The presence of headache, dizziness (non-systemic), memory loss, sleep disturbances, noise in the head, ringing in the ears, blurred vision, general weakness, increased fatigue, decreased performance and emotional lability, in addition to chronic cerebral circulatory failure, may indicate other diseases and conditions . In addition, these subjective sensations sometimes simply inform the body of fatigue. When confirming the vascular origin of asthenic syndrome using additional methods examination and identification of focal neurological symptoms establish a diagnosis of “dyscirculatory encephalopathy”.

It should be noted that there is an inverse relationship between the presence of complaints, especially those reflecting the ability to cognitive activity (memory, attention), and the severity of chronic cerebrovascular insufficiency: the more cognitive functions suffer, the fewer complaints. Thus, subjective manifestations in the form of complaints cannot reflect either the severity or the nature of the process.

The core of the clinical picture of discirculatory encephalopathy has recently been recognized as cognitive impairment, detected already in stage I and progressively increasing towards stage III. In parallel, emotional disorders develop (emotional lability, inertia, lack of emotional reaction, loss of interests), various motor disorders (from programming and control to the execution of both complex neokinetic, higher automated, and simple reflex movements).

Stages of dyscirculatory encephalopathy

Discirculatory encephalopathy is usually divided into 3 stages.

At stage I, the above complaints are combined with diffuse microfocal neurological symptoms in the form of anisoreflexia, convergence insufficiency, and mild reflexes of oral automatism. Slight changes in gait are possible (decreased step length, slower walking), decreased stability and uncertainty when performing coordination tests. Emotional and personal disturbances (irritability,

emotional lability, anxious and depressive traits). Already at this stage, mild cognitive disorders of the neurodynamic type appear: slowdown and inertia of intellectual activity, exhaustion, fluctuations in attention, and a decrease in the amount of RAM. Patients cope with neuropsychological tests and work that do not require time tracking. The life activity of patients is not limited.

Stage II is characterized by an increase in neurological symptoms with the possible formation of a mild but dominant syndrome. Individual extrapyramidal disorders, incomplete pseudobulbar syndrome, ataxia, central-type CN dysfunction (proso- and glossoparesis) are identified. Complaints become less pronounced and less significant for the patient. Emotional disorders worsen. Cognitive dysfunction increases to a moderate degree, neurodynamic disorders are complemented by dysregulatory ones (frontal-subcortical syndrome). The ability to plan and control one’s actions deteriorates. The performance of tasks not limited by time is impaired, but the ability to compensate is preserved (recognition and the ability to use hints are preserved). At this stage, signs of decreased professional and social adaptation may appear.

Stage III is manifested by the presence of several neurological syndromes. Severe walking and balance disorders develop with frequent falls, severe cerebellar disorders, parkinsonian syndrome, and urinary incontinence. Criticism of one’s condition decreases, as a result of which the number of complaints decreases. Severe personality and behavioral disorders may appear in the form of disinhibition, explosiveness, psychotic disorders, and apathetic-abulic syndrome. Neurodynamic and dysregulatory cognitive syndromes are accompanied by operational disorders (memory, speech, praxis, thinking, visual-spatial function defects). Cognitive disorders often reach the level of dementia, when maladjustment manifests itself not only in social and professional activities, but also in everyday life. Patients are incapacitated and in some cases gradually lose the ability to care for themselves.

Neurological syndromes in dyscirculatory encephalopathy

Most often, in chronic cerebrovascular insufficiency, vestibulocerebellar, pyramidal, amyostatic, pseudobulbar, psychoorganic syndromes, as well as their combinations, are identified. Sometimes cephalgic syndrome is isolated separately. The basis of all syndromes characteristic of dyscirculatory encephalopathy is the disconnection of connections due to diffuse anoxic-ischemic damage to the white matter.

With vestibulocerebellar (or vestibuloatactic) syndrome subjective complaints of dizziness and instability when walking are combined with nystagmus and coordination disorders. Disorders can be caused by both cerebellar-stem dysfunction due to circulatory insufficiency in the vertebrobasilar system, and disconnection of the frontal-stem tracts with diffuse damage to the white matter cerebral hemispheres brain due to disruption of cerebral blood flow in the internal carotid artery system. Ischemic neuropathy of the vestibulocochlear nerve is also possible. Thus, ataxia in this syndrome can be of 3 types: cerebellar, vestibular, frontal. The latter is also called apraxia of walking, when the patient loses locomotion skills in the absence of paresis, coordination, vestibular disorders, and sensory disorders.

Pyramid syndrome in dyscirculatory encephalopathy it is characterized by high tendon and positive pathological reflexes, often asymmetrical. Paresis is mildly expressed or absent. Their presence indicates a previous stroke.

Parkinsonian syndrome within the framework of dyscirculatory encephalopathy, it is represented by slow movements, hypomimia, mild muscle rigidity, often in the legs, with the phenomenon of “counteraction”, when muscle resistance involuntarily increases when performing passive movements. Tremor is usually absent. Gait disturbances are characterized by a slower walking speed, a decrease in the size of the step (microbasia), a “sliding”, shuffling step, small and rapid trampling in place (before starting to walk and when turning). Difficulties when turning while walking are manifested not only by marking time, but also by turning the whole body with a violation of balance, which can be accompanied by a fall. Falls in these patients occur with phenomena of propulsion, retropulsion, lateropulsion and may also precede walking due to impaired initiation of locomotion (symptom of “stuck legs”). If there is an obstacle in front of the patient (a narrow door, a narrow passage), the center of gravity shifts forward, in the direction of movement, and the legs mark time, which can cause a fall.

The occurrence of vascular parkinsonian syndrome in chronic cerebral circulatory failure is caused by damage not to the subcortical ganglia, but to the corticostriatal and cortical-stem connections, therefore treatment with drugs containing levodopa does not bring significant improvement to this group of patients.

It should be emphasized that in chronic cerebrovascular insufficiency, motor disorders are manifested primarily by walking and balance disorders. The genesis of these disorders is combined, caused by damage to the pyramidal, extrapyramidal and cerebellar systems. Not least important is the disruption of the functioning of complex motor control systems provided by the frontal cortex and its connections with subcortical and brainstem structures. When motor control is damaged, they develop dysbasia and astasia syndromes(subcortical, frontal, frontal-subcortical), otherwise they can be called apraxia of walking and maintaining a vertical posture. These syndromes are accompanied by frequent episodes of sudden falls (see Chapter 23, “Walking Disorders”).

Pseudobulbar syndrome, the morphological basis of which is bilateral damage to the cortical-nuclear pathways, occurs in chronic cerebrovascular insufficiency very often. Its manifestations in discirculatory encephalopathy do not differ from those in other etiologies: dysarthria, dysphagia, dysphonia, episodes of forced crying or laughter and reflexes of oral automatism arise and gradually increase. The pharyngeal and palatal reflexes are preserved and even high; the tongue is without atrophic changes and fibrillary twitching, which makes it possible to differentiate pseudobulbar syndrome from bulbar, caused by damage to the medulla oblongata and/or CNs emerging from it and clinically manifested by the same triad of symptoms (dysarthria, dysphagia, dysphonia).

Psychoorganic (psychopathological) syndrome can manifest itself as emotional and affective disorders (asthenodepressive, anxiety-depressive), cognitive (cognitive) disorders - from mild mnestic and intellectual disorders to various degrees of dementia (see Chapter 26 “Impaired cognitive functions”).

Expressiveness cephalgic syndrome decreases as the disease progresses. Among the mechanisms for the formation of cephalalgia in patients with chronic cerebrovascular insufficiency, one can consider myofascial syndrome against the background of osteochondrosis cervical spine spine, as well as headache Tension (TN) is a variant of psychalgia, often occurring against the background of depression.

DIAGNOSTICS

To diagnose chronic cerebral circulatory failure, it is necessary to establish a connection between clinical manifestations and pathology of cerebral vessels. For the correct interpretation of the identified changes, careful collection of anamnesis with an assessment of the previous course of the disease and dynamic monitoring of patients are very important. One should keep in mind the inverse relationship between the severity of complaints and neurological symptoms and the parallelism of clinical and paraclinical signs during the progression of cerebral vascular insufficiency.

It is advisable to use clinical tests and scales taking into account the most common clinical manifestations of this pathology (assessment of balance and gait, identification of emotional and personality disorders, neuropsychological testing).

Anamnesis

When collecting anamnesis from patients suffering from certain vascular diseases, one should pay attention to the progression of cognitive disorders, emotional and personal changes, focal neurological symptoms with the gradual formation of full-blown syndromes. Identification of these data in patients at risk of developing cerebrovascular accidents or who have already suffered a stroke and transient ischemic attacks, with a high degree of probability allows us to suspect chronic cerebral circulatory failure, especially in the elderly.

From the anamnesis it is important to note the presence coronary disease heart, myocardial infarction, angina pectoris, atherosclerosis of the peripheral arteries of the extremities, arterial hypertension with damage to target organs (heart, kidneys, brain, retina), changes in the valvular apparatus of the heart chambers, cardiac arrhythmias, diabetes mellitus and other diseases specified in the section “Etiology” "

Physical examination

A physical examination can reveal pathology of the cardiovascular system. It is necessary to determine the safety and symmetry of pulsation in the main and peripheral vessels of the limbs and head, as well as the frequency and rhythm of pulse oscillations. Blood pressure should be measured in all 4 limbs. It is imperative to auscultate the heart and abdominal aorta to identify murmurs and heart rhythm disturbances, as well as the main arteries of the head (vessels of the neck), which makes it possible to determine the noise above these vessels, indicating the presence of a stenotic process.

Atherosclerotic stenoses usually develop in the initial segments of the internal carotid artery and in the area of ​​bifurcation of the common carotid artery. This localization of stenoses allows you to hear a systolic murmur during auscultation of the vessels of the neck. If there is noise above the patient's vessel, the patient should be referred for duplex scanning of the main arteries of the head.

Laboratory research

Main stream laboratory research- clarification of the causes of the development of chronic cerebrovascular insufficiency and its pathogenetic mechanisms. Explore clinical analysis blood with reflection

Instrumental studies

The task of instrumental methods is to clarify the level and degree of damage to blood vessels and brain matter, as well as to identify underlying diseases. These problems are solved using repeated ECG recordings, ophthalmoscopy, echocardiography (according to indications), cervical spondylography (if pathology in the vertebrobasilar system is suspected), ultrasound research methods (USDG of the main arteries of the head, duplex and triplex scanning of extra- and intracranial vessels).

Structural assessment of the brain substance and cerebrospinal fluid pathways is carried out using imaging studies (MRI). To identify rare etiological factors, non-invasive angiography is performed, which makes it possible to identify vascular abnormalities, as well as determine the state of collateral circulation.

An important place is given to ultrasound research methods, which make it possible to identify both disturbances in cerebral blood flow and structural changes in the vascular wall that cause stenosis. Stenoses are usually divided into hemodynamically significant and insignificant. If a decrease in perfusion pressure occurs distal to the stenotic process, this indicates a critical or hemodynamically significant narrowing of the vessel, which develops when the lumen of the artery decreases by 70-75%. In the presence of unstable plaques, which are often found with concomitant diabetes mellitus, hemodynamically significant will be the overlap of the vessel lumen by less than 70%. This is due to the fact that with an unstable plaque, the development of arterio-arterial embolisms and hemorrhages into the plaque is possible with an increase in its volume and an increase in the degree of stenosis.

Patients with such plaques, as well as with hemodynamically significant stenoses, should be referred for consultation to an angiosurgeon to resolve the issue of prompt restoration of blood flow through the main arteries of the head.

We should not forget about asymptomatic ischemic disorders of cerebral circulation, detected only when additional examination methods are used in patients without complaints and clinical manifestations. This form of chronic cerebral circulatory failure is characterized by atherosclerotic lesions of the main arteries of the head (with plaques, stenoses), “silent” cerebral infarctions, diffuse or lacunar changes in the white matter of the brain and atrophy of brain tissue in individuals with vascular damage.

It is believed that chronic cerebral circulatory failure exists in 80% of patients with stenotic lesions of the main arteries of the head. Obviously, this indicator can reach an absolute value if an adequate clinical and instrumental examination is carried out to identify signs of chronic cerebral ischemia.

Considering that in chronic cerebrovascular insufficiency, the white matter of the brain is primarily affected, preference is given to MRI rather than CT. MRI in patients with chronic cerebrovascular insufficiency reveals diffuse changes in the white matter, cerebral atrophy, and focal changes in the brain.

MR tomograms visualize the phenomena of periventricular leukoaraiosis (rarefaction, decreased tissue density), reflecting ischemia of the white matter of the brain; internal and external hydrocephalus (enlargement of the ventricles and subarachnoid space), caused by atrophy of brain tissue. Small cysts (lacunae), large cysts, as well as gliosis, can be detected, indicating previous cerebral infarctions, including clinically “silent” ones.

It should be noted that all of the listed signs are not considered specific; It is incorrect to diagnose dyscirculatory encephalopathy only based on imaging examination data.

Differential diagnosis

The above-mentioned complaints characteristic initial stages chronic cerebrovascular insufficiency, can also occur during oncological processes, various somatic diseases, be a reflection of the prodromal period or asthenic “tail” of infectious diseases, be part of the symptom complex of borderline diseases mental disorders(neuroses, psychopathy) or endogenous mental processes (schizophrenia, depression).

Signs of encephalopathy in the form of diffuse multifocal brain damage are also considered nonspecific. Encephalopathies are usually defined by the main etiopathogenetic feature (posthypoxic, posttraumatic, toxic, infectious-allergic, paraneoplastic, dysmetabolic, etc.). Dyscirculatory encephalopathy most often has to be differentiated from dysmetabolic, including degenerative processes.

Dysmetabolic encephalopathy, caused by disorders of brain metabolism, can be either primary, resulting from a congenital or acquired metabolic defect in neurons (leukodystrophy, degenerative processes, etc.), or secondary, when disorders of brain metabolism develop against the background of an extracerebral process. The following variants of secondary metabolic (or dismetabolic) encephalopathy are distinguished: hepatic, renal, respiratory, diabetic, encephalopathy with severe multiple organ failure.

Causes great difficulties differential diagnosis discirculatory encephalopathy with various neurodegenerative diseases, in which, as a rule, cognitive disorders and certain focal neurological manifestations are present. Such diseases include multisystem atrophy, progressive supranuclear palsy, corticobasal degeneration, Parkinson's disease, diffuse Lewy body disease, frontotemporal dementia, and Alzheimer's disease. Differentiation between Alzheimer's disease and discirculatory encephalopathy is far from a simple task: discirculatory encephalopathy often initiates subclinical Alzheimer's disease. In more than 20% of cases, dementia in older people is of a mixed type (vascular-degenerative).

Dyscirculatory encephalopathy must be differentiated from such nosological forms as brain tumor (primary or metastatic), normal pressure hydrocephalus, manifested by ataxia, cognitive disorders, impaired control of pelvic functions, idiopathic dysbasia with impaired gait and stability.

One should keep in mind the presence of pseudodementia (dementia syndrome disappears during treatment of the underlying disease). As a rule, this term is used in relation to patients with severe endogenous depression, when not only mood worsens, but also motor and intellectual activity weakens. It is this fact that gave rise to the inclusion of a time factor in the diagnosis of dementia (symptoms persisting for more than 6 months), since symptoms of depression are relieved by this time. It is likely that this term can be applied to other diseases with reversible cognitive impairment, in particular, secondary dysmetabolic encephalopathy.

TREATMENT

Treatment Goals

The goal of treatment of chronic cerebrovascular insufficiency is stabilization, suspension of the destructive process of cerebral ischemia, slowing down the rate of progression, activation of sanogenetic mechanisms of function compensation, prevention of both primary and recurrent stroke, therapy of major background diseases and accompanying somatic processes.

Treatment of an acutely occurring (or exacerbation of) chronic somatic disease is considered mandatory, since against this background the phenomena of chronic cerebral circulatory failure are significantly increasing. They, in combination with dysmetabolic and hypoxic encephalopathy, begin to dominate the clinical picture, leading to incorrect diagnosis, non-core hospitalization and inadequate treatment.

Indications for hospitalization

Chronic cerebral circulatory failure is not considered an indication for hospitalization if its course is not complicated by the development of a stroke or severe somatic pathology. Moreover, hospitalization of patients with cognitive disorders and removal from their usual environment can only worsen the course of the disease. Treatment of patients with chronic cerebrovascular insufficiency is assigned to the outpatient clinic service; if cerebrovascular disease has reached stage III of discirculatory encephalopathy, home patronage is necessary.

Drug treatment

The choice of medications is determined by the main areas of therapy noted above.

The main ones in the treatment of chronic cerebral circulatory failure are considered to be 2 areas of basic therapy - normalization of brain perfusion by influencing different levels of the cardiovascular system (systemic, regional, microcirculatory) and influencing the platelet component of hemostasis. Both of these directions, optimizing cerebral blood flow, simultaneously perform a neuroprotective function.

Basic etiopathogenetic therapy affecting the main pathological process, implies, first of all, adequate treatment of arterial hypertension and atherosclerosis.

Antihypertensive therapy

A major role in preventing and stabilizing the manifestations of chronic cerebrovascular insufficiency is assigned to maintaining adequate blood pressure. There is information in the literature about the positive effect of normalizing blood pressure on the resumption of an adequate response of the vascular wall to the gas composition of the blood, hyper- and hypocapnia (metabolic regulation of blood vessels), which affects the optimization of cerebral blood flow. Maintain blood pressure at 150-140/80 mm Hg. prevents the increase in mental and motor disorders in patients with chronic cerebrovascular insufficiency. In recent years, it has been shown that antihypertensive drugs have a neuroprotective property, that is, they protect surviving neurons from secondary degenerative damage after a stroke and/or chronic cerebral ischemia. In addition, adequate antihypertensive therapy helps prevent the development of primary and repeated acute cerebrovascular accidents, the background of which is often chronic cerebral circulatory failure.

It is very important to start antihypertensive therapy early, before the development of a pronounced “lacunar state”, which determines the disconnection of cerebral structures and the development of the main neurological syndromes of dyscirculatory encephalopathy. When prescribing antihypertensive therapy, sharp fluctuations in blood pressure should be avoided, since with the development of chronic cerebral circulatory failure, the mechanisms of autoregulation of cerebral blood flow are reduced, which will depend to a greater extent on systemic hemodynamics. In this case, the autoregulation curve will shift towards higher systolic blood pressure, and arterial hypotension (<110 мм рт.ст.) - неблагоприятно влиять на мозговой кровоток. В связи с этим назначаемый препарат должен адекватно контролировать системное давление.

Currently, a large number of antihypertensive drugs from different pharmacological groups have been developed and introduced into clinical practice to provide blood pressure control. However, the data obtained on the important role of the renin-angiotensin-aldosterone system in the development of cardiovascular diseases, as well as on the connection between the content of angiotensin II in the central nervous system and the volume of ischemia of brain tissue, allow today in the treatment of arterial hypertension in patients with cerebrovascular pathology to give preference to drugs that affect renin-angiotensin-aldosterone system. These include 2 pharmacological groups - angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists.

Both angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists have not only antihypertensive, but also organoprotective effects, protecting all target organs affected by arterial hypertension, including the brain. The PROGRESS (prescription of the angiotensin-converting enzyme inhibitor perindopril), MOSES and OSCAR (prescription of the angiotensin II receptor antagonist eprosartan) studies have proven the cerebroprotective role of antihypertensive therapy. The improvement in cognitive functions while taking these drugs should be especially emphasized, given that cognitive disorders are present to one degree or another in all patients with chronic cerebrovascular insufficiency and are the dominant and most dramatic disabling factors in severe stages of dyscirculatory encephalopathy.

According to the literature, it is possible that angiotensin II receptor antagonists influence degenerative processes occurring in the brain, in particular in Alzheimer’s disease, which significantly expands the neuroprotective role of these drugs. It is known that recently most types of dementia, especially in old age, are considered as combined vascular-degenerative cognitive disorders. It should also be noted the putative antidepressant effect of angiotensin II receptor antagonists, which is of great importance in the treatment of patients with chronic cerebrovascular insufficiency, who often develop affective disorders.

In addition, it is very important that angiotensin-converting enzyme inhibitors are indicated for patients with signs of heart failure, nephrotic complications of diabetes mellitus, and angiotensin II receptor antagonists can have angioprotective, cardioprotective, and also renoprotective effects.

The antihypertensive effectiveness of these groups of drugs increases when they are combined with other antihypertensive drugs, often with diuretics (hydrochlorothiazide, indapamide). The addition of diuretics is especially indicated in the treatment of elderly women.

Lipid-lowering therapy (treatment of atherosclerosis)

For patients with atherosclerotic lesions of cerebral vessels and dyslipidemia, in addition to a diet with limited animals and the predominant use of vegetable fats, it is advisable to prescribe lipid-lowering drugs, in particular statins (atorvastatin, simvastatin, etc.), which have a therapeutic and preventive effect. Taking these drugs in the early stages of dyscirculatory encephalopathy is more effective. Their ability to reduce cholesterol content, improve endothelial function, reduce blood viscosity, stop the progression of the atherosclerotic process in the main arteries of the head and coronary vessels of the heart, have an antioxidant effect, and slow down the accumulation of β-amyloid in the brain has been shown.

Antiplatelet therapy

It is known that ischemic disorders are accompanied by activation of the platelet-vascular component of hemostasis, which determines the mandatory prescription of antiplatelet drugs in the treatment of chronic cerebrovascular insufficiency. Currently, the effectiveness of acetylsalicylic acid is most well studied and proven. Enteric-soluble forms are used predominantly at a dose of 75-100 mg (1 mg/kg) daily. If necessary, other antiplatelet agents (dipyridamole, clopidogrel, ticlopidine) are added to treatment. Prescribing drugs in this group also has a preventive effect: it reduces the risk of developing myocardial infarction, ischemic stroke, and peripheral vascular thrombosis by 20-25%.

A number of studies have shown that only basic therapy (antihypertensive, antiplatelet) is not always sufficient to prevent the progression of vascular encephalopathy. In this regard, in addition to the constant intake of the above groups of drugs, patients are prescribed a course of treatment with agents that have antioxidant, metabolic, nootropic, and vasoactive effects.

Antioxidant therapy

As chronic cerebral circulatory failure progresses, there is an increasing decrease in protective sanogenetic mechanisms, including the antioxidant properties of plasma. In this regard, the use of antioxidants such as vitamin E, ascorbic acid, ethylmethylhydroxypyridine succinate, Actovegin* is considered pathogenetically justified. Ethylmethylhydroxypyridine succinate can be used in tablet form for chronic cerebral ischemia. The initial dose is 125 mg (one tablet) 2 times a day with a gradual increase in dose to 5-10 mg/kg per day (maximum daily dose - 600-800 mg). The drug is used for 4-6 weeks, the dose is reduced gradually over 2-3 days.

Use of combination drugs

Considering the variety of pathogenetic mechanisms underlying chronic cerebral circulatory failure, in addition to the above-mentioned basic therapy, patients are prescribed drugs that normalize the rheological properties of blood, microcirculation, venous outflow, and have antioxidant, angio-protective, neuroprotective and neurotrophic effects. To exclude polypharmacy, preference is given to drugs that have a combined effect, a balanced combination of medicinal substances in which eliminates the possibility of drug incompatibility. Currently, quite a large number of such drugs have been developed.

Below are the most common drugs with a combined effect, their doses and frequency of use:

Ginkgo biloba leaf extract (40-80 mg 3 times a day);

Vinpocetine (Cavinton) (5-10 mg 3 times a day);

Dihydroergocriptine + caffeine (4 mg 2 times a day);

Hexobendine + etamivan + etophylline (1 tablet contains 20 mg hexobendine, 50 mg etamivan, 60 mg etophylline) or 1 tablet forte, which contains 2 times more content of the first 2 drugs (taken 3 times a day);

Piracetam + cinnarizine (400 mg piracetam and 25 mg cinnarizine, 1-2 tablets 3 times a day);

Vinpocetine + piracetam (5 mg of vinpocetine and 400 mg of piracetam, one capsule 3 times a day);

Pentoxifylline (100 mg 3 times a day or 400 mg 1 to 3 times a day);

Trimethylhydrazinium propionate (500-1000 mg 1 time per day);

Nicergoline (5-10 mg 3 times a day).

These drugs are prescribed in courses of 2-3 months, 2 times a year, alternating them for individual selection.

The effectiveness of most drugs that affect blood flow and brain metabolism is manifested in patients with early, that is, stages I and II dyscirculatory encephalopathy. Their use in more severe stages of chronic cerebrovascular insufficiency (in stage III discirculatory encephalopathy) can give a positive effect, but it is much weaker.

Despite the fact that they all have the above-described set of properties, one can focus on some selectivity of their action, which may be important in the choice of drug, taking into account the identified clinical manifestations.

Ginkgo biloba leaf extract accelerates vestibular compensation processes, improves short-term memory, spatial orientation, eliminates behavioral disorders, and also has a moderate antidepressant effect.

Dihydroergocryptine + caffeine acts primarily at the level of microcirculation, improving blood flow, tissue trophism and their resistance to hypoxia and ischemia. The drug helps improve vision, hearing, normalize peripheral (arterial and venous) circulation, reduce dizziness and tinnitus.

Hexobendine + etamivan + etophylline improves concentration, integrative brain activity, normalizes psychomotor and cognitive functions, including memory, thinking and performance. It is advisable to slowly increase the dose of this drug, especially in elderly patients: treatment begins with 1/2 tablet per day, increasing the dose by 1/2 tablet every 2 days, bringing it to 1 tablet 3 times a day. The drug is contraindicated in epileptic syndrome and increased intracranial pressure.

Metabolic therapy

Currently, there are a large number of drugs that can influence the metabolism of neurons. These are drugs of both animal and chemical origin that have a neurotrophic effect, chemical analogues of endogenous biologically active substances, agents affecting cerebral neurotransmitter systems, nootropics, etc.

Such drugs as solcoseryl* and cerebrolysin* and polypeptides of the cerebral cortex of livestock (polypeptide cocktails of animal origin) have a neurotrophic effect. It must be taken into account that in order to improve memory and attention in patients with cognitive disorders caused by cerebral vascular pathology, fairly large doses should be administered:

Cerebrolysin * - 10-30 ml intravenously, 20-30 infusions per course;

Livestock cerebral cortex polypeptides (cortexin*) - 10 mg intramuscularly, 10-30 injections per course.

Solcoseryl(Sokoseryl) is a deproteinized hemodialysate that contains a wide range of low-molecular components of cell mass and blood serum of dairy calves. Solcoseryl contains factors that, under hypoxic conditions, help improve metabolism in tissues, accelerate reparative processes and rehabilitation periods. Solcoseryl is a universal drug that has a complex effect on the body: neuroprotective, antioxidant, activates neuronal metabolism, improves microcirculation and has an endotheliotropic effect.

At the molecular level, the following mechanisms of action of the drug are distinguished. Solcoseryl increases the utilization of oxygen by tissues under hypoxic conditions, enhances the transport of glucose into the cell, increases the synthesis of intracellular ATP, and increases the proportion of aerobic glycolysis. According to experimental data, Solcoseryl improves cerebral blood flow, leads to a decrease in blood viscosity by increasing the deformability of erythrocytes, which increases microcirculation.

The above mechanisms of action of the drug increase the functional potential of the tissue under ischemic conditions, which leads to less damage to brain tissue during ischemia.

The clinical effectiveness of Solcoseryl in patients with cerebral pathology was confirmed by double-blind, placebo-controlled studies (1, 2).

Indications: ischemic, hemorrhagic stroke, traumatic brain injury, dyscirculatory encephalopathy, diabetic neuropathy and other neurological complications of diabetes, peripheral vascular diseases, peripheral trophic disorders.

Dosage: 10-20 ml intravenously drip, 5-10 ml intravenously slowly (in saline), 2-4 ml intramuscularly (total course duration - up to 4-8 weeks), topically (in the form of ointment or gel) - for trophic disorders, damage to the skin and mucous membranes.

Bibliography

1. Ito K. et al. A double-blind study of the clinical effects of solcoseryl infusion on cerebral arteriosclerosis // Kiso to Rinsho. - 1974. - N 8(13). - P. 4265-4287.
2. Mihara H. et al. A double-blind evaluation of pharmaceutical effect of solcoseryl on cerebrovascular accidents // Kiso to Rinsho. - 1978. - N 12(2). - P. 311-343.

Domestic drugs glycine and Semax* are chemical analogues of endogenous biologically active substances. In addition to their main effect (improving metabolism), glycine can produce a slight sedative effect, and Semax * can produce an stimulating effect, which should be taken into account when choosing a drug for a particular patient. Glycine is a non-essential amino acid that affects the glutamergic system. The drug is prescribed at a dose of 200 mg (2 tablets) 3 times a day, the course is 2-3 months. Semax* is a synthetic analogue of adrenocorticotropic hormone, its 0.1% solution is administered 2-3 drops into each nasal passage 3 times a day, the course is 1-2 weeks.

The concept of “nootropic drugs” combines various drugs that can cause an improvement in the integrative activity of the brain and have a positive effect on memory and learning processes. Piracetam, one of the main representatives of this group, has the noted effects only when given in large doses (12-36 g / day). It should be borne in mind that the use of such doses by elderly people may be accompanied by psychomotor agitation, irritability, sleep disturbance, as well as provoke an exacerbation of coronary insufficiency and the development of epileptic paroxysm.

Symptomatic therapy

With the development of vascular or mixed dementia syndrome, background therapy is enhanced with agents that affect the exchange of the main neurotransmitter systems of the brain (cholinergic, glutamatergic, dopaminergic). Cholinesterase inhibitors are used - galantamine 8-24 mg/day, rivastigmine 6-12 mg/day, glutamate NMDA receptor modulators (memantine 10-30 mg/day), D2/D3 dopamine receptor agonist with a 2 -noradrenergic activity piribedil 50-100 mg/day. The last of these drugs is more effective in the early stages of dyscirculatory encephalopathy. It is important that, along with improving cognitive functions, all of the above drugs are able to slow down the development of affective disorders, which may be resistant to traditional antidepressants, and also reduce the severity of behavioral disorders. To achieve the effect, the drugs should be taken for at least 3 months. You can combine these means, replace one with another. If the result is positive, taking an effective drug or drugs for a long time is indicated.

Dizziness significantly impairs the quality of life of patients. Some of the above drugs, such as vinpocetine, dihydroergocriptine + caffeine, ginkgo biloba leaf extract, can eliminate or reduce the severity of vertigo. If they are ineffective, otoneurologists recommend taking betahistine 8-16 mg 3 times a day for 2 weeks. The drug, along with reducing the duration and intensity of dizziness, reduces the severity of autonomic disorders and noise, and also improves motor coordination and balance.

Special treatment may be required if affective disorders (neurotic, anxiety, depressive) occur in patients. In such situations, antidepressants that do not have an anticholinergic effect (amitriptyline and its analogues), as well as intermittent courses of sedatives or small doses of benzodiazepines, are used.

It should be noted that the division of treatment into groups according to the main pathogenetic mechanism of the drug is very arbitrary. For broader acquaintance with a specific pharmacological agent, there are specialized reference books; the task of this guide is to determine directions in treatment.

Surgery

In case of occlusive-stenotic lesions of the main arteries of the head, it is advisable to raise the question of surgical elimination of the obstruction of vascular patency. Reconstructive operations are often performed on the internal carotid arteries. This is carotid endarterectomy, stenting of the carotid arteries. The indication for their implementation is the presence of hemodynamically significant stenosis (overlapping more than 70% of the vessel diameter) or a loose atherosclerotic plaque, from which microthrombi can break off, causing thromboembolism of small vessels of the brain.

Approximate periods of incapacity for work

The disability of patients depends on the stage of dyscirculatory encephalopathy.

At stage I, patients are able to work. If temporary disability occurs, it is usually due to intercurrent illnesses.

Stage II of dyscirculatory encephalopathy corresponds to disability group II-III. Nevertheless, many patients continue to work, their temporary disability can be caused by both a concomitant disease and an increase in the phenomena of chronic cerebral circulatory failure (the process often occurs in stages).

Patients with stage III dyscirculatory encephalopathy are disabled (this stage corresponds to disability group I-II).

Further management

Patients with chronic cerebrovascular insufficiency require constant background therapy. The basis of this treatment is blood pressure correcting drugs and antiplatelet drugs. If necessary, substances are prescribed that eliminate other risk factors for the development and progression of chronic cerebral ischemia.

Non-drug methods of influence are also of great importance. These include adequate intellectual and physical activity, feasible participation in social life. For frontal dysbasia with disorders of gait initiation, freezing, and the threat of falls, special gymnastics are effective. Stabilometric training based on the principle of biofeedback helps reduce ataxia, dizziness, and postural instability. For affective disorders, rational psychotherapy is used.

Patient Information

Patients should follow the doctor’s recommendations for both continuous and course use of medications, control blood pressure and body weight, stop smoking, follow a low-calorie diet, and eat foods rich in vitamins (see Chapter 13 “Lifestyle Modification”).

It is necessary to carry out health-improving exercises, use special gymnastic exercises aimed at maintaining the functions of the musculoskeletal system (spine, joints), and take walks.

It is recommended to use compensatory techniques to eliminate memory disorders, write down the necessary information, and draw up a daily plan. Intellectual activity should be maintained (reading, memorizing poems, talking on the phone with friends and family, watching television, listening to music or radio programs of interest).

It is necessary to perform feasible household duties, try to lead an independent lifestyle for as long as possible, maintain physical activity while taking precautions to avoid falling, and, if necessary, use additional means of support.

It should be remembered that in older people, after a fall, the severity of cognitive impairment increases significantly, reaching the severity of dementia. To prevent falls, it is necessary to eliminate risk factors for their occurrence:

Remove carpets that could cause the patient to trip;
use comfortable non-slip shoes;
if necessary, rearrange the furniture;
attach handrails and special handles, especially in the toilet and bathroom;
Showers should be taken in a sitting position.

Forecast

The prognosis depends on the stage of dyscirculatory encephalopathy. Using these same stages, it is possible to evaluate the rate of disease progression and the effectiveness of treatment. The main unfavorable factors are severe cognitive disorders, often paralleled by an increase in episodes of falls and the risk of injury, both TBI and limb fractures (primarily the femoral neck), which create additional medical and social problems.

Four (4) degrees of cerebral vascular insufficiency (Pokrovsky A.V., Kiyashko V.A., RMAPO, A.V. Vishnevsky Institute of Surgery, Moscow):

Ι degree– asymptomatic cerebral vascular insufficiency;

Asymptomatic course is those conditions when the patient completely lacks any complaints indicating cerebral circulatory insufficiency, but upon physical examination (auscultation) or according to instrumental diagnostic methods there are indications of varying degrees of damage to the arteries supplying the brain.

ΙΙ degree– transient cerebrovascular accidents (TCI) or transient ischemic attacks (TIA) lasting no more than a day;

Transient cerebrovascular accidents - this group of patients is often encountered in the practice of a neurologist, since the patient develops clear neurological symptoms indicating ischemia of the carotid or vertebral basin. The frequency of episodes ranges from 10–20 times a day to 1–2 times a month and even less frequently. Paroxysms are provoked by physical activity and changes in body position. In addition to purely neurological symptoms, patients may also experience visual impairment. Transient blindness in one eye, that is, “amaurosis fugax,” is one of the leading symptoms of carotid artery stenosis, but, unfortunately, doctors (including ophthalmologists) are poorly aware of this.

ΙΙΙ degree– chronic brain failure – discirculatory encephalopathy;

Disculatory encephalopathy - characterized by constant headaches, a sharp decrease in performance, and sleep disorders. A neurological examination reveals pseudobulbar, pyramidal and extrapyramidal symptoms of varying severity.

ΙV degree– ischemic stroke and its consequences (circulatory disorders can occur in various vascular areas of the brain: carotid and vertebral).

Ischemic stroke in the carotid region develops much more often than in the vertebral region. It should be especially noted that in almost 70% of cases, a stroke in the carotid region develops suddenly, without any previous ischemic attacks. In case of stroke, symptoms persist for more than 24 hours. The clinical picture of severe residual symptoms of stroke is observed in patients with occlusion of the internal carotid artery and continued thrombosis from the bifurcation of the common carotid artery into its intracranial parts.

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Cerebrovascular disease is a frequently diagnosed disease that doctors face today. It has been scientifically proven that acute disease is one of the common causes of death in many countries.

Symptoms of the pathological condition are expressed in causeless headaches, nausea, dizziness and other unpleasant manifestations. It is worth visiting a specialist immediately, because the earlier therapy is started, the lower the risk of negative consequences.

Acute cerebral circulatory failure can lead to death

The brain is supplied with blood through 2 paired main arteries of the head: the internal carotid and vertebral. Approximately 2/3 of the plasma fills the brain through internal arteries and 1/3 through vertebral arteries. The former in their complex form the basis of the carotid system, and the latter – the vertebrobasilar system.

The internal arteries are branches of the common carotid artery, enter the cranial region through the internal opening of the carotid canal of the temple bone, penetrate the cavernous sinus, forming an S-shaped bend. This area of ​​the internal artery is called the siphon or pars cavernosum.

Next, the internal artery passes through the dura mater of the brain, where it divides into several branches. One of them is the ophthalmic one, passing into the orbit along with the optic nerve. Other branches are the posterior connective and anterior villous.

Lateral to the optic junction, the internal artery contains a division into 2 other branches - the anterior and middle. The first supplies blood to the anterior frontal lobe and the inner surface of the hemisphere, the second – to the frontal cortex, parietal and temporal lobes, subcortical nuclei, and internal capsule.

Causes of pathology

Chronic high blood pressure may cause cerebrovascular insufficiency

The scientific term "cerebrovascular accident" refers to difficulties in the flow of blood in the cavities of blood vessels. If the arteries and veins that are responsible for blood flow are affected, vascular insufficiency occurs.

Among the vascular pathological conditions that cause disruption in the blood flow of the brain, experts identify the following:

• thrombus neoplasm
• loops, bend
• narrowing
• protrusion of the artery wall when it thins or stretches

The pathological condition of the vessel is diagnosed when the blood entering the brain has a volume less than acceptable. In most cases, failure in this process develops as a consequence of sclerotic vascular lesions. The type of neoplasm does not allow blood to pass normally through the internal cavity of the vessel, thereby causing such a pathology.

If therapy is not started in a timely manner, the plaque-like formation can constantly accumulate platelets and increase in size, subsequently contributing to the formation of a blood clot. The latter will either block the vessel, thereby disrupting the blood flow in the vessel, or it may break off and enter the brain artery with the blood. In this section, a blockage of the vessel will occur, contributing to the occurrence of acute circulatory disorders, that is.

Another source of brain pathology is chronic. People who suffer from this pathology must follow all doctor's instructions. At the same time, the possibility of developing the disease is reduced significantly.

Blood flow is also hampered due to the development of osteochondrosis of the neck. This compresses the artery that supplies the brain. Therefore, it is important to treat osteochondrosis as soon as possible in order to avoid both pain and negative complications.

Chronic fatigue does not have the best effect on the condition of many organs and systems, including blood vessels and the human brain.

Another source of the disease is head injury: a concussion, a bruise, which causes compression of the brain centers, and thereby a disruption in blood flow.

Symptoms accompanying the pathology

Dizziness may be one of the symptoms of cerebrovascular insufficiency

At each stage of the pathological condition of blood vessels, a specific clinical picture is observed. Common manifestations of circulatory disorders are:

• constant headaches
• nausea and vomiting syndrome
• memory loss (partial)
• malfunction of the visual and auditory systems
• impaired motor coordination

Additional symptoms of pathology include:

• insensibility of one half of the body (opposite to the source of the disease)
• weakness in arms and legs
• failure of speech function
• hallucinations of vision
• general malaise
• tinnitus
• increased sweating

Considering that with this pathological condition of the cerebral vessels, speech impairment occurs and weakness in the limbs increases, this pathology can be confused with a stroke. A characteristic difference is the disappearance of acute symptoms with NMC within a day, which cannot be said about a stroke.

Experts divide all manifestations of pathology into stages. At the initial stage of the disease, the following symptoms occur:

• headache
• general malaise even after minor exertion
• increased irritability
• absent-mindedness
• forgetfulness (partial)

As the pathology develops, namely at stage 2, other clinical manifestations join:

• motor function is impaired
• gait becomes shaky and unsteady
• concentration is impaired
• mood changes often
• aggression arises
• dizziness occurs
• performance deteriorates

At stage 3 of the pathology, the following clinical manifestations occur:

• tremors of hands and feet
• failure in memory and speech processes

At the last stage of pathology, a person almost completely degrades and is no longer able to care for himself. At this time, the development of irreversible pathological phenomena occurs, which can no longer be corrected by generally accepted methods of therapy. The neurons of the brain simply die off, and the person faces a quick death outcome.

Diagnostics

To diagnose cerebrovascular insufficiency, ultrasound of the vessels of the neck and head is used

In order not to doubt the correct diagnosis, the specialist carries out certain diagnostic measures.

Using these, you can determine the exact location of the lesion, the predisposing factor and the degree of manifestation of symptoms.

Differential analysis is carried out to identify or refute the presence of another pathology that occurs with similar symptoms.

Standard methods for identifying disorders in cerebral circulation include:

1. Neuroimaging
2. cervical and head region
3. Daily blood pressure monitoring
4. X-ray of the vertebral bodies of the neck
5. Determination of plasma lipid volume
6. Determination of plasma sugar levels

In addition, pathological conditions in the vessels that the person previously suffered from (atherosclerotic lesions or others) are taken into account. The doctor also asks the person about the complaints and how long ago they occurred.

Specific diagnostic methods include:

1. Neuropsychological examination (it detects cognitive impairment)
2. Ophthalmological examination (detects fundus angiopathy)
3. (visualizes atherosclerotic lesions of cerebral vessels, vascular malformations, venous encephalopathy)
4. (detects hypodense foci, changes in the liquor-containing compartment, atrophy of the cerebral cortex and post-stroke changes)

Treatment of the disease

Various types of drugs are used to treat cerebrovascular insufficiency

As soon as the first alarming manifestations of this pathological condition of the blood vessels appear, it is recommended to seek the help of a specialist as soon as possible in order to prevent the progression of the disease and the occurrence of irreversible consequences.

After carrying out diagnostic measures and clarifying the diagnosis, the doctor will prescribe the most effective therapy.

Antihypertensive treatment

To slow down the progression of pathology, it is necessary to constantly monitor indicators and keep them normal. This will help eliminate disturbances in the motor and mental systems and an increase in its intensity.

Antihypertensive treatment consists of prescribing specific medications - angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists. Such medications help reduce blood pressure and protect organs that suffer from high blood pressure (including the brain).

The effectiveness of such drugs can be increased by taking other antihypertensive drugs in combination, for example, (or Hydrochlorothiazide).

Lipid-lowering treatment (with concomitant atherosclerosis)

Combination drugs

Treatment of vascular pathology in the brain is carried out with means that have a combined effect on the body. They participate in the normalization of the rheological qualities of blood, the passage of blood through the veins, and have antioxidant, angio-protective, neuroprotective and neurotrophic effects.

Similar medications include Piracezin, Pentoxifylline, Instenon, etc.

Metabolic treatment

To improve metabolic processes in brain tissues that suffer from hypoxia, various medications of animal or chemical origin are prescribed. Some of the most effective drugs include Cerebrolysin, Cortexin, and Solcoseryl.

Folk remedies

To improve cerebral circulation, you can use folk remedies.

For example, ordinary alfalfa is often used, namely its seeds: 1 tsp. Pour 100 g of boiling water over the crushed seeds and leave to steep for an hour. Strain the finished product and take it orally before meals 3 times a day.

You can prepare an infusion of mulberry: 10 leaves of the plant are poured with hot water (half a liter) and left to infuse for an hour. Strain the finished product and use it internally instead of tea.

An excellent remedy for normalizing blood circulation is a decoction of periwinkle: chop the leaves in equal parts, boil in water at a ratio of 1 part raw material to 10 parts liquid for 5 minutes. After removing from the heat, the product is infused for another 3 hours, then filtered and taken orally, 100 ml at a time three times a day.

Nutrition

When treating cerebrovascular insufficiency, it is very important to maintain a drinking regime.

In combination with the main drug therapy, it is recommended to follow a special diet, which will only enhance the main therapy. Principles of nutrition for vascular pathology in the brain:

1. Limiting salt intake. The daily amount of salt consumed should not exceed 4.5 g. This is not only salt as a seasoning, but also products containing it (canned food, smoked meats, etc.).
2. Limiting the consumption of animal fats. This includes butter, milk, fatty dairy products, fatty meats and lard. The daily volume is calculated taking into account the person’s weight: 1 g per 1 kg of weight.
3. Limiting the consumption of fast carbohydrates. These include sweets, confectionery products, and baked goods.
4. Limit foods rich in vitamin K, namely: green tea, kale, spinach, lettuce, eggs and dairy products.
5. Enrich your daily diet with a sufficient amount of lean meat, legumes, seafood and fish, vegetables and fruits, which help improve blood flow in the brain.
6. It is recommended to follow a drinking regime. Insufficient fluid intake often causes blood clots, which is considered one of the sources of impaired blood flow in the brain. The daily volume of liquid consumed is within 1.5-2.5 liters.

Prevention

In order to prevent the occurrence of cerebrovascular insufficiency, it is necessary to constantly monitor blood pressure levels.

Prevention of the pathological condition of cerebral vessels is as follows:

• with the exception of smoking, drinking alcoholic beverages, taking drugs
• constant monitoring of pressure indicators
• taking antihypertensive medications
• proper diet with limited consumption of fatty, fried, smoked, salt, as well as foods that contribute to blood thickening
• eliminating stressful situations and emotional overload
• avoiding increased physical activity
• timely treatment of any heart disease

Cerebrovascular insufficiency is an insidious pathology, which often becomes the source of assigning a disability group to a person, and sometimes even death.

Watch a video about cerebrovascular accidents:

That is why it is important to immediately contact a specialist at the first warning signs and begin appropriate therapy.

Catad_tema Chronic cerebral ischemia - articles

Chronic cerebrovascular accidents

Published in the magazine:
"PHARMATEKA"; Current reviews; No. 15; 2010; pp. 46-50.

O.V. Kotova
Department of Pathology of the Autonomic Nervous System, Research Center of the First Moscow State Medical University named after. THEM. Sechenov, Moscow

Chronic cerebrovascular accidents (CVA) are a progressive form of cerebrovascular pathology with the gradual development of a complex of neurological and neuropsychological disorders. The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension, atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. In the complex treatment of patients with CNM, drugs are used that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. One of these drugs is Vasobral (dihydroergocriptine + caffeine) - an effective and safe treatment for CNM.
Keywords: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular disease (CCVD) is a progressive form of cerebrovascular pathology with gradual development of neurological and neuropsychological disorders. The main causes leading to chronic hypoperfusion of the brain are hypertension, atherosclerosis, and heart disease accompanied by chronic heart failure. In the complex treatment of patients with CCVD, drugs with comprehensive antioxidant, angioprotective, neuroprotective and neurotrophic action are usually used. One these drugs is Vazobral (dihydroergocryptine + coffein), effective and safe preparation for treatment of CCVD.
Key words: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular accidents (CVA) are a progressive form of cerebrovascular pathology, characterized by multifocal or diffuse ischemic brain damage with the gradual development of a complex of neurological and neuropsychological disorders. This is one of the most common forms of cerebrovascular pathology, usually occurring against the background of general cardiovascular diseases.

Etiology of CNMK
There are many extracerebral causes leading to pathology of cerebral circulation. First of all, these are diseases accompanied by a disorder of systemic hemodynamics, leading to a chronic decrease in adequate blood supply - chronic cerebral hypoperfusion. The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension (AH), atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. Other causes include diabetes mellitus, vasculitis in systemic connective tissue diseases, other diseases accompanied by vascular damage, blood diseases leading to changes in its rheology (erythremia, macroglobulinemia, cryoglobulinemia, etc.).

Pathomorphological changes in CNM
A high level of perfusion is required for adequate brain function. The brain, whose mass is 2.0-2.5% of body weight, consumes 15-20% of the blood circulating in the body. The main indicator of brain perfusion is the level of blood flow per 100 g of brain matter per minute. The average value of hemispheric cerebral blood flow (CBF) is approximately 50 ml/100 g/min, but there are significant differences in the blood supply to individual brain structures. The magnitude of MK in gray matter is 3-4 times higher than in white matter. At the same time, in the anterior parts of the hemispheres, blood flow is higher than in other areas of the brain. With age, the value of MB decreases, and frontal hyperperfusion also disappears, which is explained by diffuse atherosclerotic changes in cerebral vessels. It is known that with CNM, the subcortical white matter and frontal structures are more affected, which may be explained by the indicated characteristics of the blood supply to the brain. Initial manifestations of insufficiency of cerebral blood supply to the brain occur if the blood flow to the brain is less than 30-45 ml/100 g/min. The advanced stage is observed when the blood supply to the brain decreases to a level of 20-35 ml/100 g/min. The threshold of regional blood flow within 19 ml/100 g/min (functional threshold of blood supply to the brain), at which the functions of the corresponding areas of the brain are impaired, is considered critical. The process of death of nerve cells occurs when regional arterial cerebral blood flow is reduced to 8-10 ml/100 g/min (infarction threshold of cerebral blood supply).

In conditions of chronic brain hypoperfusion, which is the main pathogenetic link of CNM, compensation mechanisms are depleted, the energy supply of the brain becomes insufficient, as a result, first functional disorders develop, and then irreversible morphological damage. In chronic cerebral hypoperfusion, a slowdown in cerebral blood flow, a decrease in oxygen and glucose levels in the blood, a shift in glucose metabolism towards anaerobic glycolysis, lactic acidosis, hyper-osmolarity, capillary stasis, a tendency to thrombus formation, depolarization of cells and cell membranes, activation of microglia, which begins to produce neurotoxins, which, along with other pathophysiological processes, leads to cell death.

Damage to small penetrating cerebral arteries (cerebral microangiopathy), on which the blood supply to the deep parts of the brain depends, in patients with CNM is accompanied by various morphological changes in the brain, such as:

diffuse damage to the white matter of the brain (leukoencephalopathy);

multiple lacunar infarctions in the deep parts of the brain;

microinfarctions;

microhemorrhages;

atrophy of the cerebral cortex and hippocampus.

To implement autoregulation of cerebral circulation, it is necessary to maintain certain values ​​of blood pressure (BP) in the main arteries of the head. On average, systolic blood pressure (SBP) in the main arteries of the head should range from 60 to 150 mm Hg. Art. With long-term hypertension, these limits shift slightly upward, so autoregulation does not become impaired for a long time and MB remains at a normal level. Adequate brain perfusion is maintained by increasing vascular resistance, which in turn leads to an increase in the load on the heart. Chronic uncontrolled hypertension leads to secondary changes in the vascular wall - lipohyalinosis, which is observed mainly in the vessels of the microvasculature. The resulting arteriolosclerosis leads to changes in the physiological reactivity of blood vessels. Under these conditions, a decrease in blood pressure as a result of the addition of heart failure with a decrease in cardiac output or as a result of excessive antihypertensive therapy, or as a result of physiological circadian changes in blood pressure leads to the occurrence of hypoperfusion in the areas of the terminal circulation. Acute ischemic episodes in the basin of deep penetrating arteries lead to the occurrence of small-diameter lacunar infarcts in the deep parts of the brain. If the course of hypertension is unfavorable, repeated acute episodes lead to the emergence of the so-called. lacunar state, which is one of the variants of multi-infarct vascular dementia.

In addition to repeated acute disorders, the presence of chronic ischemia in the areas of terminal circulation is also assumed. A marker of the latter is a rarefaction of the periventricular or subcortical white matter (leukoaraiosis), which pathomorphologically represents a zone of demyelination, gliosis and expansion of the perivascular spaces. In some cases of an unfavorable course of hypertension, subacute development of diffuse damage to the white matter of the brain with a clinical picture of rapidly progressing dementia and other manifestations of disconnection is possible, which is sometimes referred to in the literature as “Binswanger’s disease.”

Another significant factor in the development of CNM is atherosclerotic damage to cerebral vessels, which is usually multiple, localized in the extra- and intracranial parts of the carotid and vertebral arteries, as well as in the arteries of the circle of Willis and their branches, forming stenoses. Stenoses are divided into hemodynamically significant and insignificant. If a decrease in perfusion pressure occurs distal to the atherosclerotic process, this indicates a critical or hemodynamically significant narrowing of the vessel.

It has been shown that hemodynamically significant stenoses develop when the vessel lumen narrows by 70-75%. But cerebral blood flow depends not only on the severity of stenosis, but also on the mechanisms that prevent the development of ischemia: the state of collateral circulation, the ability of cerebral vessels to dilate. These hemodynamic reserves of the brain allow “asymptomatic” stenoses to exist without complaints or clinical manifestations. However, the obligatory development of chronic cerebral hypoperfusion during stenosis leads to CNM, which is detected by magnetic resonance imaging (MRI). MRI visualizes periventricular leukoaraiosis (reflecting ischemia of the white matter of the brain), internal and external hydrocephalus (caused by atrophy of brain tissue); Cysts may be detected (as a consequence of previous cerebral infarctions, including clinically “silent” ones). It is believed that CNMC is present in 80% of patients with stenotic lesions of the main arteries of the head. Atherosclerotic changes in the vessels of the brain are characterized not only by local changes in the form of plaques, but also by hemodynamic restructuring of the arteries in the area distal to atherosclerotic stenoses and occlusions. All this leads to the fact that “asymptomatic” stenoses become clinically significant.

The structure of the plaques is also of great importance: the so-called. unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents - often of a transient type. When hemorrhaging into such a plaque, its volume quickly increases with an increase in the degree of stenosis and worsening of the signs of CNM. In the presence of such plaques, blocking the lumen of the vessel up to 70% will be hemodynamically significant.

In the presence of damage to the main arteries of the head, cerebral blood flow becomes very dependent on systemic hemodynamic processes. Such patients are especially sensitive to arterial hypotension, which can occur when moving to a vertical position (orthostatic hypotension), with cardiac arrhythmias leading to a short-term decrease in cardiac output.

Clinical manifestations of CNM
The main clinical manifestations of CNM are disturbances in the emotional sphere, balance and gait disorders, pseudobulbar disorders, impairment of memory and learning ability, neurogenic urination disorders, which gradually lead to maladjustment of patients.

During CNM, three stages can be distinguished:

At stage I, the clinic is dominated by subjective disorders in the form of general weakness and fatigue, emotional lability, sleep disturbances, decreased memory and attention, and headaches. Neurological symptoms do not form distinct neurological syndromes, but are represented by anisoreflexia, discoordination, and symptoms of oral automatism. Violations of memory, praxis and gnosis can be identified, as a rule, only when special tests are carried out.

At stage II, there are more subjective complaints, and neurological symptoms can already be divided into distinct syndromes (pyramidal, discoordination, amyostatic, dysmnestic), with one neurological syndrome usually dominating. Professional and social adaptation of patients decreases.

At stage III, neurological symptoms increase, a distinct pseudobulbar syndrome appears, and sometimes paroxysmal conditions (including epileptic seizures); Severe cognitive impairment leads to disruption of social and everyday adaptation and complete loss of working capacity. Ultimately, CNMK contributes to the formation of vascular dementia.

Cognitive impairment is a key manifestation of CNM, which largely determines the severity of the patient’s condition. They often serve as the most important diagnostic criterion for CNM and are a sensitive marker for assessing the dynamics of the disease. It is worth noting that the location and extent of vascular changes detected by MRI or computed tomography are only partially correlated with the presence, type and severity of neuropsychological findings. In case of CNMC, there is a more pronounced correlation between the severity of cognitive impairment and the degree of brain atrophy. Correcting cognitive impairment is often critical to improving the quality of life of the patient and his relatives.

Methods for diagnosing cognitive impairment
To assess the overall severity of cognitive defect, the Mini-Mental State Examination scale is most widely used. However, this method is not an ideal screening tool, since its results are significantly influenced by the patient's premorbid level and type of dementia (the scale is less sensitive to frontal cortex dysfunction and therefore better detects the early stages of Alzheimer's disease than the early stages of vascular dementia). In addition, its implementation requires more than 10-12 minutes, which the doctor does not always have at an outpatient appointment.

Clock drawing test: subjects are asked to draw a clock with its hands pointing to a specific time. Normally, the subject draws a circle, places the numbers from 1 to 12 inside it in the correct order at equal intervals, draws 2 hands (the hour hand is shorter, the minute hand is longer), starting in the center and showing the specified time. Any deviation from correct test performance is a sign of fairly severe cognitive dysfunction.

Speech activity test: subjects are asked to name as many names of plants or animals as possible in a minute (semantically mediated associations) and words starting with a certain letter, for example “l” (phonetically mediated associations). Normally, most elderly people with secondary and higher education name from 15 to 22 plants and from 12 to 16 words starting with “l” per minute. Naming fewer than 12 semantically mediated associations and fewer than 10 phonetically mediated associations usually indicates significant cognitive dysfunction.

Visual memory test: patients are asked to remember 10-12 images of simple, easily recognizable objects presented on one sheet; Subsequently, the following are assessed: 1) immediate reproduction, 2) delayed reproduction after interference (a verbal association test can be used as an interfering effect), 3) recognition (the patient is asked to recognize previously presented objects among other images). Failure to remember more than half of previously presented images may be considered a sign of severe cognitive dysfunction.

Main directions in the treatment of CNM
The main directions in the treatment of CNM stem from the etiopathogenetic mechanisms that led to this process. The main goal is to restore or improve brain perfusion, which is directly related to the treatment of the underlying disease: hypertension, atherosclerosis, heart disease with the elimination of heart failure.

Taking into account the diversity of pathogenetic mechanisms underlying CNM, preference should be given to agents that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. In this regard, the use of drugs that combine several mechanisms of action is justified. Among such drugs, I would like to mention Vasobral, a combined drug that has both nootropic and vasoactive effects. It contains an ergot derivative (dihydroergocryptine) and caffeine. Dihydroergocriptine blocks α1 and α2 adrenergic receptors of vascular smooth muscle cells, platelets, and erythrocytes, and has a stimulating effect on dopaminergic and serotonergic receptors of the central nervous system.

When using the drug, the aggregation of platelets and erythrocytes decreases, the permeability of the vascular wall decreases, blood supply and metabolic processes in the brain improve, and the resistance of brain tissue to hypoxia increases. The presence of caffeine in Vasobral determines the stimulating effect on the central nervous system, mainly on the cerebral cortex, respiratory and vasomotor centers, and increases mental and physical performance. Studies have shown that Vasobral has a vegetative stabilizing effect, which manifests itself in increased pulse blood filling, normalization of vascular tone and venous outflow, which is due to the positive effect of the drug on the sympathetic nervous system while reducing the activity of the parasympathetic system. A course of treatment with Vasobral leads to a decrease or disappearance of symptoms such as dizziness, headache, palpitations, and numbness of the extremities. Positive dynamics of the neuropsychological status of the patient with CNM are noted: increased attention span; improving orientation in time and space, memory for current events, intelligence; increased mood, decreased emotional lability. The use of Vasobral helps reduce fatigue, lethargy, and weakness; there is a feeling of cheerfulness.

The drug is prescribed in a dose of 2-4 ml (1-2 pipettes) or 1/2-1 tablet 2 times a day for 2-3 months. The drug is taken with a small amount of water. Side effects occur rarely and are mild. It should be noted that due to the presence of liquid and tablet forms, double dosing and good tolerability, Vasobral is convenient for long-term use, which is extremely important in the treatment of chronic diseases.

Non-drug ways to correct the manifestations of CNM should include:

proper organization of work and rest, avoidance of night shifts and long business trips;

moderate physical activity, therapeutic exercises, measured walking;

diet therapy: limiting the total calorie content of food and salt consumption (up to 2-4 g per day), animal fats, smoked meats; introduction of fresh vegetables and fruits, fermented milk and fish products into the diet;

climatic treatment at local resorts, in low altitudes and at sea resorts; balneotherapy, which has a positive effect on central hemodynamics, contractile function of the heart, and the state of the autonomic nervous system; the means of choice are radon, carbon dioxide, sulfide, iodine-bromine baths.

In general, an integrated approach to the treatment of CNM and repeated pathogenetically based course treatment can contribute to better adaptation of the patient in society and prolong the period of his active life.

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