Vascular Dementia

What is Vascular Dementia?

Dementia is an acquired mental disorder, manifested by a decrease in intelligence and violating the social adaptation of the patient (making him incapable of professional activity, the possibility of self-care is limited) and not accompanied by impaired consciousness. An intellectual defect in dementia is characterized by a complex disorder of several cognitive (cognitive) functions, such as memory, attention, speech, gnosis, praxis, thinking, the ability to plan, make decisions, and control one’s actions. In contrast to mental retardation, in which disorders are noted from birth, dementia develops with acquired organic lesions of the brain. Dementia also does not include isolated violations of individual cognitive functions (aphasia, amnesia, agnosia, etc.), in which the intellect as such does not significantly suffer.

Vascular dementia accounts for 15-20% of all cases of dementia and is the second most common in Western Europe and the United States. But in some countries of the world, such as Russia, Finland, China and Japan, vascular dementia takes the 1st place and is more common than Alzheimer’s disease. In 20% of cases of vascular dementia, Alzheimer’s disease resembles with the course, and in 10-20% of cases there is a combination of them. Modern basic research suggests that cerebral vascular insufficiency is one of the important factors in the pathogenesis of Alzheimer’s disease. The risk of Alzheimer’s disease and the rate of progression of cognitive impairment associated with this disease is higher in the presence of cardiovascular pathology, such as atherosclerosis of cerebral arteries and hypertension. On the other hand, deposits of b amyloid associated with Alzheimer’s disease in the vascular wall can lead to the development of amyloid microangiopathy, which exacerbates the lack of blood supply to the brain. Thus, the main forms of dementia (Alzheimer’s disease and vascular dementia), according to modern concepts, are pathogenetically very closely related.

The problem of vascular dementia is not only medical, but also social, since this disease not only affects the quality of life of patients, but also leads to large economic losses due to the need for constant monitoring of patients with severe forms of vascular dementia. In Ukraine, the main burden of caring for the sick is his relatives. With the aggravation of the patient’s condition, the load on the guardian also increases, which leads to a deterioration in the mental state of the caregiver, and subsequently to the emergence or exacerbation of chronic somatic diseases. In 1994, R. Ernst and J. Hay showed that caregivers were 46% more likely to visit a general practitioner and 71% more were using medications than people of the same age who were not caring for patients .

The significance of the problem of vascular dementia is also determined by the fact that the life expectancy of patients is much less than in the corresponding age-related population without dementia, and less than with Alzheimer’s disease. So, according to Skoog et al, the mortality rate among patients with vascular dementia at an advanced age over 3 years was 66.7%, while in Alzheimer’s disease – 42.2%, and among non-cement probands – 23.1%. The highest risk of dementia is observed in patients with stroke (8.4% per year). Dementia develops in 26.3% after 2 months and in 31.8% of patients 3 months after a stroke. And the mortality rate of patients with post-stroke dementia in the coming years after a stroke is 3 times higher than in post-stroke patients without dementia.

Causes of Vascular Dementia

Vascular genesis dementia is understood to mean a decrease in cognitive functions as a result of ischemic or hemorrhagic brain damage due to the primary pathology of cerebral vessels or diseases of the cardiovascular system.

The most common etiological factors of vascular dementia are:

  • ischemic strokes (atherothrombotic, embolic with large vessels, lacunar);
  • intracerebral hemorrhages (with arterial hypertension, amyloid angiopathy);
  • subshell hemorrhages (subarachnoid, subdural);
  • repeated embolization due to cardiac pathology (endocarditis, atrial myxoma, atrial fibrillation and others);
  • autoimmune vasculitis (systemic lupus erythematosus, erythematosis, etc.);
  • infectious vasculitis (neurosyphilis, Lyme disease, etc.);
  • non-specific vasculopathies.

Risk Factors for Vascular Dementia
Risk factors for the development of vascular dementia include: over 60 years of age, arterial hypertension, hypotension, diabetes mellitus, dyslipidemia, heart disease (atrial fibrillation, coronary heart disease, heart defects), peripheral vascular disease, smoking, male, black and Asian race, heredity and others. It is interesting to emphasize that the alleged risk factors include low educational level and the profession of a worker. A higher level of education may reflect greater brain abilities and reserves, thus delaying the onset of cognitive impairment over time.

Arterial hypertension is a major risk factor for the development and progression of vascular dementia. This is due to both the high prevalence of hypertension among elderly people, and the nature of the specific damage to the vessels of the brain in arterial hypertension.

Long-term epidemiological studies have shown that hypertension is associated with cognitive impairment, such as the Honolulu-Asia Aging Study, and that blood pressure lowering therapy can reduce the risk of dementia. These data were convincingly confirmed in the studies of Systolic Hypertension in Europe trials, PROGRESS, LIFE, SCOPE, MOSES.

Pathogenesis during Vascular Dementia

The leading role in the formation of dementia in vascular lesions of the brain is played by the defeat of the white matter of the brain and the basal ganglia, the thalamus, which leads to a disruption in the connection of the frontal sections and subcortical structures (the phenomenon of cortical-subcortical separation).

The main pathogenetic factor in the development of this phenomenon is arterial hypertension, which leads to changes in the vascular wall (microateromatosis, lipogialinosis), mainly in the vessels of the microvasculature. As a result, arteriolosclerosis develops, which causes a change in the physiological reactivity of the vessels. This vascular pathology (vascular remodeling) leads to a decrease in perfusion, the development of ischemia of the white matter of the brain and multiple lacunar infarction. As a result of their cumulative effect, brain tissue is lost.

Large single cerebral infarctions are also important; cerebral infarction, even small, but in the “strategic” areas. Among these “strategic” zones, the thalamus, hippocampus, angular gyrus and caudate nucleus should be noted.

Symptoms of Vascular Dementia

Acute-onset dementia is characterized by the occurrence of cognitive impairment during the first month (but not more than three months) after the first or repeated strokes. Multi-infarction vascular dementia is predominantly cortical, it develops gradually (over 3-6 months) after a series of small ischemic episodes. With multi-infarction dementia, an “accumulation” of heart attacks occurs in the brain parenchyma. The subcortical form of vascular dementia is characterized by the presence of arterial hypertension and signs (clinical, instrumental) of damage to the deep sections of the white matter of the cerebral hemispheres. Subcortical dementia often resembles dementia in Alzheimer’s disease. The distinction between cortical and subcortical dementia itself seems extremely conditional, since pathological changes in dementia affect to one degree or another both subcortical departments and cortical structures.

Recently, attention has been focused on variants of vascular dementia that are not directly related to cerebral infarction. The concept of “non-infarction” vascular dementia is of great clinical importance, since most of these patients are mistakenly diagnosed with Alzheimer’s disease. Thus, these patients do not receive timely and adequate treatment, and vascular damage to the brain progresses. The reason for including patients in the group of “non-infarction” vascular dementia is the presence of a prolonged (more than 5 years) vascular history, the absence of clinical and computed tomographic signs of cerebral infarction.

One form of vascular dementia is Binswanger’s disease (subcortical arteriosclerotic encephalopathy). First described by Binswanger in 1894, it is characterized by progressive dementia and episodes of acute development of focal symptoms or progressive neurological disorders associated with damage to the white matter of the cerebral hemispheres. Previously, this disease was classified as rare and diagnosed almost exclusively posthumously. But with the introduction of clinical methods of neuroimaging, it turned out that Binswanger’s encephalopathy is quite common. It makes up about a third of all cases of vascular dementia. Most neurologists suggest that this disease should be considered one of the options for the development of hypertensive angioencephalopathy, in which diffuse and small focal changes are observed, mainly in the white matter of the hemispheres, which is clinically manifested by progressive dementia syndrome.

Based on round-the-clock monitoring of blood pressure, features of the course of arterial hypertension in such patients were revealed. It was found that in patients with Binswangerian type vascular dementia, higher average and maximum systolic blood pressure and its pronounced fluctuations during the day are observed. In addition, in such patients there is no physiological decrease in blood pressure at night and there is a significant rise in blood pressure in the morning.

A feature of vascular dementia is the clinical variety of disorders and the frequent combination of several neurological and neuropsychological syndromes in a patient.

Patients with vascular dementia are characterized by a slowdown, rigidity of all mental processes and their lability, narrowing of the circle of interests. Patients have a decrease in cognitive functions (memory, attention, thinking, orientation, etc.) and difficulties in performing functions in everyday life and everyday life (serving yourself, cooking, shopping, filling out financial documents, orientation in a new environment, etc.), loss of social skills, adequate assessment of their disease. Among cognitive impairments, it is first of all worth noting the disorders of memory and attention, which are already observed at the stage of initial vascular dementia and are steadily progressing. Decreased memory for past and current events is a characteristic symptom of vascular dementia, however, mnemonic disorders are more mild in comparison with dementia in AD. Memory impairments are manifested mainly during training: memorization of words, visual information, and the acquisition of new motor skills are difficult. Mostly active reproduction of the material suffers, while simpler recognition is relatively safe. At later stages, disturbances in abstract thinking and judgment may develop. A pronounced narrowing of the volumes of voluntary attention, significant violations of its functions — concentration, distribution, and switching — are determined. In vascular dementia, attention deficit syndromes are modal-nonspecific and increase as cerebrovascular insufficiency progresses.

In patients with vascular dementia, there are disorders of the counting functions, with the progression of the disease reaching the degree of acalculia. Various speech disorders, reading and writing disorders are detected. Most often there are signs of semantic and amnestic forms of aphasia. At the stage of initial dementia, these signs are determined only during special neuropsychological tests.

In more than half of patients with vascular dementia, so-called emotional incontinence (weak-heartedness, violent crying) is observed, in some patients – depression. Perhaps the development of affective disorders, psychotic symptoms. For vascular dementia, a fluctuating type of disease course is characteristic. Vascular dementia is inherent in long periods of stabilization and even a known reverse development of mental-intellectual disorders, and therefore the degree of its severity fluctuates in one direction or another, which often correlates with the state of cerebral blood flow.

In addition to cognitive impairment, patients with vascular dementia also have neurological manifestations: pyramidal, subcortical, pseudobulbar, cerebellar syndromes, paresis of limb muscles, usually not severe, impaired gait of the apraxic-atactic or parkinsonian type. Most patients, especially the elderly, have impaired pelvic function control (most often urinary incontinence).

Often there are paroxysmal conditions – falls, epileptic seizures, syncope.

It is a combination of cognitive and neurological disorders that distinguishes vascular dementia from Alzheimer’s disease.

Diagnosis of Vascular Dementia

Diagnostic criteria for vascular dementia and clinical forms
In ICD-10, vascular dementia is classified as a mental illness, is interpreted as the result of cerebral infarction due to cerebrovascular disease and has the code F 01. Psycho-diagnostic tests, which include testing on the Mini-mental State Examination (MMSE), Khachinsky scale, are required to diagnose dementia. and etc.

The diagnosis of vascular dementia includes 3 criteria:

  1. the presence of dementia (psychodiagnostic testing);
  2. the presence of cerebrovascular disease, which is confirmed by clinical, biochemical data, dopplerography of cerebral vessels, computed tomography (CT), magnetic resonance imaging (MRI) of the brain;
  3. the relationship of the 1st and 2nd criteria with each other.

There are some subtypes of vascular dementia:

  1. acute onset dementia;
  2. multi-infarction dementia;
  3. subcortical dementia;
  4. mixed cortical and subcortical;
  5. “indefinite” forms of vascular dementia.

Neuroimaging methods in the diagnosis of vascular dementia
In patients with vascular dementia, characteristic intravital changes in the brain are detected using modern methods of neuroimaging. In case of multi-infarction dementia, infarcts on tomograms are detected both in the gray and white matter of the cerebral hemispheres, with subcortical – mainly in the white matter, usually in combination with diffuse changes in the white matter (leukoaraiosis) and expansion of the lateral ventricles and furrows. The severity of leukoaraiosis and the expansion of the ventricular system correlate with the severity of clinical disorders, but the full relationship between the neuroimaging picture and the clinic is not always observed. MRI, especially performed in T 2 mode, is a more sensitive method for detecting these changes in the brain compared to CT. Leukoaraiosis is detected by MRI in almost all patients with vascular dementia. Its severity is moderate or severe, and its prevalence can reach more than 1/4 of the area of ​​the white matter.

In addition to clarifying the nature of structural brain damage for the development of vascular dementia, the value of fluctuations in cerebral blood flow was also shown. It turned out that for vascular dementia a typically pronounced decrease (almost 2 times compared with the age norm) of cerebral blood flow and metabolism. At the same time, the total indicators of hypometabolism are more strongly correlated with indicators of cognitive deficit than indicators of the value of destruction of the brain substance.

Treatment of Vascular Dementia

Knowledge of the etiopathogenetic mechanisms of the formation of vascular dementia, risk factors, evidence-based medicine made it possible to formulate the basic principles of treatment and prevention of vascular dementia. The first step is to confirm the diagnosis of dementia. In this case, the identification of predementic conditions, the therapeutic possibilities of which are much wider, is of particular importance.

The principles of treatment of vascular dementia:

  1. etiopathogenetic;
  2. drugs to improve cognitive function;
  3. symptomatic therapy;
  4. preventive.

Treatment of vascular dementia is differentiated, which is determined by the heterogeneity of the pathological process. Due to the large number of etiopathogenetic mechanisms, there is no single and standardized method of treatment for this category of patients. Treatment of vascular dementia should include measures aimed at the underlying disease, against which dementia develops, and the correction of existing risk factors. Given that the main risk factor is AH, an important role is given to its normalization, since adequate antihypertensive therapy is accompanied by a significant reduction in the risk of dementia of any etiology. Considering the fact that vascular dementia often develops in patients who have already suffered acute cerebrovascular accident, the optimal blood pressure in these patients is within 120/80 mm Hg. Taking into account evidence-based medicine, the use of ACE inhibitors (perindopril, lisinopril, etc.) is recommended, preferably in combination with diuretics.

Based on the peculiarities of pharmacokinetics and pharmacodynamics, lisinopril is a priority for combination of hypertension with diabetes mellitus (EUCLID), in individuals with varying severity of acute hepatocellular insufficiency and chronic diseases of the hepatobiliary system (the only representative of the group of ACE inhibitors, which is recommended for a single dose and at the same time represents finished dosage form that does not need additional biotransformation). Metabolic neutrality recommends lisinopril for the treatment of patients with manifestations of the metabolic syndrome and obesity (hydrophilic substance). The pharmacological properties of lisinopril have been studied in sufficient detail (7 trials with “intermediate” endpoints (53,435 patients), and 5 trials with “solid” endpoints (53,030 patients), which is not inferior in scope to studies of representatives of the previous classes – captopril and enalapril, and also exceeds the breadth of tests of perindopril, fosinopril and moexipril). Based on this, one can welcome the expansion of the Ukrainian market of lisinopril due to the emergence of highly effective and affordable drugs of European quality in a variety of dosages (Lopril 5, 10, 20 mg) and combinations (Lopril N 10, 20 mg).

Calcium antagonists and AT II receptor antagonists have an independent neuroprotective effect, including the prevention of dementia, in addition to lowering blood pressure.

In order to prevent the development of repeated disorders of cerebral circulation and other cardiovascular complications (myocardial infarction, etc.), which contribute to the development and progression of vascular dementia, the use of antiplatelet drugs is recommended. First-line drugs currently are: acetylsalicylic acid (ASA) – 50-325 mg 1 time per day, or clopidogrel – 75 mg 1 time per day, or a combination of ASA – 25 mg 2 times a day and a prolonged form of dipyridamole – 200 mg 2 times a day. The purpose of each of these drugs is individual and depends on tolerance and the presence of risk factors in each patient. With intolerance or inefficiency of ASA, clopidogrel is recommended – 75 mg per day.

Since cerebral infarction due to heart disease (primarily atrial fibrillation) is a common cause of the development of vascular dementia, the use of oral anticoagulants (warfarin) under the control of the international normalization ratio (INR) is recommended.

Surgical treatment (carotid endarterectomy, angioplasty) is indicated for patients with critical carotid artery stenosis of more than 70%, as well as atherosclerotic plaques, which are the source of embolism.

Patients with hypercholesterolemia are recommended statins.

Since the basis of vascular dementia is cognitive impairment, it is recommended to take different groups of drugs to improve cognitive function:

  • preparations based on Ginkgo Biloba (tanakan, memoplant, etc.);
  • anticholinesterase drugs (amiridine, rivastigmine, galantamine, gliatilin, etc.);
  • neurotrophic drugs (cerebrolysin);
  • MAO inhibitors (selegiline);
  • nootropics (piracetam, pramiracetam);
  • neuropeptides (solcoseryl, actovegin, lipocerebrin);
  • membrane stabilizing (citicoline);
  • NMDA receptor antagonists (memantine);
  • antioxidants (vitamins C, E, carotenoids, flavonoids);
  • substances that affect the GABA system (aminalon, pantogam, noofen, etc.);
  • vasoactive drugs (nicergoline, vinpocetine, instenon, etc.);
  • combined (Fezam, etc.).

It should be emphasized that drugs that improve cerebral blood flow and neuronal metabolism are more effective if they are prescribed in the early stages of cerebral vascular insufficiency, when the severity of cognitive impairment does not yet reach the degree of dementia.

Separate treatment may require the occurrence of depression, anxiety, hallucinations, psychomotor agitation in patients. In the presence of depression in patients with dementia, serotonin reuptake inhibitors are currently preferred, since, unlike tricyclic antidepressants, they have less anticholinergic side effects and do not inhibit cognitive functions.

The response to treatment should be carefully evaluated in each patient, taking into account the relatively frequent occurrence of paradoxical reactions and side effects of therapy. Treatment should be reviewed periodically, avoiding without good reason long-term use of drugs that impair cognitive function (benzodiazepines, anticonvulsants, antipsychotics, central anticholinergics, digitalis drugs).

Adequate therapy of concomitant somatic diseases that significantly affect the neuropsychic state of patients should be carried out in conjunction with other specialists. The psychological support of the patient is important.

Prevention of Vascular Dementia

The development of vascular dementia can be prevented by detecting risk factors for its development and correcting, in the first place, hypertension, hyperlipidemia, diabetes mellitus, and heart diseases. These preventive measures should be carried out by doctors of various profiles.

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