About health, for example, what is dementia. Dementia - what is this disease? Symptoms and course of senile vascular dementia

Dementia is a persistent disorder of higher nervous activity, accompanied by the loss of acquired knowledge and skills and a decrease in learning ability. There are currently more than 35 million people suffering from dementia worldwide. It develops as a result of brain damage, against the background of which a marked breakdown of mental functions occurs, which generally makes it possible to distinguish this disease from mental retardation, congenital or acquired forms of dementia.

What kind of disease is this, why dementia often occurs at an older age, as well as what symptoms and first signs are characteristic of it - let's look further.

Dementia - what is this disease?

Dementia is insanity, expressed in the breakdown of mental functions, which occurs due to brain damage. The disease must be differentiated from oligophrenia - congenital or acquired infantile dementia, which is a mental underdevelopment.

For dementia patients are not capable of understanding what is happening to them, the disease literally “erases” everything from their memory that accumulated in it during the previous years of life.

Dementia syndrome manifests itself in many ways. These are speech, logic, memory disorders, causeless depressive states. People with dementia are forced to leave work because they need help permanent treatment and supervision. The disease changes the life of not only the patient, but also his loved ones.

Depending on the degree of the disease, its symptoms and the patient’s reaction are expressed differently:

  • With mild dementia, he is critical of his condition and is able to take care of himself.
  • With a moderate degree of damage, there is a decrease in intelligence and difficulties in everyday behavior.
  • Severe dementia – what is it? The syndrome means a complete breakdown of personality, when an adult cannot even relieve himself or eat on his own.

Classification

Taking into account the predominant damage to certain areas of the brain, four types of dementia are distinguished:

  1. Cortical dementia. The cerebral cortex is predominantly affected. It is observed in alcoholism, Alzheimer's disease and Pick's disease (frontotemporal dementia).
  2. Subcortical dementia. Subcortical structures suffer. Accompanied by neurological disorders (trembling limbs, muscle stiffness, gait disorders, etc.). Occurs with Huntington's disease and hemorrhages in the white matter.
  3. Cortical-subcortical dementia is a mixed type of lesion, characteristic of pathology caused by vascular disorders.
  4. Multifocal dementia is a pathology characterized by multiple lesions in all parts of the central nervous system.

Senile dementia

Senile dementia (dementia) is severe dementia that manifests itself at the age of 65 years and older. The disease is most often caused by rapid atrophy of cells in the cerebral cortex. First of all, the patient’s reaction speed and mental activity slow down and short-term memory deteriorates.

Mental changes that develop with senile dementia are associated with irreversible changes in the brain.

  1. These changes occur at the cellular level; neurons die due to lack of nutrition. This condition is called primary dementia.
  2. If there is a disease due to which the nervous system is damaged, the disease is called secondary. Such diseases include Alzheimer's disease, Huntington's disease, spastic pseudosclerosis (Creutzfeldt-Jakob disease), etc.

Senile dementia, being among mental illness, is the most common disease among older people. Senile dementia occurs almost three times more often in women than in men. In most cases, the age of patients is 65-75 years, on average, in women the disease develops at 75 years, in men - at 74 years.

Vascular dementia

Vascular dementia is understood as a disorder of mental acts, which is caused by problems with blood circulation in the vessels of the brain. Moreover, such disorders significantly affect the patient’s lifestyle and activity in society.

This form of the disease usually occurs after a stroke or heart attack. Vascular dementia - what is it? This is a whole complex of symptoms that are characterized by a deterioration in a person’s behavioral and mental abilities after damage to the blood vessels of the brain. With mixed vascular dementia, the prognosis is the most unfavorable, since it affects several pathological processes.

In this case, as a rule, dementia that develops after vascular accidents, such as:

  • Hemorrhagic stroke (vascular rupture).
  • (blockage of a vessel with cessation or deterioration of blood circulation in a certain area).

Most often, vascular dementia occurs hypertension, less often - with severe diabetes mellitus and some rheumatic diseases, even less often - with embolism and thrombosis due to skeletal injuries, increased blood clotting and peripheral venous diseases.

Elderly patients should monitor their underlying medical conditions that may cause dementia. These include:

  • hypertension or hypotension,
  • atherosclerosis,
  • ischemia,
  • diabetes etc.

Dementia is promoted by a sedentary lifestyle, lack of oxygen, and addictions.

Alzheimer's type dementia

The most common type of dementia. It refers to organic dementia (a group of dementive syndromes that develop against the background of organic changes in the brain, such as cerebrovascular diseases, traumatic brain injuries, senile or syphilitic psychoses).

In addition, this disease is quite closely intertwined with types of dementia with Lewy bodies (a syndrome in which the death of brain cells occurs due to Lewy bodies formed in neurons), having many common symptoms with them.

Dementia in children

The development of dementia is associated with the influence of various factors on the child’s body that can cause disturbances in the functioning of the brain. Sometimes the disease is present from birth, but manifests itself as the child grows.

In children there are:

  • residual organic dementia,
  • progressive.

These types are divided depending on the nature of the pathogenetic mechanisms. With meningitis, a residual organic form may appear; it also occurs with significant traumatic brain injuries and poisoning of the central nervous system with medications.

The progressive type is considered an independent disease, which may be part of the structure of hereditary degenerative defects and diseases of the central nervous system, as well as cerebral vascular lesions.

With dementia, a child may develop depression. Most often, this is characteristic of the early stages of the disease. The progressive disease impairs children's mental and physical abilities. If you do not work to slow down the disease, the child may lose a significant part of his skills, including household skills.

For any type of dementia, loved ones, relatives and household members should treat the patient with understanding. After all, it’s not his fault that he sometimes does inappropriate things, it’s the illness that does it. We ourselves should think about preventive measures so that the disease does not affect us in the future.

Causes

After the age of 20, the human brain begins to lose nerve cells. Therefore, minor problems with short-term memory are quite normal for older people. A person may forget where he put his car keys, or the name of the person he was introduced to at a party a month ago.

These age-related changes happen to everyone. They usually do not cause problems in Everyday life. In dementia, the disorders are much more pronounced.

The most common causes of dementia:

  • Alzheimer's disease (up to 65% of all cases);
  • vascular damage caused by atherosclerosis, impaired circulation and properties of blood;
  • alcohol abuse and drug addiction;
  • Parkinson's disease;
  • Pick's disease;
  • traumatic brain injuries;
  • endocrine diseases (thyroid problems, Cushing's syndrome);
  • autoimmune diseases (multiple sclerosis, lupus erythematosus);
  • infections (AIDS, chronic encephalitis, etc.);
  • diabetes;
  • serious illnesses internal organs;
  • a consequence of complications of hemodialysis (blood purification),
  • severe renal or liver failure.

In some cases, dementia develops from multiple causes. A classic example of such a pathology is senile (senile) mixed dementia.

Risk factors include:

  • age over 65 years;
  • hypertension;
  • elevated blood lipid levels;
  • obesity of any degree;
  • lack of physical activity;
  • lack of intellectual activity for a long time (from 3 years);
  • low estrogen levels (applies only to female) and etc.

First signs

The first signs of dementia are a narrowing of horizons and personal interests, a change in the patient’s character. Patients develop aggression, anger, anxiety, and apathy. The person becomes impulsive and irritable.

The first signs you need to pay attention to:

  • The first symptom of any type of disease is memory disorder, which progresses rapidly.
  • The individual's reactions to the surrounding reality become irritable and impulsive.
  • Human behavior is filled with regression: rigidity (cruelty), stereotyping, sloppiness.
  • Patients stop washing and dressing, and professional memory is impaired.

These symptoms rarely signal to others about an impending illness; they are attributed to current circumstances or a bad mood.

Stages

In accordance with the patient’s social adaptation capabilities, three degrees of dementia are distinguished. In cases where the disease that causes dementia has a steadily progressive course, we often speak of the stage of dementia.

Lightweight

The disease develops gradually, so patients and their relatives often do not notice its symptoms and do not consult a doctor in time.

For mild stage characterized by significant violations intellectual sphere, however, the patient’s critical attitude towards his own condition remains. The patient can live independently and also perform household activities.

Moderate

The moderate stage is marked by the presence of more severe intellectual impairment and a decrease in critical perception of the disease. Patients have difficulty using household appliances ( washing machine, stove, TV), as well as door locks, telephone, latches.

Severe dementia

At this stage, the patient is almost completely dependent on loved ones and needs constant care.

Symptoms:

  • complete loss of orientation in time and space;
  • it is difficult for the patient to recognize relatives and friends;
  • requires constant care late stages the patient cannot eat himself or perform simple hygiene procedures;
  • behavioral disturbances increase, the patient may become aggressive.

Symptoms of dementia

Dementia is characterized by its manifestation from many sides simultaneously: changes occur in the patient’s speech, memory, thinking, and attention. These, as well as other body functions, are disrupted relatively evenly. Even the initial stage of dementia is characterized by very significant impairments, which certainly affects the person as an individual and as a professional.

In a state of dementia, a person not only loses ability demonstrate previously acquired skills, but also loses the opportunity gain new skills.

Symptoms:

  1. Memory problems. It all starts with forgetfulness: a person does not remember where he put this or that object, what he just said, what happened five minutes ago (fixation amnesia). At the same time, the patient remembers in every detail what happened many years ago, both in his life and in politics. And if I’ve forgotten something, I almost involuntarily begin to include fragments of fiction.
  2. Thought disorders. There is a slowness in the pace of thinking, as well as a decrease in the ability to logical thinking and abstraction. Patients lose the ability to generalize and solve problems. Their speech is detailed and stereotypical in nature, its scarcity is noted, and as the disease progresses, it is completely absent. Dementia is also characterized possible appearance delusional ideas in patients, often with absurd and primitive content.
  3. Speech . At first it becomes difficult to select the right words, then you may get stuck on the same words. In later cases, speech becomes intermittent and sentences are not completed. Although he has good hearing, he does not understand speech addressed to him.

Common cognitive disorders include:

  • memory impairment, forgetfulness (most often this is noticed by people close to the patient);
  • difficulties in communication (for example, problems with choosing words and definitions);
  • obvious deterioration in the ability to solve logical problems;
  • problems with making decisions and planning your actions (disorganization);
  • impaired coordination (unsteady gait, falls);
  • disorders motor functions(inaccuracy of movements);
  • disorientation in space;
  • disturbances of consciousness.

Psychological disorders:

  • , depressed state;
  • unmotivated feeling of anxiety or fear;
  • personality changes;
  • behavior that is unacceptable in society (constant or episodic);
  • pathological excitement;
  • paranoid delusions (experiences);
  • hallucinations (visual, auditory, etc.).

Psychosis—hallucinations, mania, or—occurs in approximately 10% of people with dementia, although in a significant percentage of patients the onset of these symptoms is temporary.

Diagnostics

Image of a normal brain (left) and with dementia (right)

Manifestations of dementia are treated by a neurologist. Patients are also advised by a cardiologist. If severe mental disorders occur, the help of a psychiatrist is required. Often such patients end up in psychiatric institutions.

The patient must undergo comprehensive examination, which includes:

  • conversation with a psychologist and, if required, with a psychiatrist;
  • dementia tests (brief mental status assessment scale, FAB, BPD and others) electroencephalography
  • instrumental diagnostics (blood tests for HIV, syphilis, thyroid hormone levels; electroencephalography, CT and MRI of the brain and others).

When making a diagnosis, the doctor takes into account that patients with dementia are very rarely able to adequately assess their condition and are not inclined to note the degradation of their own mind. The only exceptions are patients with dementia early stages. Consequently, the patient’s own assessment of his condition cannot become decisive for the specialist.

Treatment

How to treat dementia? Currently, most types of dementia are considered incurable. However, developed healing techniques, allowing to control a significant part of the manifestations of this disorder.

The disease completely changes a person’s character and his desires, so one of the main components of therapy is harmony in the family and in relation to loved ones. At any age, you need help and support, the sympathy of loved ones. If the situation around the patient is unfavorable, then it is very difficult to achieve any progress and improvement in the condition.

When prescribing medications, you need to remember the rules that must be followed so as not to harm the patient’s health:

  • All medications have their own side effects which must be taken into account.
  • The patient will need assistance and supervision to take medications regularly and on time.
  • The same drug can act differently at different stages, so therapy needs periodic adjustment.
  • Many of the drugs can be dangerous if taken in large quantities.
  • Some drugs may not combine well with each other.

Patients with dementia are poorly trained, it is difficult to interest them in new things in order to somehow compensate for lost skills. When treating, it is important to understand that this is an irreversible disease, that is, incurable. Therefore, the question arises about the patient’s adaptation to life, as well as quality care for him. Many devote a certain period of time to caring for the sick, look for caregivers, and quit their jobs.

Prognosis for people with dementia

Dementia usually has a progressive course. However, the rate (speed) of progression varies widely and depends on a number of reasons. Dementia shortens life expectancy, but survival estimates vary.

Activities that ensure safety and provide appropriate environmental conditions are extremely important in treatment, as is the assistance of a caregiver. Some medications may be helpful.

Prevention

In order to prevent the occurrence of this pathological condition, doctors recommend prevention. What will it take?

  • Observe healthy image life.
  • Refuse bad habits: smoking and alcohol.
  • Control blood cholesterol levels.
  • Eat well.
  • Control blood sugar levels.
  • Treat emerging ailments in a timely manner.
  • Spend time on intellectual activities (reading, doing crossword puzzles, etc.).

This is all about dementia in older people: what kind of disease it is, what are its main symptoms and signs in men and women, is there any treatment. Be healthy!

Department of Neurology of the Russian medical academy postgraduate education, Moscow

Mixed dementia occurs as a result of two or more simultaneously developing pathological processes. This article examines the most common form of mixed dementia, which occurs as a result of a combination of Alzheimer's disease and cerebrovascular disease; criteria for diagnosing mixed dementia are proposed, and rational approaches to treatment are discussed.
Keywords: mixed dementia, vascular dementia, Alzheimer's disease, diagnosis, treatment.

About the author:
Levin Oleg Semenovich – Doctor of Medical Sciences, Professor, Head of the Department of Neurology, State Budgetary Educational Institution of Further Professional Education of the Russian Medical Academy of Postgraduate Education, member of the executive committee of the European section of the Movement Disorders Society, Member of the Board of the All-Russian Society of Neurologists, member of the Presidium of the National Society for the Study of Parkinson's Disease and Movement Disorders

Current Approaches to Diagnostics and Treatment of Mixed Dementia

O.S. Levin

Neurology Department, Russian Medicine Academy of Postgraduate Training, Moscow

Mixed dementia results from two or several simultaneous pathological processes. This article discusses the most common form of mixed dementia, resulting from a combination of Alzheimer’s disease and cerebrovascular disease, proposes diagnostic criteria for mixed dementia, and discusses rational approaches to treatment.
Keywords: mixed dementia, vascular dementia, Alzheimer’s disease, diagnostics, treatment.

Mixed dementia is usually understood as dementia that occurs as a result of two or more simultaneously developing pathological processes. In recent years, ideas about the incidence of mixed dementia have changed significantly, and some experts consider it to be the most common form of dementia. In clinical practice, this has been reflected in a clear tendency towards overdiagnosis of mixed dementia, which often leads to inadequate treatment. This article examines the most common form of mixed dementia, resulting from a combination of asthma and cerebrovascular disease, offers criteria for diagnosing mixed dementia, and discusses rational approaches to its treatment.

Although dementia that occurs when a combination of Alzheimer's disease (AD) and cerebrovascular disease is most often called mixed, in the literature one can find examples of other variants of mixed dementia that occur when a combination of:

  • AD with Lewy body disease (“variant of AD with Lewy bodies”);
  • Lewy body disease with cerebrovascular disease;
  • consequences of traumatic brain injury with cerebrovascular or degenerative disease, etc. . In some patients, a combination of not two but three pathological processes is possible, for example, AD, neurodegeneration with the formation of Lewy bodies and cerebrovascular disease.

Alzheimer's disease and cerebrovascular disease

The exact prevalence of mixed dementia is unknown. According to pathological data, mixed dementia can account for 6 to 60% of dementia cases. According to J. Schneider et al. (2008), in 38% of cases, post-mortem examination reveals a combination of Alzheimer's and vascular changes, in 30% of cases, dementia can be associated with Alzheimer's changes, and only in 12% of cases - with isolated vascular damage to the brain. According to pathomorphological studies, at least 50% of patients with asthma have one or another cerebrovascular pathology, but whether it has clinical significance remains unclear. On the other hand, about 80% of patients with vascular dementia have Alzheimer's changes of varying severity. Even with dementia developing after a stroke, only about 40% of cases could be attributed to vascular disease, while in at least a third of patients it was due to concomitant asthma.

The likelihood of detecting mixed pathology in a patient with dementia clearly depends on his age. If “pure” forms of diseases may predominate in young and middle age, then dementia that begins in senile age is especially often of a mixed nature.

Such a frequent combination of asthma and cerebrovascular disease can be explained in various ways. First of all, the commonality of risk factors - arterial hypertension, atrial fibrillation, hyperlipidemia, diabetes mellitus, metabolic syndrome, excess body weight, smoking and, possibly, hyperhomocysteinemia predispose to the development of not only vascular brain damage, but also asthma (although with asthma the latent period of their action may be significantly higher). Epidemiological studies also show that patients with asthma have an increased incidence of stroke and other cerebrovascular disease, while patients with cerebrovascular disease have an increased risk of asthma.

Relationship between vascular and degenerative processes

Degenerative and vascular changes may:

  • do not interact if one or both components are asymptomatic;
  • have an additive effect (the clinical picture becomes the result of the summation of the manifestations of both processes);
  • have a synergistic effect (the manifestation of one pathological process enhances the manifestations of another, or both processes mutually enhance the manifestations of each other);
  • have a competing effect (the symptoms of one pathological process “mask” the manifestation of another pathological process).

In older adults without dementia, asymptomatic microvascular changes and some Alzheimer's changes, such as senile plaques associated with amyloid deposition, are common. In this regard, even the statement of the presence of vascular and degenerative changes during pathomorphological examination in itself, apparently, does not yet provide grounds for diagnosing mixed dementia. Both components must have clinical significance, as evidenced by their severity, localization, and connection with clinical manifestations. According to R.Kalaria et al. (2004), mixed dementia should be diagnosed in the presence of at least three cerebral infarctions and neurofibrillary tangles, the distribution of which corresponds to at least the fourth stage according to Braak - starting from this stage, characterized by the involvement of limbic structures, the degenerative process is clinically manifested by dementia. K. Jellinger (2010), based on a pathomorphological examination of more than a thousand patients with dementia, concluded that cerebrovascular changes are much more common in patients with AD than in dementia with Lewy bodies and Parkinson's disease. Moreover, in AD they do not appear to significantly affect the level of cognitive decline (except in cases of severe multifocal vascular brain damage).

On the other hand, mixed dementia can be diagnosed pathomorphologically in the case when vascular lesions and Alzheimer's changes in their quantitative expression are insufficient to cause dementia, and only their interaction can explain the development of severe cognitive impairment. The importance of the interaction of degenerative and vascular processes has been shown in a number of studies, which have determined that the persistence of cognitive impairment after stroke depends more on the severity of cerebral atrophy than on the size or location of the infarction. Cases have been described where a stroke only contributed to the identification of a previously subclinical degenerative disease - the total volume of the lesion in this case exceeded the threshold for the clinical manifestation of dementia.

In other cases, degenerative and vascular processes can cause damage to the same neural circuits, but at different levels; infarctions in this case are usually localized in strategic areas of the brain. Thus, vascular damage to the dorsomedial region of the thalamus, associated with cholinergic neurons of the anterior basal regions, and primarily with Meynert’s nucleus, can aggravate the defect in patients with subclinically developing AD. Although, with pure lesions of the thalamus, the defect is relatively limited and associated primarily with impaired attention.

Modern ideas about the mechanisms of development of AD and vascular dementia suggest that the interaction between vascular and degenerative processes goes beyond the additive effect and acquires the character of synergy due to interaction at the level of intermediate links in pathogenesis. As a result, cerebrovascular disease and asthma can form a kind of vicious circle, the main pathogenetic links of which are: decreased microvascular reactivity (observed both in cerebrovascular pathology and, to a lesser extent, in asthma), ischemia, neurogenic inflammation, impaired clearance and accumulation of beta -amyloid, which, on the one hand, initiates a violation of the metabolism of tau protein with the formation of neurofibrillary tangles in neurons, and, on the other hand, leads to aggravation of microvascular disorders. This vicious circle predetermines more extensive damage to the brain in mixed dementia.

A special variant of mixed dementia, according to some authors, should be considered cases of AD in which there are diffuse changes in the periventricular white matter, which in some cases may be associated with concomitant cerebrovascular disease (for example, hypertensive microangiopathy), and in others reflect the presence of cerebral amyloid angiopathy . In both cases, brain damage can be represented not only by ischemic changes, but also by macro- or microhemorrhages, which can contribute to cognitive decline. A model where one pathological process “masks” the clinical manifestations of another pathological process has been noted in patients who simultaneously have signs of the Alzheimer’s process and degeneration with the formation of Lewy bodies. In patients with concomitant Alzheimer's changes, some typical clinical manifestations of degeneration with Lewy bodies were less pronounced.

How to clinically diagnose mixed dementia?

Mixed dementia is usually diagnosed with the simultaneous identification of clinical and/or neuroimaging signs of both AD and cerebrovascular disease. However, a simple statement of the simultaneous presence of vascular foci (both ischemic and hemorrhagic) or leukoaraiosis and cerebral atrophy, according to CT or MRI, cannot serve as a basis for diagnosing mixed dementia, since, for example, a stroke can only accompany asthma without significantly affecting way on the patient's cognitive functions. Moreover, there is no reason to diagnose it in a patient with clinical asthma if he has vascular risk factors (for example, arterial hypertension) or atherosclerotic stenosis of the carotid arteries or has anamnestic indications of stroke that are not confirmed by neuroimaging data.

Apparently, the diagnosis of mixed dementia is justified only when, based on the concept of one disease, it is impossible to explain the clinical picture or features of the process in a given patient.

It should be taken into account that BA is a more hidden process that does not manifest itself as a dramatic picture of a stroke or easily detectable specific changes on CT and MRI. However, its presence can be judged by the characteristic cognitive profile, reflecting the predominant involvement of the temporoparietal structures, the progressive course of the disease with a characteristic evolution of the neuropsychological status. The possibility of asthma should also be considered if there is a family history of indications for this disease.

According to the neuropsychological profile, patients with mixed dementia usually occupy an intermediate position between patients with “pure” AD and “pure” vascular dementia, but in most cases they are closer to patients with AD than to patients with vascular dementia. Thus, the presence of a “vascular component” may contribute to an earlier onset of AD and the development of a more pronounced dysregulatory (frontal) defect, but at a later stage of development it is Alzheimer’s changes that decisively determine the rate of cognitive decline and the neuropsychological profile.

In agreement with this are the data of D. Lisbon et al. (2008), according to which patients with extensive leukoaraesis exhibit a neuropsychological profile characteristic of DEP, that is, a pronounced dysregulatory defect with relative preservation of memory (assessed not by reproduction, but by recognition), while for patients with mild leukoaraesis the opposite relationship is characteristic: pronounced memory loss with moderate impairment in performing tests assessing mental control, which is more typical for AD. It can be assumed that the development of mixed dementia can be explained Alzheimer's phenomenon neuropsychological profile in some patients with dyscirculatory encephalopathy.

The rate of cognitive decline may have important diagnostic implications. The results of the meta-analysis by G. Frisoni et al. have already been mentioned. (2007), the increase in the severity of leukoencephalopathy (leukoaresis) can explain the decrease in the Mini-Mental State Examination (MMSE) score by an average of 0.28 points per year (for comparison: with natural aging the MMSE score per year decreases by less than one thousandth of a point, that is, it remains practically stable, and with AD it decreases by about 3 points). It is not surprising that according to the results of prospective studies, mixed dementia occupies an intermediate position in terms of the rate of cognitive decline between AD, characterized by a higher rate of cognitive decline (2-4 points on the MMSE per year) and pure diabetes (0.5-1.0 points per year). year) .

On the other hand, the cerebrovascular process is not always obvious, which, especially with cerebral microangiopathy, can occur covertly, without episodes of stroke, but, nevertheless, accelerate the onset or modify the course of parallel developing BA. In the latter case, the neuropsychological profile, generally characteristic of AD, may acquire a subcortical-frontal component in the form of impaired attention and regulatory functions, slowed mental activity, and/or be accompanied by an earlier development of walking disorders, postural instability, dysarthria, and neurogenic urination disorders. Although neuroimaging techniques play a key role in identifying the vascular component of mixed dementia, some microvascular lesions (eg, cortical microinfarcts) remain “invisible” to modern methods structural neuroimaging and can only be detected during pathomorphological examination. This blurs clinical and neuroimaging correlations and makes it difficult to identify the mixed nature of dementia. The nosological diagnosis of dementia is also complicated by the existence of atypical forms of AD, primarily its “frontal form,” characterized by the early development of regulatory cognitive impairment.

In clinical practice, mixed dementia is most often diagnosed in 3 situations. Firstly, with a rapid increase in cognitive defect after a stroke in a patient who previously suffered from asthma. Secondly, with the development of progressive dementia with a pronounced cortical (temporo-parietal) component within several months after a stroke in an initially safe patient (already mentioned, in about a third of cases post-stroke dementia is explained by the addition or acceleration of the development of Alzheimer's degeneration). Thirdly, mixed dementia may be characterized by the parallel development of diffuse ischemic lesion deep white matter of the cerebral hemispheres and degeneration of the temporal lobe, which can be identified using neuroimaging.

Once again, it should be emphasized that the main principle for diagnosing mixed dementia should be the correspondence between the nature, degree and localization of neuroimaging changes and clinical (cognitive, behavioral, motor) disorders - taking into account established clinical and neuroimaging correlations. For example, the severity of atrophy of the temporo-parietal region and hippocampus should correspond to certain impairments of memory, speech and visuospatial functions, and the presence of leukoaraiosis should correspond to cognitive or motor impairments of the subcortical (fronto-subcortical) type. In addition, assessment of the course is important: for example, the persistence of acutely developed cognitive impairment, disproportionate to the vascular focus, also indicates the possibility of mixed dementia. Thus, simultaneous analysis of clinical and neuroimaging manifestations contributes to the diagnosis of “mixed” dementia and assessment of the “contribution” of each disease to the final clinical picture.

Based on these data, the criteria for mixed dementia in the most general form can be formulated as follows:

1) The presence of cognitive deficits, the profile and dynamics of which are characteristic of asthma, in combination with anamnestic data and/or neurological deficits indicating cerebrovascular disease.
And/or
2) A combination of MRI changes characteristic of AD (primarily hippocampal atrophy) and diabetes (leukoaraiosis, lacunae, infarction), especially if neuroimaging signs of cerebrovascular disease are insufficient to explain the patient’s cognitive deficit.

Features that may be suggestive of mixed dementia in patients with clear clinical evidence of AD or cerebrovascular disease are summarized in the table.

A similar approach was proposed in 2010 by the already mentioned international group of experts led by B. Dubois. According to it, “mixed asthma” should be diagnosed if the typical clinical phenotype of asthma has one or more elements, including anamnestic indications of a recent or previous stroke, early-onset walking disorders or parkinsonism, psychotic disorders or cognitive fluctuations, sufficiently pronounced neuroimaging signs of cerebrovascular diseases.

It was hoped that identification of biomarkers of AD and other degenerative dementias (eg, CSF levels of amyloid beta and tau protein) would in the future lead to a more accurate diagnosis of mixed dementia. However, according to recent publications, even in pure vascular dementia, elevated levels of total tau protein may be detected in the CSF, which was considered typical of AD. Although a low level of beta-amyloid is more likely to indicate AD or mixed dementia with an Alzheimer's component, its differential diagnostic significance has not been adequately assessed. Thus, these biomarkers can undoubtedly contribute to the early diagnosis of AD, differentiating it from age norm, however, their significance in the differential diagnosis of AD, vascular and mixed dementia remains unclear today.

Principles of treatment

Based on general considerations, treatment of mixed dementia should be aimed at all pathological processes detected in the patient. Even if the cerebrovascular process is not a leading factor in the development of dementia, it can contribute to the progression of cognitive defect and needs correction to the same extent as in purely vascular dementia. Accordingly, treatment should include measures to correct vascular risk factors, including the use of antihypertensive drugs, statins, etc., and the prevention of recurrent ischemic episodes (for example, antiplatelet agents). Of particular importance may be the use of statins, which not only contribute to the normalization lipid profile, but also, as experimental data show, they have an anti-inflammatory and antithrombogenic effect, reduce the accumulation of beta-amyloid in the brain, improve endothelial function and increase the reactivity of cerebral vessels.

At the same time, a series of studies evaluating the effectiveness of antihypertensive drugs, statins, and aspirin in patients with already developed BA gave negative results. Hyperhomocysteinemia is also a risk factor for dementia, which can be corrected with folic acid, vitamins B12 and B6. Although the role of homocysteine ​​as a risk factor for both vascular and degenerative dementia is well established, it has not yet been possible to prove that a decrease in homocysteine ​​levels is accompanied by a decrease in the risk of cerebrovascular lesions and cognitive impairment. This leads to the conclusion that hyperhomocysteinemia may be a marker of increased risk of dementia rather than a cause.

Endothelial dysfunction, which disrupts the functioning of neurovascular units in microvascular pathology, can be considered one of the most promising targets for therapeutic intervention in mixed dementia. To date, experiments have shown that statins, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and cholinomimetics can increase the reactivity of small vessels and improve brain perfusion, but whether this effect has clinical significance remains unclear. Antioxidants (particularly Neurox), which block the action of free radicals generated due to ischemia, can also potentially increase functional hyperemia by promoting the coupling of neurons and the small vessels that supply them.

Unfortunately, at the moment, there are no proven possibilities for etiopathogenetic effects on the degenerative component of mixed dementia, which would at least slow down the process of degeneration and cell death. Despite the widespread popularity of so-called “vasoactive agents,” their role in the treatment of mixed dementia remains unproven. Their long-term ability to improve brain perfusion and disease prognosis is seriously questionable. The weakening of the reactivity of affected small vessels can be a serious obstacle to their therapeutic effect.

However, modern antidementia drugs (cholinesterase inhibitors and memantine) make it possible to slow down the process of cognitive decline and delay the development of behavioral disorders and complete loss of everyday autonomy in patients with AD. These drugs, as shown in controlled studies, can also reduce the cognitive deficits characteristic of vascular dementia.

The basis for the use of cholinesterase inhibitors in asthma is the deficiency of the cholinergic system identified in this disease. With regard to cerebrovascular pathology, data on the state of the cholinergic system are more contradictory. As some studies show, a deficit of the cholinergic system is more or less predictably detected in cerebrovascular pathology only in the presence of additional Alzheimer's changes. In this regard, the use of cholinesterase inhibitors in patients with mixed dementia seems promising.

Currently in controlled clinical trials in mixed dementia, the effectiveness of the cholinesterase inhibitor galantamine, which also enhances cholinergic transmission through modulation of central H-cholinergic receptors, has been proven. An analysis of the results of a study of rivastigmine in patients with vascular dementia showed that the drug was more effective in cases where the dementia was more likely to be mixed (in patients over 75 years of age, as well as in the presence of atrophy medial sections temporal lobes). However, even in this category of patients, rivastigmine improved cognitive function rather than the state of daily activity.

These data confirm that cholinergic deficit in patients with vascular dementia most likely reflects the presence of a concomitant Alzheimer's component. On the other hand, one of the earlier studies of rivastigmine showed that patients with AD who had arterial hypertension responded better to the drug than patients without hypertension, which further justifies the use of cholinomimetic agents in mixed dementia.

In addition to influencing cognitive functions, as experimental data show, cholinomimetics can inhibit the accumulation of beta-amyloid and the formation of amyloid deposits in the brain, which contribute to the “Alzheimerization” of cognitive impairment in cerebrovascular pathology, protect cell cultures from the toxic effects of amyloid and free radicals, enhance brain perfusion, having a vasodilating effect on the vessels of the cerebral cortex. Moreover, it has been shown that cholinergic drugs are capable of increasing the reactivity of small vessels, enhancing the phenomenon of working hyperemia, and the vasoactive component of their action can be mediated by an effect on the nitric oxide production system, a key link in the regulation of vascular tone. In addition, cholinomimetics can affect another intermediate link in the vascular and degenerative process - the process of neuroinflammation, which is controlled by the cholinergic pathway and through increasing the level of extracellular (extrasynaptic) acetylcholine can be weakened.

Two controlled studies lasting 6 months showed a positive effect of memantine on cognitive function in patients with mild to moderate vascular dementia. In both studies, the drug better helped patients who did not have macrostructural changes in the brain according to neuroimaging, which can be interpreted as higher effectiveness of the drug in patients with microvascular and mixed dementia.

One of the promising approaches that can improve the effectiveness of mixed dementia is the use of acetylcholine precursors, in particular choline alfoscerate (ceretone). A group of acetylcholine precursors that historically were the first cholinomimetic drugs to be used for cognitive impairment. However, clinical trials of first-generation acetylcholine precursors, choline and phosphatidylcholine (lecithin), were unsuccessful (both as monotherapy and in combination with a cholinesterase inhibitor). Their ineffectiveness may have been due to the fact that they increased acetylcholine levels in the brain, but did not stimulate its release, and also did not penetrate the blood-brain barrier well.

Second generation drugs (including choline alfoscerate) do not have this drawback. Choline alphoscerate, when entering the body, is broken down into choline and glycerophosphate. Thanks to rapid increase plasma concentrations and electrical neutrality, choline released during the breakdown of choline alfoscerate penetrates the blood-brain barrier and participates in the biosynthesis of acetylcholine in the brain. The result is an increase in cholinergic activity, both due to increased acetylcholine synthesis and its release.

According to experimental data, choline alfoscerate enhances the release of acetylcholine in the hippocampus of rats, improves memory impaired by the administration of scopolamine, restores markers of cholinergic transmission in old rats, and has a neuroprotective effect, improving tissue survival. Along with drugs of some other groups (serotonergic antidepressants, small doses of levodopa), choline alfoscerate is able to stimulate the activity of progenitor cells in the hippocampus and subventricular zone and the processes of neoneurogenesis. Controlled clinical trials have shown that choline alfoscerate may be useful in post-stroke dementia, including in combination with cholinesterase inhibitors and memantine. A similar approach may be promising for mixed dementia.

Literature

1. Gavrilova S.I. Pharmacotherapy of Alzheimer's disease. M.: 2003; 319.
2. Damulin I.V. Vascular dementia and Alzheimer's disease. M.: 2002; 85.
3. Levin O.S. Clinical magnetic resonance imaging study of dyscirculatory encephalopathy with cognitive impairment. Diss. Ph.D. med. sc. M.: 1996.
4. Levin O.S. Diagnosis and treatment of dementia in clinical practice. M.: Medpress-inform, 2009; 255.
5. Ferstl G., Melike A., Weichel K. Dementia. Per with him. M.: Medpress-inform, 2010; 250.
6. Yakhno N.N. Cognitive disorders in a neurological clinic. Neurol. magazine 2006; 11: Adj. 1:4–13.
7. Ballard C., Sauter M., Scheltens P. et al. Efficacy, safety and tolerability of rivastigmine capsules in patients with probable vascular dementia: the VantagE study. Current Medical Research and Opinion. 2008; 24:2561–2574.
8. Baor K.J., Boettger M.K., Seidler N.et al Influence of galantamine on vasomotor reactivity in Alzheimer’s disease and vascular dementia due to cerebral microangiopathy. Stroke. 2007; 38:3186–3192.
9. Benarroch E. Neurovascular unit dysfunction: a vascular component of Alzheimer disease? Neurology. 2007; 68:1730–1732.
10. Blessed G., Tomlinson B.E., Roth M. The association between quantitative measures of dementia and of senile change in the cerebral gray matter of elderly subjects. Br. J. Psychiatry. 1968; 114:797–811.
11. Bruandet A., Richard F., Bombois S. Alzheimer disease with cerebrovascular disease compared with Alzheimer disease and vascular dementia. J. Neurol. Neurosurg. Psychiatry. 2009; 80: 133–139.
12. Dubois B., Feldman H., Jacova C. et al. Revising the definition of Alzheimer's disease: a new lexicon. Lancet Neurology. 2010; 9: 1118–1127.
13. Erkinjuntti T., Kurz A., Gauthier S. et al. Efficacy of galantamine in probable vascular dementia and Alzheimer’s disease combined with cerebrovascular disease: a randomized trial. Lancet. 2002; 359:1283–1290.
14. Erkinjuntti T., Kurz A., Small G.W. et al. An open-label extension trial of galantamine in patients with probable vascular dementia and mixed dementia. Clin Ther. 2003; 25: 1765–1782.
15. Erkinjuntti T., Skoog I., Lane R., Andrews C. Rivastigmine in patients with Alzheimer’s disease and concurrent hypertension. Int. J. Clin. Pract. 2002; 56:791–796.
16. Feldman H.H., Doody R.S., Kivipelto M. et al. Randomized controlled trial of atorvastatin in mild to moderate Alzheimer disease. Neurology. 2010; 74:956–964.
17. Frisoni G.B., Galluzzi S., Pantoni L. et al. The effect of white matter problems on cognition in the elderly. Nat.Clin.Pract.Neurology. 2007; 3: 620–627.
18. Girouard H., Iadecola C. Neurovascular coupling in the normal brain and in hypertension. Stroke and Alzheimer's disease. J.Appl.Physiol. 2006; 100:328–335.
19. Iadecola C. Neurovascular regulation in the normal brain and in Alzheimer’s disease. Nat. Rev. Neurosci. 2004; 5:347–360.
20. Jellinger KA. The enigma of vascular cognitive disorder and vascular dementia. Acta Neuropathol (Berl). 2007; 113:349–388.
21. Jellinger K.A., Attems J. Is there pure vascular dementia in old age? J Neurol Sci. 2010; 299; 150–155.
22. Jellinger K.A. Prevalence and Impact of Cerebrovascular Lesions in Alzheimer and Lewy Body Diseases. Neurodegenerative Dis. 2010; 7: 112–115.
23. Kalaria R.N., Kenny R.A., Ballard C. et al. Towards defining neuropathological substrates of vascular dementia. J. Neurol Sci. 2004; 226:75–80.
24. Leys D., Henon H., Mackowiak-Cordoliani M.A., Pasquier F. Poststroke dementia. Lancet Neurol. 2005; 752–759.
25. Libon D., Price C., Giovannetti T. et al Linking MRI hyperintensities with patterns of neuropsychological impairment. Stroke. 2008; 39:806–813.
26. McGuinness B., Todd S., Passmore A. P. et al. Systematic review: blood pressure lowering in patients without prior cerebrovascular disease for prevention of cognitive impairment and dementia. J. Neurol. Neurosurg. Psychiatry. 2008; 79:4–5.
27. Mesulam M, Siddique T, Cohen B. Cholinergic denervation in a pure multi-infarct state: observations on CADASIL. Neurology. 2003; 60: 1183–1185.
28. O'Brien J.T., Erkinjuntti T., Reisberg B. et al. Vascular cognitive impairment. Lancet Neurology. 2003; 2:89–98.
29. O'Connor D. Epidemiology. / A. Burns et al (eds). Dementia. 3-d ed. New York, Holder Arnold, 2005; 16–23.
30. Orgogozo J.M., Rigaud A.S., Stöffler A, et al. Efficacy and Safety of Memantine in Patients With Mild to Moderate Vascular Dementia: A Randomized, Placebo-Controlled Trial (MMM 300). Stroke. 2002; 33: 1834–1839.
31. Rockwood K., Wentzel C., Hachinski V. et al. Prevalence and outcomes of vascular cognitive impairment. Neurology. 2000; 54:447–451.
32. Roman G.C., Tatemichi T.K., Erkinjuntti T., et al. Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology. 1993; 43: 250–260.
33. Román GC, Royall DR. Executive control function: a rational basis for the diagnosis of vascular dementia. Alzheimer's Dis Assoc Disord. 1999; 13: Suppl 3: 69–80.
34. Roman G.C., Kalaria R.N. Vascular determinants of cholinergic deficits in Alzheimer disease and vascular dementia. Neurobiol aging. 2006; 27: 1769–1785.
35. Schneider J.A., Arvanitakis Z., Bang W., Bennett D.A. Mixed brain pathologies account for most dementia cases in community-dwelling older persons. Neurology. 2007; 69:2197–2204.
36. Shanks M., Kivipelto M., Bullock R. Cholinesterase inhibition: there is evidence for
disease-modifying effects? Current Medical Research and Opinion. 2009; 25:2439–2446.
37. Snowdon D.A., Greiner L.H., Mortimer J.A., et al. Brain infarction and the clinical expression of Alzheimer disease: the Nun Study. JAMA. 1997; 277:813–817.
38. Sparks D. L., Sabbagh M. N., Connor D. J., et al. Atorvastatin for the treatment of mild to moderate Alzheimer disease: preliminary results. Arch Neurol. 2005; 62:753–757.
39. Staekenborg S., Van der Flier W., Van Straaten E. et al. Neurological signs in relation to type of cerebrovascular disease in vascular dementia. Stroke. 2008; 39: 317–322.
40. Wilcock G., Möbius H.J., Stöffler A. A double-blind, placebo-controlled multicentre study of memantine in mild to moderate vascular dementia (MMM 500). Int. Clin. Psychopharmacol. 2002; 17: 297–305.
41. Woodward M., Brodaty H., Boundy K. Does executive impairment define a frontal variant of Alzheimer’s disease? International Psychogeriatrics. 2010; 22: 1280–1290.
42. Zekry D., Hauw J.J., Gold G. Mixed dementia: epidemiology, diagnosis, and treatment. J Am Geriatr Soc. 2002; 50: 1431–1438.
43. Zekry D., Gold G. Management of Mixed Dementia. Drugs and Aging. 2010; 27: 715–728.

Dementia defines an acquired form of dementia, in which patients experience a loss of previously acquired practical skills and acquired knowledge (which can occur in varying degrees of intensity of manifestation), while at the same time a persistent decrease in their cognitive activity. Dementia, the symptoms of which, in other words, manifest themselves in the form of a breakdown of mental functions, is most often diagnosed in old age, but the possibility of its development at a young age cannot be ruled out.

general description

Dementia develops as a result of brain damage, against which a marked decline in mental functions occurs, which generally makes it possible to distinguish this disease from mental retardation, congenital or acquired forms of dementia. Mental retardation (also known as oligophrenia or dementia) implies a stop in personality development, which also occurs with brain damage as a result of certain pathologies, but predominantly manifests itself in the form of damage to the mind, which corresponds to its name. Wherein mental retardation differs from dementia in that with it the intelligence of a person, a physically adult, does not reach normal levels corresponding to his age. In addition, mental retardation is not a progressive process, but is the result of a disease suffered by a sick person. However, in both cases, both when considering dementia and when considering mental retardation, there is the development of a disorder of motor skills, speech and emotions.

As we have already noted, dementia overwhelmingly affects people in old age, which determines its type as senile dementia (it is this pathology that is usually defined as senile insanity). However, dementia also appears in youth, often as a result of addictive behavior. Addiction means nothing more than addictions or addictions - a pathological attraction in which there is a need to perform certain actions. Any type of pathological attraction increases the risk of developing mental illness in a person, and often this attraction is directly related to social problems or personal problems that exist for him.

Addiction is often used in connection with such phenomena as drug addiction and drug dependence, but more recently another type of addiction has been defined for it - non-chemical addictions. Non-chemical addictions, in turn, define psychological addiction, which itself acts as an ambiguous term in psychology. The fact is that predominantly in the psychological literature this kind of dependence is considered in a single form - in the form of dependence on narcotic substances (or intoxicants).

However, if we consider this type of addiction at a deeper level, this phenomenon also arises in the everyday mental activity that a person encounters (hobbies, interests), which, thereby, defines the subject of this activity as an intoxicating substance, as a result of which he, in in turn, is considered as a substitute source that causes certain missing emotions. These include shopaholism, Internet addiction, fanaticism, psychogenic overeating, gambling addiction, etc. At the same time, addiction is also considered as a method of adaptation, through which a person adapts to conditions that are difficult for himself. The elementary agents of addiction are drugs, alcohol, and cigarettes, which create an imaginary and short-term atmosphere of “pleasant” conditions. A similar effect is achieved when performing relaxation exercises, while resting, as well as through actions and things that bring short-term joy. In any of these options, after their completion, a person has to return to reality and conditions from which he managed to “escape” in such ways, as a result of which addictive behavior is considered as a rather complex problem of internal conflict, based on the need to escape from specific conditions, against the background of which and there is a risk of developing mental illness.

Returning to dementia, we can highlight the current data provided by WHO, based on which it is known that global incidence rates number about 35.5 million people with this diagnosis. Moreover, it is expected that by 2030 this figure will reach 65.7 million, and by 2050 it will be 115.4 million.

With dementia, patients are not capable of realizing what is happening to them; the disease literally “erases” everything from their memory that accumulated in it during the previous years of life. Some patients experience the course of such a process at an accelerated pace, which is why they quickly develop total dementia, while other patients can linger for a long time at the stage of the disease within the framework of cognitive-mnestic disorders (intellectual-mnestic disorders) - that is, with disorders mental performance, decreased perception, speech and memory. In any case, dementia not only determines the result for the patient in the form of problems of an intellectual scale, but also problems in which he loses many human personality traits. The severe stage of dementia determines for patients dependence on others, maladaptation, they lose the ability to perform simple actions related to hygiene and eating.

Causes of dementia

The main causes of dementia are the presence of Alzheimer's disease in patients, which is defined, respectively, as Alzheimer's type dementia, as well as with actual vascular lesions to which the brain is exposed - the disease in this case is defined as vascular dementia. Less commonly, the causes of dementia are any neoplasms that develop directly in the brain; this also includes traumatic brain injuries ( non-progressive dementia ), diseases of the nervous system, etc.

The etiological significance in considering the causes leading to dementia is assigned to arterial hypertension, disorders of the systemic circulation, lesions great vessels against the background of atherosclerosis, arrhythmias, hereditary angiopathy, repeated disorders relevant to cerebral circulation (vascular dementia).

The etiopathogenetic variants leading to the development of vascular dementia include its microangiopathic variant, macroangiopathic variant and mixed variant. This is accompanied by multi-infarct changes occurring in the brain substance and numerous lacunar lesions. In the macroangiopathic variant of the development of dementia, pathologies such as thrombosis, atherosclerosis and embolism are distinguished, against the background of which occlusion develops in a large artery of the brain (a process in which narrowing of the lumen and blockage of the vessel occurs). As a result of this course, a stroke develops with symptoms corresponding to the affected pool. As a result, vascular dementia subsequently develops.

As for the next, microangiopathic development option, here angiopathy and hypertension are considered as risk factors. The characteristics of the lesion in these pathologies lead in one case to demyelination of the white subcortical matter with the simultaneous development of leukoencephalopathy, in another case they provoke the development of lacunar lesion, against which Binswanger's disease develops, and because of which, in turn, dementia develops.

In about 20% of cases, dementia develops against the background of alcoholism, the appearance of tumor formations and the previously mentioned traumatic brain injuries. 1% of the incidence is due to dementia due to Parkinson's disease, infectious diseases, degenerative diseases of the central nervous system, infectious and metabolic pathologies, etc. Thus, a significant risk has been identified for the development of dementia due to actual diabetes mellitus, HIV, infectious diseases of the brain (meningitis, syphilis) , dysfunction of the thyroid gland, diseases of internal organs (renal or liver failure).

Dementia in older people, by the nature of the process, is irreversible, even if the possible factors that provoked it are eliminated (for example, taking medications and their withdrawal).

Dementia: classification

Actually, based on a number of listed features, types of dementia are determined, namely senile dementia And vascular dementia . Depending on the degree of social adaptation that is relevant for the patient, as well as the need for supervision and receiving outside help in combination with his ability to self-care, corresponding forms of dementia are distinguished. So, in the general course, dementia can be mild, moderate or severe.

Mild dementia implies a condition in which a sick person is faced with degradation in terms of his existing professional skills; in addition, his social activity also decreases. Social activity in particular means a reduction in the time spent on everyday communication, thereby spreading to the immediate environment (colleagues, friends, relatives). In addition, in a state of mild dementia, patients also have a weakened interest in the conditions of the outside world, as a result of which it is important to abandon their usual options for spending free time and hobbies. Mild dementia is accompanied by the preservation of existing self-care skills; in addition, patients adequately navigate within the confines of their home.

Moderate dementia leads to a condition in which patients can no longer remain alone with themselves for a long period of time, which is caused by the loss of skills in using technology and devices surrounding them (remote control, telephone, stove, etc.), difficulties even using door locks. Constant monitoring and assistance from others is required. As part of this form of the disease, patients retain the skills to self-care and perform actions related to personal hygiene. All this, accordingly, makes life more difficult for those around the patients.

As for such a form of the disease as severe dementia then here we are talking about the absolute disadaptation of patients to what surrounds them with the simultaneous need to provide constant assistance and control, which are necessary even for performing the simplest actions (eating, dressing, hygiene measures, etc.).

Depending on the location of the brain damage, the following types of dementia are distinguished:

  • cortical dementia - the lesion predominantly affects the cerebral cortex (which occurs against the background of conditions such as lobar (frontotemporal) degeneration, alcoholic encephalopathy, Alzheimer's disease);
  • subcortical dementia - in this case, subcortical structures are predominantly affected (multi-infarct dementia with white matter lesions, supranuclear progressive palsy, Parkinson's disease);
  • cortical-subcortical dementia (vascular dementia, cortical-basal form of degeneration);
  • multifocal dementia - many focal lesions are formed.

The classification of the disease we are considering also takes into account dementia syndromes that determine the corresponding variant of its course. In particular this could be lacunar dementia , which implies a predominant memory loss, manifested in the form of a progressive and fixation form of amnesia. Compensation for such a defect by patients is possible due to important notes on paper, etc. The emotional-personal sphere in this case is slightly affected, because the core of the personality is not subject to damage. Meanwhile, the appearance of emotional lability (instability and changeability of moods), tearfulness and sentimentality in patients is not excluded. An example of this type of disorder is Alzheimer's disease.

Alzheimer's type dementia , the symptoms of which appear after the age of 65 years, in the initial (initial) stage occurs in combination with cognitive-mnestic disorders with increasing disturbances in the form of orientation in place and time, delusional disorders, the appearance of neuropsychological disorders, subdepressive reactions in relation to one’s own incompetence . At the initial stage, patients are capable of critically assessing their condition and taking measures to correct it. Moderate dementia within this condition is characterized by progression of the listed symptoms, especially gross violation functions inherent in intelligence (difficulties in conducting analytical and synthetic activities, reduced level judgments), loss of opportunities to perform professional duties, and the emergence of a need for care and support. All this is accompanied by the preservation of basic personal characteristics, a feeling of one’s own inferiority while adequately responding to the existing disease. In the severe stage of this form of dementia, memory decay occurs completely; support and care are needed in everything and at all times.

The next syndrome is considered total dementia. It means the appearance of gross forms of disorders of the cognitive sphere (impaired abstract thinking, memory, perception and attention), as well as personality (here we already distinguish moral disorders, in which such forms as modesty, correctness, politeness, sense of duty, etc.) disappear. . In the case of total dementia, as opposed to lacunar dementia, the destruction of the core of the personality becomes relevant. Vascular and atrophic forms of damage are considered as the causes leading to the condition in question. frontal lobes brain. An example of such a condition is Pick's disease .

This pathology is diagnosed less frequently than Alzheimer's disease, mainly among women. Among the main characteristics are: current changes within the emotional-personal sphere and the cognitive sphere. In the first case, the state implies rough forms personality disorder, complete lack of criticism, spontaneity, passivity and impulsiveness of behavior; hypersexuality, foul language and rudeness are relevant; the assessment of the situation is impaired, there are disorders of desires and will. In the second, with cognitive disorders, severe forms of thinking impairment are present, and automated skills are retained for a long time; Memory disorders are noted much later than personality changes; they are not as pronounced as in the case of Alzheimer's disease.

Both lacunar and total dementia are in general terms atrophic dementia, and there is also a variant of a mixed form of the disease (mixed dementia) , which implies a combination of primary degenerative disorders, which mainly manifests itself in the form of Alzheimer's disease, and vascular type brain lesions.

Dementia: symptoms

In this section we will look at a generalized view of the signs (symptoms) that characterize dementia. The most characteristic of them are considered disorders associated with cognitive functions, and this kind of impairment is the most pronounced in its own manifestations. Emotional disorders in combination with behavioral disorders are no less important clinical manifestations. The development of the disease occurs gradually (often), its detection most often occurs as part of an exacerbation of the patient’s condition, arising due to changes in the environment surrounding him, as well as during an exacerbation of a somatic disease that is relevant to him. In some cases, dementia can manifest itself in the form of aggressive behavior of the sick person or sexual disinhibition. In the event of personality changes or changes in the patient’s behavior, the question is raised about the relevance of dementia for him, which is especially important if he is over 40 years old and does not have a mental illness.

So, let’s take a closer look at the signs (symptoms) of the disease we are interested in.

  • Disorders related to cognitive functions. In this case, disorders of memory, attention and higher functions are considered.
    • Memory disorders. Memory disorders in dementia consist of damage to both short term memory, and long-term memory; in addition, confabulations are not excluded. Confabulations in particular involve false memories. Facts from them that occurred earlier in reality or facts that previously occurred but underwent a certain modification are transferred to the patient at another time (often in the near future) with their possible combination with events that were completely fictitious by them. A mild form of dementia is accompanied by moderate memory impairment, mainly associated with events occurring in the recent past (forgetting conversations, phone numbers, events that occurred within a certain day). Cases more severe course Dementia is accompanied by retention in memory of only previously learned material while quickly forgetting newly received information. Final stages diseases may be accompanied by forgetting the names of relatives, one’s own occupation and name, this manifests itself in the form of personal disorientation.
    • Attention disorder. In the case of the disease we are interested in, this disorder implies a loss of the ability to respond to several relevant stimuli at once, as well as a loss of the ability to switch attention from one topic to another.
    • Disorders associated with higher functions. In this case, the manifestations of the disease are reduced to aphasia, apraxia and agnosia.
      • Aphasia implies a speech disorder in which the ability to use phrases and words as a means of expressing one’s own thoughts is lost, which is caused by actual damage to the brain in certain areas of its cortex.
      • Apraxia indicates a violation of the patient's ability to perform purposeful actions. In this case, the skills previously acquired by the patient are lost, and those skills that have been formed over many years (speech, household, motor, professional).
      • Agnosia determines a violation of various types of perception in the patient (tactile, auditory, visual) with the simultaneous preservation of consciousness and sensitivity.
  • Disorientation. This type of disorder occurs over time, and mainly within the initial stage of development of the disease. In addition, disruption of orientation in temporal space precedes disruption of orientation on the scale of orientation in place, as well as within the framework of one’s own personality (here the difference between a symptom in dementia and delirium is manifested, the features of which determine the preservation of orientation within the framework of considering one’s own personality). The progressive form of the disease with advanced dementia and pronounced manifestations of disorientation on the scale of the surrounding space determines for the patient the likelihood that he can freely get lost even in an environment that is familiar to him.
  • Behavioral disorders, personality changes. The onset of these manifestations is gradual. The main features characteristic of the individual gradually intensify, transforming into conditions inherent to this disease as a whole. Thus, energetic and cheerful people become restless and fussy, and people who are thrifty and neat, accordingly, become greedy. Transformations inherent in other traits are considered similarly. In addition, there is an increase in selfishness in patients, a disappearance of responsiveness and sensitivity to the environment, they become suspicious, conflictual and touchy. Sexual disinhibition is also detected; sometimes patients begin to wander and collect various rubbish. It also happens that patients, on the contrary, become extremely passive, they lose interest in communication. Untidyness is a symptom of dementia that occurs in accordance with the progression of the general picture of the course of this disease; it is combined with a reluctance to self-care (hygiene, etc.), with uncleanliness and a general lack of reaction to the presence of people next to you.
  • Thinking disorders. There is a slowness in the pace of thinking, as well as a decrease in the ability for logical thinking and abstraction. Patients lose the ability to generalize and solve problems. Their speech is detailed and stereotypical in nature, its scarcity is noted, and as the disease progresses, it is completely absent. Dementia is also characterized by the possible appearance of delusional ideas in patients, often with absurd and primitive content. So, for example, a woman with dementia with a thought disorder before the appearance of delusional ideas may claim that her mink coat was stolen, and such an action may go beyond her environment (i.e. family or friends). The crux of the nonsense in this idea is that she never had a mink coat at all. Dementia in men within this disorder often develops according to a scenario of delusion based on the jealousy and infidelity of the spouse.
  • Decreased critical attitude. We are talking about the attitude of patients both to themselves and to the world around them. Stressful situations often lead to the appearance of acute forms anxiety-depressive disorders (defined as a “catastrophic reaction”), in which there is a subjective awareness of intellectual inferiority. Partially preserved criticism in patients determines the possibility for them to maintain their own intellectual defect, which may look like a sharp change in the topic of conversation, turning the conversation into a humorous form, or distracting from it in other ways.
  • Emotional disorders. In this case, it is possible to determine the diversity of such disorders and their overall variability. Often these are depressive states in patients combined with irritability and anxiety, anger, aggression, tearfulness or, conversely, a complete lack of emotions in relation to everything that surrounds them. Rare cases determine the possibility of developing manic states in combination with a monotonous form of carelessness, with gaiety.
  • Perception disorders. In this case, the conditions of the appearance of illusions and hallucinations in patients are considered. For example, with dementia, a patient is sure that he hears the screams of children being killed in the next room.

Senile dementia: symptoms

In this case, a similar definition of the state of senile dementia is the previously mentioned senile dementia, senile insanity or senile dementia, the symptoms of which arise against the background of age-related changes occurring in the structure of the brain. Such changes occur within neurons; they arise as a result of insufficient blood supply to the brain, the impact on it during acute infections, chronic diseases and other pathologies, which we discussed in the corresponding section of our article. Let us also repeat that senile dementia is an irreversible disorder that affects each of the areas of the cognitive psyche (attention, memory, speech, thinking). As the disease progresses, all skills and abilities are lost; It is extremely difficult, if not impossible, to acquire new knowledge during senile dementia.

Senile dementia, being among the mental illnesses, is the most common disease among older people. Senile dementia occurs almost three times more often in women than in men. In most cases, the age of patients is 65-75 years, on average, in women the disease develops at 75 years, in men - at 74 years.
Senile dementia manifests itself in several varieties of forms, manifesting itself in a simple form, in a presbyophrenic form and in a psychotic form. The specific form is determined by the current rate of atrophic processes in the brain, somatic diseases associated with dementia, as well as factors of a constitutional-genetic scale.

Simple form characterized by inconspicuousness, occurring in the form of disorders generally inherent in aging. With an acute onset, there is reason to assume that pre-existing mental disorders have been intensified due to one or another somatic disease. There is a decrease in mental activity in patients, which is manifested in a slowdown in the pace of mental activity, in its quantitative and qualitative deterioration (implying a violation of the ability to concentrate attention and switch it, its volume is narrowed; the ability to generalize and analyze, to abstract and in general weakens imagination is impaired; the ability to be inventive and resourceful in solving problems that arise in everyday life is lost).

To an increasing extent, a sick person adheres to conservatism in terms of his own judgments, worldview and actions. What happens in the present tense is seen as unimportant and not worth a look, and is often completely rejected. Returning to the past, the patient primarily perceives it as a positive and worthy example in certain life situations. Characteristic feature there becomes a tendency to edify, intractability bordering on stubbornness and increased irritability that arise when there are contradictions or disagreement on the part of the opponent. Interests that previously existed are significantly narrowed, especially if they are in one way or another related to general issues. Increasingly, patients focus their attention on their physical condition, especially with regard to physiological functions (i.e. bowel movements, urination).

Patients also have a decrease in affective resonance, which is manifested in an increase in complete indifference to what does not directly affect them. In addition, attachments weaken (this even applies to relatives), and in general, understanding of the essence of relationships between people is lost. Many people lose their modesty and sense of tact, and the range of shades of mood is also subject to narrowing. Some patients may show carelessness and general complacency, sticking to monotonous jokes and a general tendency to joke, while other patients are dominated by dissatisfaction, pickiness, capriciousness and pettiness. In any case, the patient’s past characterological traits become scarce, and awareness of the personality changes that have arisen either disappears early or does not occur at all.

The presence of pronounced forms of psychopathic traits before the disease (especially those that are sthenic, this concerns power, greed, categoricalness, etc.) leads to their aggravation in manifestation at the initial stage of the disease, often to a caricatured form (which is defined as senile psychopathization ). Patients become stingy, begin to accumulate rubbish, and they increasingly make various reproaches towards their immediate environment, especially regarding irrationality, in their opinion, of expenses. Also subject to censure on their part are the morals that have developed in public life, especially with regard to marital relations, intimate life etc.
Initial psychological changes, combined with the personal changes that occur with them, are accompanied by memory deterioration, in particular with regard to current events. They are usually noticed by those around the patients later than the changes that have occurred in their character. The reason for this is the revival of past memories, which is perceived by the environment as a good memory. Its decay actually corresponds to those patterns that are relevant for a progressive form of amnesia.

So, first, memory associated with differentiated and abstract topics (terminology, dates, titles, names, etc.) comes under attack, then a fixation form of amnesia is added here, manifesting itself in the form of an inability to remember current events. Amnestic disorientation regarding time also develops (i.e., patients are unable to indicate a specific date and month, day of the week), and chronological disorientation also develops (impossibility of determining important dates and events tied to a specific date, regardless of whether such dates relate to personal life or public life). To top it off, spatial disorientation develops (manifests itself, for example, in a situation where, when leaving home, patients cannot return back, etc.).

The development of total dementia leads to impairment of self-recognition (for example, when viewing oneself in reflection). Forgetting the events of the present is replaced by the revival of memories relating to the past, often this can concern youth or even childhood. Often, such a substitution of time leads to the fact that patients begin to “live in the past,” while considering themselves young or children, depending on the time in which such memories occur. Stories about the past in this case are reproduced as events relating to the present time, while it is not excluded that these memories are generally fiction.

The initial periods of the course of the disease can determine the mobility of patients, the accuracy and speed of performing certain actions, motivated by random necessity or, conversely, by habitual performance. Physical insanity is observed already within the framework of an advanced disease (complete collapse of behavior patterns, mental functions, speech skills, often with relative preservation of somatic function skills).

In severe forms of dementia, the previously discussed states of apraxia, aphasia and agnosia are noted. Sometimes these disorders manifest themselves in a sharp form, which may resemble the course of Alzheimer's disease. Few and isolated epileptic seizures, similar to fainting, are possible. Sleep disorders appear, in which patients fall asleep and get up at an unspecified time, and the duration of their sleep ranges from 2-4 hours, reaching an upper limit of about 20 hours. In parallel with this, periods of prolonged wakefulness may develop (regardless of the time of day).

The final stage of the disease determines for patients the achievement of a state of cachexia, in which an extreme form of exhaustion occurs, in which there is a sharp weight loss and weakness, decreased activity in terms of physiological processes with accompanying changes in the psyche. In this case, the characteristic feature is the adoption of the fetal position when the patients are in a drowsy state, there is no reaction to surrounding events, and sometimes muttering is possible.

Vascular dementia: symptoms

Vascular dementia develops against the background of previously mentioned disorders that are relevant for cerebral circulation. In addition, as a result of studying the brain structures of patients after their death, it was revealed that vascular dementia often develops after a heart attack. To be more precise, the point is not so much in the transfer of this condition, but in the fact that because of it a cyst is formed, which determines the subsequent likelihood of developing dementia. This probability is determined, in turn, not by the size of the cerebral artery that has been damaged, but by the total volume of the cerebral arteries that have undergone necrosis.

Vascular dementia is accompanied by a decrease in indicators relevant for cerebral circulation in combination with metabolism, otherwise the symptoms correspond to the general course of dementia. When the disease is combined with a lesion in the form of laminar necrosis, in which glial tissue grows and neurons die, serious complications may develop (vascular blockage (embolism), cardiac arrest).

As for the predominant category of people who develop vascular form dementia, then in this case the data indicate that this predominantly includes persons aged 60 to 75 years, and one and a half times more often these are men.

Dementia in children: symptoms

In this case, the disease, as a rule, appears as a symptom of certain diseases in children, which may include mental retardation, schizophrenia and other types of mental disorders. This disease develops in children with a characteristic decrease in mental abilities, which manifests itself in impaired memorization, and in severe cases, difficulties arise even with remembering one’s own name. The first symptoms of dementia in children are diagnosed early, in the form of loss of certain information from memory. Further, the course of the disease determines the appearance of disorientation within the framework of time and space. Dementia in young children manifests itself in the form of loss of previously acquired skills and in the form of speech impairment (up to its complete loss). The final stage, similar to the general course, is accompanied by the fact that patients stop taking care of themselves; they also lack control over the processes of defecation and urination.

Within childhood, dementia is inextricably linked with oligophrenia. Oligophrenia, or, as we previously defined it, mental retardation, is characterized by the relevance of two features relating to intellectual defect. One of them is that mental underdevelopment is total, that is, both the child’s thinking and his mental activity are subject to defeat. The second feature is that with general mental underdevelopment, the “young” functions of thinking are most affected (young - when considering them on a phylo- and ontogenetic scale); insufficient development is determined for them, which makes it possible to associate the disease with oligophrenia.

Persistent intellectual disability, which develops in children after 2-3 years of age against the background of trauma and infection, is defined as organic dementia, the symptoms of which appear due to the collapse of relatively mature intellectual functions. Such symptoms, due to which it is possible to differentiate this disease from oligophrenia, include:

  • lack of mental activity in its purposeful form, lack of criticism;
  • pronounced type of memory and attention impairment;
  • emotional disturbances in a more pronounced form, not correlating (i.e. not associated) with the actual degree of decline in intellectual abilities for the patient;
  • frequent development of disorders relating to instincts (perverted or increased forms of desire, performance of actions under the influence of increased impulsiveness, weakening of existing instincts (instinct of self-preservation, lack of fear, etc.) is not excluded);
  • Often the behavior of a sick child does not adequately correspond to a specific situation, which also happens if a pronounced form of intellectual disability is irrelevant for him;
  • in many cases, the differentiation of emotions is also subject to weakening, there is a lack of attachment in relation to close people, and the child’s complete indifference is noted.

Diagnosis and treatment of dementia

Diagnosis of the patient’s condition is based on a comparison of the symptoms that are relevant to them, as well as on the recognition of atrophic processes in the brain, which is achieved through computed tomography (CT).

Regarding the issue of treating dementia, now effective way There is no cure, particularly when considering cases of senile dementia, which, as we have noted, is irreversible. Meanwhile, proper care and the use of therapy measures aimed at suppressing symptoms can, in some cases, seriously alleviate the patient’s condition. It also discusses the need to treat concomitant diseases (with vascular dementia in particular), such as atherosclerosis, arterial hypertension, etc.

Treatment of dementia is recommended within the home environment, hospitalization or psychiatric department relevant for severe disease development. It is also recommended to create a daily routine so that it includes a maximum of vigorous activity while periodically performing household chores (with an acceptable form of load). Psychotropic drugs are prescribed only in case of hallucinations and insomnia; in the early stages it is advisable to use nootropic drugs, then nootropic drugs in combination with tranquilizers.

Prevention of dementia (in its vascular or senile form), as well as effective treatment of this disease is currently excluded due to the practical absence of appropriate measures. If symptoms indicating dementia appear, it is necessary to visit specialists such as a psychiatrist and a neurologist.

– acquired dementia caused by organic brain damage. It may be a consequence of one disease or be of a polyetiological nature (senile or senile dementia). Develops in vascular diseases, Alzheimer's disease, trauma, brain tumors, alcoholism, drug addiction, central nervous system infections and some other diseases. Persistent intellectual disorders, affective disorders and decreased volitional qualities are observed. The diagnosis is established based on clinical criteria and instrumental studies (CT, MRI of the brain). Treatment is carried out taking into account the etiological form of dementia.

General information

Dementia is a persistent disorder of higher nervous activity, accompanied by the loss of acquired knowledge and skills and a decrease in learning ability. There are currently more than 35 million people suffering from dementia worldwide. The prevalence of the disease increases with age. According to statistics, severe dementia is detected in 5%, mild – in 16% of people over 65 years of age. Doctors assume that the number of patients will increase in the future. This is due to an increase in life expectancy and an improvement in the quality of medical care, which makes it possible to prevent death even in cases of severe injuries and diseases of the brain.

In most cases, acquired dementia is irreversible, so the most important task of doctors is timely diagnosis and treatment of diseases that can cause dementia, as well as stabilization of the pathological process in patients with acquired dementia. Treatment of dementia is carried out by specialists in the field of psychiatry in collaboration with neurologists, cardiologists and doctors of other specialties.

Causes of dementia

Dementia occurs when organic damage brain as a result of injury or disease. Currently there are more than 200 pathological conditions that can provoke the development of dementia. The most common cause of acquired dementia is Alzheimer's disease, accounting for 60-70% of total number cases of dementia. In second place (about 20%) are vascular dementias caused by hypertension, atherosclerosis and other similar diseases. In patients suffering from senile dementia, several diseases that provoke acquired dementia are often detected at once.

In young and middle age, dementia can occur with alcoholism, drug addiction, traumatic brain injury, benign or malignant neoplasms. In some patients, acquired dementia is detected due to infectious diseases: AIDS, neurosyphilis, chronic meningitis or viral encephalitis. Sometimes dementia develops with severe diseases of internal organs, endocrine pathology and autoimmune diseases.

Classification of dementia

Taking into account the predominant damage to certain areas of the brain, four types of dementia are distinguished:

  • Cortical dementia. The cerebral cortex is predominantly affected. It is observed in alcoholism, Alzheimer's disease and Pick's disease (frontotemporal dementia).
  • Subcortical dementia. Subcortical structures suffer. Accompanied by neurological disorders (trembling limbs, muscle stiffness, gait disorders, etc.). Occurs in Parkinson's disease, Huntington's disease and white matter hemorrhages.
  • Cortico-subcortical dementia. Both the cortex and subcortical structures are affected. Observed when vascular pathology.
  • Multifocal dementia. Multiple areas of necrosis and degeneration form in various parts of the central nervous system. Neurological disorders are very diverse and depend on the location of the lesions.

Depending on the extent of the lesion, two forms of dementia are distinguished: total and lacunar. With lacunar dementia, the structures responsible for certain types of intellectual activity suffer. Short-term memory disorders usually play a leading role in the clinical picture. Patients forget where they are, what they planned to do, what they agreed on just a few minutes ago. Criticism of one’s condition is preserved, emotional and volitional disturbances are weakly expressed. Signs of asthenia may be detected: tearfulness, emotional instability. Lacunar dementia is observed in many diseases, including in the early stages of Alzheimer's disease.

With total dementia, there is a gradual disintegration of the personality. Intelligence decreases, learning abilities are lost, and the emotional-volitional sphere suffers. The circle of interests narrows, shame disappears, and previous moral and moral norms become insignificant. Total dementia develops with space-occupying formations and circulatory disorders in the frontal lobes.

The high prevalence of dementia in the elderly led to the creation of a classification of senile dementias:

  • Atrophic (Alzheimer's) type– provoked by primary degeneration of brain neurons.
  • Vascular type– damage to nerve cells occurs secondary, due to disturbances in the blood supply to the brain due to vascular pathology.
  • Mixed type– mixed dementia - is a combination of atrophic and vascular dementia.

Symptoms of dementia

The clinical manifestations of dementia are determined by the cause of acquired dementia and the size and location of the affected area. Taking into account the severity of symptoms and the patient’s ability to socially adapt, three stages of dementia are distinguished. With mild dementia, the patient remains critical of what is happening and of his own condition. He retains the ability to self-service (can do laundry, cook, clean, wash dishes).

With moderate dementia, criticism of one's condition is partially impaired. When communicating with the patient, a clear decrease in intelligence is noticeable. The patient has difficulty caring for himself, has difficulty using household appliances and mechanisms: cannot answer the phone call, open or close the door. Care and supervision required. Severe dementia is accompanied by a complete collapse of personality. The patient cannot dress, wash, eat, or go to the toilet. Constant monitoring is required.

Clinical variants of dementia

Alzheimer's type dementia

Alzheimer's disease was described in 1906 German psychiatrist Alois Alzheimer. Until 1977, this diagnosis was made only in cases of dementia praecox (aged 45-65 years), and when symptoms appeared after the age of 65 years, senile dementia was diagnosed. It was then found that the pathogenesis and clinical manifestations of the disease are the same regardless of age. Currently, the diagnosis of Alzheimer's disease is made regardless of the time of onset of the first clinical signs acquired dementia. Risk factors include age, the presence of relatives suffering from this disease, atherosclerosis, hypertension, excess weight, diabetes mellitus, low physical activity, chronic hypoxia, traumatic brain injury and lack of mental activity throughout life. Women get sick more often than men.

The first symptom is a pronounced impairment of short-term memory while maintaining criticism of one’s own condition. Subsequently, memory disorders worsen, and a “movement back in time” is observed - the patient first forgets recent events, then what happened in the past. The patient ceases to recognize his children, mistakes them for long-dead relatives, does not know what he did this morning, but can talk in detail about the events of his childhood, as if they had happened quite recently. Confabulations may occur in place of lost memories. Criticism of one's condition decreases.

In the advanced stage of Alzheimer's disease, the clinical picture is complemented by emotional and volitional disorders. Patients become grouchy and quarrelsome, often demonstrate dissatisfaction with the words and actions of others, and become irritated by every little thing. Subsequently, delirium of damage may occur. Patients claim that loved ones deliberately leave them in dangerous situations, add poison to their food in order to poison them and take over the apartment, say nasty things about them in order to ruin their reputation and leave them without public protection, etc. Not only family members are involved in the delusional system, but also neighbors, social workers and other people interacting with patients. Other behavioral disorders may also be detected: vagrancy, intemperance and indiscriminateness in food and sex, senseless disorderly actions (for example, shifting objects from place to place). Speech becomes simplified and impoverished, paraphasia occurs (the use of other words instead of forgotten ones).

At the final stage of Alzheimer's disease, delusions and behavioral disorders are leveled out due to a pronounced decrease in intelligence. Patients become passive and inactive. The need to take fluids and food disappears. Speech is almost completely lost. As the disease worsens, the ability to chew food and walk independently is gradually lost. Due to complete helplessness, patients require constant professional care. Death occurs as a result of typical complications (pneumonia, bedsores, etc.) or the progression of concomitant somatic pathology.

The diagnosis of Alzheimer's disease is made based on clinical symptoms. Treatment is symptomatic. There are currently no drugs or non-drug treatments that can cure patients with Alzheimer's disease. Dementia progresses steadily and ends with complete collapse of mental functions. The average life expectancy after diagnosis is less than 7 years. The earlier the first symptoms appear, the faster the dementia worsens.

Vascular dementia

There are two types of vascular dementia - those that arose after a stroke and those that developed as a result of chronic insufficiency of blood supply to the brain. In post-stroke acquired dementia, the clinical picture is usually dominated by focal disorders (speech disorders, paresis and paralysis). The nature of neurological disorders depends on the location and size of the hemorrhage or area with impaired blood supply, the quality of treatment in the first hours after a stroke and some other factors. In chronic circulatory disorders, symptoms of dementia predominate, and neurological symptoms are quite monotonous and less pronounced.

Most often, vascular dementia occurs with atherosclerosis and hypertension, less often with severe diabetes mellitus and some rheumatic diseases, and even less often with embolism and thrombosis due to skeletal injuries, increased blood clotting and peripheral venous diseases. The likelihood of developing acquired dementia increases with illness of cardio-vascular system, smoking and excess weight.

The first sign of the disease is difficulty trying to concentrate, distracted attention, fatigue, some rigidity of mental activity, difficulty planning and decreased ability to analyze. Memory disorders are less severe than in Alzheimer's disease. Some forgetfulness is noted, but when given a “push” in the form of a leading question or offered several answer options, the patient easily recalls the necessary information. Many patients exhibit emotional instability, low mood, depression and subdepression are possible.

Neurological disorders include dysarthria, dysphonia, gait changes (shuffling, decreased step length, “sticking” of the soles to the surface), slowing of movements, impoverishment of gestures and facial expressions. The diagnosis is made on the basis of the clinical picture, ultrasound and MRA of cerebral vessels and other studies. To assess the severity of the underlying pathology and draw up a pathogenetic therapy regimen, patients are referred for consultation to the appropriate specialists: therapist, endocrinologist, cardiologist, phlebologist. Treatment is symptomatic therapy, therapy of the underlying disease. The rate of development of dementia is determined by the characteristics of the leading pathology.

Alcoholic dementia

The cause of alcoholic dementia is long-term (over 15 years or more) abuse of alcoholic beverages. Along with the direct destructive effect of alcohol on brain cells, the development of dementia is caused by disruption of the activity of various organs and systems, severe metabolic disorders and vascular pathology. Alcoholic dementia is characterized by typical personality changes (coarsening, loss of moral values, social degradation) combined with a total decrease in mental abilities (distracted attention, decreased ability to analyze, plan and abstract thinking, memory disorders).

After complete failure Partial recovery from alcohol and alcoholism treatment is possible, however, such cases are very rare. Due to a pronounced pathological craving for alcoholic beverages, decreased volitional qualities and lack of motivation, most patients are unable to stop taking ethanol-containing liquids. The prognosis is unfavorable; the cause of death is usually somatic diseases caused by alcohol consumption. Often such patients die as a result of criminal incidents or accidents.

Diagnosis of dementia

The diagnosis of dementia is made if five mandatory signs are present. The first is memory impairment, which is identified based on a conversation with the patient, special research and interviews with relatives. The second is at least one symptom indicating organic brain damage. These symptoms include the “three A” syndrome: aphasia (speech disorders), apraxia (loss of the ability to perform purposeful actions while maintaining the ability to perform elementary motor acts), agnosia (perceptual disorders, loss of the ability to recognize words, people and objects while maintaining the sense of touch , hearing and vision); reducing criticism of one’s own condition and the surrounding reality; personality disorders (unreasonable aggressiveness, rudeness, lack of shame).

The third diagnostic sign of dementia is a violation of family and social adaptation. The fourth is the absence of symptoms characteristic of delirium (loss of orientation in place and time, visual hallucinations and delusions). Fifth – the presence of an organic defect, confirmed by instrumental studies (CT and MRI of the brain). A diagnosis of dementia is made only if all of the above symptoms are present for six months or more.

Dementia most often has to be differentiated from depressive pseudodementia and functional pseudodementia resulting from vitamin deficiency. If a depressive disorder is suspected, the psychiatrist takes into account the severity and nature of affective disorders, the presence or absence of daily mood swings and feelings of “painful insensibility.” If vitamin deficiency is suspected, the doctor examines the medical history (malnutrition, severe intestinal damage with prolonged diarrhea) and excludes symptoms characteristic of a deficiency of certain vitamins (anemia due to a lack of folic acid, polyneuritis due to a lack of thiamine, etc.).

Prognosis for dementia

The prognosis for dementia is determined by the underlying disease. With acquired dementia resulting from traumatic brain injury or space-occupying processes (hematomas), the process does not progress. Often there is a partial, less often a complete reduction of symptoms due to the compensatory capabilities of the brain. In the acute period, it is very difficult to predict the degree of recovery; the outcome of extensive damage can be good compensation with preservation of ability to work, and the outcome of minor damage can be severe dementia leading to disability and vice versa.

In dementia caused by progressive diseases, there is a steady worsening of symptoms. Doctors can only slow down the process by adequate treatment main pathology. The main goals of therapy in such cases are maintaining self-care skills and adaptability, prolonging life, providing proper care and eliminating unpleasant manifestations of the disease. Death occurs as a result of a serious impairment of vital functions associated with the patient's immobility, his inability to perform basic self-care and the development of complications characteristic of bedridden patients.

- extensive, persistent, usually irreversible impairment of mental functioning resulting from a combination of two or more diseases. Most often develops with a combination of Alzheimer's disease and vascular damage to the brain. Mixed dementia is manifested by memory impairment, cognitive impairment, behavioral disorders, decreased intellectual productivity and signs of atherosclerosis or hypertension. The diagnosis is made on the basis of anamnesis, a combination of symptoms characteristic of different types of dementia and additional research data. Treatment is pharmacotherapy.

General information

dementia, which occurs when two or more pathological processes are combined. The development is usually caused by cerebrovascular disease and neurodegenerative brain damage. The prevalence of mixed dementia is unknown, but it is believed to be the most common type of dementia. According to researchers, 50% of patients with Alzheimer's disease have vascular diseases of the brain, and 75% of patients with vascular dementia have manifestations of neurodegeneration, but it is not always possible to assess the clinical significance of the second pathological process. Treatment of mixed dementia is carried out by specialists in the field of neurology and psychiatry.

Causes of mixed dementia

Most often, mixed dementia develops with a combination of vascular pathology and Alzheimer's disease (AD), however, there are publications indicating other possible combinations. Sometimes, with such dementia, three pathological processes are detected at once, for example, vascular pathology, neurodegeneration and the consequences of injury. The frequent combination of AD and vascular pathology in mixed dementia is explained by a number of circumstances. Both pathological processes have the same risk factors: excess weight, smoking, persistent increase in blood pressure, diabetes mellitus, hyperlipidemia, atrial fibrillation, physical inactivity, metabolic syndrome and the presence of the apoE4 gene. Changes in the brain resulting from one disease create the preconditions for the development of another, which causes the rapid development of mixed dementia.

A healthy brain has a reserve of cells. This reserve, to a certain extent, makes it possible to compensate for the disorders that occur after the death of some cells during vascular diseases. The disease is hidden for some time, the brain continues to function within normal limits. The addition of Alzheimer's disease causes additional damage to neurons; in the absence of reserve, rapid decompensation of brain functions occurs, and symptoms of mixed dementia occur.

In AD, senile plaques (accumulations of beta-amyloid) are deposited in the brain matter and the walls of cerebral vessels. The presence of such plaques causes the development of angiopathy, which causes rapid extensive vascular damage when cerebrovascular disease is associated. The likelihood of mixed dementia directly depends on the age of the patient. In middle-aged patients, dementia caused by a single disease predominates. In older people, dementia caused by two or more diseases is more common.

Symptoms of mixed dementia

Clinical symptoms are determined by the characteristics of the course of diseases that provoke mixed dementia. There are four types of relationships between pathological processes. The first is that one of the diseases occurs latently and is detected only during special studies; all manifestations of dementia are caused by the second disease. Second, the symptoms of diseases in mixed dementia are summed up. Third, the manifestations of one disease intensify the symptoms of another, or their mutual intensification is observed. Fourth, the symptoms compete with each other, the manifestations of one disease mask the signs of another.

Most often, with mixed dementia, symptoms of two dementias are detected. Cognitive and memory impairments characteristic of AD are observed. A history of hypertension, stroke, or atherosclerosis is found. Typical symptoms of mixed dementia include memory impairment, difficulty concentrating, difficulty planning activities, decreased productivity, and slower intellectual functioning. Spatial orientation disorders are usually absent or mild.

Diagnosis of mixed dementia

The diagnosis of mixed dementia is established on the basis of anamnesis, clinical picture and the results of additional studies indicating the simultaneous presence of two pathological processes. At the same time, MRI of the brain or CT scan of the brain, confirming the presence of focal vascular lesions and areas of cerebral atrophy, is not yet a basis for diagnosing mixed dementia. Experts believe that a diagnosis is justified only when the manifestations or dynamics of the course of dementia cannot be explained by one disease.

In practice, the diagnosis of “mixed dementia” is made in three cases. The first is the rapid worsening of cognitive impairment after a stroke in a patient with AD. The second is progressive dementia with signs of damage to the temporoparietal region with a recent stroke and the absence of symptoms of dementia before the stroke. The third is the simultaneous presence of symptoms of dementia in AD and dementia of vascular origin in combination with signs of cerebrovascular disease and a neurodegenerative process according to neuroimaging data.

When making a diagnosis, it is taken into account that Alzheimer's disease (especially in the early stages) occurs relatively latently, without dramatic manifestations of a stroke and obvious changes when additional studies are carried out. Evidence of mixed dementia with damage to the cerebral vessels is a characteristic history, including progressive disorders of cognitive functions and memory impairment. As an additional indication of the possibility of developing mixed dementia with vascular pathology, the presence of close relatives who suffered or are suffering from AD is considered.

Treatment and prognosis of mixed dementia

Treatment for mixed dementia should be comprehensive, aimed at possible compensation of all existing disorders and prevention of further progression of diseases that cause damage to brain cells. Even if one of the processes occurs latently or with minor clinical symptoms, in the future it can cause the rapid development of a major defect, and therefore needs correction along with the disease that caused the main symptoms of mixed dementia.

Measures are taken to normalize blood pressure. They use statins and medicines, reducing the risk of ischemia (antiplatelet agents). Patients suffering from mixed dementia are prescribed cholinomimetics and other drugs that help improve cerebral circulation. To slow down the development of cognitive defects and behavioral disorders in AD, antidementia drugs are used.

Combined with measures to ensure safety and improve the quality of life of patients with mixed dementia. At home, if necessary, they install a video surveillance system, block the inclusion of electrical and gas appliances, and hire a nurse. Create a comfortable environment with a sufficient number of stimuli (watch with a simple large dial, good lighting, radio, TV) to maintain activity and maintain orientation in the surrounding space. Where possible, patients with mixed dementia are referred to music therapy, occupational therapy and group psychotherapy to maintain motor and social skills.

Loading...Loading...