Ministry of Education of the Russian Federation

St. Petersburg State Pedagogical

University named after A.I. Herzen

Faculty of Law

Department of Criminal Procedure

Forensic psychiatry Lecture No. 12

Diseases of old age.

Alzheimer's disease.

Pick's disease.

Senile sclerosis.

Forensic psychiatric examination.

Ph.D. M.T.Chernukhin

Saint Petersburg

Among patients with mental disorders caused by organic brain damage and pathology of other body systems, patients of senile (76 years or more) and presenile age (55-75 years) make up the majority.

The aging of the body is accompanied by changes in all its functions - both biological and mental. However, the nature of these changes and the time of their manifestation have individual characteristics and vary widely: mental age-related changes do not always correlate with the somatic manifestations of aging of the body.

Changes in mental functioning due to age can manifest themselves selectively and at different age periods. Thus, a person’s ability to imagine—its brightness, imagery—begins to weaken relatively early; the mobility of mental processes and the ability to quickly switch attention also deteriorate. Somewhat later, the assimilation of new knowledge deteriorates.

Emotional manifestations also change with age. Emotional instability and anxiety develop. There is a tendency to get stuck on unpleasant experiences, an anxious - depressive mood. The time of manifestation of age-related changes in the psyche is relatively individual.

The age that is usually considered the onset of mental changes associated with involution is 50-60 years. Mental disorders in elderly and senile people can manifest themselves both in the form of borderline mental disorders and in the form of severe mental disorders - severe memory disorders, dementia, delirium, etc.

Among people over 65 years of age, mental disorders of varying degrees account for 30-35%, of which psychosis with severe disorders accounts for 3-5%. Borderline disorders include neurosis-like disorders, mood disorders, and personality changes.

Neurosis-like disorders manifest themselves in the form of sleep disturbances, various unpleasant sensations in the body, emotionally unstable mood, irritability, unaccountable anxiety and fears for the well-being of loved ones, one’s health, etc.

The ongoing changes in the patient's personality affect both his characterological and intellectual properties. In characterological features, there is a kind of sharpening and exaggeration of individual personality traits that were previously characteristic of the patient. Thus, distrust turns into suspicion, frugality into stinginess, perseverance into stubbornness, etc. Intellectual processes lose their brightness, associations become poor, the quality and level of generalization of concepts decreases. Understanding new events and phenomena requires a lot of effort and time. New information is either not assimilated at all or is assimilated with great difficulty. First of all, memory for current events is impaired. For example, it is difficult to remember the events of the past day. There is also a decrease in criticism - the ability to correctly evaluate one’s own mental condition and the changes taking place.

The leading changes in the clinical picture of elderly and senile people are: weakening of memory, from mild disorders to amnestic (Korsakoff) syndrome, deterioration of intellectual abilities up to dementia, disturbance of emotions - weakness, tearfulness, apathy, etc.

Severe mental disorders that occur in a number of elderly and old age, are associated with degenerative and atrophic changes in the brain and changes in the functioning of other body systems.

All these changes are accompanied by typical mental disorders, called Alzheimer's disease, Pick's disease (named after the psychiatrists who first described them), senile dementia etc.

Content: PSYCHOSES OF LATE AGE:
ATROPHIC DISEASES OF THE BRAIN:

Alzheimer's disease - primary endogenous degenerative dementia, beginning in presenile age and characterized by progressive impairment of memory, speech, and intellect, resulting in total dementia with severe disorders of higher cortical functions (speech, praxis, optical-spatial perception) - aphato-apractic-agnostic dementia.

The first description of such a disease was given by A. Alzheimer (1906). The woman, who became ill at the age of 51, showed memory deterioration, and later there were disturbances in spatial orientation, speech disorders and increasing loss of skills. Gradually, total dementia developed: the patient became helpless, unkempt, she developed contractures, and four and a half years later death occurred. When examining the brain, A. Alzheimer discovered for the first time, in addition to abundant senile plaques characteristic changes neurofibrils, later called Alzheimer's neurofibril changes.

In accordance with modern neuromorphological data, at the early stage of the disease, characteristic neurohistological changes are found only in the hippocampus, amygdala nucleus and adjacent parts of the temporal lobe cortex. With moderate dementia at the next stage, damage to the posterior temporal and parietal parts of the cortex and the posterior part of the angular gyrus is noted. In the final stage of severe dementia, the frontal parts of the brain are also involved in the disease process (A. Brun, I. Gustafson, 1976, 1993).

Prevalence. According to a multicenter study, the indicators for the age groups 60-69 years, 70-79 years, 80-89 years of the female population in the EEC were 0.4, respectively; 3.6; 11.2%, and male - 0.3; 2.5; 10%. In Moscow (data from S.I. Gavrilova, 1995) the frequency is 4.4%. The ratio of female patients to male patients is, according to various sources, from 3:1 to 5:1.

Clinical manifestations. In most cases, the disease begins between the ages of 45 and 65; very rarely, an earlier onset (about 40 years) or a later onset (over 65 years) is observed. Initial symptoms are signs of gradual development of memory impairment. Absent-mindedness and forgetfulness appear, patients forget where they put this or that thing, sometimes they do not immediately remember the name of this or that object. In the first years of the disease, senile-like features predominate: stupidity, fussiness, excessive talkativeness. Memory disorders progress from more complex and abstract to simpler, more concrete, from later acquired and less firmly fixed to earlier acquired and more firmly fixed material. The ability to form new connections is lost. Memory impairments due to fixation amnesia resemble the picture, but develop against the background of gradually increasing dementia. This leads to difficulties in recording past experiences and to phenomena of amnestic disorientation in the environment, time, and sequence of events. At the same time, the ability to selectively reproduce the material needed at the moment suffers. Memory materials, its reserves are destroyed in sequence from newer connections to older ones. Patients forget their address, place of residence, calling their previous address, etc. In advanced cases, they can no longer give any information about themselves.

With the progression of mnestic disorders, attention and perception disorders occur in parallel. Visual, auditory, tactile perceptions become less clear, unclear, remain scattered, not connected into one whole. Instead of real recognition of the situation, false recognitions appear more and more often, although there is no such pronounced “shift of the situation into the past” as in senile dementia. Only at the final stage of the disease do false recognitions reach an extreme degree, so that patients do not recognize themselves in the mirror, mistake their image for a stranger, can communicate with him, argue (“mirror symptom”). In contrast to the amnestic syndrome in Alzheimer's disease, it is not accompanied by such a pronounced revival of past experiences; these phenomena do not always occur and are scanty, fragmentary, and there are no manifestations of “senile delirium.” Very rare (only in slowly progressing cases). Main clinical feature- This is the leading role of memory impairment. Characterized by the appearance of special confusion, affective disorders(confused-suppressed affect). Early orientation disorders are typical for Alzheimer's disease, as are manifested praxis disorders. Patients seem to “forget how” to sew, cut, cook, wash, iron. Loss of skills serves as a harbinger of the future, just as disruption of orientation is a harbinger of the future. Symptoms that in the early stages of the disease represent specific but typical manifestations of dementia, psychotic symptoms, then develop into more specific neurological, that is, focal, symptoms. Early orientation disorders turn into distinct optical-agnostic disorders. Loss of skills and general stupidity are then transformed into more specific non-practical symptoms. Similar dynamics are observed in relation to the motor skills and behavior of patients. Motor revival and fussiness subsequently become the basis for the development of increasingly monotonous activity, acquire the character of monotony, become rhythmic, patients rub something, knead something, nod rhythmically, bend and straighten their arm, etc. (go to more simple forms motor disorders based on neurological pathology).

At the same time, many patients experience a long-lasting well-known feeling of alteration (sometimes patients’ statements are surprising: “there is no memory,” “the brain is not the same,” etc.).

Speech decay. Features of the dynamics coincide with memory pathology. The disintegration of speech proceeds, as it were, from the higher and less fixed aspects of the speech function to simpler, more primitive ones. In the early stages of the disease, there is an unclear pronunciation of individual words (dysarthria), then the decay process leads to the appearance of sensory aphasia (88%), amnestic aphasia is detected with almost the same frequency (78%). The fact that sensory aphasia is transcortical in nature is indicated by the high frequency of preservation of repeated speech, i.e. phonemic awareness and echolalic speech. The rarity of paraphasias is also characteristic. Speech activity can turn into speech aspontaneity. Later, spontaneous speech begins to disintegrate with dysarthria and logoclonia.

Etiology and pathogenesis. Biological and neurobiological research in psychiatry has led to Lately to a number of advances in the study of the molecular genetics of Alzheimer's disease. The data showed the progressive role of the concept of clinical and genetic heterogeneity of this pathology. At the same time, it becomes clear that we are talking about etiologically various forms DATE For example, familial forms of the disease were shown in the work of G. Lauter, who described a family in which 13 of its members were sick.

Currently, three genes have been identified, localized on three different chromosomes: on chromosome 21 - the gene for the amyloid B-precursor protein (B-APP); on chromosome 14 - presenilin 1 (PSN1), and on chromosome 1 - presenilin 2 (PSN2) (E.I. Rogaev, 1996). These genes play important role in the occurrence of familial (hereditary) forms of Alzheimer's disease. Carriers of mutations in the PSN1 gene were responsible for 60 - 80% of early presenile cases of familial Alzheimer's disease. Mutations in the PSN2 gene are more rare and are currently found only in families of people from the Volga region of German origin.

Now only one genetic factor has been identified - E4 or an isomorphic variant of apo-lipoprotein E (Apo E4) in the gene of chromosome 19, confirmed in independent studies as a risk factor for senile dementia of the Alzheimer's type (E.I. Rogaev, 1996; A.D. Rossis et al., 1996).

It was found that some mutations in the B-APP gene are responsible for an increase in the production of B-amyloid, from the aggregates of which senile or amyloid plaques are formed. Senile plaques have been found to be toxic, so nerve cells brains undergo degeneration, which leads to their massive death (cortical atrophy). The severity of dementia is even more strongly correlated with neurofibrillary tangle density and synaptic loss. The severity of dementia is facilitated by the accumulation of hyperphosphorylated insoluble t-protein, which forms the basis of pairwise twisted filaments that form neurofibrillary tangles.

Alzheimer's disease is a syndrome that has its relevance to neurology and psychiatry, as well as psychotherapy. During medical measures aimed at reducing negative factors, it is possible to use the most different methods, including various physiotherapy treatments, massage and others.

Alzheimer's disease is a common form of dementia, most often found in people over 65 years of age.

The disease is associated with this area primarily due to the fact that its neurodegenerative nature has been established. The reasons for the death of brain cells associated with pathogenesis have not been fully established. It is known that during the process of tissue destruction, accumulation occurs amyloid plaques and neurofibrillary tangles in brain tissue. Plaques are dense and insoluble deposits of beta-amyloid and cellular material in and near neurons. During their formation, folded proteins - beta-amyloids and tau proteins - accumulate in the brain tissue. Other processes and their consequences are also identified.

Alzheimer's disease: psychiatry

All detected somatic changes lead to dementia. This is dementia that increases as the disease progresses. It is expressed in the form of an amnestic syndrome and a decrease in cognitive abilities. Delirium is also possible. This already suggests that in some cases antidepressants, antipsychotics, etc. may be required. Well, all this is already from the field of psychiatry. In addition, correction of the condition itself is important from the point of view of general psychotherapy.

Which doctor treats Alzheimer's disease?

All at once or none at all, but a nurse with experience working specifically with patients of this profile. In the West, due to the prevalence of the disease, even the specialization of Alzheimer's doctors has appeared. This also exists in Russia, but to a much lesser extent. In our district clinics There may be no offices for urologists, psychiatrists, or many specialized specialists at all. Let's add to this the fact that the disease cannot be cured, its symptoms cannot even be stopped. Only conditions are created for the least negative development factors. Clinical guidelines in Alzheimer's disease are complex. Therapy is mainly aimed at reducing the development of dementia.

There is no cure for Alzheimer's disease, but therapy can eliminate some of the symptoms of the disease.

At the initial stage, a psychotherapist can play a large role. At the same time, working not only with patients, but also with their relatives. When working with patients themselves, the following methods are used:

• reminiscence therapy;
• presence simulation;
• orientation in reality.

They are included in general direction cognitive retraining, and were developed mainly in the USA, where this disease is most often found. It is believed that this approach allows one to revive memory and improve adaptation... There will be one sad definition here. Not to life, but to the disease itself, since during therapy it is necessary to take into account reality, and there are no adequate treatment methods for it.

Early pharmacological interventions include the use of:

• anticholinesterase symptomatic drugs;
• memantine.

The clinical pharmacology of Alzheimer's disease is of course much broader. It should be noted that on different people Some drugs have different effects.

Typically, a neurologist gets involved in therapy at the moment when some bodily difficulties arise. These are urinary incontinence, difficulty swallowing and the like. Often patients fall and break their limbs, in which case the intervention of an orthopedic traumatologist is necessary.

For the therapeutic treatment of Alzheimer's disease, methods of psychosocial intervention, presence simulation, etc. are used.

Alzheimer's disease: psychosomatics

Considering that the real reason pathological changes, like diseases in general, are still unknown, it is impossible to say anything definite about psychosomatics. Because of this, the problem is constantly overgrown with a number of conjectures and hypotheses that go beyond the boundaries of the scientific range. Even books are published dedicated to the mental status of patients and the problems of their relatives. It is impossible to draw an unambiguous conclusion about the benefits of such research. On the one hand, they smack of amateurism, but on the other hand, they can be very useful in some ways.

One of the authors is Liz Burbo. She devoted the topic to psychosomatics of this disease an entire book that deduces a certain mental status of the average patient. There are constant calls for them from their relatives. In general, all this comes down to the formula “get up and go!” It would be good, of course, if one of the patients gets inspired, reads it and tries to become more active. True, this is not relevant for everyone and, of course, does not make any sense at the final stage of the disease.

If the conversation is about psychosomatics, then the question arises about what methods can be used, aimed not at teaching how to live with it, but at therapy. What is the main difficulty? Let us assume that relatively healthy man decided that he needed to take care of himself, practice physical exercises and combine them with mental training. Goal: improve health and increase stress resistance. This is quite achievable. The other one does the same thing, but in an enhanced mode, and at the same time wants to become enlightened and immortal. Well, God knows, maybe it will work out. However, we will still retain some skepticism. So, for a patient with such a diagnosis, ordinary memory development exercises can be extremely difficult. And the goal of recovery is an analogue of enlightenment and immortality for a healthy person.

Therefore, we do not recommend rushing to any training, especially on a paid basis. We are all for psychotherapy, but we don’t want to give false hopes in the style of “sign up for a training and you will become healthy.” If only it were that simple...

One of the test tasks when diagnosing is sometimes a request to draw a dial, and its hands should show the current time. All patients fail to cope with this task. Nobody asks for graphic masterpieces; the drawing can be simple. But patients may not even have numbers on the dial, and instead they draw some zeros and squiggles. In general, if a person begins to experience difficulty writing words and numbers with a pen, then this is one of the warning signs. Letters run over each other, or lines go up or down and run over others.

Patients with disorders that are more common in old age should not be given any overly difficult tasks. By too complex we mean banal and ordinary for healthy people.

Liz Bookrbo, already mentioned by us, put forward a rather strange concept. It’s as if patients are trying to get rid of responsibility and manipulate other people. One might even agree with this. For example, a person with the diagnosis we are considering cannot leave his bed. He whinily asks someone to do something for him, then scolds him - you see, it seemed to him that they did it wrong. But after an hour he gets up and does something himself. Just what I asked for. You might think that it was an senile whim, some kind of mockery of others. This is a wrong opinion. Until the very last phase, the disease manifests itself in waves. At some point, the head was “rubbery” and the patient could not think correctly, do something, said senile things, but was not delirious. Or maybe he was delirious, anything can happen. But now there has been some improvement and he remembered what he wanted. Uninitiated people think that he was playing a trick on them. No, I didn't play it. This is what people call “memory lapses.” Sometimes we remember, and sometimes we don’t. We remembered, and then forgot that we remembered the very fact that we remembered.

Real specialists and professionals in their field should take part in the process of treatment and care for patients.

Therefore, specialists should take part in the treatment and care of patients. Without preparation, without receiving information about what is actually happening to patients, relatives experience much more discomfort. Usually people know very little about this disease. They may even ask whether head tremors lead to Alzheimer's disease.

The manual includes a detailed presentation of the course of lectures on private psychiatry in accordance with the standard program in the discipline “psychiatry and narcology” for specialties 1–79 01 01 General Medicine, 1–79 01 02 Pediatrics. The manual covers clinical issues, diagnosis, and treatment of mental and behavioral disorders in accordance with the diagnostic criteria of ICD-10 and taking into account the characteristics of childhood.

Book:

Sections on this page:

Dementia due to Alzheimer's disease

Etiology and pathogenesis

Alzheimer's disease is a primary degenerative cerebral disease of unknown etiology with characteristic neuropathological and neurochemical features. In 1901, German psychiatrist Alois Alzheimer noted a case of the disease that was later named after him. The clinical picture of AD was characterized by gradually developing deep memory damage, weakening of intelligence with the appearance of focal symptoms - speech disorders, agnosia and apraxia - already in the early stages of the disease. AD is characterized by the following brain changes: a significant decrease in the population, especially in the hippocampus, substantia innominata, locus coeruleus; changes in the temporoparietal region and frontal cortex; the appearance of neurofibrillary tangles consisting of paired spiral filaments; neuritic (argentophilic) plaques, predominantly amyloid, showing a certain tendency towards progressive development (although there are plaques without amyloid); granulocular bodies. Neurochemical changes were also detected, which included a significant decrease in the enzyme acetylcholine transferase, acetylcholine itself, and other neurotransmitters and neuromodulators.

Clinic

The disease usually has a gradual onset and progresses slowly but steadily over several years. In time it can be 2 or 3 years, but sometimes much longer. Onset may be in middle age or even earlier (presenile-onset AD), but incidence is higher in late age and older (senile-onset AD). In cases with the onset of the disease before 65–70 years of age, there is a likelihood of a family history of similar forms of dementia, a faster rate of progression and characteristic features brain damage in the temporal and parietal regions, including symptoms of dysphasia and dyspraxia. In cases with a later onset, there is a tendency towards slower development; the disease in these cases is characterized by a more general lesion of higher cortical functions. Patients with Down syndrome are at high risk of developing asthma.

The progressive development of clinical and organic changes does not always go in parallel: there may be an undeniable presence of some symptoms with a minimal presence of others. Nevertheless, Clinical signs AD is such that very often a presumptive diagnosis can be made only on the basis of clinical data.

The following features support the diagnosis, but are not necessary elements: involvement of cortical functions, as evidenced by aphasia, apraxia, or agnosia; decreased motivation and drive, leading to apathy and lack of spontaneity; irritability and disinhibition in social behavior; data from a special examination about the presence of cerebral atrophy, especially if it increases over time. In severe cases, Parkinson-like extrapyramidal phenomena, logoclonus, and epileptic seizures may occur.

For a reliable diagnosis, the following signs must be present:

1. Presence of dementia.

2. Gradual onset with slowly increasing dementia.

Although the time of onset of the disease is difficult to determine, detection of existing defects by others may occur suddenly. There may be some plateau in the development of the disease.

3. Lack of clinical or special research data that could suggest that the mental state is caused by other systemic or brain diseases leading to dementia (hypothyroidism, hypercalcemia, vitamin B-12 deficiency, nicotinamide deficiency, neurosyphilis, hydrocephalus normal pressure, subdural hematoma).

4. Absence of sudden apoplectic onset or neurological symptoms associated with brain damage, such as hemiparesis, loss of sensitivity, changes in visual fields, loss of coordination, occurring early in the development of the disease (however, such symptoms may further develop against the background of dementia).

Currently, asthma is irreversible.

Diagnostics

The diagnosis is confirmed by postmortem findings of neurofibrillary tangles and neuritic plaques in quantities greater than those observed during normal aging of the brain.

Genetic testing is performed using markers that help identify early-onset AD. Mutations in the presenilin 1 gene (PS1, chromosome 14) cause the most common early familial forms of AD and are apparently the most “aggressive” genetic factors. Their pathological manifestation is characterized by high penetrance and does not depend on other environmental factors or genotype. To date, more than 45 different missense mutations have been identified along the entire length of the coding part of the gene, and one “splicing” mutation associated with familial AD. It is known that the e4 allele of the apolipoprotein E gene (on chromosome 19) is also associated with AD. Although the e4 allele is associated with a high risk of AD, the extent of the increased risk is not clearly defined. Moreover, it is not clear whether this increased risk is specific to AD or whether it is shared by other forms of dementia (the e4 allele is also associated with an increased risk of coronary artery disease). In addition, the APOE e4 mutation does not cause AD; it can be found in older people who have not developed dementia.

As follows from the above, genetic testing of the APOE genotype has no diagnostic value in the case of AD. The presence or absence of the e4 allele cannot indicate the presence of AD. Currently, most AD specialists believe that the use of APOE genotyping in unaffected individuals is not justified except for research purposes. Due to the fact that patients with the APOE e4 variant may not suffer from asthma, and patients with APOE e3 are diagnosed with asthma, APOE genotyping is not considered as evidence in the diagnosis of this disease.

Diagnostic CT signs that confirm the diagnosis of AD are signs of total and regional atrophy of the brain substance, the presence of which is judged by the degree of expansion of the subarachnoid spaces and ventricles.

Conducting standard MRI in dementia is associated with pulse sequences of fast spin echo (FSE) to obtain T1-weighted images (T1WI) and T2-weighted images (T2WI), as well as an inversion-recovery sequence in the FLAIR modification. T1WI, T2WI, and FLAIR images have good contrast between the brain tissue and the cerebrospinal fluid, and therefore make it possible to determine the degree of brain atrophy. The methods of MRI described by O. V. Bozhko (2003) for diagnosing brain pathology in the elderly have the following features: axial T2WI and FLAIR images are used to assess the periventricular and subcortical white matter, identify cortical infarcts or infarcts of the deep gray matter, thalamic, stem, cerebellar changes; thin (2 mm) coronal T1WI slices obtained in a projection orthogonal to the long axis of the hippocampus are used to assess the degree of atrophy of the medial temporal lobes and hippocampus.

When analyzing MRI results in the elderly, age-related (involutional) changes in the brain are taken into account, primarily cerebral atrophy, manifested by expansion of the ventricles and sulci of the brain. However, it should be noted that the external and internal hydrocephalus, as a manifestation of atrophy, may be associated not only with AD, but also with other degenerative diseases late age accompanied by dementia (Pick's disease, amyloid angiopathy, Huntington's chorea, etc.), and may also be a consequence of injury or, for example, radiation therapy. In addition, expansion of the liquor spaces is also observed during a number of physiological and pathological processes (meningitis, starvation) and is reversible.

Quantitative techniques based on MRI results are being developed to assess atrophy. This approach includes linear and volumetric measurements of the ventricles, volumetric measurements of the cerebrospinal fluid spaces, gray and white matter. The specificity of these techniques in detecting dementia is low, since atrophy occurs in both dementia and normal aging, and the measurement results partially overlap. An exception is the medial parts of the temporal lobes. A decrease in their volume is already typical for early manifestations BA. Measurements were made of various structures located in the medial temporal lobes based on MRI data in AD and normal aging. It was possible to most accurately differentiate between AD and the norm using volumetric measurements of the entorhinal cortex and hippocampus. However, given the difficulty in defining the boundaries of the entorhinal cortex compared to the hippocampus, measurements of the latter are more often used in research.

Functional radioisotope methods are single-photon emission computed tomography (SPECT with excametazyme (99mTc isotope), positron emission tomography (PET).

Brain SPECT is used to assess regional cerebral blood flow. In AD, a decrease in hemoperfusion in the parietotemporal region is detected. PET is a method that evaluates the level of glucose metabolism in the brain after intravenous administration radiopharmaceutical fluoro-2-deoxyglucose. PET scans are performed both at rest and during cognitive tests. AD is characterized by a decrease in the level of metabolism in the parietotemporal region; the magnitude of this decrease correlates with the degree of cognitive decline.

However, the listed methods genetic testing, PET, SPECT, perfusion MRI, diffusion-weighted MRI, MR spectroscopy are not widely used due to the complexity of the research procedure and the high cost of both equipment and consumables.

Currently, scientists are paying increasing attention to the neuropsychological analysis of disorders in different options cognitive disorders. Neuropsychological research methods include various tests and tests for memorizing and reproducing words and pictures, recognizing images, solving intellectual problems, studying movements, etc. Psychometric scales are used in diagnosing AD: Mini-Mental State Examination (MMSE); Khachinsky ischemic scale; Battery frontal dysfunction(Frontal Assessment Battery - FAB); Clock Drawing Test (CDT); neuropsychological examination technique adapted for this group of patients by A. R. Luria et al.

Differential diagnosis dementia in AD is carried out with the following diseases: depressive disorders, delirium, organic amnestic syndrome, other primary dementias (Pick, Creutzfeldt-Jakob, Huntington's disease), secondary dementia in somatic diseases, intoxication, forms mental retardation, but most often it is necessary to differentiate AD from SoD. A third of patients with asthma have significant cerebrovascular pathology caused by damage to small vessels; Cerebral amyloid angiopathy, microvascular degeneration, hyaline fibrosis of arterioles and small vessels are common.

Treatment

Experimental data accumulated over the past decades show that the progressive degeneration of cholinergic neurons and disruption of associative connections with the areas of their projections into the parietotemporal and frontal regions of the cerebral cortex are the main causative factors of memory disorders and other cognitive functions, which ultimately lead to the development of severe cognitive deficits, social maladaptation and behavioral disorders, i.e. to the formation of dementia syndrome. Therefore, the first attempts at pathogenetic therapy for AD were associated with the use of acetylcholine precursors, such as choline and lecithin, as well as acetylcholinesterase (AChE) blockers, which prevent the destruction of acetylcholine in the synaptic cleft. However, acetylcholine precursors, like first-generation AChE inhibitors (physostigmine, tacrine), did not live up to therapeutic expectations either due to unproven clinical efficacy or severe side effects.

In recent years, new generation AChE inhibitors have been developed that have reversible action, selectivity for brain AChE and, accordingly, significantly less severity of unwanted peripheral side effects and lack of hepatotoxic properties. Representatives of the new generation of AChE inhibitors are rivastigmine and donepezil.

Rivastigmine is a pseudoreversible carbamate-type AChE inhibitor with a selective effect on acetylcholinesterase in the central nervous system, which has successfully passed clinical trials in the USA and several European countries in two large multicenter studies (R. Anand, G. Gharabawi, 1996). The clinical study of rivastigmine also yielded extremely encouraging results regarding both therapeutic efficacy and clinical safety of long-term (6 months) use of the drug in patients with mild and moderate asthma. A feature of the use of rivastigmine is the individual selection of optimal therapeutic dosages at the level of maximum tolerated doses in the range from 3 to 12 mg/day in 2 doses and the possibility of its combination with other medications, often necessary for elderly patients.

Another representative of the new generation of drugs of this type is donepezil, a reversible AChE inhibitor, a piperidine derivative. It has a high selectivity of action against brain AChE compared to butyrylcholine sterase, which minimizes the risk of peripheral side effects. The reversibility of the drug's action reduces the risk of accumulation and acetylcholinesterase toxicity. Do-nepezil has a long-lasting effect, which makes it possible to limit it to a single dose during the day. The effectiveness and safety of donepezil treatment in AD patients with early and moderate severity of dementia was established in multicenter, double-blind trials lasting 30 weeks. (S. Roger et al., 1996). The drug is recommended to be used in a daily dose of 5 to 10 mg/day (single dose). During the 1st month of therapy, the dosage is 5 mg/day; if well tolerated, from the 2nd month of therapy the dose is increased to 10 mg/day. The course of treatment ranges from 3 to 6 months.

Amiridine also belongs to the group of AChE inhibitors and, in addition, has the ability to activate potassium conduction of nerve fibers. Amiridine is recommended for clinical use in the treatment of dementia of the Alzheimer's type, as well as cerebrovascular dementia. The drug improves the mnestic-intellectual functions of patients, increases spontaneous activity with a simultaneous positive effect on the organization of behavior, smoothes out manifestations of irritability and fussiness. A decrease in confusion was also noted. Recommended doses are from 40 to 100 mg per day (in 2 divided doses, average daily dose 60 mg). The duration of the course of treatment is at least 2 months. The effectiveness of the drug depends on the severity of dementia: the drug is ineffective or ineffective in the stage of severe dementia. The drug is well tolerated and does not cause serious side effects. Long-term (14 months) use of amiridine in patients with moderate severity of asthma showed a positive effect or prevents the progression of the disease (E. E. Bukatina, I. V. Grigorieva, 1991).

In addition to the pronounced cholinergic deficiency, which is the earliest and most pronounced manifestation of AD, insufficiency of other neurotransmitter systems has also been established, in particular, serotonergic, glutamatergic, as well as impaired activity of monoamine oxidase (MAO) type B. Correction of these types of neurotransmitters requires other types of thorn failure are directed replacement therapy. Selegeline, a selective inhibitor of MAO-B oxidase, was proposed for the treatment of AD due to the increase in MAO-B oxidase activity in the brain of patients established in various studies. Small pilot clinical trials have been conducted and have shown some improvement in cognitive function and behavior in patients. However, the drug needs further research regarding the effectiveness and safety of use in asthma. Protective therapy is aimed at preserving and increasing the viability (survival) of neurons and includes therapy with nootropics, vasoactive agents and drugs with neurotrophic properties.

The use of nootropics such as piracetam, pyriditol, drugs that improve cerebral metabolism, did not give reliable positive results in the treatment of patients suffering from asthma. Large doses of these drugs in some cases even have a negative effect, since there is evidence of possible neurotransmitter depletion with their use.

Nursing

Inpatient treatment in itself already has a maladaptive effect on patients of late age (weakening of self-care skills, impairment social contacts). Hospitalization with a sharp change in habitual life patterns and the entire environment often worsens the mental state, causes depressive reactions and even (in patients with psychoorganic syndrome) a state of confusion. Therefore, the most important part of treatment and rehabilitation work is the creation of a special psychological microclimate, a therapeutic environment that helps prevent maladaptation and stimulate mental abilities and social activity, encouragement to expand social contacts and train self-care skills, prepare for life outside the hospital. A clear daily routine eliminates “empty” periods of time when the patient is left to his own devices; contacts and participation in various types of employment are encouraged (self-care, department cleaning, cultural and entertainment activities). When placing patients in wards, their mutual sympathies and the possibility of mutual assistance are taken into account. It is allowed to wear personal clothing and use familiar toiletries. On the first day of admission, the patient is given the necessary explanations about the need for treatment, he is introduced to the department and the location of the main premises. It is important to have safe and spacious rooms where patients can move, since constraint itself is often the cause of behavioral disorders. Creating a therapeutic environment begins with maximum compliance with hygienic requirements, which is especially important when working with geriatric patients. These include cleanliness of the premises, the use of disposable linen, a cozy interior, and a convenient arrangement of furniture. IN warm time years, patients walk on fresh air– in the department’s walking gardens or in the hospital park. Close interaction with relatives of patients, involving them in patient care, and periodically conducting surveys of patients and their relatives allows us to optimize work and improve patient care. Two main points reflect the peculiarities of the staff's work. Firstly, the organization of close interaction, team work of various specialists (psychiatrist, psychotherapist, neurologist, social worker, etc.). Secondly, special training for middle and junior medical staff to work with the elderly (service techniques, special tact and patience).

Caring for patients with asthma requires professional approach, and if it falls on relatives, it exposes them to great emotional stress. Close people watch with pain how the person they love and close to them deteriorates, but they often cannot help him. But the helplessness of relatives has the most negative impact not only on the health of their ward, but also on their own. In this regard, nurses and social workers It is necessary to provide psychological support to those who provide primary care for the patient at home, to teach them special techniques that will help prevent many problems.

Unfortunately, vascular brain lesions and primary degenerative disorders are often combined. In these cases, it is customary to talk about mixed dementia.

According to numerous studies, at least half of patients with Alzheimer's disease suffer from disorders circulatory system brain. Along with this, approximately 75% of patients diagnosed with vascular dementia experience symptoms of neurodegenerative processes.

This connection is quite understandable. Alzheimer's disease for a long time(on average about 20 years) is asymptomatic. The brain is a fairly flexible instrument and for a long time compensates for the negative processes associated with the death of neurons. Stroke and ischemic disease reduce the reserve and accelerate the onset of Alzheimer's type dementia. The inverse relationship is also quite obvious. Alzheimer's disease increases the risk of vascular diseases of the brain, since the deposition of beta-amyloid (senile plaques) occurs both in the substance of the brain and on the walls blood vessels, leading to their damage (angiopathy).

What causes mixed dementia?

Primary degenerative processes and vascular diseases have many common prerequisites. These include:

• carriage of the APOE4 gene;
• high blood pressure;
• cerebral atherosclerosis;
• arrhythmias;
• high cholesterol;
• bad habits (poor diet, smoking);
• physical inactivity.

Thus, frequent combination Alzheimer's disease and vascular dementia are quite natural.

Diagnosis of the disease

Suspicion of mixed dementia is appropriate in cases where the appearance of cognitive disorders of the Alzheimer's type (primarily memory impairment) is preceded by cardiovascular diseases(hypertension, atherosclerosis).

An atypical set of symptoms allows one to suspect mixed dementia. For example, if memory problems are not combined with disturbances in spatial orientation, as often happens in Alzheimer's disease, but are accompanied by problems more characteristic of diseases associated with dysfunction of the frontal lobes: these are difficulties concentration, impaired ability to plan one’s actions, slowness when performing intellectual work.

Treatment

Treatment of mixed dementia combines correction of vascular factors (primarily gradual normalization of blood pressure, antiplatelet therapy) and the use of anti-dementia drugs.

The material was prepared by the Memini project.

Alexander Sonin