Home Hygiene Tiganov A.S. (under

Tiganov A.S. (under

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 risk vascular diseasĕ brain, since the deposition of beta-amyloid (senile plaques) occurs both in the substance of the brain itself 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 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 blood pressure, antiplatelet therapy) and the use of anti-dementia drugs.

The material was prepared by the Memini project.

Alexander Sonin

We will get acquainted with a case of Alzheimer's disease immediately after analyzing the difficult ending of the treatment of the previous patient, we will also get acquainted because the initial and clinical diagnosis This patient had Alzheimer's disease. This disease in the Soviet psychiatric school was considered more narrowly as an example of presenile, endogenously caused dementia with a typical pathological and anatomical picture, a unique clinical picture, distinguishable from senile and vascular dementia, and in Western psychiatry the disease is considered more broadly, with the criteria being blurred, almost all cases of senile and presenile dementia, many cases atherosclerotic dementia classified as Alzheimer's disease.

We have just seen the importance of distinguishing vascular dementia from Alzheimer's disease when considering the previous history of the disease. What is characteristic of Alzheimer's disease according to the domestic psychiatric school?<

Case 25. Alzheimer's disease

S.Z.E., born in 1921.

Anamnesis from the outpatient card: lives in a rural village, alone with her husband, has 3 sons who have their own families. She graduated from a pedagogical institute and worked as a school director. Currently she is a pensioner. She first contacted a psychiatrist on December 18, 1987 with complaints of sleep disturbances, memory loss, and fear of being left alone at home. A mild decline in memory has been observed over the past 5 years.

(Note that the first mental disorders began in the sixty-second year of life; five years later the patient turned to a psychiatrist with complaints of memory impairment, worsening sleep, fear, i.e. the initial period of the disease - asthenic disorders and mild memory loss - began long before stationary level of symptoms.)

Since March 1988, she regularly visited the local psychiatrist and took Relanium, amitriptyline, haloperidol, and piracetam. There was some improvement, she came to the appointment on her own. In October 1988, she began to lock herself at home, felt afraid, and stopped going to the store because she could not find her way. At the reception she talked to the point and was oriented. On November 28, 1988, I was at a reception with my husband, according to whom, “he doesn’t understand anything at all.” She was sent to hospital treatment.

From the anamnesis (according to her husband): she graduated from a pedagogical school in Elabuga and a pedagogical institute in Kazan. Retired since age 56. Memory impairment has been noted over the past year, she became forgetful, could not find things that she herself put away. But I did everything at home, went to stores, cooked. In August 1988, she did not stay alone at home, she went everywhere with her husband, saying that she was scared alone. In October, she changed dramatically, couldn’t do housework, didn’t take care of herself, started eating often, saying she was hungry. At the end of November, I pulled hot coals out of the stove, put them in a bowl, got ready to eat, stopped sleeping at night, put things in bundles, wanted to go somewhere, said “ridiculous things.”

Has 3 sons, the 4th died in 1977 in a car accident. One of the patient's 8 sisters died,

“She has become just as weak-minded.” Another of the sisters was admitted to the PND twice.

(Assessing the obtained data from the objective anamnesis, one should first of all pay attention to the hereditary burden - two sisters had mental illnesses, one had dementia, and the second had an unknown diagnosis. The second feature of the anamnesis given by the husband is a significant discrepancy in the assessment of the time of onset of the disorders memory. Subjectively, the patient noted memory impairments five to six years before hospitalization, but according to her husband, only in the last year. What does this mean? Objective manifestations were hidden by outwardly orderly behavior in the first years of the disease and remained insignificant for the husband.)

She was in hospital treatment from 11/30/88 to 01/03/89. At the hospital, upon admission, the following mental status was noted: emotionally labile, upon entering the office, she burst into tears, talking about some money that was missing. Doesn't know the current date. Where is? - “At an institute or technical school.” The doctor is called a clerk or a student. How long has she been here - “yes, as soon as they called, she came right away.”

(So, from the first lines of reading the mental state described upon admission of the patient, we record disorientation in time, place of stay, environment. She is oriented correctly in her own personality, which is mentioned later.)

He believes that all the people here are teachers. I wrote my full name correctly. She says that she worked as a school director - “She has been retired since the New Year.” She gave the correct home address, but could not remember the names of her sons or their ages. “They were born every 2 months.” He doesn’t know when the Great Patriotic War, the revolution took place - “But not everyone knows that now.” November 7 is “the end of all work,” May 1 is “the first step of Soviet power.” 100- 7=106. When asked if she is in the hospital, she answers in the negative.

Mental status in the hospital over time: given accompanied by staff. At the invitation, she sat down on a chair. Disoriented in place and time, calls herself correctly, does not know her age. At the request, I wrote my full name correctly, but it took me a long time to concentrate, my handwriting was changed, the letters were uneven.

(Not only amnestic disorientation is noted, but also handwriting disorders, which is called agraphia; in combination with elements of apraxia and acalculia, this suggests the presence of Alzheimer’s disease.)

She couldn’t remember her husband’s name, then she said Stepan. I couldn't remember my sons' names. She says that she lives in the village. Tatarstan, on Kalinin street. The revolution took place in 1919, the war - “everyone knows this, began on May 25, ended in January.” I had difficulty remembering that I taught Russian. He doesn’t know who Alexander Sergeevich is. To the question - who is Pushkin, she answered - “everyone knows this from childhood.” 2x2=4; 2x3=6; 6x7=9. He often answers inappropriately and loses his thoughts. There is an almost constant smile on my face. There is no criticism of my condition.

(Lack of criticism and inadequate emotional background are also more typical of total presenile dementia than of vascular dementia.)

But she said, “You probably take me for an abnormal person, but I’m telling you the truth.” In the person of the doctor, whom I saw for the first time, I recognized an acquaintance whom I had met “a couple of times.” The doctors stated in their conclusion to the VKK: given the constant memory impairment over the last year, the loss of work and self-care skills over the last 2-3 months, individual violations (believes that she retired 2 years ago, that she is at a meeting of teachers) ; a sharp decline in memory over the last month, progressive dementia, one can think of Alzheimer's disease. General restorative treatment and tranquilizers were recommended, which was done. She was readmitted to the women's department of the PND on January 23, 1990 and was hospitalized from January 23, 1990 to March 5, 1990. Mental status: disoriented in place and time. Makes contact. Sensitive, cries, says that she has become an asshole, doesn’t know anything, doesn’t remember anything. He calls himself correctly, the year of birth is 1921. He cannot give his age, “it’s already a lot, now it’s already 1922.” He answers that his husband’s name is Pavel, he doesn’t know his middle name, “Yes, I don’t call him by his middle name.” She says that she has 2 daughters and 2 sons (actually 3 sons), but she couldn’t remember their names. She answers that she sleeps very well, there are no fears, that now she is at home, but does not know anyone around her. Coming out of the staff room, I started crying again, “I need to go home, I have a small child crying.”

According to unofficial data in Russia, 80% of patients over the age of 65 suffer from dementia. Considering the fact that more than 2.5 million elderly people live in the capital, the treatment of Alzheimer's disease in Moscow is becoming a serious problem.

Symptoms

The disease is a form of progressive dementia (dementia), leading to loss of ability to learn new things. An elderly patient loses all previously acquired skills and experiences:

  • forgetfulness;
  • incoherent speech and speech disorders;
  • inability to communicate;
  • delusions, hallucinations;
  • aggressiveness or, conversely, complete apathy;
  • loss of orientation in familiar places;
  • inability to recognize family and friends.

In addition, the person experiences urinary and fecal incontinence, difficulty walking, and difficulty performing usual daily activities.

Typically, Alzheimer's disease develops in several stages in older people. The first stage, when the only characteristic feature is the inability to remember new information, is often mistaken for natural age-related changes. Gradually the symptoms worsen. The last stage - the patient loses speech functions, cannot perform any actions and practically does not get out of bed, physical and mental exhaustion and disability occur.

Causes

The disease is a consequence of a dysfunction of the central nervous system. Until now, medicine has not been able to identify the exact cause of degenerative changes. There is a theory that this disorder is a pathology of chromosomes, in particular the 1st, 14th, 19th, 21st. But since the phenomenon has not been fully studied, it is generally accepted that the development of the disease can be triggered by:

  • heredity;
  • arterial hypertension;
  • cerebral atherosclerosis;
  • diabetes;
  • Down syndrome.

According to the observations of doctors, people with a low level of intelligence, insufficient physical activity, who are overweight, and with frequent depression are most susceptible to the disease.

There is currently no way to cure Alzheimer's disease. In Moscow, according to official data, over 100 people die from this disease every year; the real picture is 5-6 times higher.

Diagnosis and supportive therapy

Prevention of the development of the disease in old age is intellectual activity, dietary nutrition, and timely treatment of cardiovascular diseases. But if prevention does not produce a positive result, it is very important to consult a psychotherapist if you notice signs of changes in cognitive behavior or memory impairment in an elderly person.

To diagnose the disease, the medical history of the patient and his relatives is studied. A psychotherapist conducts neuropsychological testing to identify the patient’s intellectual abilities. X-ray studies (CT, MRI, PET scan, puncture) help identify signs of pathology in the brain and spinal cord.

If a specialist says he knows how to treat Alzheimer's disease, run away from him. Because when a positive diagnosis is made, the doctor’s efforts are aimed at slowing the progression of the disorder and nothing more. For this purpose, medications are prescribed and psychological sessions are conducted. These measures are not treatment as such. They are intended to alleviate symptoms and adapt to the disease.

Providing proper care is the foundation of the entire program. Creating a constant routine, safety, proper nutrition, timely reminders of physiological needs and other actions will ensure comfort and peace for the elderly person and his family.

If you don’t know which doctor treats Alzheimer’s disease, contact psychotherapist I.G. Gernet (Moscow). Many years of experience in psychiatry allows him to give effective recommendations regarding the prevention of the initial stage, use proven diagnostic methods, proven methods of psychotherapy and effective medications. The doctor will give practical advice on patient care, help an elderly patient adapt to new conditions, make a home visit if necessary, and give advice over the phone. By using the services of a specialist, you can give your elderly loved ones a few more years of normal life.

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

Alzheimer's disease is a primary endogenous degenerative dementia that begins in presenile age and is characterized by progressive impairment of memory, speech, and intelligence, 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 in neurofibrils, which later became known as Alzheimer's changes in neurofibrils.

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. The 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). The main clinical feature is the leading role of memory impairment. The appearance of special confusion and affective disorders (confused-suppressed affect) is characteristic. 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. (transition to simpler forms of 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 recently led 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. It becomes clear that we are talking about etiologically different forms of DAT. 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 an 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. It has been discovered that senile plaques are toxic, so the nerve cells of the brain 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.

The main problem associated with Alzheimer's disease- inattention of the patient’s relatives to the first alarming symptoms, which they frivolously attribute to banal aging. In order to avoid catastrophic consequences, we recommend immediately contacting the National Center for Clinical Psychiatry, where all conditions have been created for an in-depth diagnosis of the stage of the disease and the nature of the pathological process, as well as the most effective treatment, allowing the patient to prolong his stay in society as a full-fledged member of it.

Diagnosis of Alzheimer's disease at the National Center for Clinical Psychiatry.

If you suspect Alzheimer's disease The NDC patient will first of all undergo an examination and... His medical history will be carefully analyzed, as well as information about the mental health of his relatives. The primary diagnostic criterion in this case is gradual memory loss and weakening of cognitive abilities. It is necessary to establish the current functional state of the brain, and, if necessary, the thyroid gland. The Center's staff includes highly qualified diagnostic doctors, whose experience largely determines the further success of treatment. List of diagnostic measures to identify Alzheimer's disease and the development of individual tactics for its treatment includes, and, a blood test for thyroid hormones, and neuropsychological tests.

Treatment of Alzheimer's disease.

The NDC does not reassure patients’ relatives, giving empty promises: yes, Alzheimer's disease truly incurable. But by adequately and competently constructing the therapeutic process, one can (and should) achieve a significant mitigation of symptoms, slowing down further progression of the disease and the maximum possible socio-psychological adaptation of the patient in society under the current circumstances. cornerstone Alzheimer's disease treatment at the NDC of Clinical Psychiatry is drug therapy: based on a series of diagnostic tests, the patient is offered an individual drug regimen that meets his individual needs and current condition. Depending on the situation, combinations are used, including monoamine oxidase type B inhibitors, 2nd generation acetylcholinesterase inhibitors, neuroprotectors (memantine), NSAIDs, vitamins, and symptomatic therapy. The National Center for Clinical Psychiatry is in close contact with the best Israeli clinics, exchanging experiences and their own best practices. Examples of such productive cooperation are the Israeli computer program Savion, the purpose of which is to help the patient remember individual episodes from the past, and the NeuroAD electromagnetic therapy device, which allows restoring some behavioral functions.

Prevention of Alzheimer's disease.

NDC guarantees all its patients constant psychological support, which is very important for patients suffering from Alzheimer's disease, and is an important part of the prevention of this disease. Ours will not let the brain of an elderly person with Alzheimer's disease, constantly training him and keeping him in constant tone. To do this, we use memorizing poetry, solving crosswords, and learning foreign languages. This should also include moderate physical activity and dietary adjustments (our “secret weapon” for prevention of Alzheimer's disease- so-called Mediterranean diet).

In conclusion, it should be noted that NDC specialists are constantly searching for effective methods Alzheimer's disease treatment, which undoubtedly inspires optimism and gives hope to our patients and their relatives.



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