Childish behavior

Introduction Behavioral action naive stupidity is the clinical manifestation of Alzheimer's disease dementia. The patient's appearance is old, dry and wrinkled, pigmentation, white teeth and muscle atrophy. It may be too neat, organized, disciplined, or informal, with a euphoric or violent or dull expression, and nasty and stupid. The key to the prevention of this disease is the application of various methods, including drugs, nursing, psychology, physical therapy, etc., to delay the aging process of the entire body. At the same time, we will actively prevent various infectious diseases and trauma, treat various chronic physical diseases, and continuously improve the health level and quality of life.

Cause

Causes:

From the current epidemiological data, Alzheimer's disease dementia (AD) may be a heterogeneous disease that occurs under the influence of a variety of factors, including biological and psychosocial factors. Although AD neuropathology, especially molecular biology research, has made great progress, which lays a foundation for the study of pathophysiology and etiology of AD, it is still in the exploratory stage, and the etiology of AD is far from being elucidated. Epidemiological studies have analyzed the risk factors for AD, providing clues for finding the cause, but the risk factors are not the cause. From the current research, there are more than 30 possible factors and hypotheses of AD, such as family history, female, head trauma, low education level, thyroid disease, too high or too low maternal age, virus infection, etc. The discussion of different aspects of a problem may be correct and not mutually exclusive. From the current research, there may be different reasons for AD. The following factors are related to the pathogenesis of this disease:

Family history

Most epidemiological studies suggest that family history is a risk factor for AD. In some patients, members of the family members who suffer from the same disease are higher than the general population, and the risk of congenital disease is also increased. Further genetic studies have confirmed that the disease may be caused by autosomal dominant genes. Recently, through gene mapping studies, it was found that the pathogenic gene of amyloid in the brain is located on chromosome 21. It can be seen that dementia is related to heredity, but it is hard to be sure how big the genetic effect is. Due to the late onset of AD, there are no reports of twins based on the general population. The same prevalence reported in a small number of elderly single-ovary twins (MT) studies is not very high. Most reports suggest that there is a family aggregation phenomenon in AD, and the relationship between AD and the positive family history of first-degree relatives is also quite positive. According to available data, in eight case-control studies, AD was associated with a history of dementia in first-degree relatives, and no association was found in the other. A reanalysis of 11 case-control studies in Europe showed that if at least one first-degree relative had dementia, the risk of dementia increased more than three-fold. The study of the distribution frequency of apolipoprotein E (Apo E) genotype in the population further supports the pathogenesis of genetic factors on AD. The Apo E allele 4 has been shown to be an important risk factor for AD. The frequency of the Apo E 4 gene was significantly increased in both familial and sporadic AD. The frequency of Apo E 4 gene in autopsy-recognized AD patients is about 40%, compared with about 16% in normal control population, and the risk of AD with an 4 allele is two to three times that of the general population. The risk of carrying two 4 alleles is about eight times that of the general population. It is now clear that the Apo E4 allele is not a necessary factor in the pathogenesis of AD, and its predictive effect on the pathogenesis of AD remains to be confirmed by prospective studies. The author's analysis may be associated with the collection of late-onset AD, suggesting that family aggregation may be an important risk factor for early-onset AD. However, this interpretation of positive results should be cautious, and family aggregation is not a true genetic factor. Thus, genetic factors are not the only factor in the pathogenesis of AD.

2. Some physical diseases

Such as thyroid disease, immune system diseases, epilepsy, migraine, etc., have been studied as a risk factor for AD. In patients with a history of hypothyroidism, the relative risk of developing AD is 2.3. There was a history of seizures before the onset of AD (relative risk was 1.6). The history of migraine or severe headache has nothing to do with AD. Many studies have found that the history of depression, especially the history of depression in the elderly, is a risk factor for AD. A recent case-control study suggests that other functional disorders such as schizophrenia and paranoid psychosis are associated with depression. A comparison of early history of central nervous system infections, such as encephalitis, meningitis, herpes virus infection, and history of exposure to livestock, and animal history of eating animals have failed to demonstrate that these factors are associated with AD. Chemicals that have been studied as risk factors for AD include heavy metal salts, organic solvents, pesticides, and pharmaceuticals. The role of aluminum has been a concern because animal experiments have shown that aluminum salts have an impact on learning and memory; epidemiological studies suggest that the prevalence of dementia is related to the amount of aluminum in drinking water. According to preliminary results of a study on the prevalence of dementia in France, Michel et al. reported that aluminum was a risk factor for AD, but further analysis denied this result. Flaten et al. (1990) reported that aluminum in drinking water is associated with dementia. Since then, several studies have failed to confirm that aluminum is a risk factor for AD. Case-control studies of people with a history of heavy metal exposure, including exposure to aluminum, did not find any heavy metals associated with AD. It may be due to the accumulation of neurotoxins such as aluminum or silicon in the body, which accelerates the aging process. However, although aluminum is a neurotoxic substance, it has not been considered as a risk factor for AD in the existing studies. It has been reported that smoking is not a risk factor for AD, but instead protects AD. And some authors did not find the relationship between the two. Smokers suffering from less AD may be due to their short life expectancy and they will die if they are old.

3. Education level

There are more and more reports about the low level of education and the increased prevalence of dementia. Shanghai reported that the prevalence of dementia and AD was 6.9%, and that school age was 1.2% more than 6 years. A recent Italian epidemiological survey has similar findings. However, in a Japanese case-control study, no association was found between education levels and dementia and/or dementia subtypes. There is no reasonable explanation for this. Some scholars believe that this is caused by systematic errors. Since most epidemiological studies use a two-stage screening test, a diagnostic test is performed on patients who are positive for screening, so that people with low illiteracy or low education may have low scores in the screening test and easy to enter the diagnosis. The stage of sexual examination is diagnosed as dementia, which increases the prevalence, and in fact these people may not have cognitive decline at all. It is believed that this is due to the biological characteristics of illiterate itself, not to education, and that education is related to the socio-economic situation, further complicating this issue. However, Zhang Mingyuan et al. (1990) used different screening cut-off values according to the different educational levels of screening subjects during screening to avoid such systematic errors. As a result, the prevalence of dementia was still high in low-educational people. Several studies have confirmed this result since then. The low level of education and the etiology of AD are still unclear. The possible explanation is that early education and training promoted the development of cortical synapses, increased the number of synapses and increased the brain reserve, thus delaying dementia. Diagnostic time. This hypothesis is supported by some clinical observations. For example, patients with high levels of AD can retain some cognitive functions even in advanced stages, and their duration from diagnosis to death is relatively short. Low levels of education have a similar relationship with vascular dementia and other secondary dementias.

4. Head trauma

Head trauma refers to head trauma with conscious disturbance, and brain trauma has been reported as a risk factor for AD. Of the 12 case-control studies, 3 were found to be significantly associated; 4 AD had more traumatic history than the control group, but there was no statistical significance, and the other 5 did not find any association. However, a recent follow-up study of a severe brain injury has attracted more interest. Robert et al. followed the average follow-up of patients with severe traumatic brain injury for 25 years. As a result, approximately one-third of patients had amyloid-like deposition similar to AD in brain tissue. Clinical and epidemiological studies suggest that severe brain injury may be one of the causes of certain AD. According to current data, head trauma may be a risk factor for AD, but it is not certain.

5. Pregnant mothers are too high or too low (more than 40 years old or younger than 20 years old)

Due to Down's syndrome (DS), it may be a risk factor for AD, and DS risk increases with the increase of maternal age. There were 9 case-control studies, some of which were found to be related, some found to be different but not statistically significant, or none of them were found at all, and some were considered to be only risk factors for some sporadic AD.

6. Other

Progressive failure of the immune system, impaired detoxification of the body and lentivirus infection, as well as social and psychological factors such as widowhood, solitary, economic difficulties, and life bumps can be the cause of the disease.

an examination

Related inspection

Whole body condition check

Neuropsychological test

Simple Mental Scale (MMSE): The content is concise, the measurement time is short, and it is easy to be accepted by the elderly. It is the most common scale for clinically measuring the degree of intelligent damage of this disease. The total score of the scale is related to the level of cultural education. If the illiteracy is 17 points; the primary school level is 20 points; the secondary school level is 22 points; the university degree is 23 points, indicating the existence of cognitive impairment. Further detailed neuropsychological tests, including memory, executive function, language, application, and visual spatial ability, should be evaluated. For example, the AD Rating Scale Cognitive Part (ADAS-cog) is a cognitive ability test that contains 11 items specifically designed to detect changes in the severity of AD, but is primarily used in clinical trials.

Assessment of daily living ability: For example, the Daily Living Ability Assessment (ADL) scale can be used to assess the degree of impairment of a patient's daily life function. The scale has two parts: one is the physical self-care ability scale, which measures the patient's ability to take care of their own life (such as dressing, undressing, combing and brushing); the second is the tool use ability scale, which measures the patient's use. The ability to use everyday tools (such as making calls, taking a bus, cooking by yourself, etc.). The latter is more susceptible to the decline in cognitive function in the early stages of the disease.

Assessment of behavioral and psychiatric symptoms (BPSD): including the Alzheimer's Disease Behavioral Pathology Rating Scale (BEHAVE-AD), the Neuropsychiatric Symptom Questionnaire (NPI), and the Cohen-Mansfield Agitated Questionnaire (CMAI), often based on informed individuals The baseline information provided provides not only the presence or absence of symptoms, but also the frequency and severity of symptoms, and the burden on the comparators. Repeated assessments can also monitor treatment outcomes. The Cornell Dementia Depression Scale (CSDD) focuses on the evaluation of agitation and depression in dementia, and 15 geriatric depression scales can be used to evaluate AD depressive symptoms. CSDD has higher sensitivity and specificity, but has nothing to do with the severity of dementia.

2. Hematology examination

It is mainly used to detect the presence of accompanying diseases or complications, to identify potential risk factors, and to exclude dementia caused by other causes. Including blood routine, blood sugar, blood electrolytes including blood calcium, renal function and liver function, vitamin B12, folic acid levels, thyroxine and other indicators. For high-risk groups or those suggesting clinical symptoms, syphilis, human immunodeficiency virus, and Borrelia burgdorferi serology should be performed.

3. Neuroimaging

Structural imaging: specific imaging findings used to rule out other underlying diseases and to detect AD.

Head CT (thin-thickness scan) and MRI (coronal) examinations can show significant cerebral cortical atrophy, especially hippocampus and medial temporal lobe, supporting the clinical diagnosis of AD. Compared with CT, MRI detects subcortical vascular changes (such as infarcts at critical sites) and suggests specific diseases (such as multiple sclerosis, progressive supranuclear palsy, multiple system atrophy, cortical basal ganglia degeneration, prion disease, amount) Changes in temporal lobe dementia, etc. are more sensitive.

Functional neuroimaging: such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) can improve the reliability of dementia diagnosis.

The 18F-deoxyribose glucose positron emission scan (18FDG-PET) showed a decrease in glucose metabolism in the apical and superior/posterior temporal region, posterior cingulate cortex and anterior cranial lobes, revealing specific abnormal changes in AD. The level of frontal lobe metabolism is reduced in the late AD. 18FDG-PET has a sensitivity of 93% and a specificity of 63% for the pathological diagnosis of AD. It has become a practical tool, especially suitable for the differential diagnosis of AD and other dementia.

Amyloid PET imaging is a very promising technology, but it has not yet been routinely applied.

4. Electroencephalogram (EEG)

The EEG of AD is characterized by a decrease in alpha wave, an increase in theta wave, and a decrease in the average frequency. However, 14% of patients had normal EEG in the early stages of the disease. EEG is used for the differential diagnosis of AD, providing early evidence of prion disease, or suggesting the possible presence of poisoning-metabolic abnormalities, transient epileptic amnesia or other epilepsy.

5. Cerebrospinal fluid testing

Cerebrospinal fluid cell count, protein, glucose and protein electrophoresis analysis, suspected vasculitis, infection or demyelinating disease should be tested. Patients with rapidly progressing dementia should undergo a 14-3-3 protein test to aid in the diagnosis of prion disease.

Detection of -amyloid and Tau protein in cerebrospinal fluid: Decreased -amyloid (A42) level in cerebrospinal fluid of AD patients (decreased A42 content in cerebrospinal fluid due to deposition of A42 in the brain), elevated total Tau protein or phosphorylated Tau protein . Studies have shown that the sensitivity of A42 diagnosis is 86%, specificity is 90%; the sensitivity of total Tau protein diagnosis is 81%, the specificity is 90%; the sensitivity of phosphorylated Tau protein diagnosis is 80% and the specificity is 92%; A42 and total Tau protein combination The sensitivity of the diagnosis of AD compared with the control can reach 85% to 94%, and the specificity is 83% to 100%. These markers can be used to support the diagnosis of AD, but the specificity of AD and other dementia diagnoses is low (39% to 90%). There is currently no uniform detection and sample processing method.

6. Genetic testing

Can provide a reference for diagnosis. The amyloid precursor protein gene (APP), presenilin 1, 2 gene (PS1, PS2) mutations accounted for 50% of familial early-onset AD. Apolipoprotein APOE4 gene detection can be used as a reference for sporadic AD.

Differential diagnosis

Differential diagnosis:

Behavior disorder and peculiarity: behavioral disorder and peculiarity is one of the clinical manifestations of mental disorders associated with intracranial tumors. A mental disorder associated with an intracranial tumor refers to an intracranial tumor that invades the brain tissue or cerebral blood vessels of the brain parenchyma, causing damage to the brain parenchyma or increased intracranial pressure. Patients suffering from intracranial tumors have 40% to 100% of people can have mental symptoms.

Behavioral and emotional abnormalities: When children show deviations from the mood, personality and social behavior of the age, it seriously affects the development of the child itself and the interference of the learner. The life of the person is called behavior and emotional abnormality. Children with behavioral and emotional abnormalities are divided into extroverted and introverted surnames. Extroverts are their non-stop activities, their attention is very short-lived, they are distracted and unable to learn, or they are aggressive, unable to obey authority, and have more aggressive behaviors. This type of child often destroys group order in a group. Introverted children often have deep fears, often feel anxious, insecure, unable to bear frustration or blows, and sometimes cry, depression or sadness, so that they can't learn normally. Such children are also classified into mild and moderate to severe due to different biased behavioral intensity. The extremes of this type are autism, schizophrenia, and the like.

Mechanically repeating the speech or behavior of the surrounding people: it is a behavioral disorder of the will, found in schizophrenia. Sometimes the patient mechanically performs any external request (passive obedience) and allows anyone to place his or her own posture. For example, if the patient raises one leg, the patient can maintain the posture given for a period of time (wax-like flexion), or Mechanically repeat the words or behaviors of the people around you (imitation of language, imitation of movements).

Stupid Lu: Stupid, that is stupid and rude. It is a manifestation of mental retardation. Mental retardation (MR) is a group of diseases in which the general intellectual function is significantly lower than the same age level and the same amount is accompanied by adaptive behavioral defects. There are also multiple claims such as mental retardation, mental dysplasia, mental defects, mental retardation, mental retardation, mental retardation, mental retardation, mental retardation and intellectual disability.

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