Alzheimer's disease
Introduction
Introduction to Alzheimer's disease Alzheimer's disease (AD) is a dementia caused by chronic progressive central nervous system degeneration, the most common cause of dementia and the most common senile dementia. AD is characterized by neuropsychological symptoms such as progressive memory impairment, cognitive dysfunction, personality changes, and language disorders. Often in the elderly or early premature, more slowly onset, and gradually progress, with dementia as the main performance, before the onset of the elderly or more, with a family history of the same disease, the disease develops faster. Patients with AD with genetic quality and genetic mutations of 10% have a clear family history, especially those before the age of 65, so family history is an important risk factor. Some people think that AD first-degree relatives are about 50% of the disease when they are 80-90 years old. The risk is There is no family history of AD 2 to 4 times, early onset autosomal dominant AD is relatively rare, currently only 120 families in the world carry certain pathogenic genes, and genes related to FAD pathogenesis include No. 21, No. 14, 1 No. and chromosome 19, it has been found so far that FAD is an autosomal dominant genetic disease with genetic heterogeneity. basic knowledge The proportion of sick people: up to 0.1%--0.5% of the elderly over 60 years old Susceptible people: good for the elderly Mode of infection: non-infectious Complications: depression, anxiety, paranoia
Cause
Causes of Alzheimer's disease
(1) Causes of the disease
The etiology of Alzheimer's disease has not been known so far. AD is generally considered to be a complex heterogeneous disease, and many factors may be involved in the pathogenesis, such as genetic factors, neurotransmitters, immune factors and environmental factors.
1. Neurotransmitter AD patients with hippocampus and neocortex acetylcholine (Ach) and choline acetyltransferase (ChAT) were significantly reduced, Ach was synthesized by ChAT, cortical cholinergic neurotransmitter dysfunction is considered to be memory impairment And one of the causes of other cognitive dysfunction, Meynert basal ganglia is the main source of neocortical cholinergic fibers, the early cholinergic neurons in this area of AD decreased, is the main site of early damage in AD, there is a significant sustained Ach synthesis Insufficient; ChAT reduction is also related to the severity of dementia, the increase in the number of senile plaques and the number of neurofibrillary tangles in the amygdala and cerebral cortex, but this view is still controversial. The muscarinic M2 receptor and nicotine in the brain of AD patients Receptors are significantly reduced, M1 receptors are relatively retained, but incomplete, combined with the G protein second messenger system; in addition, non-cholinergic transmitters, such as serotonin (5-HT), gamma -Aminobutyric acid (GABA) is reduced by 50%, somatostatin, norepinephrine and 5-HT receptor, glutamate receptor, and somatostatin receptor are all reduced, but these changes are Primary or secondary to the nerve Reduction has not been determined, given acetylcholine precursors such as choline or lecithin and degradation inhibitors physostigmine, or a muscarinic antagonist drug acts directly on postsynaptic receptors, and not improved.
2. Genetic quality and genetic mutations in 10% of patients with AD have a clear family history, especially in patients before the age of 65, so family history is an important risk factor, some people think that AD first-degree relatives 80 to 90 years old when about 50% of the disease, The risk is 2 to 4 times that of family-free AD. Early-onset autosomal dominant AD is relatively rare. Currently, only 120 families in the world carry certain pathogenic genes. Genes related to the pathogenesis of FAD include No. 21 and No. 14 , chromosomes 1 and 19, it has been found that FAD is an autosomal dominant genetic disease with genetic heterogeneity.
(1) Some families have mutations in the amyloid protein precursor (APP) gene on chromosome 21, and several APP gene mutations have been found in early-onset FAD. The age of onset is <65 years old, which is rare.
(2) Some families are associated with the transmembrane protein presenilin 1 (PS1) gene mutation on chromosome 14, FAD is early onset, and is associated with 30% to 50% of early-onset AD. The main cause of FAD is a malignant course.
(3) It has been found that a German national FAD is associated with a mutation in the presenilin 2 (PS2) gene located on chromosome 1, which may be caused by an excess of A142.
(4) The apolipoprotein E-4 (Apo E4) allele polymorphism on chromosome 19 is present in the normal population, and the Apo E4 allele can significantly increase the risk of late-onset FAD or sporadic AD over 60 years of age. ApoE has three alleles: 2, 3, 4, which can form genotypes such as 4/4, 4/3, 4/2, 3/3, 3/2 and 2/2, and 4 increases the risk of AD. And to make the age of onset, 2 reduce the risk of AD and delay the onset age, ApoE4/4 genotype 80 years after the onset of AD is three times the risk of non-4 genotype, often in the 60 to 70 years old, the above are statistical results It does not indicate a necessary relationship. The interpretation of these results must be cautious and can only be regarded as a sensitive factor. Apo E 4 cannot be simply used for the diagnosis of AD.
(5) Other proteins such as 2 macroglobulin and its receptor, low-density lipoprotein receptor related protein, also significantly increased the risk of AD in the elderly.
3. Immunomodulation Abnormal immune system activation may be a component of AD pathological changes, such as AD brain tissue B lymphocyte aggregation, serum brain-reactive antibodies, anti-NFT antibodies, human brain S100 protein antibodies, -AP The antibody and myelin basic protein (MBP) antibody are increased, and the B cell pool of AD is enlarged, which may reflect the immune response caused by neuronal degeneration and nerve tissue damage. The total number of peripheral blood lymphocytes, T cells and B cells are normal. Scope, many patients with increased CD4 / CD8 cell ratio, suggesting immunoregulatory T cell defects, increased IL-1, IL-2 and IL-6 production in AD patients, IL-2 production is related to the severity of the disease, peripheral blood of AD patients The MBP and lipid-containing protein (PLP)-reactive IFN- secreting T cells were significantly higher than the control group. The MBP-reactive IFN- secreting T cells in CSF were 180 times that of peripheral blood, but this self-responsive T The significance of cellular responses remains unclear.
4. Environmental factors Epidemiological studies suggest that the occurrence of AD is also affected by environmental factors, low level of education, smoking, brain trauma and heavy metal exposure history, the age of the mother when pregnant and the first-degree relatives suffering from Down syndrome can increase the disease Risk; Apo E2 allele, long-term use of estrogen and non-steroidal anti-inflammatory drugs may have a protective effect on the disease, age is an important risk factor for AD, the prevalence of AD increases by a factor of five every five years after age 60, The prevalence rate of 60 to 64 years old is about 1%, from 65 to 69 years old to about 2%, 70 to 74 years old is about 4%, 75 to 79 years old is about 8%, 80 to 84 years old is about 16%, and 85 years old or older is about 85%. 35% to 40%, the incidence rate has also increased similarly, AD patients with more women, may be related to women's longevity, the skull contains small neurons and less synapses, may be a risk factor for AD.
Prevention
Alzheimer's disease prevention
Alzheimer's disease is one of the most harmful diseases in the elderly. As people's life expectancy continues to increase, the prevention of this disease is very important for the elderly.
Primary prevention: Prevention of AD Since the cause has not been known so far, some risk factors have been mentioned in the cause, and some can be prevented and interfered with, such as preventing viral infection, reducing aluminum poisoning, strengthening cultural accomplishment, and reducing head trauma. Wait.
Secondary prevention: Because of the difficulty in diagnosis of AD, it is necessary to strengthen early diagnosis techniques and early treatment. It is generally believed that AD is the acceleration of the aging process, and Jobst et al. determine the deterministic and probable AD and the elderly with no cognitive impairment. Do a head CT examination, the thickness of the middle temporal lobe is measured by the undiagnosed clinical diagnosis. The result is that the axillary atrophy of the AD patients with large and high probability is significantly faster than that of the elderly without cognitive impairment. Therefore, the disease is suspected and determined. It is very necessary for the elderly in this disease to do this check regularly and give positive treatment.
Tertiary prevention: Although the cognitive function of patients with AD is diminished, patients should be encouraged to participate in daily social activities, including mental and physical activities, especially in early patients. As many activities as possible can maintain and retain their abilities, such as playing Musical instruments, dancing, playing cards, typing and painting all contribute to the patient's life and have the potential to delay the progression of the disease, as severe dementia patients can also respond to familiar social life and familiar music.
The specific practices are as follows:
First, we must strengthen prevention from the aspects of internal and external environmental factors such as psychology, personality, diet and nutrition, air quality, etc. Among them, psychological factors are particularly important, we must pay attention to maintain a good mentality and ensure the balance of mental and mental state.
Second, establish a scientific and rational lifestyle and develop a good living habit.
Third, we must pay attention to exercise and persevere, and we must combine static and dynamic, work and rest, such as chess and calligraphy, fishing and other travel.
Fourth, for postmenopausal women, in the early menopause, under the guidance of gynecologists, estrogen and progesterone replacement therapy, estrogen + progesterone replacement therapy can protect endothelial function, better than estrogen alone.
5. Men from the beginning of their prime, they should apply appropriate amount of Chinese herbal medicine (food therapy or medicine) to nourish yin and tonify kidneys under the guidance of traditional Chinese medicine to increase androgen secretion and protect endothelium by regulating endocrine hormone balance.
Sixth, the application of antioxidants, such as ginkgo preparations, vitamin C, E, -carotene, superoxide dismutase (SOD), etc., in order to resist the accumulation of oxygen free radicals.
Seven, the application of folic acid, vitamin B6, B12 and other drugs that promote homocysteine metabolism.
Eight, the application of anti-inflammatory agents, such as aspirin, indomethacin and so on.
Nine, eat foods rich in L-arginine, less methionine, such as a variety of nuts, black sesame, black beans, oats and so on.
The above measures can prevent and delay the occurrence and development of Alzheimer's disease, and may have symptoms-lowering effects for early and mid-term patients.
Complication
Alzheimer's disease complications Complications depression anxiety paranoia
First, behavioral complications include unfriendly, excited, lost and uncooperative.
Second, mental complications include depression, anxiety and paranoia.
Third, pay attention to secondary lung infections, urinary tract infections, etc.
Symptom
Symptoms of Alzheimer's disease Common symptoms Ataxia convulsions Apathy Insomnia Illusion directional dysfunction Depressive myoclonus
1. The patient is insidious onset, the mental change is concealed, and the early stage is not easy to be noticed by the family. It is not clear the exact date of the onset of the disease. Occasional fever, infection, surgery, mild head trauma or medication, caused by abnormal mental disorder. Note that some patients may complain of dizziness, headaches that are difficult to express, variable physical symptoms or autonomic symptoms.
2. The gradual occurrence of memory impairment or forgetting is an important feature or first symptom of AD.
(1) The near memory disorder is obvious: the patient can't remember the daily chores that happened on the day, remember the things that have just been done or the words that have been said, forget the nouns that are rarely used, where the appointments or valuable objects are placed, and easily forget the names that are not commonly used. Frequently repeated questions, previously familiar names are easy to confuse, vocabulary is reduced, distant memories can be relatively reserved, words that are not commonly used in early years will also lose memory, Albert and other patients check the date of important political events and identify past and current important people. The photo found that memory loss included the entire life cycle to some extent.
(2) Korsakoff's Forgotten Status: It is characterized by recent forgotten, and things that have been said before 1~2min can not be remembered at all. It is easy to forget the names, places and numbers of people who have recently contacted. In order to fill the memory gap, the patient often unintentionally composes the plot. Or a distant move, misunderstanding and fiction, learning and remembering new knowledge is difficult, it takes weeks or months to repeat, in order to remember your bed and the name of the doctor or nurse, repeat a series of numbers or words during the inspection, instant Memory can often be maintained, short-term and long-term memory is incomplete, but some long-established patterns can still be performed.
3. Cognitive impairment is a characteristic manifestation of AD, which gradually becomes apparent as the disease progresses.
(1) Language dysfunction: It is characterized by fluent aphasia that cannot be distinguished from listening and comprehension. Spoken language gradually stops due to difficulty in finding words, causing language or writing to be interrupted or expressed as spoken language, lacking substantive words, and being verbose and chattering; If you can't find the words you need, you can use roundabouts or leave unfinished sentences, like naming obstacles; early retelling without difficulty, late difficulties; early maintenance of language comprehension, gradually showing incomprehension and inability to perform more complicated Instruction, the amount of spoken language is reduced, there is a wrong language, the ability to talk is diminished, the reading comprehension is impaired, the reading can be relatively reserved, and finally complete aphasia occurs. The examination method is to let the subject say as many vegetables as possible within 1 min. , tools and clothing names, AD patients often less than 50.
(2) Damaged visual space function: It can appear early, manifested as severe directional power disorder, lost or not recognized in the familiar environment, will not look at the street map, can not distinguish left, right or parking; find in the room If you don't have your own bed, you can't identify the tops and bottoms of the tops and trousers and clothes. When you wear the jacket, you can't reach the sleeves. When you spread the tablecloth, you can't match the corners of the tablecloth with the table corners; you can't describe one place and another. Directional relationship, you can't go to the familiar places you used to go to; you can't draw the simplest geometric figures in the later stage. You can't use common items or tools such as chopsticks, spoons, etc., but you can still retain muscle strength and movement coordination. The occipital dysfunction causes an imbalance between the body and the surrounding environment, and the stimulation in one side of the visual path is ignored.
(3) Loss of recognition and misuse: there may be visual disappearance and face disapproval. You may not know the faces of loved ones and acquaintances. You may also suffer from self-knowledge and mirror signs. The patient speaks in the shadow of his own in the mirror. Intentional disuse, can still brush their teeth every morning, but can not do the brushing action according to the instructions; and conceptual misuse, can not correctly complete the continuous and complex use of actions, such as cigarettes, matches and cigarettes.
(4) Computational power disorder: often the price of the wrong item, miscalculated or paid the wrong money, can not balance the bank account, and finally the simplest calculation can not be completed.
4. Mental disorders
(1) Depressed mood, apathy, anxiety, anxiety, euphoria and loss of control, less initiative, distraction, talking to yourself or talking loudly during the day, afraid to stay alone at home, a small number of patients appear inappropriate or frequent Laugh.
(2) Some patients have thinking and behavioral disorders, such as hallucinations, illusions, fragmentary delusions, fiction, eccentric behavior, aggressiveness and personality changes, such as suspicion that their old and weak spouse has an affair, suspecting that their children steal their own money. Or items, hiding valuable things as treasures, thinking that family members are hostile and hostile, unreasonably changing their will, continuing anxiety, nervousness and irritability, refusing old friends to visit, words and actions out of control, risky investment or pornography Wait.
(3) Bulimia behavior, or often ignore eating, most patients suffer from insomnia or nighttime paralysis.
5. Check that the early patients still maintain the usual instruments, forgetting, aphasia and other symptoms when the patient's activities are mild, behavior and social interactions are not obvious abnormal; in severe cases, the performance is uneasy, irritating or less moving, not paying attention to clothing, not trimming, personal Poor health; later still retain habitual autonomic activities, but can not perform command actions, usually without pyramidal tract signs and sensory disturbances, normal gait, visual acuity, relatively complete vision, such as hemiplegia or unilateral blindness in the course of the disease, should pay attention to Whether combined with stroke, tumor or subdural hematoma, can be seen in the late stages of the disease, limb stiffness, pyramidal tract signs, small gait, balance disorders and urinary incontinence, about 5% of patients with seizures and Parkinson's syndrome, Patients with Parkinson's syndrome often cannot stand and walk, stay in bed all day, and rely entirely on care.
Examine
Alzheimer's disease check
1. Laboratory tests, as part of the assessment of dementia, are indispensable for determining the etiology of dementia and common comorbidities in the elderly. Thyroid function tests and serum vitamin B12 levels are other specific causes of dementia. The necessary check items should also be examined as follows: complete blood count; blood urea nitrogen, serum electrolytes and blood glucose levels; liver function tests 15, when the history of the disease or clinical conditions suggest that the cause of dementia may be infection, inflammatory disease or When exposed to toxic substances, special laboratory tests such as syphilis serology, erythrocyte sedimentation rate, human immunodeficiency virus antibody test or heavy metal screening should also be performed.
2. Enzyme-linked immunosorbent assay (ELISA) sandwich detection of cerebrospinal fluid tau protein, AB protein, biochemical detection of CSF dopamine, norepinephrine, 5-HT and other neurotransmitters and metabolite levels.
3. PCR-RFLP detection of APP, PS-1 and PS-2 gene mutations can help diagnose early-onset familial AD. Carriers with significantly increased Apo E4 gene may be sporadic AD patients, but these indicators are not yet available. Clinical diagnosis of the disease.
4. Determination of Apo E phenotype ApoE polymorphism is an important determinant of Alzheimer's disease (AD) risk, Shimaro et al (1989) first described the relationship between AD and 4, they used IEF study found that AD patients 4 frequency is higher than the control group Two times, since then, Rose's research group has reported an increase in the frequency of 4 in patients with delayed familial AD (FAD). These studies have described and confirmed the relationship between 4 and AD. Schachter et al. (1994) first reported on centenarians. The 2 allele is commonly carried, and the number of 2 in older people is twice that of young people. Therefore, the 2 gene seems to protect not only AD, but also longevity.
5. In the EEG topographic map of patients with EEG, the diffuse symmetry of delta and theta is enhanced, and the alpha power decreases in most areas.
6. Brain CT In the CT diagnosis of diffuse brain atrophy, the temporal lobe and hippocampus are atrophy, and the lower horn enlargement (transverse diameter > 7.7 mm) is helpful for the differentiation of AD patients from normal brain aging. Brain CT can exclude hydrocephalus. Chronic subdural hematoma, brain tumors and cerebral infarction and other symptoms similar to AD, such as dementia and clinical course of organic encephalopathy, AD may be normal in early brain CT, AD is hippocampus type dementia, autopsy and CT visible Hippocampal atrophy, hippocampal atrophy is associated with early memory impairment, which indicates that AD may occur. Therefore, CT shows that hippocampal atrophy can be used as a marker for early diagnosis. The Meese cerebrospinal fluid linear measurement method is used to compare the brain CT values of the two groups, and the A±D patient group is found. Compared with the normal elderly group, there was obvious cortical atrophy and sulcal widening. Between the patient group and the control group: the frontal angle width was (5.78±1.82) cm and (5.25±0.60) cm, and the width of the third ventricle was (8.93±2.72) mm and 5.18±1.82) mm, ventricle brain ratio was 3.06±0.61, 5.14±0.61, lateral split width was (9.46±3.84) mm and (6.16±1.37) mm, frontal groove width was (5.45±2.05) mm and (3.71± 1.49) mm, longitudinal crack width is (5.88±1.91) mm and (3.61±1.78) mm, and the top crack width is (5.61±2.02) mm. (4.23±1.69) mm, P value <0.05, the case group white matter low density of 21 cases, accounting for 70% of AD, brain CT findings in the diagnosis of AD is only a reference, but the quantitative analysis of brain CT index helps To identify brain atrophic dementia and normal age-related brain atrophy, and to help predict the prognosis of the disease, but also provide an objective basis for brain morphological changes in AD patients. 3. Brain MRI Brain MBI can provide structural changes in the brain. Updated diagnostic information, using MRI to measure the volume of the anterior and posterior hippocampal formation, found that the volume of AD patients was significantly smaller than the control group, MRI measured the degree of structural atrophy in the middle of the temporal lobe, to distinguish between AD and the same age control group, the sensitivity is 81.0%, specificity was 67.0%, and the vertical diameter of the papillary body was measured by MRI. It was found that the papillary body of the AD group had obvious atrophy.
7. Single photon emission computed tomography - SPECT study has shown that the cerebral blood flow of AD is constantly reduced, and the degree of reduction is related to the severity of dementia. The combined cortex of the sacral, apical and occipital levels is important in cognition and learning. The follow-up study of 132 cases of cognitive impairment found that: the double apical perfusion reduction, AD coincidence rate of 80%, observed clinical diagnosis of AD patients with CT and SPECT, 86% of patients with CT found hippocampus and At the same time that the surrounding structure is atrophy, SPECT shows that the blood flow of the temporal lobe is reduced, and it is positively correlated with the degree of atrophy. Among them, 10 cases have been confirmed by pathology as AD. It is speculated that the atrophy of hippocampal formation and surrounding tissues can lead to the projection of fibers. Destruction and loss result in reduced metabolism and cerebral blood flow in the corresponding cerebral cortex.
8. Positron emission tomography - PET PET proves that the metabolic activity of AD is decreased, and the decline of the combined cortex is most obvious; the decline of cerebral glucose metabolism in 95 patients is consistent with the severity of dementia, degenerative dementia, especially Is AD, metabolic disorders have occurred before neuroimaging found morphological changes, can cause memory and cognitive changes, the typical metabolic reduction region is prominently distributed in the top-sacral cortex, followed by the frontal cortex, not Affecting the primitive cortex, basal ganglia, thalamus and cerebellum, as the disease progresses, the decrease in the cerebral metabolic rate (CMRgl) in the characteristic regions of the sputum-top and frontal contact areas is further aggravated, and is associated with the severity of dementia. These typical distributions contribute to The identification of AD and other diseases, depending on the typical affected and non-invasive areas, distinguishes between AD and non-AD, with extremely high sensitivity and specificity. PET can use these specific metabolic rates in the early stages. Only mild functional abnormalities, memory impairment and mild dementia were found in AD, among the various experimental values, glucose metabolic rate and clinical symptoms The degree of severity is most closely related. However, the CMRglu of the sensorimotor cortex does not change according to the degree of dementia. The unique neuropsychological disorder is clearly related to the local metabolic disorder of typical AD distribution: when the memory is reduced, the bilateral temporal lobe Decreased metabolism; language barrier is associated with decreased left cerebral cortex metabolism; visual structural behavior changes and misuse have right apical dysfunction.
9. Neuropsychology and scale examination are useful for the diagnosis and differentiation of dementia. Commonly used mini-mental state examination (MMSE), Wechsler Adult Intelligence Scale (WAIS-RC), clinical dementia assessment The Neurological Test can determine the degree of memory, cognition, language and visual spatial dysfunction, establish the diagnosis of dementia, and the Hachinski Ischemic Score (HIS) scale is used for the scale (CDR) and Blessed Behavior Scale (BBBS). Identification with vascular dementia.
Diagnosis
Diagnosis and diagnosis of Alzheimer's disease
diagnosis
1. Currently, the clinically widely used NINCDS-ADRDA diagnostic criteria are recommended by the NINCDS-ADRDA Task Force (1984) established by the National Institute of Neurological Disorders and Strokes (NINCDS) and the Alzheimer's Disease and Related Diseases Association (ADRDA). 1. Probable Alzheimer's disease 1 clinical examination confirmed dementia, neuropsychological test MMSE and Blessed dementia scale support; 2 must have 2 or more cognitive dysfunction; 3 progressively exacerbated memory and Other mental disorders; 4 unconscious disorder, may be associated with mental and behavioral abnormalities; 5 onset age 40 to 90 years old, mostly after 65 years of age; 6 exclude other brain diseases that can lead to progressive memory and cognitive dysfunction.
2. Possible Alzheimer's disease (common Alzheimer's disease) 1 Special cognitive dysfunction progressive, such as language (aphasia), motor skills (missing) and perception (abandonment); 2 daily living ability decline and behavioral abnormalities; Similar family history of the disease, and neuropathological evidence; 4 laboratory examination: lumbar puncture routine examination, EEG showed non-specific changes such as increased slow activity, CT examination showed brain atrophy, if necessary, can be reviewed.
3. Exclude other brain diseases that cause dementia, clinical characteristics of Alzheimer's disease 1 There may be a stable period during disease progression; 2 Concomitant symptoms include depression, insomnia, urinary incontinence, delusions, illusions, hallucinations, emotional or behavioral disorders, weight loss Etc. 3 Some patients have signs of the nervous system, especially in the later stages of the disease, such as changes in muscle tone, myoclonus or gait disorders; 4 may have seizures in the later stages of the disease; 5CT examination of the brain is normal.
4. Does not support the clinical features of possible Alzheimer's disease 1 sudden stroke-like onset. 2 focal neurological signs such as hemiplegia, loss of sensation, visual field defects and ataxia, especially in the early stages of the disease. 3 convulsions and gait disturbances occurred early in the course of the disease.
5. Consider the clinical symptoms of Alzheimer's disease. 1 The patient has a manifestation of dementia syndrome, but lacks evidence of neurological, mental or physical illness sufficient to cause dementia. 2 patients may be associated with physical or brain diseases, but can not lead to dementia. 3 patients presented with a single cognitive dysfunction, progressive progressive disease, lack of obvious etiology.
6. The confirmed Alzheimer's disease (definite Alzheimer's disease) 1 meets the clinical diagnostic criteria for the most likely Alzheimer's disease. 2 The pathological changes of autopsy or brain biopsy were consistent with the characteristics of Alzheimer's disease.
Differential diagnosis
1. Mild cognitive dysfunction (MCI) Only memory impairment, no other cognitive dysfunction, such as senile forgetfulness, human word memory, information storage and understanding ability usually peak at 30 years old, recent and distant Memory is relatively stable throughout the life, forgetfulness is the difficulty of starting memories, can be improved by reminding memories, forgetting is the memory process is impaired, reminders can not be recalled, AD patients are also accompanied by computational power, orientation and personality and other obstacles, this Rarely seen in normal elderly.
2. The onset of the disease is more urgent, usually caused by systemic diseases or strokes, when the time is ambiguous, and the patients with dementia have a clear consciousness.
3. Depression DSM-IV proposes depressive symptoms including depression, emotional depression, lack of interest and happiness in various things, guilty or uselessness, loss of appetite or significant weight loss, sleep disorders such as insomnia or excessive sleep, decreased activity It is easy to fatigue or decrease in physical strength. It is difficult to concentrate on thinking or indecision. Repeated thoughts of death or suicide. Clinical diagnosis of depression should have at least one symptom. More than 5 symptoms should be diagnosed in severe depression for more than 2 weeks.
4. Pick's disease Early manifestations of personality changes, poor self-knowledge and social behavior decline, forgetting, spatial orientation and cognitive impairment appear later, CT shows characteristic frontal and temporal lobe atrophy, with AD Diffuse brain atrophy is different.
5. Vascular dementia (VD) has a history of stroke. Cognitive impairment occurs within 3 months after the cerebrovascular disease event. Dementia can occur suddenly or slowly in a step-like manner. Neurological examination can reveal focal signs; special parts Such as angular gyrus, infarction of the anterior or medial thalamus can cause dementia, CT or MRI can show multiple infarcts, except for other possible causes.
6. Parkinson's disease (PD) dementia PD patients with dementia incidence can be as high as 30%, showing a near-memory memory is slightly better, poor performance, but not specific, neuroimaging no identification value, must pay attention to about 10% Lewy bodies can be found in AD patients, senile plaques and neurofibrillary tangles can be seen in 20% to 30% of PD patients. Patients with Guamanian Parkinson dementia syndrome can have both dementia and Parkinson's disease symptoms, often found in the cerebral cortex and white matter. Fibril tangles, age spots and Lewy bodies are not common.
7. Diffuse Lewy body dementia (DLB) manifested as symptoms of Parkinson's disease, visual hallucinations, fluctuating cognitive dysfunction, with attention, alertness, motor symptoms usually appear more than a year after mental disorders, Patients are prone to falls and are sensitive to psychotic drugs.
8. Frontotemporal dementia (FTD) is less common, insidious onset, slow progress, manifested as emotional loss of control, impulsive behavior or withdrawal, inappropriate treatment of people and manners, and constantly can eat or can not get Eating things in the mouth to test, appetite hyperthyroidism, mimic behavior, etc., memory loss is lighter, Pick disease is a type of frontotemporal dementia, pathology can be seen in the neocortex or hippocampal neurons cytoplasmic silver stained inclusion body Pick body .
9. Normal intracranial pressure hydrocephalus (NPH) occurs mostly in brain diseases such as subarachnoid hemorrhage, ischemic stroke, head trauma and brain infection, or is idiopathic, dementia, gait disorder and Typical triads such as dysuria, dementia mainly characterized by subcortical type, mild cognitive decline, decreased spontaneous activity, late emotional response, memory impairment, fiction and disorientation, etc., anxiety, aggressive behavior and Delusion, early urinary incontinence, frequent urination, incomplete urination, post-urinary urination, CT showed enlarged ventricles, and normal pressure on the lumbar cerebrospinal fluid.
10.AD still needs dementia caused by alcoholic dementia, intracranial tumor, chronic drug poisoning, liver failure, pernicious anemia, hypothyroidism or hyperthyroidism, Huntington's disease, amyotrophic lateral sclerosis, neurosyphilis, CJD, etc. Syndrome identification.
