Dementia with Lewy bodies

Introduction to Louise Dementia Dementia with Lewybodies (DLB), first described by Okazak et al. (1961), is a group that overlaps between Parkinson's disease and Alzheimer's disease in clinical and pathological manifestations, with volatility cognitive dysfunction, visual hallucinations, and Parkinson's disease. Disease syndrome is a clinical feature, a neurodegenerative disease characterized by Lewy body. basic knowledge The proportion of sickness: 0.0023% Susceptible people: no specific population Mode of infection: non-infectious Complications: loss of libido, sleep disorders

Cause of Lewy body dementia

Cause (50%):

The etiology has not been known so far. The study found that the -synuclein of the nervous system is the main component of the Lewy body structure. Some patients with DLB and familial Parkinson's disease have -synuclein gene mutations, which make the -burst. Heteronin changes from soluble to insoluble, and abnormal aggregation occurs. It is speculated that -synuclein gene mutation may be related to the pathogenesis of DLB and PD. DLB has few family genetic predispositions, but Japan has reported familial DLB patients, although There are reports that some DLB patients and AD patients have increased Apo E4 alleles, but the exact genetic mechanism remains to be studied.

Lewy body dementia prevention

A reasonable diet can take more high-fiber and fresh vegetables and fruits, balanced nutrition, including essential nutrients such as protein, sugar, fat, vitamins, trace elements and dietary fiber, with a combination of vegetarian and vegetarian foods. The complementary role of nutrients in food is also helpful in preventing this disease.

Lewy body dementia complications Complications, libido, sleep disorders

May be associated with autonomic dysfunction symptoms and depression, loss of libido, sleep disorders, anorexia, fatigue and pain.

Symptoms of dementia in Lewy body Common symptoms Dementia mental disorder Progressive dementia Cognitive dysfunction Illusion Attention Deficient subcortical dementia groping Reflex tongue-like dementia

1. Lewy body dementia is more than the elderly, only a small number of young and middle-aged patients, slowly progressing, the main clinical manifestations of progressive dementia, extrapyramidal dyskinesia and mental disorders, the main manifestations of dementia, Pa The symptoms of Jinsen's disease are mild, and in a few cases, the symptoms may fluctuate.

2. Cognitive dysfunction DLB patients have a general decline in cognitive function, and AD is a cortical dementia, there are similarities, often with memory loss, lack of orientation, but early memory impairment is light, volatility, There may also be aphasia, disuse and loss of recognition. Some patients have subcortical dementia characteristics, such as lack of concentration, alertness and fluency in the language. In the progression of dementia, there is a lack of visual space ability, and there are symptoms of frontal lobe release. Strong grip and groping reflection, cognitive dysfunction can fluctuate, can change in a few weeks or even within 1 day, abnormal and normal state alternately appear, light or heavy or irregular.

Lewy body dementia check

1. There is no characteristic change in CT and MRI examination. In some cases, diffuse brain atrophy or focal frontal atrophy can be seen, and the degree is mild. MRI coronary scanning is helpful for the differentiation of DLB and AD. AD can have axillary medial atrophy. DLB is not obvious.

2.18F-dopa PET examination revealed a decrease in dopamine uptake in the substantia nigra and striatum. PET showed a decrease in glucose metabolism rate in the sacral-apical-occipital cortex, which was more severe than AD, and may be related to DLB visual space disorder, visual hallucination, etc. AD is mainly The rate of glucose metabolism in the temporal lobe and cingulate gyrus is reduced.

3. The early EEG is mostly normal, and a few of them show that the background amplitude is reduced. It can be seen that the periodic discharge is 2~4Hz, and the basic rhythm is slowed. More patients can see the wave reduction and transient slow wave in the temporal lobe area, which may appear short-term. The temporal lobe outbreak activity, sleep EEG has a rapid eye movement abnormality, and has certain reference value for diagnosis.

Diagnosis and differentiation of Lewy body dementia

Diagnostic criteria

1. Alzheimer's disease (AD) mainly manifests as progressive cognitive decline, often due to forgetting, fiction, illusory depiction of illusion, abnormal mental behavior, intermediate and advanced patients may have extrapyramidal symptoms, difficult to distinguish from DLB. DLB cognitive impairment is characterized by volatility, visual illusory content is specific and vivid, patients can be imaged and convinced; there is obvious visual impairment, extrapyramidal appearance appears earlier, and CT and MRI show diffuse cortical atrophy.

2. Parkinson's disease (PD) Some patients with PD may develop dementia in the advanced stage. The visual hallucination may occur in drug treatment. The clinical resembles DLB, but the symptoms of dementia in PD patients often appear several years after the onset of the disease, characterized by subcortical dementia. The obstacles are prominent and the symptoms of levodopa disappear. DLB patients have volatility cognitive impairment in the early stage. The dyskinesia manifests as tonic, less movement, and rarely shows typical resting tremor; the response to levodopa is usually poor.

3. Vascular dementia often has a clear history of stroke and neurological focal signs, the disease progresses stepwise, neuroimaging clearly indicates infarct or hemorrhagic lesions, easy to identify with DLB.

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