What Is Lewy Body Dementia?

Lewy body dementia (DLB) is a group of clinical and pathological features that overlap between Parkinson's disease and Alzheimer's disease. It is characterized by fluctuating cognitive dysfunction, visual hallucinations, and Parkinson's syndrome, and is characterized by Lewy bodies. Neurodegenerative diseases. Most scholars believe that this disease has constituted an independent disease, which is more common in the elderly and slightly more in men than women.

Basic Information

English name: dementia with Lewy bodies
English alias: DLB
Visiting department: Internal medicine

Multiple groups: Older men
Common symptoms: Impaired memory, speech and visual space skills, syncope, hallucinations, myoclonus, dance-like movements, etc.

Causes of Lewy Body Dementia

The etiology and pathogenesis are unclear. It has been found that DLB and Lewy bodies of Parkinson's disease are abnormal aggregation of -synuclein from soluble to insoluble. The factors affecting the expression and metabolism of -synuclein may be related to the pathogenesis of DLB. DLB usually has few families. Genetic predisposition. Experiments have confirmed that cholinergic and monoaminergic neurotransmitter damage in DLB may be related to cognitive impairment and extrapyramidal dyskinesia.

Lewy body dementia clinical manifestations

The course of the disease progressed slowly, and eventually it became comprehensive dementia after several years. In the early stages, the cognitive function of most cases is the temporal parietal lobe type, which manifests as impairment of memory, speech, and visual spatial skills, similar to the performance of Alzheimer's disease (AD). Impaired cognitive function in DLB. Most patients with DLB have true visual hallucinations, which are often vivid and vivid. The hallucinations are mostly characters or animals familiar to patients. These visual images are often active, talking or sounding, and occasionally the hallucinations are distorted. Some DLB patients may have motor abnormalities such as myoclonus and dance-like movements. DLB patients often experience syncope.

Lewy body dementia test

1. Cerebrospinal fluid measurement

Quantitative amyloid fragments of APOE polymorphic Tau protein in serum have diagnostic and differential significance.

2.CT and MRI examination

There were no characteristic changes, and diffuse brain atrophy or focal frontal atrophy was mild in some cases. Coronal MRI can help distinguish DLB from AD. AD may have atrophy of the medial temporal lobe, but DLB is not obvious.

3. ¹⁸ F-dopaPET inspection

It can be found that dopamine uptake in the substantia nigra and striatum is reduced. PET shows that the reduction of the glucose metabolism rate of the temporal-parietal-occipital cortex is more severe than AD, which may be related to DLB visual spatial disorder and visual hallucinations. AD is mainly a decrease in glucose metabolism in the temporal lobe and cingulate gyrus.

4. Early EEG

Most of them are normal, a few of them show a decrease in background amplitude, periodic discharge at 2 to 4 Hz, and slowing of the basic rhythm. Most patients can see a decrease in alpha waves and transient slow waves in the temporal lobe, and transient frontotemporal burst activity can occur. The abnormal EEG during sleep EEG has certain reference value for diagnosis.

Lewy body dementia diagnosis

1. Essential conditions for clinical diagnosis of DLB

Including progressive cognitive decline, affecting social and work ability; having 2 of the following 3 items:

(1) Volatile cognitive dysfunction, the most obvious fluctuations in attention and alertness;

(2) recurrent visual hallucinations;

(3) Parkinson's syndrome occurs at the same time or later.

2. Support DLB diagnostic conditions

(1) Repeated falls;

(2) syncope;

(3) temporary loss of consciousness;

(4) sensitive to stabilizers;

(5) Other forms of hallucinations.

3.MRI Coronal Scan

DLB temporal lobe atrophy is not obvious, and AD temporal lobe atrophy helps to identify. The early EEG of DLB is mostly normal, and a few background wave amplitudes are reduced. It can be seen that 2 to 4 Hz periodic discharge, reduced temporal alpha wave and transient slow wave. The abnormal EEG during sleep EEG is valuable for diagnosis.

Lewy body dementia differential diagnosis

1. Alzheimer disease (AD)

Mainly manifested by progressive cognitive decline, often ambiguous portrayal of hallucinations due to forgetfulness and fiction, abnormal mental behavior, patients with advanced pyramidal symptoms, difficult to distinguish from DLB, DLB cognitive impairment manifested as fluctuation The hallucinations are specific and vivid, and the patient can be described and convinced. He has obvious visual impairment, early appearance of extrapyramidal system, and CT and MRI examinations show diffuse cortical atrophy.

2. Parkinson's disease (PD)

Some patients with PD may develop dementia at an advanced stage, and visual hallucinations may occur during drug treatment, which is clinically similar to DLB. However, the symptoms of dementia in PD patients are often characterized by subcortical dementia several years after the onset of the disease. The dyskinesia is prominent and the symptoms of levodopa disappear. DLB patients have fluctuant cognitive impairment in the early stage, dyskinesia manifests as rigidity and less movement, rarely has typical resting tremor, and usually has a poor response to levodopa treatment.

3. Vascular dementia

There is often a clear history of stroke and focal signs of the nervous system. The disease progresses in steps, and the neuroimaging is clear, suggesting infarct or hemorrhagic lesions, which are easily distinguished from DLB.

4. Creutzfeldt-Jakob Disease (CJD)

It is characterized by dementia and extrapyramidal damage. The disease progresses rapidly. The extrapyramidal signs are diverse. Myoclonus and seizures can occur. Typical EEG changes are helpful for diagnosis.

5. Progressive supranuclear palsy (PSP)

Before the occurrence of eye movement disorders, PSP and DLB were difficult to distinguish. PSP dementia was a subcortical dementia with no volatility and rare visual hallucinations.

Lewy Body Dementia Treatment

The principle of treatment of DLB is the same as that of other dementias. The main purpose is to improve cognitive function, relieve mental and behavioral symptoms, and improve social living ability. However, psychiatric and extrapyramidal symptoms are more prominent in DLB patients and often become the main focus of treatment.

At present, there is no specific therapy for DLB. Patients may respond well to anticholinesterase drugs such as tacrine and donepezil, which may improve cognitive function and behavioral disorders. DLB is particularly sensitive to side effects of antipsychotics and antipsychotics. It is prone to drowsiness and coma, which is different from other types of dementia. It is not used or used with caution. New antipsychotic drugs such as Vestone and Olanzapine have better effects on visual hallucinations. Depressive symptoms can use selective 5-HT receptor reuptake inhibitors, such as fluoxetine, citalopram and so on.