Vascular dementia

Introduction Dementia caused by cerebral infarction due to vascular disease, including hypertensive cerebrovascular disease. Dementia can occur after multiple transient ischemic attacks or continuous acute cerebrovascular accidents, and individuals can also occur after a severe stroke. Infarcts are generally small, but the effects can be additive. It usually starts in old age, including multiple cerebral infarction dementia. Cerebral vascular dementia can be caused by ischemic stroke, hemorrhagic stroke, and cerebral ischemia and hypoxia. Older age, smoking, family history of dementia, history of recurrent stroke, and hypotension are prone to vascular dementia.

Cause

Causes of vascular dementia

Vascular dementia (VaD) is the second cause of senile dementia, accounting for 10% to 50% of dementia. VaD is a syndrome, not a single disease. Different vascular pathological changes can cause VaD symptoms, including large and small arterial lesions, diffuse ischemic white matter lesions, embolization of cardiac detachment emboli, and hemodynamic changes. Bleeding, hematological factors and hereditary diseases. Pathophysiological mechanisms associated with VaD include focal ischemic damage (localization, morphology, number, volume), white matter lesions (type, location, size), and other factors associated with ischemia (incomplete ischemic necrosis) And pathological changes in the tissues surrounding the infarct, local brain tissue selectivity and susceptibility to ischemia, and functional factors (local and distant functional impairment of infarction). Which of these mechanisms plays a major role is unclear, but it is likely that multiple mechanisms work together to cause VaD.

an examination

Related inspection

Radiological allergen adsorption test (RAST) for cerebral CT examination 133Xe cerebral blood flow measurement and imaging cerebral blood flow measurement

Neuropsychological examination

The commonly used mental state scale, the Hasegawa dementia scale, the blessed dementia scale, the daily life function scale, the clinical dementia rating scale, etc., establish dementia and its degree, and the Hachinski ischemic scale 7 points supports VD diagnosis.

2. Neuroimaging

Brain CT showed multiple low-density infarcts of varying sizes in the cerebral cortex and white matter, showing a broad low-density area of subcortical white matter or lateral paraventricular white matter. Brain MRI showed bilateral long basal ganglia, cerebral cortex and multiple long T1 and long T2 lesions in the white matter. Brain atrophy was observed around the lesion.

Differential diagnosis

1. Alzheimer's disease (AD)

AD onset is concealed, progress is slow, memory and other cognitive dysfunction are prominent, personality can be changed, neuroimaging is marked by significant cortical atrophy, Hachacinski ischemic scale 4 points (modified Hachacinski ischemic scale 2 points ) Support for AD diagnosis.

2.Pick disease

Progressive dementia, in the early stage, has obvious personality changes and social behavior disorders, impaired language function, and cognitive impairments such as memory are relatively late. CT or MRI is primarily atrophy of the frontal and/or temporal lobe.

3. Lewy body dementia (DLB)

Cognitive impairment of volatility, repeated visual hallucinations, and extrapyramidal symptoms. However, there was no infarction in imaging, and no signs of localization in the nervous system examination.

4. Parkinson's disease dementia

In the early stage of Parkinson's disease dementia, symptoms of extrapyramidal involvement such as resting tremor and myotonia were observed. Focus on attention, computational power, visual space, memory and other damage. There is usually no history of stroke.

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