痴呆诊断标准-update(福州).pptVIP

* Gary--I would change the display range so they can more easily see the deficits in ther normal memory APOE-4 patient. They only get a quick look need to easily see this. A 14 6 % change is a big one should seen easily in the was it is displayed. * Key Points Over the years, the medical community’s attitude and approach to dementia and its treatment has evolved immensely. Prior to the late 1800s, dementia was considered a part of the normal aging process. Senility, as it was referred to then, was expected to occur in every individual, should they live long enough to experience it. By the end of the 19th century, opinions on senility and dementia were starting to shift. It was recognized that dementia was in fact an abnormal process. And in the first few years, it was thought to be due to heart disease and atherosclerosis. Arteriosclerotic dementia became synonymous with senile dementia, albeit incorrectly. Cortical atrophy in the elderly was thought to result from declining cerebral perfusion causing neuronal death due to hypoxia.1 Vasodilators were therefore used to treat this condition. By the mid 1970s, AD was demonstrated to be the main cause of cerebral atrophy and dementia.1 Slightly later, the cholinergic hypothesis of AD became widely accepted together with the suggestion that cholinomimetics might be useful for the symptomatic treatment of AD.2 Arteriosclerotic dementia was thought to be caused by multiple infarcts (multi-infarct dementia [MID]), and should, thus, be treated by preventing further cerebrovascular damage.3,4 Now it is accepted that VaD is caused by more than MID, which represents only a small portion of all cases. Therefore, the management of VaD currently focuses on reducing cardiovascular risk factors such as hypertension, smoking, and hyperlipidemia. Recent data shows that patients with VaD also suffer from a cholinergic deficit and therefore may benefit from the same treatments that are currently approved for use in AD. References