EPIDEMIOLOGIC STUDY OF THE RISK OF DEMENTIA AFTER STROKE

脑血管疾病（CVD）被认为是第二大常见原因 老年人的智力衰退。与阿尔茨海默病不同，CVD是 可以治疗的在第一个研究期间，中风和衰老研究 该项目完成了其目标，以确定患病率，发病率， 与中风有关的痴呆症的危险因素，导致新的信息 以前没有的。我们建议继续的中心目标是 是扩展先前的研究结果的风险因素和过程中使用纵向 研究（目标1和2），并研究有关症状特征的新问题 和解剖风险（目标3和4）。一是 将确定中风患者发生痴呆的危险因素 基线时最初非痴呆，持续随访原始 队列（n=500）和新卒中样本的组装（n=300）。在我们之前的 研究，把握度足以识别基于交叉的风险因素， 分段分析，但不适合发病率研究。分析 现有的纵向数据表明， 一项旨在检验脑萎缩和 复发性中风会增加痴呆症的风险。其他因素 将作为次要假设进行检验。第二，我们将描述 中风后认知功能的变化在我们之前的研究中， 患者表现出稳定或改善的过程，而一些患者表现出 认知能力下降更长的随访和更大的样本将使我们 检验基线时心脏病与以下因素相关的假设： 一些患者的测试分数下降的斜率更大。三是 检查新中风患者的执行功能或额叶功能的缺陷， 抽样并检验这些缺陷在以下国家更常见的假设 与CT扫描上的皮质下梗死相比， 执行功能受损被认为是 皮质下卒中引起的痴呆;然而， 尚未在大型卒中队列中检查与病变类型的关系。 第四，我们将评估痴呆的解剖危险因素， 亚组的新样本与皮层下梗死，并测试 假设尾状核、前囊膜或 丘脑与中风发作时痴呆的风险增加有关 与其他皮层下位置相比。在我们之前的研究中，一些患者 出现额叶综合征和痴呆， 脑梗死，证明术语“战略性梗死性痴呆”。 功能成像显示，皮质分离是一种机制， 对于痴呆症，由于对投射到大脑的结构的损害， 额叶我们新的解剖学研究将确立 协会 虽然痴呆症是一种常见的和致残的后果心血管疾病，在我们的国家， 人口迅速老龄化，很少有研究探讨这些问题。 综合征和解剖学风险因素的信息将提高诊断 精确性和明确的病理生理学。关于风险因素和 课程将具有预防意义，并可能有助于设计 旨在延缓认知衰退的临床试验。CVD的。

Cerebrovascular disease (CVD) is considered the second most common cause of mental deterioration in th elderly. Unlike Alzheimer's disease, CVD is treatable. During the first study period, the Stroke and Aging Research Project accomplished its aims to determine the prevalence, incidence, and risk factors for dementia related to stroke, resulting in new information not previously available. The central goals of our proposed continuation are to extend prior findings on risk factors and course using longitudinal studies (Aims l and 2) and to examine new questions on syndromic profiles and anatomic risks using cross-sectional studies (Aims 3 and 4). First, we will identify risk factors for incident dementia in stroke patients initially nondemented at baseline by continued followup of the original cohorts (n=500) and assembly of a new stroke sample (n=300). In our prior study, power was sufficient to identify risk factors based on cross- sectional analysis, but suboptimal for incidence studies. Analysis of existing longitudinal data indicates that power will be sufficient in the proposed study to test the primary hypothesis that cerebral atrophy and recurrent stroke increase the risk of incident dementia. Other factors will be examined as secondary hypotheses. Second, we will characterize the course of cognitive function after stroke. In our prior study, most stroke patients showed a stable or improving course, while some patients showed cognitive decline. The extended followup and larger sample will allow us to test the hypothesis that cardiac disease at baseline is associated with a steeper slope of decline in test scores in some patients. Third, we will examine deficits in executive or frontal lobe function in the new stroke- sample and test the hypothesis that these deficits are more frequent in patients with subcortical compared to cortical infarcts on CT scan. Impaired executive function is considered to be a common manifestation of dementia from subcortical stroke; however, syndrome specificity in relation to lesion type has not been examined in a large stroke cohort. Fourth, we will evaluate an anatomic risk factor for dementia in a subgroup of the new sample with subcortical infarcts and test the hypothesis that involvement of the caudate, anterior capsule-genu, or thalamus is associated with an increased risk of dementia at stroke onset compared to other subcortical locations. In our prior study, some patients presented with a frontal lobe syndrome and dementia from isolated capsular genu infarction, justifying the term "strategic-infarct dementia". Functional imaging suggested that cortical disconnection was a mechanism for dementia, resulting from damage to structures that project to the frontal lobe. Our new anatomic studies will establish the strength of the association. Although dementia is a frequent and disabling consequence of CVD in our rapidly aging population, few studies have examined these issues. Information on syndromes and anatomic risk factors will improve diagnostic precision and clarify pathophysiology. Information on risk factors and course will have preventive implications and may assist in the design of clinical trials aimed at delaying cognitive deterioration. from CVD.