Pendlebury Sarah T, Rothwell Peter M
Stroke Prevention Research Unit, University Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK.
Lancet Neurol. 2009 Nov;8(11):1006-18. doi: 10.1016/S1474-4422(09)70236-4. Epub 2009 Sep 24.
Reliable data on the prevalence and predictors of post-stroke dementia are needed to inform patients and carers, plan services and clinical trials, ascertain the overall burden of stroke, and understand its causes. However, published data on the prevalence and risk factors for pre-stroke and post-stroke dementia are conflicting. We undertook this systematic review to assess the heterogeneity in the reported rates and to identify risk factors for pre-stroke and post-stroke dementia.
Studies published between 1950 and May 1, 2009, were identified from bibliographic databases, reference lists, and journal contents pages. Studies were included if they were on patients with symptomatic stroke, were published in English, reported on a series of consecutive eligible patients or volunteers in prospective cohort studies, included all stroke or all ischaemic stroke, measured dementia by standard criteria, and followed up patients for at least 3 months after stroke. Pooled rates of dementia were stratified by study setting, inclusion or exclusion of pre-stroke dementia, and by first, any, or recurrent stroke. Pooled odds ratios were calculated for factors associated with pre-stroke and post-stroke dementia.
We identified 22 hospital-based and eight population-based eligible cohorts (7511 patients) described in 73 papers. The pooled prevalence of pre-stroke dementia was higher (14.4%, 95% CI 12.0-16.8) in hospital-based studies than in population-based studies (9.1%, 6.9-11.3). Although post-stroke (<or=1 year) dementia rates were heterogeneous overall, 93% of the variance was explained by study methods and case mix; the rates ranged from 7.4% (4.8-10.0) in population-based studies of first-ever stroke in which pre-stroke dementia was excluded to 41.3% (29.6-53.1) in hospital-based studies of recurrent stroke in which pre-stroke dementia was included. The cumulative incidence of dementia after the first year was little greater (3.0%, 1.3-4.7) per year in hospital-based studies than expected on the basis of recurrent stroke alone. Medial temporal lobe atrophy, female sex, and a family history of dementia were strongly associated with pre-stroke dementia, whereas the characteristics and complications of the stroke and the presence of multiple lesions in time and place were more strongly associated with post-stroke dementia.
After study methods and case mix are taken into account, reported estimates of the prevalence of dementia are consistent: 10% of patients had dementia before first stroke, 10% developed new dementia soon after first stroke, and more than a third had dementia after recurrent stroke. The strong association of post-stroke dementia with multiple strokes and the prognostic value of other stroke characteristics highlight the central causal role of stroke itself as opposed to the underlying vascular risk factors and, thus, the likely effect of optimum acute stroke care and secondary prevention in reducing the burden of dementia.
None.
需要有关卒中后痴呆患病率及预测因素的可靠数据,以便为患者及照料者提供信息、规划服务及临床试验、确定卒中的总体负担并了解其病因。然而,关于卒中前和卒中后痴呆患病率及危险因素的已发表数据相互矛盾。我们进行了这项系统评价,以评估所报告率的异质性,并确定卒中前和卒中后痴呆的危险因素。
从书目数据库、参考文献列表及期刊目录页中识别1950年至2009年5月1日期间发表的研究。纳入标准为:研究对象为有症状性卒中患者;以英文发表;在前瞻性队列研究中报告了一系列连续的合格患者或志愿者;纳入所有卒中或所有缺血性卒中;采用标准标准测量痴呆;卒中后对患者随访至少3个月。痴呆的合并率按研究环境、是否纳入卒中前痴呆以及首次、任何一次或复发性卒中进行分层。计算与卒中前和卒中后痴呆相关因素的合并比值比。
我们在73篇论文中识别出22个基于医院的合格队列和8个基于人群的合格队列(7511例患者)。基于医院的研究中卒中前痴呆的合并患病率(14.4%,95%可信区间12.0 - 16.8)高于基于人群的研究(9.1%,6.9 - 11.3)。尽管卒中后(≤1年)痴呆率总体上存在异质性,但93%的变异可由研究方法和病例组合解释;其范围从排除卒中前痴呆的基于人群的首次卒中研究中的7.4%(4.8 - 10.0)到纳入卒中前痴呆的基于医院的复发性卒中研究中的41.3%(29.6 - 53.1)。在基于医院的研究中,第一年之后痴呆的累积发病率每年仅略高于(3.0%,1.3 - 4.7)仅基于复发性卒中预期的发病率。颞叶内侧萎缩、女性性别及痴呆家族史与卒中前痴呆密切相关,而卒中的特征和并发症以及在时间和部位上存在多个病灶与卒中后痴呆的相关性更强。
在考虑研究方法和病例组合后,所报告的痴呆患病率估计值是一致的:10%的患者在首次卒中前患有痴呆,10%在首次卒中后不久出现新发痴呆,超过三分之一的患者在复发性卒中后患有痴呆。卒中后痴呆与多次卒中的强关联以及其他卒中特征的预后价值突出了卒中本身而非潜在血管危险因素的核心因果作用,因此,最佳急性卒中治疗和二级预防在减轻痴呆负担方面可能具有的作用。
无。