Background: 

Chronic cerebrovascular pathology accelerates the incidence of poststroke dementia (PSD). Whether the risk of PSD varies according to different types of chronic cerebrovascular pathology remains unclear.

Objectives: 

We investigated whether PSD is associated with a unique pattern of interactions between chronic cerebrovascular pathologies and acute stroke lesions.

Materials and Method: 

In this case-control study of acute mild stroke patients (n=185), cases included patients who developed PSD at a 6-month poststroke follow-up, and controls included patients who remained nondemented at 6 months, matched on prestroke cognitive status. Magnetic resonance imaging was performed at initial stroke presentation; neuropsychological assessments were performed 6 months after the stroke.

Results: 

White matter hyperintensities (WMH), chronic lacunes, microbleeds, and acute infarcts were not associated with PSD after controlling for demographics, cardiovascular risk, and global cortical atrophy. The risk of PSD was largest for patients with acute large subcortical infarcts (>15 mm) and concomitant periventricular WMH compared with patients with large subcortical infarcts and punctate/absent periventricular WMH [odds ratio (OR)=5.85, 95% confidence interval (CI)=1.85-40.04]. A moderate risk of PSD was observed for patients with acute multiple small infarcts (3 to 15 mm) and concomitant lacunes (OR=2.48, 95% CI=0.94-6.51) or concomitant lobar microbleeds (OR=2.20, 95% CI=0.89-5.41), compared with patients with acute multiple small infarcts and absent lacunes or microbleeds. Single small infarcts did not interact with cerebrovascular pathology to affect PSD.

Conclusions: 

The risk of PSD varies depending on the presence of chronic cerebrovascular pathologies and type of acute infarcts. Clinical implications support a precision medicine approach for stratifying those at highest risk of PSD.

中文翻译：

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急性梗塞与脑血管病理之间的相互作用可预测中风后痴呆。

背景： 

慢性脑血管病理会加速卒中后痴呆（PSD）的发生。PSD的风险是否根据慢性脑血管病理的不同类型而变化尚不清楚。

目标： 

我们调查了PSD是否与慢性脑血管病变和急性中风病变之间的相互作用的独特模式有关。

材料与方法： 

在这项对急性轻度中风患者（n = 185）的病例对照研究中，病例包括在卒中后6个月随访中发展为PSD的患者，对照组包括在卒中前6个月保持无痴呆且与卒中前认知状态相匹配的患者。初次卒中时进行磁共振成像；脑卒中后6个月进行神经心理评估。

结果： 

在控制了人口统计学，心血管疾病风险和整体皮质萎缩之后，白质高信号（WMH），慢性腔腔出血，微出血和急性梗死与PSD无关。急性大皮层下梗死（> 15 mm）和伴发室周WMH的患者与大皮层下梗塞且点状/不存在脑室周WMH的患者相比，PSD的风险最大[比值比（OR）= 5.85，95％置信区间（CI） ）= 1.85-40.04]。急性多发性小梗死患者观察到中等程度的PSD风险（3到15 mm）和伴随的腔隙（OR = 2.48，95％CI = 0.94-6.51）或伴随的肺叶微出血（OR = 2.20，95％CI = 0.89-5.41），与急性多发性小梗死且无梗死的患者相比腔隙或微出血。单个小梗死并没有与脑血管病理学相互作用影响PSD。

结论： 

PSD的风险取决于慢性脑血管病变的存在和急性梗死的类型。临床意义支持一种精确的医学方法，用于对那些罹患PSD最高风险的人群进行分层。