Department of Neurology, National Neuroscience Institute.
Centre for Healthy Brain Ageing (CHeBA), School of Psychiatry, University of New South Wales, Sydney, NSW, Australia.
Alzheimer Dis Assoc Disord. 2020 Jul-Sep;34(3):206-211. doi: 10.1097/WAD.0000000000000384.
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.
We investigated whether PSD is associated with a unique pattern of interactions between chronic cerebrovascular pathologies and acute stroke lesions.
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.
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.
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.
慢性脑血管病会加速脑卒中后痴呆(PSD)的发生。PSD 的风险是否因不同类型的慢性脑血管病而有所不同尚不清楚。
我们旨在研究 PSD 是否与慢性脑血管病和急性脑卒中病灶之间独特的相互作用模式有关。
这是一项对急性轻度脑卒中患者(n=185)的病例对照研究,病例组为在脑卒中后 6 个月随访时发生 PSD 的患者,对照组为在 6 个月时认知状态仍正常的患者,匹配了发病前的认知状态。所有患者在初次脑卒中时均进行了磁共振成像检查,在脑卒中后 6 个月进行了神经心理学评估。
在控制了人口统计学、心血管风险和全脑皮质萎缩等因素后,脑白质高信号(WMH)、慢性腔隙、微出血和急性梗死与 PSD 无关。与仅有大皮质下梗死和点状/无皮质下 WMH 的患者相比,伴有急性大皮质下梗死(>15mm)和伴有脑室周围 WMH 的患者 PSD 风险最大[比值比(OR)=5.85,95%置信区间(CI)=1.85-40.04]。伴有急性多发性小梗死(3-15mm)和伴有腔隙(OR=2.48,95%CI=0.94-6.51)或伴有脑叶微出血(OR=2.20,95%CI=0.89-5.41)的患者 PSD 风险中等,与伴有急性多发性小梗死且无腔隙或微出血的患者相比。单个小梗死与脑血管病之间无相互作用,不会影响 PSD。
PSD 的风险取决于慢性脑血管病的存在情况和急性梗死的类型。临床意义支持采用精准医学方法对 PSD 风险最高的患者进行分层。