Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK.
Int Psychogeriatr. 2012 Apr;24(4):568-76. doi: 10.1017/S1041610211002195. Epub 2011 Dec 12.
The neurobiological basis of increased risk of dementia in stroke patients is unclear, though there are several related pathological changes, including white matter hyperintensities (WMH), and medial temporal atrophy. Subcortical gray matter structures have also been implicated in dementia resulting from vascular pathology, particularly vascular dementia. This study aimed to investigate the contribution of changes in subcortical gray matter structures to post-stroke dementia (PSD).
T1- and T2-weighted images and T2-weighted fluid-attenuated inversion recovery (FLAIR) images were obtained on a 3-Tesla magnetic resonance (MR) system, in four groups aged over 75 years: post-stroke with dementia (PSD; 8), post-stroke no dementia (PSnoD; 33), Alzheimer's disease (AD; 26) and controls (30). Automated software was used to measure the volume of thalamus, putamen, caudate nucleus, and hippocampus as well as total WMH volume. The number of subcortical lacunes was also counted.
The number of caudate lacunes was higher in the PSnoD group, compared with AD (p = 0.029) and controls (p = 0.019). The putamen volume was smaller in the stroke and AD groups, when compared with controls. In the whole stroke group, putamen lacunes were correlated with impairment in memory (Rey test; ρ = -0.365; p = 0.031), while WMH and hippocampal volume both correlated with global dysfunction.
Our findings implicate a variety of neurobiological substrates of dementia, such as small vessel disease and Alzheimer pathology, which develop after stroke in an old older population, with a contribution from subcortical brain structures.
中风患者痴呆风险增加的神经生物学基础尚不清楚，但存在几种相关的病理变化，包括脑白质高信号（WMH）和内侧颞叶萎缩。皮质下灰质结构也与血管病理学引起的痴呆有关，特别是血管性痴呆。本研究旨在探讨皮质下灰质结构变化对中风后痴呆（PSD）的影响。
在 3T 磁共振（MR）系统上获得 T1 和 T2 加权图像以及 T2 加权液体衰减反转恢复（FLAIR）图像，分为四组：年龄均超过 75 岁的中风后伴痴呆（PSD；8 例）、中风后不伴痴呆（PSnoD；33 例）、阿尔茨海默病（AD；26 例）和对照组（30 例）。使用自动软件测量丘脑、壳核、尾状核和海马的体积以及总 WMH 体积。还计数了皮质下腔隙的数量。
PSnoD 组的尾状核腔隙数高于 AD 组（p = 0.029）和对照组（p = 0.019）。与对照组相比，中风和 AD 组的壳核体积较小。在整个中风组中，壳核腔隙与记忆障碍（ Rey 测试；ρ = -0.365；p = 0.031）相关，而 WMH 和海马体积均与整体功能障碍相关。
我们的研究结果表明，在老年人群中，中风后会出现多种痴呆的神经生物学基础，如小血管疾病和阿尔茨海默病病理学，这些都会对皮质下脑结构产生影响。
