Cortical thickness and hippocampal shape in pure vascular mild cognitive impairment and dementia of subcortical type.

Cortical thickness and hippocampal shape in pure vascular mild cognitive impairment and dementia of subcortical type.
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DOI:
10.1111/ene.12376
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发表时间:
2014-05
影响因子:
5.1
通讯作者:
Seo SW
Seo SW
中科院分区:
医学3区
文献类型:
--
作者:
Kim HJ;Ye BS;Yoon CW;Noh Y;Kim GH;Cho H;Jeon S;Lee JM;Kim JH;Seong JK;Kim CH;Choe YS;Lee KH;Kim ST;Kim JS;Park SE;Kim JH;Chin J;Cho J;Kim C;Lee JH;Weiner MW;Na DL;Seo SW

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孤立性脑血管病(CVD)患者脑结构改变的进展模式尚不清楚。为探讨单纯性脑血管病在认知损害中的作用,对单纯皮质下血管性轻度认知损害(SvMCI)和单纯皮质下血管性痴呆(SVaD)患者的皮质变薄和海马区萎缩进行了特征分析。选择匹兹堡化合物B(PIB)正电子发射断层显像阴性的45例svMCI和46例SVaD患者和75例正常认知(NC)者作为研究对象。与正常对照组相比,PIB(−)svMCI患者表现为额叶、语言和提取型记忆功能障碍,而PIB(−)SVaD患者则进一步受损,并伴有视觉空间和再认记忆功能障碍。与NC相比,PIB(−)svMCI患者的额叶、穹隆周围、颞底及扣带后区皮质变薄。在PIB(−)SVaD患者中,这种萎缩更加明显,并进一步向外侧顶区和内侧颞区延伸。与NC组相比,PIB(−)svMCI患者表现为侧体的海马体形态畸形,而PIB(−)SVaD患者表现为额外的侧头和下体畸形。我们的发现表明,没有阿尔茨海默病病理的脑血管病患者可以患有痴呆,表现为多个领域的认知障碍,这与皮质变薄和海马形态畸形的地形图相一致。
The progression pattern of brain structural changes in patients with isolated cerebrovascular disease (CVD) remains unclear. To investigate the role of isolated CVD in cognitive impairment patients, patterns of cortical thinning and hippocampal atrophy in pure subcortical vascular mild cognitive impairment (svMCI) and pure subcortical vascular dementia (SVaD) patients were characterized. Forty-five patients with svMCI and 46 patients with SVaD who were negative on Pittsburgh compound B (PiB) positron emission tomography imaging and 75 individuals with normal cognition (NC) were recruited. Compared with NC, patients with PiB(−) svMCI exhibited frontal, language and retrieval type memory dysfunctions, which in patients with PiB(−) SVaD were further impaired and accompanied by visuospatial and recognition memory dysfunctions. Compared with NC, patients with PiB(−) svMCI exhibited cortical thinning in the frontal, perisylvian, basal temporal and posterior cingulate regions. This atrophy was more prominent and extended further toward the lateral parietal and medial temporal regions in patients with PiB(−) SVaD. Compared with NC subjects, patients with PiB(−) svMCI exhibited hippocampal shape deformities in the lateral body, whilst patients with PiB(−) SVaD exhibited additional deformities within the lateral head and inferior body. Our findings suggest that patients with CVD in the absence of Alzheimer’s disease pathology can be demented, showing cognitive impairment in multiple domains, which is consistent with the topography of cortical thinning and hippocampal shape deformity.
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