Fiber Connectivity Density in Cerebral Small-Vessel Disease Patients With Mild Cognitive Impairment and Cerebral Small-Vessel Disease Patients With Normal Cognition
Fiber Connectivity Density in Cerebral Small-Vessel Disease Patients With Mild Cognitive Impairment and Cerebral Small-Vessel Disease Patients With Normal Cognition
复制标题
轻度认知障碍脑小血管病患者和认知正常脑小血管病患者的纤维连接密度
DOI：
10.3389/fnins.2020.00083
复制
发表时间：
2020-02-12
影响因子：
4.3
通讯作者：
Wang, Defeng
中科院分区：
文献类型：
--
作者：
Liu, Chengxia;Shi, Lin;Wang, Defeng
脑小血管病（CSVD）的结构连接异常与认知功能障碍有关。但在早期CSVD患者中，结构连接的不同特征尚未阐明。本研究旨在探讨CSVD合并轻度认知功能障碍（MCI）患者与认知功能正常的CSVD患者脑结构连接的潜在差异。22例CSVD伴MCI患者、34例认知功能正常的CSVD患者和35例年龄、性别和教育程度匹配的对照者进行了弥散张量成像和高分辨率T1加权成像。定量评估临床特征、腔隙性梗死体积、白色高信号（WMH）体积和整体萎缩。构建了纤维连接密度（FiCD）图，并在顶点水平上对各组进行了比较。Pearson相关性用于估计控制一般特征的成像-临床关系。CSVD合并MCI组WMH和腔隙性脑梗死的病灶负荷明显高于认知功能正常组（P < 0.01），而FiCD值则明显低于认知功能正常组（P < 0.01）。腔隙性梗死（r =-0.318，P < 0.01）和WMH（r =-0.400，P < 0.01）与总体FiCD值显著相关，但与总体萎缩、年龄或性别无关。认知功能正常的CSVD患者FiCD值下降主要集中在额前区（P < 0.01）。与认知功能正常的CSVD患者相比，CSVD合并MCI患者额、顶叶增大区FiCD值显著降低（经Monte Carlo校正，P < 0.01）。组间比较显示，CSVD伴MCI患者的左上级额回、左楔前叶和右额下回眶部的连接密度受损区域增强（Monte Carlo校正P < 0.01）。额叶、顶叶区域FiCD值与认知功能相关（P < 0.01）。总之，认知正常的CSVD患者已经有结构连接的破坏。额、顶叶脑区连接性障碍的程度和强度可能是CSVD认知功能损害的机制之一。纤维连接密度测量可能有助于定量描述结构皮质连接。
Abnormal structural connectivity of cerebral small-vessel disease (CSVD) is associated with cognitive impairment. But the different characteristics of structural connectivity have not been elucidated in early CSVD patients. The current study aimed to investigate the potential differences of structural connectivity in CSVD patients with mild cognitive impairment (MCI) and CSVD patients with normal cognition. Twenty-two CSVD patients with MCI, 34 CSVD patients with normal cognition, and 35 controls, who were age, sex, and education matched underwent diffusion tensor imaging and high resolution T1-weighted imaging. Clinical characteristics, lacunar infarct volume, white matter hyperintensity (WMH) volume, and global atrophy were quantitatively evaluated. Maps of fiber connectivity density (FiCD) were constructed and compared across groups in vertex levels. Pearson correlation was used to estimate the imaging-clinical relationships with control of general characteristics. CSVD patients with MCI had higher lesion load of WMH and lacunar infarcts, and correspondingly lower global FiCD value than CSVD patients with normal cognition (P < 0.01). Lacunar infarct (r = -0.318, P < 0.01) and WMH (r = -0.400, P < 0.01), but not global atrophy, age, or sex, were significantly correlated with the global FiCD value. CSVD patients with normal cognition showed decreased FiCD value mainly in the prefrontal areas (P < 0.01 with Monte Carlo correction). Compared with CSVD patients with normal cognition, CSVD patients with MCI showed significantly decreased FiCD value in enlarged frontal and parietal areas (P < 0.01 with Monte Carlo correction). Inter-group comparisons showed regional enhanced impairment of connectivity density in CSVD patients with MCI in the left superior frontal gyrus, the left precuneus, and the orbital part of the right inferior frontal gyrus (P < 0.01 with Monte Carlo correction). Regional FiCD value of frontal and parietal areas was associated with the cognitive function (P < 0.01). In conclusion, cognitively normal CSVD patients already have disruptions of structural connectivity. The extent and intensity of connectivity disruptions in frontal and parietal areas may underlie the mechanism of cognitive impairment in CSVD. Fiber connectivity density measurements may be helpful for quantitative description of structural cortical connectivity.