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脑结构性子网络缺失与缺血性脑卒中后淡漠相关。

Deficiency of brain structural sub-network underlying post-ischaemic stroke apathy.

机构信息

Department of Experimental Psychology, University of Oxford, Oxford, UK; Department of Neurology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China.

出版信息

Eur J Neurol. 2015 Feb;22(2):341-7. doi: 10.1111/ene.12575. Epub 2014 Oct 16.

Abstract

BACKGROUND AND PURPOSE

This study aimed to reveal the structural basis of post-ischaemic stroke apathy, especially in relation to disruptions in structural connectivity.

METHODS

Eighty-eight participants were included. The Apathy Evaluation Scale, clinician version, was used to characterize the severity of apathy. Diffusion tensor imaging tractography was used to examine white matter integrity and to reconstruct white matter networks using 90 nodes based on the automated anatomical labeling atlas. The degree for each node was extracted to determine the relationship to the severity of apathy.

RESULTS

Apathy was not significantly associated with damage to any single brain region. The degrees of 24 nodes (limbic system, three nodes; frontal lobe, six; basal ganglia, two; temporal lobe, three; parietal lobe, three; insula, two; occipital lobe, five) were significantly correlated to the Apathy Evaluation Scale scores. These 24 nodes constituted an apathy-related sub-network and its global and local efficiencies were negatively correlated with apathy levels (global, r = -0.54, P < 0.01; local, r = -0.64, P < 0.01). Multivariate logistic regression indicated that decreased global efficiency of this sub-network was an independent risk factor for apathy (odds ratio 0.03, 95% confidence interval 0.01-0.04, P = 0.007). Efficiencies of the non-apathy-related sub-network (the remaining 66 nodes) did not correlate or predict the presence of apathy.

CONCLUSIONS

Post-stroke apathy is not due to the dysfunction of a single region or circuit. Rather, it results from disconnection of a complex sub-network of brain regions. This provides new insights into the neuroanatomical basis of post-stroke apathy.

摘要

背景与目的

本研究旨在揭示缺血性脑卒中后淡漠的结构基础,尤其是与结构连接中断的关系。

方法

纳入 88 名参与者。采用淡漠评估量表(临床版)来描述淡漠的严重程度。采用弥散张量成像纤维束追踪技术来检测白质完整性,并使用自动解剖标记图谱基于 90 个节点重建白质网络。提取每个节点的度数以确定其与淡漠严重程度的关系。

结果

淡漠与任何单一脑区的损伤均无显著相关性。24 个节点(边缘系统,3 个;额叶,6 个;基底节,2 个;颞叶,3 个;顶叶,3 个;脑岛,2 个;枕叶,5 个)的度数与淡漠评估量表评分显著相关。这 24 个节点构成了一个淡漠相关的子网络,其全局和局部效率与淡漠水平呈负相关(全局,r = -0.54,P < 0.01;局部,r = -0.64,P < 0.01)。多元逻辑回归表明,该子网络全局效率降低是淡漠的独立危险因素(优势比 0.03,95%置信区间 0.01-0.04,P = 0.007)。非淡漠相关子网络(其余 66 个节点)的效率与淡漠的存在无关,也无法预测淡漠的存在。

结论

脑卒中后淡漠不是由于单个区域或回路的功能障碍引起的。相反,它是由于大脑区域的一个复杂子网络的连接中断所致。这为脑卒中后淡漠的神经解剖学基础提供了新的见解。

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