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初治生长激素缺乏症儿童的小世界网络破坏:基于扩散张量成像的网络分析

Disrupted small-world networks in children with drug-naïve growth hormone deficiency: a DTI-based network analysis.

作者信息

Alimire Yasen, Cheng Yanglei, Qiu Huaqiong, Wu Liuhui, Zhang Long, Lin Liping, Qian Long, Cui Wei, Yang Zhiyun, Chen Qiuli, Xiang Xianhong, Su Shu

机构信息

Department of Radiology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

Department of Radiology, The First People's Hospital of Kashi Area, Kashi, China.

出版信息

Quant Imaging Med Surg. 2025 May 1;15(5):4101-4112. doi: 10.21037/qims-24-1927. Epub 2025 Apr 10.

DOI:10.21037/qims-24-1927
PMID:40384693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12084725/
Abstract

BACKGROUND

Growth hormone deficiency (GHD) in children results from impairment of the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis. Although GHD's effects on brain structure and function have been studied, its impact on large-scale white matter (WM) structural connectivity remains poorly understood. We aimed to investigate the topological organization of WM structural connectome in pediatric GHD using diffusion tensor imaging (DTI) and graph theoretical analysis.

METHODS

This cross-sectional study included 58 drug-naïve children with GHD and 30 typically developing (TD) controls matched for age and gender. DTI data were analyzed using deterministic tractography, and the structural connectivity between 90 cortical and subcortical regions was assessed. Graph theoretical analysis was applied to evaluate topological parameters of the resulting graphs. Between-group comparison of networks metrics was assessed. Finally, a partial correlation analysis was performed to explore the relationship between significant topologic metrics and clinical symptom severity.

RESULTS

Compared to TD groups, the GHD patients showed altered global properties, including increased characteristic path length (P<0.001), and decreased global (P<0.001) and local efficiency (P<0.001). Regarding nodal parameters, GHD showed abnormal nodal parameters (nodal degree, efficiency, betweenness) primarily in regions associated with the default mode network (DMN), central executive network (CEN), visual network (VN), salience network (SN), sensorimotor network (SMN), basal ganglia, and left thalamus. Besides, the scores of Achenbach's Child Behavior Check List (CBCL) of GHD was positively correlated with the nodal efficiency in the left middle occipital gyrus (P=0.048, uncorrected), right inferior parietal lobe (P=0.035, uncorrected), and left middle temporal gyrus (r=0.295; P=0.034, uncorrected).

CONCLUSIONS

Our findings reveal disrupted WM topological organization in children with GHD, which may potentially relate to abnormal GH/IGF-1 levels and associated with behavioral problems. These alterations in structural brain networks may underlie the behavioral challenges observed in GHD, providing new insights into the neurobiological basis of this condition.

摘要

背景

儿童生长激素缺乏症(GHD)是由生长激素/胰岛素样生长因子-1(GH/IGF-1)轴受损引起的。尽管已经研究了GHD对脑结构和功能的影响,但其对大规模白质(WM)结构连接性的影响仍知之甚少。我们旨在使用扩散张量成像(DTI)和图论分析来研究小儿GHD中WM结构连接组的拓扑组织。

方法

这项横断面研究纳入了58名未接受过药物治疗的GHD儿童和30名年龄和性别匹配的正常发育(TD)对照儿童。使用确定性纤维束成像分析DTI数据,并评估90个皮质和皮质下区域之间的结构连接性。应用图论分析来评估所得图的拓扑参数。评估网络指标的组间比较。最后,进行偏相关分析以探索显著拓扑指标与临床症状严重程度之间的关系。

结果

与TD组相比,GHD患者表现出整体属性改变,包括特征路径长度增加(P<0.001),以及全局(P<0.001)和局部效率降低(P<0.001)。关于节点参数方面,GHD主要在与默认模式网络(DMN)、中央执行网络(CEN)、视觉网络(VN)、突显网络(SN)、感觉运动网络(SMN)、基底神经节和左丘脑相关的区域表现出异常的节点参数(节点度、效率、介数)。此外,GHD儿童的阿肯巴克儿童行为检查表(CBCL)得分与左枕中回(P=0.048,未校正)、右顶下叶(P=0.035,未校正)和左颞中回的节点效率呈正相关(r=0.295;P=0.034,未校正)。

结论

我们的研究结果揭示了GHD儿童的WM拓扑组织受到破坏,这可能与GH/IGF-1水平异常有关,并与行为问题相关。脑结构网络的这些改变可能是GHD中观察到的行为挑战的基础,为这种疾病的神经生物学基础提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc4c/12084725/f589802d3010/qims-15-05-4101-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc4c/12084725/afe426de8b97/qims-15-05-4101-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc4c/12084725/8cad76293beb/qims-15-05-4101-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc4c/12084725/f589802d3010/qims-15-05-4101-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc4c/12084725/afe426de8b97/qims-15-05-4101-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc4c/12084725/8cad76293beb/qims-15-05-4101-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc4c/12084725/f589802d3010/qims-15-05-4101-f3.jpg

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