Shared and distinct intrinsic functional network centrality in autism and attention-deficit/hyperactivity disorder.

Shared and distinct intrinsic functional network centrality in autism and attention-deficit/hyperactivity disorder.
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自闭症和注意力缺陷/多动障碍中共享和独特的内在功能网络中心性

DOI:
10.1016/j.biopsych.2013.02.011
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发表时间:
2013-10-15
影响因子:
10.6
通讯作者:
Milham MP
Milham MP
中科院分区:
医学1区
文献类型:
--
作者:
Di Martino A;Zuo XN;Kelly C;Grzadzinski R;Mennes M;Schvarcz A;Rodman J;Lord C;Castellanos FX;Milham MP

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患有自闭症谱系障碍 (ASD) 的人经常表现出注意力缺陷/多动障碍 (ADHD) 的症状。在这两种疾病中,对分布式功能异常的观察表明存在异常的大规模大脑网络连接。然而,自闭症谱系障碍 (ASD) 和多动症 (ADHD) 的共同和独特的网络相关性仍未确定。在这里,我们的目的是检查患有 ASD、ADHD 的学龄儿童和完成静息态 fMRI (R-fMRI) 扫描的典型发育儿童 (TDC) 的脱节模式。我们在 56 名 ASD 儿童、45 名 ADHD 儿童和 50 名 TDC 儿童的 R-fMRI 数据中测量了体素网络中心性、功能连接指标,索引了整个大脑连接组的局部(度中心性;DC)和全局(特征向量中心性;EC)功能关系。以组为固定因素(全脑校正)的单向 ANCOVA,随后进行事后配对比较。皮质和皮质下区域表现出中心性异常;有些是 ADHD 和 ASD 共有的,例如楔前叶。其他是疾病特异性的,包括与 ADHD 相关的右侧纹状体/苍白球 DC 增加,与 ASD 相关的双侧颞边缘区 DC 增加相反。将患有 ASD 的儿童区分为患有或不患有 ADHD 样合并症的儿童(分别为 ASD+ 和 ASD−)的二次分析显示,ASD+ 组的基底神经节具有 ADHD 特异性异常。相比之下,患有自闭症谱系障碍(ASD)儿童的颞边缘区域的中心性增加,无论是否存在类似多动症(ADHD)的合并症。在簇级别特征向量中心性组模式与 DC 类似。 ADHD 和 ASD 是神经发育障碍,具有不同且重叠的临床表现。这项工作为大规模网络层面的共享和独特的底层机制提供了证据。
Individuals with autism spectrum disorders (ASD) often exhibit symptoms of Attention-Deficit/Hyperactivity Disorder (ADHD). Across both disorders, observations of distributed functional abnormalities suggest aberrant large-scale brain network connectivity. Yet, common and distinct network correlates of ASD and ADHD remain unidentified. Here, we aimed to examine patterns of dysconnection in school-age children with ASD, ADHD and typically developing children (TDC) who completed a resting state fMRI (R-fMRI) scan. We measured voxel-wise network centrality, functional connectivity metrics indexing local (degree centrality; DC) and global (eigenvector centrality; EC) functional relationships across the entire brain connectome, in R-fMRI data from 56 children with ASD, 45 children with ADHD and 50 TDC. A one-way ANCOVA, with group as fixed factor (whole-brain corrected), was followed by post-hoc pair-wise comparisons. Cortical and subcortical areas exhibited centrality abnormalities; some common to both ADHD and ASD, such as in precuneus. Others were disorder-specific and included ADHD-related increases in DC in right striatum/pallidum, in contrast with ASD-related increases in bilateral temporolimbic areas. Secondary analyses differentiating children with ASD into those with or without ADHD-like comorbidity (ASD+ and ASD−, respectively) revealed that the ASD+ group shared ADHD-specific abnormalities in basal ganglia. By contrast, centrality increases in temporolimbic areas characterized children with ASD regardless of ADHD-like comorbidity. At the cluster level eignevector centrality group patterns were similar to DC. ADHD and ASD are neurodevelopmental disorders with distinct and overlapping clinical presentations. This work provides evidence for both shared and distinct underlying mechanisms at the large-scale network level.