Connectivity-based parcellation increases network detection sensitivity in resting state fMRI: An investigation into the cingulate cortex in autism.

Connectivity-based parcellation increases network detection sensitivity in resting state fMRI: An investigation into the cingulate cortex in autism.
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DOI:
10.1016/j.nicl.2016.03.016
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发表时间:
2016
期刊:
NeuroImage. Clinical
影响因子:
--
通讯作者:
Wenderoth N
Wenderoth N
中科院分区:
其他
文献类型:
--
作者:
Balsters JH;Mantini D;Apps MAJ;Eickhoff SB;Wenderoth N

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尽管静息态功能磁共振成像 (RS-fMRI) 越来越多地用于生成精神疾病的生物标志物,但种子大小和放置等分析选择可能会导致不同的结果。种子放置对自闭症谱系障碍 (ASD) 的 RS-fMRI 研究尤其有影响,因为众所周知,患有 ASD 的个体拥有更多可变的网络拓扑。在这里,我们提出了一种使用扣带皮层作为感兴趣的示例解剖区域来分析 ASD 中 RS-fMRI 的新颖流程。我们没有使用基于先前文献或总体形态的种子,而是结合了结构信息、任务无关(RS-fMRI)和任务依赖的功能连接(元分析连接模型),将扣带皮层划分为六个具有独特连接指纹和不同行为特征的子区域。这种划分在群体之间是一致的,并且在个体之间高度可复制(高达 93% 的检测率),表明皮质-扣带回连接的组织在群体之间高度相似。然而,我们的结果显示,自闭症谱系障碍者中前中扣带皮层和右侧前额叶皮层之间的连接性随年龄增长而增加,而对照组中这种连接性则下降。还存在组 × 灰质 (GM) 相互作用,显示前扣带皮层和直肠回之间的连接性增加,与对照组中直肠回 GM 的增加相一致。通过将我们的方法与以前建立的方法进行比较,我们发现我们的方法改善了两组的网络检测,并且使用 4 毫米半径球体检测组差异的能力随着种子放置的不同而变化很大。使用我们的多模式方法,我们发现皮质-扣带脑回路被破坏,基于任务相关信息,可能会导致自闭症谱系障碍(ASD)注意力和社交互动的缺陷。此外,我们强调更灵敏的 RS-fMRI 方法对于在精神疾病中建立稳健且可重复的基于连接的生物标志物至关重要。扣带皮层连接性通常被认为是自闭症 (ASD) 的标志。然而,这些差异可能是由于种子放置等分析选择造成的。我们用于静息态功能磁共振成像的新多模态管道改善了两组的网络检测。扣带皮层分割在个体之间具有高度可复制性(高达 93% 的检测率)。我们展示了皮质-扣带脑连接的发展轨迹,这可能是自闭症谱系障碍患者注意力和社交缺陷的基础。
Although resting state fMRI (RS-fMRI) is increasingly used to generate biomarkers of psychiatric illnesses, analytical choices such as seed size and placement can lead to variable findings. Seed placement especially impacts on RS-fMRI studies of Autism Spectrum Disorder (ASD), because individuals with ASD are known to possess more variable network topographies. Here, we present a novel pipeline for analysing RS-fMRI in ASD using the cingulate cortex as an exemplar anatomical region of interest. Rather than using seeds based on previous literature, or gross morphology, we used a combination of structural information, task-independent (RS-fMRI) and task-dependent functional connectivity (Meta-Analytic Connectivity Modeling) to partition the cingulate cortex into six subregions with unique connectivity fingerprints and diverse behavioural profiles. This parcellation was consistent between groups and highly replicable across individuals (up to 93% detection) suggesting that the organisation of cortico-cingulo connections is highly similar between groups. However, our results showed an age-related increase in connectivity between the anterior middle cingulate cortex and right lateral prefrontal cortex in ASD, whilst this connectivity decreased in controls. There was also a Group × Grey Matter (GM) interaction, showing increased connectivity between the anterior cingulate cortex and the rectal gyrus in concert with increasing rectal gyrus GM in controls. By comparing our approach to previously established methods we revealed that our approach improves network detection in both groups, and that the ability to detect group differences using 4 mm radius spheres varies greatly with seed placement. Using our multi-modal approach we find disrupted cortico-cingulo circuits that, based on task-dependent information, may contribute to ASD deficits in attention and social interaction. Moreover, we highlight how more sensitive approaches to RS-fMRI are crucial for establishing robust and reproducible connectivity-based biomarkers in psychiatric disorders. Cingulate cortex connectivity is often implicated as a marker of Autism (ASD). However, these differences may be due to analytical choices such as seed placement. Our new multi-modal pipeline for resting state fMRI improved network detection in both groups. Cingulate parcellation was highly replicable across individuals (up to 93% detection). We show developmental trajectories of cortico-cingulo connectivity that may underlie attention and social deficits in ASD.