From the Department of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, the Netherlands (Wolfers, Onnink, Dammers, Hoogman, Franke); the Donders Centre for Cognitive Neuroimaging, Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, the Netherlands (Wolfers, Arenas, Hoogman, Zwiers, Franke, Marquand, Beckman); the Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, the Netherlands (Buitelaar, Marquand, Beckmann); the Centre for Functional MRI of the Brain (FMRIB), Oxford University, Oxford, UK (Beckmann); the Department of Psychiatry, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, the Netherlands (Franke); the Karakter Child and Adolescent Psychiatry University Centre, Radboud University Medical Centre, Nijmegen, the Netherlands (Buitelaar); and the Department of Neuroimaging, Institute of Psychiatry, King's College London, London, UK (Marquand).
J Psychiatry Neurosci. 2017 Nov;42(6):386-394. doi: 10.1503/jpn.160240.
Attention-deficit/hyperactivity disorder (ADHD) is biologically heterogeneous, with different biological predispositions - mediated through developmental processes - converging upon a common clinical phenotype. Brain imaging studies have variably shown altered brain structure, activity and connectivity in children and adults with ADHD. Recent methodological developments allow for the integration of information across imaging modalities, potentially yielding a more coherent view regarding the biology underlying the disorder.
We analyzed a sample of adults with persistent ADHD and healthy controls using an advanced multimodal linked independent component analysis approach. Diffusion and structural MRI data were fused to form imaging markers reflecting independent components that explain variation across modalities. We included these markers as predictors into logistic regression models on adult ADHD and put those into context with predictions of estimated intelligence, age and sex.
We included 87 adults with ADHD and 93 controls in our analysis. Participants' courses associated with all imaging markers explained 27.86% of the variance in adult ADHD. No single imaging modality dominated this result. Instead, it was explained by aggregation of relatively small effects across several modalities and markers. One of the top markers for adult ADHD was multimodal and linked to morphological and microstructural effects within anterior temporal brain regions; another was linked to cortical thickness. Several markers were also influenced by estimated intelligence, age and/or sex.
Although complex analytical approaches, such as the one applied here, provide insight into otherwise hidden mechanisms, they also increase the complexity of interpretations.
No dominant imaging modality or marker characterizes structural brain phenotypes in adults with ADHD, but we can refine our characterization of the disorder by the integration of small effects across modalities.
注意缺陷多动障碍(ADHD)具有生物学异质性,不同的生物学倾向——通过发育过程介导——汇聚到共同的临床表型。脑影像学研究表明,ADHD 儿童和成人的大脑结构、活动和连接存在不同程度的改变。最近的方法学发展允许跨成像模式整合信息,从而可能对潜在疾病生物学提供更一致的观点。
我们使用先进的多模态关联独立成分分析方法分析了一组持续性 ADHD 成年患者和健康对照组的样本。将弥散和结构 MRI 数据融合在一起,形成反映跨模态变化的独立成分的成像标记物。我们将这些标记物作为预测因子纳入成人 ADHD 的逻辑回归模型,并将其与估计智力、年龄和性别预测进行对比。
我们将 87 名 ADHD 成年患者和 93 名对照组纳入分析。参与者的病程与所有成像标记物一起解释了 27.86%的成人 ADHD 变异性。没有单一的成像模式主导这个结果。相反,这是通过聚合几个模态和标记中的相对较小的效应来解释的。成人 ADHD 的顶级标记之一是多模态的,与前颞叶脑区的形态和微观结构效应有关;另一个与皮质厚度有关。一些标记还受到估计智力、年龄和/或性别影响。
尽管复杂的分析方法,如这里应用的方法,提供了对隐藏机制的洞察,但它们也增加了解释的复杂性。
没有主导的成像模式或标记可以描述 ADHD 成年患者的大脑结构表型,但我们可以通过跨模式整合小效应来完善对该疾病的描述。