背景:行为障碍与儿童时期任何精神障碍的最高负担有关,然而其神经生物学仍不清楚。不一致的发现限制了我们对脑结构改变在行为障碍中的作用的理解。这项研究旨在确定行为障碍的最强大和可复制的大脑结构相关性。
方法:ENIGMA-反社会行为工作组对来自15个国际队列的结构MRI数据进行了协调分析。合格标准是平均样本年龄为18岁或更短,有关于性别的数据,年龄,和行为障碍的诊断,以及至少10名品行障碍参与者和10名典型发展参与者。使用ENIGMA标准化方案对所有参与者的3DT1加权MRI脑部扫描进行预处理。我们评估了皮质厚度的组间差异,表面积,和使用一般线性模型的皮层下体积,调整年龄,性别,和颅内总体积.按性别分组和按年龄分组的互动,和DSM亚型比较(儿童期发病与青春期发病,以及低水平和高水平的冷酷无情的非情感特征)进行了研究。有品行障碍经历的人没有参与这项研究。
结果:我们整理了1185名品行障碍年轻人(339[28·6%]名女性和846名[71·4%]名男性)和1253名典型发展中年轻人(446名[35·6%]名女性和807名[64·4%]名男性)的个体参与者数据。平均年龄13·5岁(SD3·0;范围7-21)。没有关于种族和族裔的信息。相对于典型的发展中的年轻人,行为障碍组的26个皮质区域表面积较低,总表面积较低(Cohen'sd0·09-0·26)。尾前扣带回皮质(d0·16)和颞上沟岸(d-0·13)的皮质厚度不同。品行障碍组的杏仁核也较小(d0·13),伏核(d0·11),丘脑(d0·14),和海马(d0·12)体积。调整ADHD合并症或智商后,大多数差异仍然显着。没有检测到按性别分组或按年龄分组的相互作用。DSM定义的行为障碍亚型之间几乎没有差异。然而,与对照组相比,具有较高的冷酷无情特征的个体比具有较低的冷酷无情特征的个体表现出更广泛的差异。
结论:我们的研究结果提供了强有力的证据,证明品行障碍在不同亚型和性别中的大脑结构发生了微妙而广泛的改变,主要是在表面区域。这些发现提供了进一步的证据,表明大脑改变可能导致行为障碍。在研究和临床实践中需要更多地考虑这种未被认识到的疾病。
背景:医学科学院和经济与社会研究理事会。
Conduct disorder is associated with the highest burden of any mental disorder in childhood, yet its neurobiology remains unclear. Inconsistent findings limit our understanding of the role of brain structure alterations in conduct disorder. This study aims to identify the most robust and replicable brain structural correlates of conduct disorder.
The ENIGMA-Antisocial Behavior Working Group performed a coordinated analysis of structural MRI data from 15 international cohorts. Eligibility criteria were a mean sample age of 18 years or less, with data available on sex, age, and diagnosis of conduct disorder, and at least ten participants with conduct disorder and ten typically developing participants. 3D T1-weighted MRI brain scans of all participants were pre-processed using ENIGMA-standardised protocols. We assessed group differences in cortical thickness, surface area, and subcortical volumes using general linear models, adjusting for age, sex, and total intracranial volume. Group-by-sex and group-by-age interactions, and DSM-subtype comparisons (childhood-onset vs adolescent-onset, and low vs high levels of callous-unemotional traits) were investigated. People with lived experience of conduct disorder were not involved in this study.
We collated individual participant data from 1185 young people with conduct disorder (339 [28·6%] female and 846 [71·4%] male) and 1253 typically developing young people (446 [35·6%] female and 807 [64·4%] male), with a mean age of 13·5 years (SD 3·0; range 7-21). Information on race and ethnicity was not available. Relative to typically developing young people, the conduct disorder group had lower surface area in 26 cortical regions and lower total surface area (Cohen\'s d 0·09-0·26). Cortical thickness differed in the caudal anterior cingulate cortex (d 0·16) and the banks of the superior temporal sulcus (d -0·13). The conduct disorder group also had smaller amygdala (d 0·13), nucleus accumbens (d 0·11), thalamus (d 0·14), and hippocampus (d 0·12) volumes. Most differences remained significant after adjusting for ADHD comorbidity or intelligence quotient. No group-by-sex or group-by-age interactions were detected. Few differences were found between DSM-defined conduct disorder subtypes. However, individuals with high callous-unemotional traits showed more widespread differences compared with controls than those with low callous-unemotional traits.
Our findings provide robust evidence of subtle yet widespread brain structural alterations in conduct disorder across subtypes and sexes, mostly in surface area. These findings provide further evidence that brain alterations might contribute to conduct disorder. Greater consideration of this under-recognised disorder is needed in research and clinical practice.
Academy of Medical Sciences and Economic and Social Research Council.