Radoeva Petya D, Bansal Ravi, Antshel Kevin M, Fremont Wanda, Peterson Bradley S, Kates Wendy R
Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, NY, USA.
Children's Hospital Los Angeles and the Keck School of Medicine at the University of Southern California, Los Angeles, CA, USA.
J Child Psychol Psychiatry. 2017 Mar;58(3):305-314. doi: 10.1111/jcpp.12657. Epub 2016 Oct 27.
22q11.2 deletion syndrome (22q11DS) is a genetic disorder that greatly increases risk of developing schizophrenia. We previously characterized cerebral surface morphology trajectories from late childhood to mid adolescence in a cohort of youth with 22q11DS. Herein, we extend the study period into early adulthood, and describe further the trajectories associated with severe psychiatric symptoms in this cohort.
Participants included 76 youth with 22q11DS and 30 unaffected siblings, assessed at three timepoints, during which high resolution, anatomic magnetic resonance images were acquired. High-dimensional, nonlinear warping algorithms were applied to images in order to derive characteristics of cerebral surface morphology for each participant at each timepoint. Repeated-measures, linear regressions using a mixed model were conducted, while covarying for age and sex.
Alterations in cerebral surface morphology during late adolescence/early adulthood in individuals with 22q11DS were observed in the lateral frontal, orbitofrontal, temporal, parietal, occipital, and cerebellar regions. An Age x Diagnosis interaction revealed that relative to unaffected siblings, individuals with 22q11DS showed age-related surface protrusions in the prefrontal cortex (which remained stable or increased during early adulthood), and surface indentations in posterior regions (which seemed to level off during late adolescence). Symptoms of psychosis were associated with a trajectory of surface indentations in the orbitofrontal and parietal regions.
These results advance our understanding of cerebral maturation in individuals with 22q11DS, and provide clinically relevant information about the psychiatric phenotype associated with the longitudinal trajectory of cortical surface morphology in youth with this genetic syndrome.
22q11.2缺失综合征(22q11DS)是一种遗传性疾病,会大幅增加患精神分裂症的风险。我们之前对一组患有22q11DS的青少年从儿童晚期到青春期中期的脑表面形态轨迹进行了特征描述。在此,我们将研究期延长至成年早期,并进一步描述该队列中与严重精神症状相关的轨迹。
参与者包括76名患有22q11DS的青少年和30名未受影响的兄弟姐妹,在三个时间点进行评估,在此期间采集了高分辨率的解剖磁共振图像。将高维、非线性变形算法应用于图像,以得出每个参与者在每个时间点的脑表面形态特征。使用混合模型进行重复测量线性回归,同时对年龄和性别进行协变量调整。
在22q11DS个体的青春期晚期/成年早期,观察到外侧额叶、眶额叶、颞叶、顶叶、枕叶和小脑区域的脑表面形态发生改变。年龄×诊断交互作用显示,与未受影响的兄弟姐妹相比,患有22q11DS的个体在额叶前皮质出现与年龄相关的表面凸起(在成年早期保持稳定或增加),而后部区域出现表面凹陷(在青春期晚期似乎趋于平稳)。精神病症状与眶额叶和顶叶区域的表面凹陷轨迹相关。
这些结果推进了我们对22q11DS个体脑成熟的理解,并提供了与该遗传综合征青少年皮质表面形态纵向轨迹相关的精神病学表型的临床相关信息。