Wiggs Kelsey, Elmore Alexis L, Nigg Joel T, Nikolas Molly A
Department of Psychological and Brain Sciences, University of Iowa, 11 Seashore Hall E., Iowa City, IA, 52242, USA.
Department of Psychiatry, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239-3098, USA.
J Abnorm Child Psychol. 2016 Nov;44(8):1473-1485. doi: 10.1007/s10802-016-0142-z.
Etiological investigations of attention-deficit hyperactivity disorder (ADHD) and disruptive behavior problems support multiple causal pathways, including involvement of pre- and perinatal risk factors. Because these risks occur early in life, well before observable ADHD and externalizing symptoms emerge, the relation between risk and symptoms may be mediated by neurodevelopmental effects that manifest later in neuropsychological functioning. However, potential dissociable effects of pre/perinatal risk elements on ADHD and familial confounds must also be considered to test alternative hypotheses. 498 youth aged 6-17 years (55.0 % male) completed a multi-stage, multi-informant assessment including parent and teacher symptom reports of symptoms and parent ratings of pre/perinatal health risk indicators. Youth completed a neuropsychological testing battery. Multiple mediation models examined direct effects of pre- and perinatal health risk on ADHD and other disruptive behavior disorder symptoms and indirect effects via neuropsychological functioning. Parental ADHD symptoms and externalizing status was covaried to control for potential familial effects. Effects of prenatal substance exposure on inattention were mediated by memory span and temporal processing deficits. Further, effects of perinatal health risk on inattention, hyperactivity-impulsivity, and ODD were mediated by deficits in response variability and temporal processing. Further, maternal health risks during pregnancy appeared to exert direct rather than indirect effects on outcomes. Results suggest that after controlling for familial relatedness of ADHD between parent and child, early developmental health risks may influence ADHD via effects on neuropsychological processes underpinning the disorder.
注意缺陷多动障碍(ADHD)及破坏性行为问题的病因学研究支持多种因果途径,包括产前和围产期风险因素的影响。由于这些风险在生命早期就已出现,远早于可观察到的ADHD及外化症状出现,风险与症状之间的关系可能由后期在神经心理功能中显现的神经发育效应介导。然而,为了检验其他假设,还必须考虑产前/围产期风险因素对ADHD的潜在可分离效应以及家族混杂因素。498名6至17岁的青少年(55.0%为男性)完成了一项多阶段、多 informant评估,包括父母和教师对症状的报告以及父母对产前/围产期健康风险指标的评分。青少年完成了一套神经心理测试。多个中介模型检验了产前和围产期健康风险对ADHD及其他破坏性行为障碍症状的直接效应,以及通过神经心理功能产生的间接效应。对父母的ADHD症状和外化状态进行了协变量分析,以控制潜在的家族效应。产前物质暴露对注意力不集中的影响由记忆广度和时间处理缺陷介导。此外,围产期健康风险对注意力不集中、多动冲动及对立违抗障碍(ODD)的影响由反应变异性和时间处理缺陷介导。此外,孕期母亲的健康风险似乎对结果产生直接而非间接影响。结果表明,在控制了父母与子女之间ADHD的家族相关性后,早期发育健康风险可能通过对该障碍基础神经心理过程的影响来影响ADHD。