| 张梦婷,谢敏,张佳硕,马小盈,韦梦菡,殷钰冰,陈洋,吴雨璐,王强.童年不良经历与儿童精神病理、睡眠及认知功能的关系：壳核体积对认知功能的中介作用[J].四川精神卫生杂志,2026,(3):263-273.Zhang Mengting,Xie Min,Zhang Jiashuo,Ma Xiaoying,Wei Menghan,Yin Yubing,Chen Yang,Wu Yulu,Wang Qiang,Association of adverse childhood experiences with psychopathology， sleep， and cognitive function in children： the mediating role of putamen volume[J].SICHUAN MENTAL HEALTH,2026,(3):263-273 |
| 童年不良经历与儿童精神病理、睡眠及认知功能的关系：壳核体积对认知功能的中介作用 |
| Association of adverse childhood experiences with psychopathology， sleep， and cognitive function in children： the mediating role of putamen volume |
| 投稿时间：2026-01-17 |
| DOI：10.11886/scjsws20260117001 |
| 中文关键词: 童年不良经历 儿童 精神病理 睡眠障碍 神经认知功能 壳核 |
| 英文关键词:Adverse childhood experiences Children Psychopathology Sleep disturbances Neurocognitive function Putamen |
| 基金项目:国家自然科学基金青年科学基金项目（项目名称：童年创伤与基因交互效应损伤精神分裂症脑白质网络的机制研究，项目编号：82401763）；四川大学华西医院专职博士后研发基金项目（项目名称：儿童青少年期环境与精神分裂症丘脑皮层环路的相关性研究，项目编号：2023HXBH084） |
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| 中文摘要: |
| 背景 童年不良经历（ACEs）是全生命周期精神病理风险的强预测因子，在个体发育早期即可对身心健康产生广泛的不良影响。ACEs不仅增加儿童精神病理的发生风险，还可能影响睡眠质量，并导致认知功能受损。然而，介导ACEs所致认知功能受损的早期神经生物学机制尚未阐明。目的 探讨ACEs暴露与儿童精神病理风险、睡眠障碍及认知功能之间的关联，并从神经发育视角考查壳核体积在ACEs与认知功能之间的中介作用。方法 使用美国青少年大脑认知发展（ABCD）研究的大样本数据，以10 572名9~10岁儿童为研究对象，根据家长及儿童报告的ACEs累积得分，将儿童分为5组：无暴露组（0种ACEs）、1种暴露组、2种暴露组、3种暴露组及高危暴露组（≥4种ACEs）。采用Logistic回归分析探究ACEs与精神病理症状（儿童行为量表T分≥65）的关联，采用多元线性回归分析探究ACEs与儿童睡眠障碍量表（SDSC）评分、美国国立卫生研究院认知功能工具箱（NIHTB-CB）以及大脑皮层及皮层下多个结构之间的关联。利用Bootstrap法检验壳核体积在ACEs与神经认知功能之间的中介效应。结果 控制混杂因素后，ACEs累积得分与儿童精神病理症状相关，且二者存在剂量-反应关系。高危暴露组出现内化问题和外化问题的风险分别为无暴露组的2.08倍（OR=2.080，95% CI：1.401~3.088）和3.13倍（OR=3.132，95% CI：1.703~5.760），品行问题的发生风险则为无暴露组的4.68倍（OR=4.681，95% CI：2.528~8.669）。ACEs累积得分对SDSC总评分具有正向预测作用（β=0.080，95% CI：0.059~0.102），对睡眠-觉醒转换障碍（β=0.086，95% CI：0.063~0.109）及入睡与维持睡眠障碍（β=0.066，95% CI：0.043~0.089）的正向预测作用相对较强。在认知功能与脑结构方面，ACEs累积得分可负向预测总体认知复合得分（β=-0.025，95% CI：-0.050~-0.001）、晶体认知复合得分（β=-0.035，95% CI：-0.060~-0.010）、左侧壳核体积（β=-0.025，95% CI：-0.046~-0.003）以及右侧壳核体积（β=-0.023，95% CI：-0.044~-0.003）。全壳核体积在ACEs与总体认知复合得分之间起部分中介作用，效应值为-0.002（95% CI：-0.004~-0.001），效应量为7.49%。结论 ACEs暴露可能增加儿童精神病理与睡眠障碍的发生风险，还可能导致神经认知功能受损。壳核体积减小可能是ACEs影响儿童认知功能的潜在神经生物学路径。 |
| 英文摘要: |
| Background Adverse childhood experiences （ACEs） are strong predictors of psychopathology across the lifespan， exerting extensive adverse effects on physical and mental health during early development. While ACEs increase the risk of childhood psychopathology， sleep quality and impair cognitive function， the early neurobiological mechanisms mediating ACE-induced cognitive impairment remain unclear.Objective To explore the association between ACEs exposure and the risk of psychopathology， sleep disorders， and cognitive function， and to examine the mediating role of the putamen volume in the relationship between ACEs and cognitive function from a neurodevelopment perspective.Methods Data were obtained from the Adolescent Brain Cognitive Development （ABCD） study， comprising 10 572 children aged 9 to 10. Participants were categorized into five groups based on the cumulative score of ACEs reported by their parents and the children themselves： no-exposure group （0 types of ACEs）， the one-exposure group， the two-exposure group， the three-exposure group， and the high-risk exposure group （≥ 4 types of ACEs）. Logistic regression analysis was employed to evaluate the association between ACEs and psychopathological symptoms ［T score of the Child Behavior Checklist （CBCL） ≥ 65］. Multiple linear regression analysis was ultilized to analyze the correlations between ACEs and the scores of the Sleep Disturbance Scale for Children （SDSC）， the NIH Toolbox Cognition Battery （NIHTB-CB）， as well as the multiple structures in the cerebral cortex and subcortex. The Bootstrap method was applied to test the mediating effect of the putamen volume between ACEs and neurocognitive function.Results After adjusting for confounders， ACEs cumulative score was correlated with children's psychopathological symptoms in a dose-response manner. Compared with the no-exposed group， the high-risk exposure group had a 2.08-fold （OR=2.080， 95% CI： 1.401–3.088） increased risk of internalizing problems and a 3.13-fold （OR=3.132， 95% CI： 1.703–5.760） increased risk of externalizing problems， and the risk of conduct problems was 4.68 times that of the no-exposed group （OR=4.681， 95% CI： 2.528–8.669）. ACEs cumulative score positively predicted the total score of SDSC （β=0.080， 95% CI： 0.059–0.102）， with relatively stronger predictive effects on sleep-wake transition disorder （β=0.086， 95% CI： 0.063–0.109） and sleep onset and maintenance disorder （β=0.066， 95% CI： 0.043–0.089）. In terms of neurocognition and brain structure， ACEs cumulative score negatively predicted the overall cognitive composite score （β=-0.025， 95% CI： -0.050–-0.001）， the crystallized cognitive composite score （β=-0.035， 95% CI： -0.060–-0.010）， the volume of the left putamen nucleus （β=-0.025， 95% CI： -0.046– 0.003）， and the volume of the right putamen nucleus （β=-0.023， 95% CI： -0.044– 0.003）. The total putamen volume played a partial mediating role between ACEs and the overall cognitive composite score， the effect value was -0.002 （95% CI： -0.004–-0.001）， accounting for 7.49% of the total effect.Conclusion ACEs exposure may increase the risk of psychopathological and sleep disturbances in children and may impair neurocognitive function. Reduced putamen volume may serve a potential neurobiological pathway underlying the impact of ACEs on childhood cognition. ［Funded by National Natural Science Foundation of China-Young Scientists Program （number， 82401763）； Sichuan University West China Hospital Full-time Postdoctoral Research and Development Fund Project （number， 2023HXBH084）］ |
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