Childhood trauma, earlier pubertal timing, and psychopathology in adolescence: The role of corticolimbic development.

Childhood trauma, earlier pubertal timing, and psychopathology in adolescence: The role of corticolimbic development.
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DOI:
10.1016/j.dcn.2022.101187
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发表时间:
2023-02
影响因子:
4.7
通讯作者:
McLaughlin, Katie A.
McLaughlin, Katie A.
中科院分区:
医学1区
文献类型:
--
作者:
Colich, Natalie L.;Hanford, Lindsay C.;Weissman, David G.;Allen, Nicholas B.;Shirtcliff, Elizabeth A.;Lengua, Liliana J.;Sheridan, Margaret A.;McLaughlin, Katie A.

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青春期早期发育似乎是童年创伤导致青春期精神病理学的一个途径。青春期相关的神经网络的变化,涉及情绪处理,即杏仁核内侧前额叶(mPFC)电路,可能是一个潜在的机制连接创伤和青少年的精神病理学。我们的参与者是227名10至13岁的青少年,他们完成了对逆境、青春期阶段以及内化和外化症状的威胁和剥夺相关经历的评估。一个子集(n = 149)也进行了功能性MRI扫描,同时被动地观看恐惧和平静的面孔。儿童创伤与精神病理学,包括早期青春期的时间和神经反应厌恶刺激的潜在机制进行了探讨。青春期发育早与儿童期创伤以及仅在男孩中增加的外部症状有关。当比较恐惧和平静的面孔时,男性和女性的青春期提前与双侧杏仁核、海马和梭状区的激活呈负相关。然而,杏仁核-mPFC连接与青春期时间或精神病理学症状无关。这些研究结果不支持加速杏仁核mPFC的发展作为一种机制,连接儿童创伤和精神病理学,而是提供支持的作用,青春期发展的边缘系统激活的正常下降的发展。青春期提前介导了男性创伤和外化问题之间的联系。青春期提前与杏仁核、海马体和梭状回对厌恶刺激的激活减少有关。青春期的时间是不相关的杏仁核mPFC连接。这些神经模式不是连接创伤和精神病理学的机制。
Earlier pubertal development appears to be one pathway through which childhood trauma contributes to psychopathology in adolescence. Puberty-related changes in neural networks involved in emotion processing, namely the amygdala-medial prefrontal (mPFC) circuit, may be a potential mechanism linking trauma and adolescent psychopathology. Our participants were 227 youth between 10 and 13 years of age who completed assessments of threat and deprivation-related experiences of adversity, pubertal stage, and internalizing and externalizing symptoms. A subset (n = 149) also underwent a functional MRI scan while passively viewing fearful and calm faces. Potential mechanisms linking childhood trauma with psychopathology, encompassing earlier pubertal timing and neural response to aversive stimuli were explored. Earlier pubertal development was associated with childhood trauma as well as increased externalizing symptoms in boys only. Earlier pubertal timing in males and females was negatively associated with activation in bilateral amygdala, hippocampal, and fusiform regions when comparing fearful and calm faces. However, amygdala-mPFC connectivity showed no association with pubertal timing or psychopathology symptoms. These findings do not support accelerated amygdala-mPFC development as a mechanism linking childhood trauma and psychopathology, but instead provide support for the role of pubertal development in normative decreases in limbic activation across development. Earlier puberty mediates the link between trauma and externalizing problems in males. Earlier puberty relates to reduced activation in amygdala, hippocampus, and fusiform gyrus to aversive stimuli. Pubertal timing was not related to amygdala-mPFC connectivity. These neural patterns are not a mechanism linking trauma and psychopathology.
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