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首页> 外文期刊>International journal of law and psychiatry >PTSD in Court II: Risk factors, endophenotypes, and biological underpinnings in PTSD
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PTSD in Court II: Risk factors, endophenotypes, and biological underpinnings in PTSD

机译：中应投入第四杆菌（Court II）：中应投灾因素，内心型和生物学基础

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The second article in the series of three for the journal on "PTSD in Court" especially concerns the biological bases that have been found to be associated with PTSD (posttraumatic stress disorder). The cohering concepts in this section relate to risk factors; candidate genes; polygenetics; "gene x environment" interactions; epigenetics; endophenotypes; biomarkers; and connective networks both structurally and functionally (in terms of intrinsic connectivity networks, ICNs, including the DMN, SN, and CEN; that is, default mode, salience, and central executive networks, respectively). Risk factors related to PTSD include pre-event, event- and post-event ones. Some of the genes related to PTSD include: FKBP5, 5-HTTLPR, and COMT (which are, respectively, FK506-binding protein 5 gene, serotonin-transporter linked polymorphic region, catechol-O-methyl-transferase). These genetic findings give an estimate of 30% for the genetic influence on PTSD. The typical brain regions involved in PTSD include the amygdala, hippocampus, and prefrontal cortex, along with the insula. Causal models of behavior are multifactorial and biopsychosocial, and these types of models apply to PTSD, as well. The paper presents a multilevel systems model of psychopathology, including PTSD, which involves three levels a top-down psychological construct one, a bottom-up symptom connection one, and a middle one involving symptom appraisal. Legally, causality refers to the event at issue needing to meet the bar of being materially contributory to the outcome. Finally, this section of the article reviews empirically-supported therapies for PTSD and the dangers of not receiving treatment for it. Crown Copyright (C) 2017 Published by Elsevier Ltd. All rights reserved.
机译：第三篇文章在“庭院中的第四次”杂志“中的三篇文章尤其涉及已发现与接触者（术后应激障碍）相关的生物基础。本节中的相干概念涉及风险因素;候选基因;多种语; “基因X环境”相互作用;表观遗传学;内噬素;生物标志物;和结构上和功能上的连接网络（以内在的连接网络，ICN，包括DMN，SN和CEN），即，分别是，默认模式，显着和中央行政网络）。与PTSD相关的危险因素包括前列前，赛事和事件后的因素。与PTSD相关的一些基因包括：FKBP5，5-HTTLPR和COMT（分别为FK506结合蛋白5基因，血清素转运蛋白连接的多晶态区域，儿茶酚-O-甲基转移酶）。这些遗传调查结果估计为PTSD的遗传影响为30％。参与PTSD的典型脑区包括杏仁醛，海马和前额叶皮质，以及insula。行为的因果模型是多因素和生物学，以及这些类型的模型也适用于PTSD。本文介绍了一种心理病理学的多级系统模型，包括PTSD，其涉及三个水平的俯卧性心理构建一个，一个自下而上的症状连接，以及涉及症状评估的中间症状。合法地，因果关系是指遇到问题的事件，以满足对结果的重要贡献的律法。最后，本文的本条审查了针对PTSD的经验支持的疗法以及未接受其待遇的危险。 Crown版权所有（c）2017由elestvier有限公司出版。保留所有权利。

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