健康与遗传心理学研究室知识库

创伤后应激障碍(posttraumatic stress disorder, PTSD)与抑郁的高共病及其不良临床后果使探索二者共病的心理病理学机制、找寻打破二者共病发展与维持的关键点显得尤为重要且迫切。目前，围绕PTSD与抑郁共病成因假说一一“二者相互影响对方的发生发展，从而导致二者共病的产生与持续”展开的研究虽己取得一定进展，但尚未厘清二者相互影响的作用方式。本论文整群抽取两所距离天津爆炸事故发生地最近的中小学在校生样本(N= 836， M年龄= 12.5，男生占比51.3070，实施三轮(事故发生后3, 8, 13个月)DSM-5 PTSD筛查量表及抑郁一焦虑一应激量表之抑郁分量表测查，采用验证性因素分析、交叉滞后模型、潜在增长模型、混合增长模型、潜在类别/转化模型及网络分析等统计方法，考察了上述时间内创伤后应激症状与抑郁症状在症状水平、发展轨迹、症状模式及症状网络层面的相互影响。

第一部分研究结果表明，创伤后应激症状与抑郁症状分别表征了两个独立的心理病理学结构;对创伤后应激症状及抑郁症状的测量具有因子结构、因子载荷以及条目截距三个水平的跨期恒等性;前期创伤后应激症状水平能够预测后期抑郁症状水平的变化，但反之则不然。第二部分研究结果表明，假定群体发展轨迹同质，创伤后应激症状与抑郁症状在上述时间内呈明显下降趋势，二者的初始水平存在关联，但二者对彼此缓解的速度无明显影响;假定群体发展轨迹异质，该样本主要存在四类创伤后应激症状发展轨迹一一心理韧性、症状缓解、症状加重和症状持续以及三类抑郁症状发展轨迹一一心理韧性、症状加重和症状持续;创伤后应激症状与抑郁症状的初始水平及其加重有关，而后者仅与前者的初始水平有关，二者对彼此缓解或加重的速度无明显影响。第三部分研究结果表明，该样本主要存在三类创伤后应激症状模式一一高症状、闯入/回避/高唤起症状和无明显症状以及三类抑郁症状模式一一高症状、情绪失调症状和无明显症状;在上述时间内，无明显症状者的症状模式转化概率较低，有明显症状者的症状模式转化概率较高且大多转化为症状更少/轻的模式;创伤后应激症状的初始水平与情绪失调相关抑郁症状的加重和持续有关，抑郁症状的初始水平与闯入/回避/高唤起相关创伤后应激症状的加重有关。第四部分研究结果表明，创伤后应激症状之间、抑郁症状之间有明显关联，但创伤后应激症状与抑郁症状之间的关联较少，主要体现在负性信念(创伤后应激症状之一)与忧郁沮丧(抑郁症状之一)之间的关联;负性信念对忧郁沮丧具有跨期预测作用，但反之则不然。

总的来说，本论文发现创伤后应激症状的初始水平能够预测抑郁症状水平的变化以及情绪失调相关抑郁症状的加重和持续，但抑郁症状对创伤后应激症状的发展影响较小，支持了PTSD与抑郁共病成因假说之一一一“PTSD导致抑郁”。本论文识别出连接创伤后应激症状与抑郁症状的“桥症状”一一负性信念和忧郁沮丧并发现仅存在前者对后者的跨期预测作用，揭示了PTSD引发抑郁的一种可能的心理病理学机制。本论文提示临床工作者在儿童青少年创伤相关心理干预中给予创伤后应激症状(特别是负性信念)更多关注，以期降低PTSD伴发抑郁的风险。

Given the high comorbidity of posttraumatic stress disorder (PTSD) and depression and its association with poor clinical outcomes, it is of great importance and urgency to explore the psychopathological mechanisms underlying this comorbidity and to identify the strategic points for obstructing the development and maintenance of this comorbidity. Considerable progress has previously been made based upon an etiological hypothesis for PTSD-depression comorbidity: PTSD and depression have reciprocal effects on each other, thereby causing their comorbidity. Nevertheless, the mechanisms behind such effects remain unclear. In a cluster sample recruited from two primary and middle schools nearest to the Tianjin explosion accident site (N=836, Mage=12.5, 51.3070 boys) and assessed by the PTSD Checklist for DSM-5 and the depression subscale of the 21-item Depression Anxiety Stress Scale at 3, 8, 13-months after the accident, this dissertation investigated the longitudinal reciprocal effects between posttraumatic stress and depressive symptoms in terms of their symptom levels, courses/trajectories, symptom patterns, and symptom networks. Multiple analytic methods were used, including confirmatory factor analysis, cross-lagged modeling, latent growth curve modeling, growth mixture modeling, latent class/transition modeling, and network analysis.

Part 1 studies found that posttraumatic stress and depressive symptoms represented two distinct psychopathological constructs. Configural, metric, and scalar invariance of measured posttraumatic stress and depressive symptoms held across time. Posttraumatic stress symptom levels at an early wave predicted later changes in depressive symptom levels, but not vice versa. Part 2 studies found that assuming a homogeneous course within the sample, both posttraumatic stress and depressive symptoms showed a marked decline over time. Their initial levels were associated, but had no substantial effect on the declining rates of each other. Assuming heterogeneous trajectories within the sample, four trajectories of posttraumatic stress symptoms were identified and named Resilience, Recovery, Worsening, and Chronicity, respectively; three trajectories of depressive symptoms were identified and named Resilience, Worsening, and Chronicity, respectively. Posttraumatic stress symptoms were associated with initial symptom levels and increased symptoms of depression, whereas depressive symptoms were only associated with initial levels of posttraumatic stress symptoms; they had no substantial effect on the recovering or worsening rates of each other. Part 3 studies identified three classes of posttraumatic stress symptoms named High Symptoms, Intrusion/Avoidance/Hyperarousal Symptoms, and Negligible Symptoms, respectively; and three classes of depressive symptoms named High Symptoms, Emotional Dysfunction Symptoms, and Negligible Symptoms, respectively. There were relatively low probabilities of migration out of Negligible Symptoms classes but relatively high probabilities of migration out of classes with significant symptoms and mainly into classes with fewer/lower symptoms over time. Initial posttraumatic stress symptom levels were associated with the worsening and chronicity of emotional dysfunction-related depressive symptoms; initial depressive symptom levels were associated with the worsening of intrusion/avoidance/hyperarousal-related posttraumatic stress symptoms. Part 4 studies found that associations were strong among posttraumatic stress symptoms and among depressive symptoms but much weaker between these two syndromes. The most sizeable between-syndrome association was found between negative beliefs (posttraumatic stress symptom) and blue/down-hearted (depressive symptom); negative beliefs was longitudinally predictive of blue/down-hearted, but not vice versa.

In conclusion, this dissertation found that initial posttraumatic stress symptom levels predicted the changes in depressive symptom levels and the worsening and chronicity of emotional dysfunction-related depressive symptoms, whereas depressive symptoms had little effect on the development of posttraumatic stress symptoms. This supports one of the etiological hypotheses for PTSD-depression comorbidity: PTSD causes depression. Negative beliefs and blue/down-hearted were identified as "bridge symptoms" that linked posttraumatic stress and depressive symptoms, and blue/down- hearted was found to be predicted by negative beliefs longitudinally and non-reciprocally. This reveals a potential way in which PTSD causes depression. To reduce the risk of PTSD-depression comorbidity, clinicians may pay more attention to posttraumatic stress symptoms, especially negative beliefs in youth's trauma-related interventions.