Berntsen Dorthe, Rubin David C, Johansen Malene Klindt
University of Aarhus.
Psychol Rev. 2008 Oct;115(4):1099-1106. doi: 10.1037/a0013730.
We address the four main points in Monroe and Mineka (2008)'s Comment. First, we first show that the DSM PTSD diagnosis includes an etiology and that it is based on a theoretical model with a distinguished history in psychology and psychiatry. Two tenets of this theoretical model are that voluntary (strategic) recollections of the trauma are fragmented and incomplete while involuntary (spontaneous) recollections are vivid and persistent and yield privileged access to traumatic material. Second, we describe differences between our model and other cognitive models of PTSD. We argue that these other models share the same two tenets as the diagnosis and we show that these two tenets are largely unsupported by empirical evidence. Third, we counter arguments about the strength of the evidence favoring the mnemonic model, and fourth, we show that concerns about the causal role of memory in PTSD are based on views of causality that are generally inappropriate for the explanation of PTSD in the social and biological sciences.
我们回应了门罗和米内卡(2008年)评论中的四个要点。首先,我们首先表明,《精神疾病诊断与统计手册》(DSM)中创伤后应激障碍(PTSD)的诊断包含一种病因,并且它基于一个在心理学和精神病学领域有着卓越历史的理论模型。该理论模型的两个原则是,对创伤的自愿(策略性)回忆是碎片化且不完整的,而不自主(自发)回忆则生动且持久,并能提供对创伤性材料的优先访问权。其次,我们描述了我们的模型与其他PTSD认知模型之间的差异。我们认为,这些其他模型与诊断共享相同的两个原则,并且我们表明这两个原则在很大程度上没有得到实证证据的支持。第三,我们反驳了关于支持记忆模型的证据力度的论点,第四,我们表明,对记忆在PTSD中的因果作用的担忧是基于因果关系的观点,而这些观点通常不适用于在社会和生物科学中对PTSD的解释。