In the mnemonic model of PTSD, the current memory of a negative event, not the event itself determines symptoms. The model is an alternative to the current event-based etiology of PTSD represented in the DSM. The model accounts for important and reliable findings that are often inconsistent with the current diagnostic view and that have been neglected by theoretical accounts of the disorder, including the following observations. The diagnosis needs objective information about the trauma and peritraumatic emotions, but uses retrospective memory reports that can have substantial biases. Negative events and emotions that do not satisfy the current diagnostic criteria for a trauma can be followed by symptoms that would otherwise qualify for PTSD. Predisposing factors that affect the current memory have large effects on symptoms. The inability-to-recall-an-importantaspect-of-the-trauma symptom does not correlate with other symptoms. Loss or enhancement of the trauma memory affects PTSD symptoms in predictable ways. Special mechanisms that apply only to traumatic memories are not needed, increasing parsimony and the knowledge that can be applied to understanding PTSD. Keywords autobiographical memory; gender; neuroticism; dissociative amnesia; trauma This paper is a about posttraumatic stress disorder (PTSD) and more specifically about its assumed etiology. We evaluate basic theoretical assumptions underlying the PTSD diagnosis and present an alternative model. By its current diagnostic criteria in the U.S.A., which we refer to as the DSM, (i.e., the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, American Psychiatric Association, 2000) and by the World Health Organization (2006), the diagnosis of PTSD requires the occurrence of a traumatic event. However, in practice, the diagnosis does not involve measuring the occurrence of an actual event, only the patient's report of the event at least one month, and sometimes years, after the Corresponding Author: David C. Rubin, Department of Psychology and Neuroscience, Box 27708-0086, Duke University, Durham, NC, 27708, U.S.A. david.rubin@duke.edu. Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at www.apa.org/journals/rev NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript event occurred. The memory report, in practice, is not questioned (McNally, 2003b). We examine the implications of a diagnosis based on a pathogenic memory rather than a pathogenic event. The change has major consequences: the event, which is not m...

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.Monroe and Mineka (2008)'s Comment has four main points, which structure our response. First, they argue that the DSM PTSD diagnosis does not imply a theoretical model, thus, we should not have contrasted our model with the DSM. Second, they criticize us for not evaluating our theoretical model against other cognitive models of PTSD. Third, they argue that some of the evidence that we presented in support of the mnemonic model is weak and may even go against the model. Fourth, they challenge the role of the traumatic memory as a causal mechanism.We counter all of these points. We first show that the DSM PTSD diagnosis implies a theoretical model, following standard definitions of what qualifies as a theoretical model, and we document that this model has a long history in psychology and psychiatry. We next describe differences between our model and other cognitive models of PTSD. Although Monroe and Mineka find these alternative cognitive models to be "much richer and more comprehensive," we show that they are largely unsupported by empirical evidence and argue that they are rooted in the same theoretical model as the diagnosis. We then clarify the evidence that Monroe and Mineka call into question, and address the notion of causality in relation to the mnemonic model Space limitations do not allow us to address the numerous more minor points raised by Monroe and Mineka, depicting aspects of our article as (in alphabetical order) inappropriate, irrelevant,

The massed, 3-week group CBT schedule proved to be effective and feasible for PD patients with outcomes comparable with that of standard, spaced group CBT.

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