The effects of extreme stress have long been recognized through syndromes such as battle fatigue and shell shock. However, it was not until 1980 that APA first included posttraumatic stress disorder (PTSD) in the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), in part because of a social demand to acknowledge and describe the insidious psychological problems experienced by many of the Vietnam veterans returning from an unpopular war. The significance of creating PTSD as a

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... sis was the recognition that responses to traumatic events formed a legitimate psychiatric condition influenced by the meaning of social events and were not merely a matter of individuals' weakness. This inclusion has allowed the identification of a broad range of psychiatric symptoms and accompanying difficulties associated with extreme stress. It has been a crucial step in providing a framework to investigate scientifically how traumatic experiences occurring at various stages of the lifespan can profoundly, and in some cases permanently, alter individuals' psychology and biology. However, there is still no clear consensus concerning the interaction of genetic and environmental factors that predispose individuals to PTSD, mechanisms underlying the development of and recovery from PTSD, or the precise role of social and cultural influences on individuals' risk or prognosis for the disorder. The variety of articles in this issue concerning PTSD attests to this complexity. The article by Wessa and Flor approaches the study of PTSD from a fear conditioning perspective. This model is widely accepted in the PTSD literature and has been supported by a considerable number of studies (1). A fear conditioning model assumes that stimuli that cause an adverse reaction (e.g., air show disaster) become linked with other, neutral stimuli (e.g., airplanes) to produce a conditioned response (fear of airplanes) to these previously neutral stimuli. Over time, the conditioned response diminishes if the conditioned (previously neutral) stimulus is not linked to the negative stimulus. In other words, there is an extinction of the association (Figure 1 ). The data presented by Wessa and Flor point to a failure of extinction in patients with PTSD and underline the need for pharmaco-and/or psychotherapeutic treatments focusing on the extinction of learned responses. The study by Litz et al. examines the outcome of an 8-week randomized, controlled trial of Internet-based self-management cognitive behavior therapy versus supportive therapy for PTSD related to attacks on the Pentagon on September 11, or the Iraq war. The rationale of the cognitive behavior therapy employed in this study again largely draws on the fear conditioning paradigm in that it utilizes graduated, self-guided, in vivo exposure designed to relearn/unlearn the association between the conditioned stimulus and the conditioned response, thus facilitating extinction. The data from this trial are promising and show reductions in PTSD, depressive, and anxiety symptoms at 6-month follow-up, thereby providing further evidence for the importance of the underlying mechanism of extinction in the treatment of PTSD. However, insofar as exposure therapy failed to eliminate all PTSD symptoms, the inference is that there are probably additional mechanisms at work. The investigation by Kilpatrick et al. indicates complex interactions among genetic factors, trauma exposure, and social aspects (social support) in the moderation of risk RUTH LANIUS, M.D., PH.D.