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Sekiguchi et al.1 demonstrated in a neuroimaging study that survivors of the Great East Japan Earthquake who had a smaller anterior cingulate cortex (ACC) volume before the earthquake and survivors with a decreased orbitofrontal cortex (OFC) volume through the earthquake disaster were likely to have symptoms of posttraumatic stress disorder (PTSD).1 As both the ACC and OFC are involved in the processing of anxiety and fear, such structural changes seem to show some similarity with the findings of epidemiological studies on peritraumatic distress (distress at the time of trauma and immediately thereafter). Fear memory becomes excessively consolidated2 in the development of PTSD and is thought to be enhanced by peritraumatic distress. Indeed, peritraumatic distress is one of the strongest predictors for PTSD.3 The presence of peritraumatic distress was shown to be a relatively weak indicator of the presence of PTSD, whereas its absence was found to be a strong indicator of the absence of PTSD.4 Recently, we in our epidemiological study, examined the predictors of PTSD among rescue workers 1 month after the Great East Japan Earthquake as, alongside survivors in the disaster area, they were deemed to be at high risk for developing PTSD. Peritraumatic distress as assessed by the Peritraumatic Distress Inventory (PDI)5, 6 and watching television for extended period of time predicted PTSD symptoms at 4 months after the earthquake.7 Moreover, in an online survey conducted by Bui et al.8 in France, Canada and the United States, within 2 weeks of the earthquake, peritraumatic distress was found to be a predictor of disruptive nocturnal behavior and PTSD symptoms among respondents, and that it significantly mediated a relationship between internet coverage of the disaster and presence of PTSD symptoms. Failure to regulate fear responses to traumatic events could be due to dysfunction in the ACC.9 As Sekiguchi et al.1 showed decreased volume of the ACC might reflect genetic and epigenetic vulnerability, and vulnerable individuals might be prone to peritraumatic distress. We suggested that the different types of peritraumatic distress occurring in response to various traumatic events might be important.7 For example, loss of emotional control and feeling shame might be more important for predicting PTSD than other types of peritraumatic distress in rescue workers after disasters, although helplessness and experiencing physical reactions might be more important in traffic accident survivors. These differences could provide insights into not only effective prevention but also future neurobiological study of PTSD. The current diagnostic criterion A2 for PTSD requires fear, helplessness or horror at the time of the event. Removal of this criterion from the fifth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-5) has been proposed.10 This change could be a reasonable one because the positive predictive value of this criterion for PTSD is relatively low, and as many patients with PTSD visit psychiatrists long after a traumatic event, recall bias would be considerable. However, assessment of peritraumatic distress, at least in settings where it could be assessed soon after a traumatic event, could screen out individuals unlikely to develop PTSD as well as contribute to elucidating the pathogenesis of PTSD. A foremost function of the OFC is its involvement in the extinction of conditioned fear.1 TV and Internet viewing for extended periods after a traumatic event might be harmful to the OFC structure and consequently impair its important functioning for the extinction of fear memory. Thus the results of Sekiguchi et al.'s1 neuroimaging study coincide with the findings from epidemiological studies, although it remains unclear whether such viewing might constitute traumatic exposure or be a part of ineffective coping. The use of longitudinal neuroimaging data to examine vulnerability factors and acquired sign of PTSD symptoms is of considerable interest for both understanding the pathogenesis of PTSD and developing preventive strategies for it. It is our mission to learn more from this latest tragic event for the future. Dr Nishi has received research support from Toray Industries, Inc. and the Foundation for Total Health Promotion, and lecture fees from Qol Co., Ltd, DHA & EPA Association and NTT DoCoMo, Inc. Dr Matsuoka has received research support from the Japan Science and Technology Agency, CREST and the Ministry of Health, Labor, and Welfare of Japan, Intramural Research Grant for Neurological and Psychiatric Disorders of NCNP and lecture fees from Suntory Wellness Ltd, Eli Lilly Japan KK and Otsuka Pharmaceutical, Ltd.

Peritraumatic distress after an earthquake: a bridge between neuroimaging and epidemiology