Reactivation of posttraumatic stress in male disaster survivors: The role of residual symptoms Hans Jakob Boe a,b , Katrine H. Holgersen a , Are Holen a,b, * a Department of Neuroscience, Faculty of Medicine, Norwegian University of Science and Technology, MTFS, NO-7489 Trondheim, Norway b Centre for Pain and Complex Disorders, St. Olav University Hospital, NO-7006 Trondheim, Norway The longitudinal course of posttraumatic stress takes multiple forms (Blank, 1993). Reactivated posttraumatic stress disorder (PTSD) is a recognized concept despite its absence in the DSM-IV. Numerous case reports have shown that posttraumatic stress can reoccur after remission (Christenson, Walker, Ross, & Maltbie, 1981; Russo, Hersen, & van Hasselt, 2001). Some studies have documented its occurrence in larger samples (Macleod, 1994; Solomon, Garb, Bleich, & Grupper, 1987). A few civilian studies (Berthier, Kulisevsky, Fera ´ ndez, & Gironell, 1998; Kinzie, Boehn- lein, Riley, & Sparr, 2002) have reported reactivation of PTSD in relation to triggers. However, the majority has been based on data from combat veterans. For example, in a 20-year longitudinal study, Solomon and Mikulincer (2006) reported reactivation in 16.0% of the combat veterans with previous combat stress reactions (CSR), and in 10.8% of the combat veterans without any prior history of CSR; the study suggests reactivation of PTSD to be rather common in combat veterans. In some survivors, new events elicit intrusions related to a primary trauma of the past. Reactivation may be precipitated by exposure to a new traumatic event, or by triggers, i.e. low grade stressors, which normally would have no impact. Precipitating events often mirror some aspect of the original trauma (Haley, 1978). Authors have reported reactivation also in association to physical illness (Macleod, 1994), retirement (Port, Engdahl, & Frazier, 2001) and aging (Archibald & Tuddenham, 1965; Christenson et al., 1981; Heuft, 1999; Hiskey, Luckie, Davies, & Brewin, 2008). When PTSD manifests itself more than 6 months after the stressor without any initial stress response, delayed onset PTSD may be diagnosed according to the DSM-IV. However, the DSM-IV criteria are ambiguous on this point (Andrews, Brewin, Philpott, & Stewart, 2007). It has been debated whether ‘‘onset of symptoms is at least 6 months after the stressor’’ should be interpreted strictly, i.e. that no immediate symptoms have been observed, or if instances of ‘‘prodromal symptoms’’ that eventually develop into full PTSD also should be classified as delayed onset. Reactivated PTSD shares these problems of definition. A narrow definition would require records of earlier PTSD episodes. Determinants of the diagnosis are not just the magnitude of symptoms, but also duration and the extent to which they lead to impaired function. Accordingly, the boundaries between delayed onset and reacti- vated PTSD are blurred, and the categorization becomes arbitrary. A core feature is a time of dormant symptoms and normal functioning before an episode of PTSD occurs. It may be argued that reactivation of PTSD and delayed onset PTSD are two designations of the same underlying phenomenon. Both imply that some survivors are left with an acquired propensity or vulnerability, which lowers their threshold for subsequent pathological response (Haley, 1978; Holen, 2007). Accordingly, the two notations may be used interchangeably (Hiskey et al., 2008). In this paper, reactivated PTSD also includes possible delayed cases. Journal of Anxiety Disorders 24 (2010) 397–402 ARTICLE INFO Article history: Received 26 August 2009 Received in revised form 2 February 2010 Accepted 6 February 2010 Keywords: Recurrence Relapse prevention Vulnerability Susceptibility Long-term Prospective ABSTRACT The aim of this study was to establish the relative distribution of resilient, remitted, chronic and reactivated posttraumatic stress disorder (PTSD) in a population of survivors from a major civilian disaster. Residual PTSD symptoms were explored to identify predictors of future reactivation. Symptoms were measured by the Impact of Event Scale (IES) 5.5 months, 14 months and 5 years after the disaster. Forty-eight survivors (79%) were interviewed after 27 years. PTSD status was determined by using the Structural Clinical Interview for DSM-IV axis I Disorders (SCID-I). The distributions were: 58.3% resilient, 14.6% remitted, 8.3% chronic, and 18.8% reactivated PTSD. Number of residual symptoms from intrusion and avoidance 14 months and 5 years past trauma predicted later reactivation. Intrusion symptoms in general, and sleep related intrusions in particular, were the most consistent predictors deserving special attention. ß 2010 Elsevier Ltd. All rights reserved. * Corresponding author at: NTNU, Dept. of Neuroscience, Faculty of Medicine, MTFS, NO-7489 Trondheim, Norway. Tel.: +47 91 89 74 66; fax: +47 73 59 87 95. E-mail address: are.holen@ntnu.no (A. Holen). Contents lists available at ScienceDirect Journal of Anxiety Disorders 0887-6185/$ – see front matter ß 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.janxdis.2010.02.003