Clinical and Neural Correlates of Alexithymia in Posttraumatic Stress Disorder Paul A. Frewen, Ruth A. Lanius, David J. A. Dozois, and Richard W. J. Neufeld University of Western Ontario Clare Pain University of Western Ontario and University of Toronto James W. Hopper Harvard Medical School and McLean Hospital Maria Densmore University of Western Ontario Todd K. Stevens University of Western Ontario and Robarts Research Institute Individuals with posttraumatic stress disorder (PTSD) often exhibit deficits in emotional experience and expression, which suggests that certain individuals with PTSD may be alexithymic. In this study, in a sample of 105 individuals with PTSD, clinical correlates of alexithymia included reexperiencing, hyperarousal, numbing, dissociative symptoms, and retrospectively reported experiences of childhood emotional neglect. In a subsample of 26 individuals with PTSD related to a motor vehicle accident, functional neural responses to trauma-script imagery were associated with severity of alexithymia, including increased right posterior-insula and ventral posterior-cingulate activation and decreased bilat- eral ventral anterior-cingulate, ventromedial prefrontal, anterior-insula, and right inferior frontal cortex activation. Clinical and theoretical implications and future research directions are discussed. Keywords: alexithymia, posttraumatic stress disorder (PTSD), script-driven imagery, neuroimaging, functional magnetic resonance imaging (fMRI) Under the current psychiatric nosological system, posttraumatic stress disorder (PTSD) is classified as an instance of the anxiety disorders (American Psychiatric Association, 1994) and therefore is chiefly construed as a condition involving elevated subjective anxiety. Accordingly, contemporary psychological models of PTSD predominantly aim to explain the information-processing mechanisms underlying individuals’ subjective anxiety (Brewin & Holmes, 2003; Dalgleish, 2004), and fear conditioning and extinc- tion models represent the principal theoretical platform for current studies of the psychobiology of PTSD (see Yehuda, 2006, for recent reviews). Notwithstanding the centrality of anxiety symptomatology to PTSD, clinical studies have revealed that anxiety symptoms represent only a fraction of the psychopathological sequelae that may ensue as a consequence of prolonged exposure to traumatic stressors (e.g., van der Kolk, Roth, Pelcovitz, Sunday, & Spinazzola, 2005). For example, individuals with PTSD may display extreme anger (Orth & Wieland, 2006), shame, guilt, dysphoria, and dissociation (e.g., Andrews, Brewin, Rose, & Kirk, 2000; Ehlers, Mayou, & Bryant, 1998; Feeny, Zoellner, Fitzgibbons, & Foa, 2000). Conversely, studies have increas- ingly documented the presence of emotional numbing symp- toms in the PTSD population, which are characterized by a restricted range of affect (e.g., Kashdan, Elhai, & Frueh, 2006; Litz, Orsillo, Kaloupek, & Weathers, 2000). A key finding is that hyperarousal and emotional numbing symptoms are posi- tively rather than negatively correlated in PTSD populations and may be functionally related (e.g., Buckley, Blanchard, & Hickling, 1998; S. Taylor, Kuch, Koch, Crockett, & Passey, 1998; Simms, Watson, & Doebbelling, 2002). Paul A. Frewen, Department of Psychology, University of Western Ontario, London, Ontario, Canada; Ruth A. Lanius, Departments of Psy- chiatry and Neuroscience, University of Western Ontario; David J. A. Dozois and Richard W. J. Neufeld, Departments of Psychology, Psychia- try, and Neuroscience, University of Western Ontario; Clare Pain, Depart- ment of Psychiatry, University of Western Ontario, and Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada; James W. Hopper, Department of Psychiatry, Harvard Medical School, and McLean Hospital, Belmont, Massachusetts; Maria Densmore, Department of Psy- chiatry, University of Western Ontario; Todd K. Stevens, Department of Medical Biophysics, University of Western Ontario, and Imaging Research Laboratories, Robarts Research Institute, London, Ontario, Canada. We acknowledge the support of Canadian Institutes of Health Research Grant MOP49543, Ontario Mental Health Foundation Grant M931D5, Canadian Psychiatric Research Foundation Grant MA94A7, and the Social Sciences and Humanities Research Council of Canada (in the form of a Canada Graduate Scholarship to Paul A. Frewen). Preliminary analyses of these data were presented at the meeting of the New York Academy of Sciences in New York, New York in September 2005 and at the meeting of the International Society for Traumatic Stress Studies in Toronto, Ontario, Canada in November 2005. We gratefully acknowledge the con- tributions of participant “W. H.,” described in the general Discussion. Correspondence concerning this article should be addressed to Ruth A. Lanius, London Health Sciences Centre, 339 Windermere Road, PO Box 5339, London, Ontario N6A 5A5, Canada. E-mail: ruth.lanius@lhsc.on.ca Journal of Abnormal Psychology Copyright 2008 by the American Psychological Association 2008, Vol. 117, No. 1, 171–181 0021-843X/08/$12.00 DOI: 10.1037/0021-843X.117.1.171 171