J Psychiatry Neurosci 2011;36(1):6-14
Marla J.S. Mickleborough, MA;* Judith K. Daniels, PhD;* Nicholas J. Coupland, MD; Raymond Kao, MD; Peter C. Williamson, MD; Ulrich F. Lanius, PhD; Kathy Hegadoren, PhD; Allan Schore, PhD; Maria Densmore, BSc; Todd Stevens, PhD; Ruth A. Lanius,MD, PhD
Mickleborough, Densmore — Neuroscience Program, University of British Columbia, Vancouver, BC; Daniels, Williamson, R.A. Lanius — Department of Psychiatry, University of Western Ontario, London, Ont.; Coupland — Department of Psychiatry, University of Alberta, Edmonton, Alta.; Kao — Department of Medicine, University of Western Ontario, and Critical Care Medicine, London Health Sciences Centre, London, Ont.; Williamson, R.A. Lanius — Department of Neuroscience, University of Western Ontario, London, Ont.; U.F. Lanius — the Sensorimotor Psychotherapy Institute, Boulder, Colo.; Hegadoren — Faculty of Nursing, University of Alberta, Edmonton, Alta.; Schore — Department of Psychiatry and Biobehavioral Sciences and Center for Culture, Brain and Development, University of California Los Angeles, Calif.; Stevens — Department of Chemistry, University of California, Berkeley, Calif.
*M.J.S. Mickleborough and J.K. Daniels contributed equally to this work.
Background: Imaging studies of pain processing in primary psychiatric disorders are just emerging. This study explored the neural correlates of stress-induced analgesia in individuals with posttraumatic stress disorder (PTSD). It combined functional magnetic resonance imaging (fMRI) and the traumatic script-driven imagery symptom provocation paradigm to examine the effects of trauma-related cues on pain perception in individuals with PTSD.
Methods: The study included 17 patients with PTSD and 26 healthy, trauma-exposed controls. Participants received warm (nonpainful) or hot (painful) thermal stimuli after listening to a neutral or a traumatic script while they were undergoing an fMRI scan at a 4.0 T field strength.
Results: Between-group analyses revealed that after exposure to the traumatic scripts, the blood oxygen level–dependent (BOLD) signal during pain perception was greater in the PTSD group than the control group in the head of the caudate. In the PTSD group, strong positive correlations resulted between BOLD signal and symptom severity in a number of brain regions previously implicated in stress-induced analgesia, such as the thalamus and the head of the caudate nucleus. Trait dissociation as measured by the Dissociative Experiences Scale correlated negatively with the right amygdala and the left putamen.
Limitations: This study included heterogeneous traumatic experiences, a different proportion of military trauma in the PTSD versus the control group and medicated patients with PTSD.
Conclusion: These data indicate that in patients with PTSD trauma recall will lead in a state-dependent manner to greater activation in brain regions implicated in stress-induced analgesia. Correlational analyses lend support to cortical hyperinhibition of the amygdala as a function of dissociation.
Submitted Nov. 19, 2008; Revised Feb. 16, May 5, 2010; Accepted May 6, 2010.
Acknowledgments: This work was supported by grants from the Department of National Defence, the Canadian Institute of Health Research and Psychiatry Seed Funding from the University of Western Ontario Psychiatry Department. We thank Stephanie Nevill and Suzy Southwell for screening and assessing the participants and Nancy Mazza for preparation of the manuscript.
Competing interests: None declared.
Contributors: This work was supported by grants from the Department of National Defence, the Canadian Institute of Health Research and Psychiatry Seed Funding from the University of Western Ontario Psychiatry Department. We thank Stephanie Nevill and Suzy Southwell for screening and assessing the participants and Nancy Mazza for preparation of the manuscript.
Correspondence to: Dr. R.A. Lanius, Department of Psychiatry, The University of Western Ontario, 339 Windermere Rd., University Hospital, London ON N6A 2A2; email@example.com