J Psychiatry Neurosci 2010;35(2):80-89
Ruth A. Lanius, MD, PhD; Chris R. Brewin, PhD; J. Douglas Bremner, MD; Judith K Daniels, PhD; Matthew J. Friedman, MD; Israel Liberzon, MD; Alexander McFarlane, MD; Paula P. Schnurr, PhD; Lisa Shin, PhD; Murray Stein, MD; Eric Vermetten, MD, PhD
Lanius, Daniels — Department of Psychiatry, University of Western Ontario, London, Ont.; Brewin — University College London, London, United Kingdom; Bremner — Emory University School of Medicine, Atlanta, Ga.; Friedman, Schnurr — Dartmouth Medical School, Hanover, NH; Liberzon — University of Michigan, Ann Arbor, Mich.; McFarlane — The University of Adelaide, Adelaide, Australia; Shin — Tufts University, Medford, Mass.; Stein — University of California, San Diego, La Jolla, Calif; Vermetten — Central Military Hospital, Utrecht, the Netherlands
Background: In an attempt to avoid unknown influence, most neuroimaging studies examining the pathophysiology of posttraumatic stress disorder (PTSD) exclude patients taking medications. Here we review the empirical evidence for relevant medications having a confounding effect on task performance or cerebral blood flow (CBF) in this population. The evidence for potentially confounding effects of psychotherapy in PTSD are also discussed.
Methods: The literature that we reviewed was obtained through a PubMed search from 1980 to 2009 using the search terms posttraumatic stress disorder, PTSD, psychotropic medications, neuroimaging, functional magnetic resonance imaging, positron emission tomography, cerebral blood flow, CBF, serotonin-specific reuptake blocker, benzodiazepine, ketamine, methamphetamine, lamotrigine and atypical antipsychotic agents.
Results: The empirical evidence for relevant medications having a confounding effect on task performance or CBF in relevant areas remains sparse for most psychotropic medications among patients with PTSD. However, considerable evidence is accumulating for 2 of the most commonly prescribed medication classes (serotonin-specific reuptake inhibitors and benzodiazepines) in healthy controls. Compelling data for the potentially confounding effects on brain areas relevant to PTSD for psychotherapeutic interventions are also accumulating.
Conclusion: Neuroimaging studies examining the pathophysiology of PTSD should ideally recruit both medicated (assuming that the medication treatment has not resulted in the remission of symptoms) and unmedicated participants, to allow the findings to be generalized with greater confidence to the entire population of patients with PTSD. More research is needed into the independent effects of medications on task performance and CBF in regions of interest in PTSD. Neuroimaging studies should also take into account whether patients are currently engaged in psychotherapeutic treatment.
Submitted Apr. 16, 2009; Revised Sept. 3, 2009; Accepted Oct. 16, 2009.
Acknowledgments: The authors gratefully acknowledge advice and suggestions by Roger K. Pitman. The authors thank Nancy Mazza for helping prepare the manuscript for publication.
Competing interests: None declared for Drs. Lanius, Brewin, Bremner, Daniels, Liberzon, McFarlane, Schnurr, Shin, Stein and Vermetten. Dr. Friedman received speaker fees from AstraZeneca in 2008.
Contributors: Drs. Brewin, Friedman, Liberzon, Schnurr, Shin and Stein designed the study. Drs. Lanius and Liberzon acquired the data, which Drs. Lanius, Daniels, Friedman, McFarlane, Schnurr, Shin, Stein and Vermetten analyzed. Drs. Lanius, Brewin, Daniels, Friedman, Liberzon and Stein wrote the article. All authors reviewed the article and approved the final version submitted for publication.
Correspondence to: Dr. R.A. Lanius, Department of Psychiatry, University of Western Ontario, 339 Windermere Rd., PO Box 5339, London ON N6A 5A5; fax 519 663-3927; firstname.lastname@example.org