Resting-state functional connectivity after hydrocortisone administration in patients with post-traumatic stress disorder and borderline personality disorder |
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| Institution: | 1. Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Klinik für Psychiatrie und Psychotherapie, Campus Benjamin Franklin, Berlin, Germany;2. MSB Medical School Berlin, Berlin, Germany;3. Department of Psychiatry, Psychotherapy and Psychosomatics, Psychiatric Hospital, University of Zurich, Switzerland;4. Institute of Cognitive Neuroscience, Department of Cognitive Psychology, Ruhr University Bochum, Germany;1. Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany;2. Department of Neurophysiology, Centre for Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany;1. Mood Disorders Psychopharmacology Unit (MDPU), University Health Network, University of Toronto, Toronto, Canada;2. University of Toronto, Toronto, Canada;3. Department of Psychiatry and Behavioral Sciences, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, USA;4. Reference Center for Alcohol, Tobacco and Other Drugs (CRATOD), São Paulo State Secretariat of Health, São Paulo, SP, Brazil;5. Endocrinology & Metabolism Division, Sunnybrook Health Sciences Centre, University of Toronto, Canada;6. Department of Affective Disorders, the Affiliated Hospital of Guangzhou Medical University and GMU-HKU Mood and Brain Sciences Center, Guangzhou, China;7. Psychiatric Center Copenhagen, University of Copenhagen, Copenhagen, Denmark;8. Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore;9. Department of Psychiatry, Universidade Federal de São Paulo, São Paulo, Brazil;10. Research Group in Molecular and Behavioral Neuroscience of Bipolar Disorder, Departament of Psychiatry, Universidade Federal de São Paulo, SP, Brazil;1. School of Psychological Sciences, Tel Aviv University, Tel-Aviv, Israel;2. Department of Life Sciences and the Zlotowski Center for Neuroscience, Ben-Gurion University, Be''er-Sheva, Israel;3. Sackler Faculty of Medicine, Tel Aviv University, Tel-Aviv, Israel;1. Department of Psychiatry, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, The Netherlands;2. Department of Translational Neuroscience, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, The Netherlands;3. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, USA;4. Ter Gooi Hospital, Department of Psychiatry, Blaricum, The Netherlands;5. Department of Psychology, Utrecht University, Utrecht, The Netherlands;6. Department of Medical Genetics, University Medical Centre Utrecht, Utrecht University, The Netherlands;7. MRC Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, Psychology & Neuroscience, King’s College London, UK;8. UCLA Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA;9. Neuroimmunology, Netherlands Institute for Neuroscience, An institute of the royal academy of arts and sciences, Amsterdam, The Netherlands;1. Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy;2. Laboratoire de Psychologie Médicale, Université Libre de Bruxelles and PsyPluriel, Brussels, Belgium;3. Université Libre de Bruxelles, Brussels, Belgium;4. Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria;5. Imperial College, University of London, London, United Kingdom;6. Expert Platform on Mental Health, Focus on Depression, Tel-Aviv University, Tel Aviv, Israel;1. Department of Psychiatry and Division of Medical Psychology, University of Bonn, 53105 Bonn, Germany;2. MOE Key Laboratory for Neuroinformation, Center for Information in Medicine, Clinical Hospital of the Chengdu Brain Science Institute, University of Electronic Science and Technology of China, Xiyuan Ave 2006, 611731 Chengdu, China;3. Department of Addiction and Psychotherapy, LVR-Clinic Bonn, 53111 Bonn, Germany;4. German Center for Neurodegenerative Diseases (DZNE), 53175 Bonn, Germany;5. Department of Epileptology, Center for Economics and Neuroscience, University of Bonn, Germany;6. Department of NeuroCognition, Life & Brain Center, 53105 Bonn, Germany;7. State Key Laboratory of Cognitive Neuroscience and Learning, IDG/McGovern Institute of Brain Research, Beijing Normal University, 100875 Beijing, China |
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| Abstract: | In a previous study, we found that - in contrast to healthy individuals - patients with borderline personality disorder (BPD) and post-traumatic stress disorder (PTSD) showed better memory retrieval performance after hydrocortisone administration compared to placebo. As these results suggest an altered function of corticosteroid receptors in the brain in PTSD and BPD, we examined the effect of hydrocortisone on brain activation in both disorders. We recruited 40 female healthy controls, 20 female unmedicated patients with PTSD and 18 female unmedicated patients with BPD. We conducted a placebo-controlled cross-over study, in which all participants underwent two resting state MRI measurements after they received either a placebo or 10 mg hydrocortisone orally and in randomized order. There was a time interval of one week between the measurements. We analysed resting state functional connectivity (RSFC) with the hippocampus and the amygdala as seed regions. Compared to healthy controls, both patient groups showed reduced hippocampus RSFC to dorsomedial prefrontal cortex (dmPFC). Positive hippocampus dmPFC RSFC correlated negatively with childhood trauma (r = -0.47) and with severity of clinical symptoms, measured with the Borderline Symptom List (r = -0.44) and the Posttraumatic Stress Diagnostic Scale (r = -0.45). We found neither differences in amygdala RSFC nor an effect of hydrocortisone administration. Childhood trauma might lead to decreased positive hippocampus dmPFC RSFC. This might explain symptoms of PTSD and BPD that are characterized by dysfunctional fear regulation. |
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