J Psychiatry Neurosci 2013; 39(2):127-34
Erlend Bøen, MD; Lars T. Westlye, PhD*; Torbjørn Elvsåshagen, MD*; Benjamin Hummelen, MD, PhD; Per K. Hol, MD, PhD; Birgitte Boye, MD, PhD; Stein Andersson, PhD; Sigmund Karterud, MD, PhD; Ulrik F. Malt, MD, PhD
Bøen, Elvsåshagen, Boye, Andersson, Malt — Department of Psychosomatic Medicine, Oslo University Hospital, Oslo; Bøen, Malt — Norwegian Research Network On Mood Disorders, Oslo; Bøen, Elvsåshagen, Karterud, Malt — Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, Oslo; Westlye — K.G. Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital, Oslo; Westlye, Andersson — Department of Psychology, University of Oslo, Oslo; Hummelen, Karterud — Department for Personality Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital, Oslo; Hummelen — Department for Research and Education, Division of Mental Health and Addiction, Oslo University Hospital, Oslo; Hol — The Intervention Centre, Oslo University Hospital, Oslo, Norway
*L.T Westlye and T. Elvsåshagen share second authorship.
Background: Animal and human studies have suggested that hippocampal subfields are differentially vulnerable to stress, but subfield volume has not been investigated in patients with borderline personality disorder (BPD). Based on the putative role of stressful life events as vulnerability factors for BPD, we hypothesized that patients with BPD would exhibit reduced volumes for the stress-sensitive dentate gyrus (DG) and the cornu ammonis (CA) 3 subfields volumes, and that these volumes would be associated with traumatic childhood experiences.
Methods: All participants underwent 3 T magnetic resonance imaging. Hippocampal subfield volumes were estimated using an automated and validated segmentation algorithm implemented in FreeSurfer. Age and total subcortical grey matter volume were covariates. We assessed traumatic childhood experiences using the Childhood Trauma Questionnaire (CTQ).
Results: A total of 18 women with BPD and 21 healthy control women were included in the study. Only 1 patient had comorbid posttraumatic stress disorder (PTSD). The volumes of the left (p = 0.005) and right (p = 0.011) DG-CA4 and left (p = 0.007) and right (p = 0.005) CA2–3 subfields were significantly reduced in patients compared with controls. We also found significant group differences for the left (p = 0.032) and right (p = 0.028) CA1, but not for other hippocampal subfields. No associations were found between CTQ scores and subfield volumes.
Limitations: The self-reported CTQ might be inferior to more comprehensive assessments of traumatic experiences. The sample size was moderate.
Conclusion: The volumes of stress-sensitive hippocampal subfields are reduced in women with BPD without PTSD. However, the degree to which childhood trauma is responsible for these changes is unclear.
Submitted Apr. 19, 2013; Revised July 12, Aug. 23, 2013; Accepted Aug. 30, 2013.
Acknowledgments: We are grateful for the cooperation of all study participants and the assistance of Dr. Yasuhiko Sudo, Dr. Yoichiro Takasaka, and all the staff of Tosa Hospital, Hosogi Unity Hospital and Aki General Hospital. This work was supported by the Kochi Medical School Alumni Association.
Funding: Funding for this study was provided by the South-Eastern Norway Regional Health Authority through the Norwegian Research Network On Mood Disorders, Oslo University Hospital, and Research Council of Norway grant 204966/F20 to L.T. Westlye.
Competing interests: E. Bøen has received honoraria from Lundbeck and AstraZeneca for lecturing to psychiatrists and psychologists about clinical and biological aspects of mood and personality disorders. T. Elvsåshagen has received honoraria for lecturing from Glaxo SmithKline and Pfizer. S. Karterud is on the board of directors and is a shareholder of the Norwegian Institute for Mentalization. U.F. Malt has received honoraria from AstraZeneca, Bristol Myers Squibb, Eli Lilly, Glaxo Smith Kline, Schering-Plough and Lundbeck for lectures about the diagnostic assessment and treatment of mood disorders. None declared by L.T. Westlye, B. Hummelen, P.K. Hol, B. Boye and S. Andersson.
Contributors: E.Bøen, T. Elvsåshagen, P.K. Hol, B. Hummelen, S. Andersson, S. Karterud, and U.F. Malt designed the study. E. Bøen, T. Elvsåshagen, B. Hummelen and B. Boye collected the data, which E. Bøen and L.T. Westlye analyzed. E.Bøen, T. Elvsåshagen and L.T. Westlye wrote the manuscript, which all authors reviewed and approved for publication.
Correspondence to: E. Bøen, Department of Psychosomatic Medicine, Oslo University Hospital, Post Box 4950 Nydalen, 0424 Oslo, Norway; email@example.com