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Journal of Neural Transmission

, Volume 125, Issue 10, pp 1433–1447 | Cite as

Longitudinal brain volume changes in major depressive disorder

  • Dilara Yüksel
  • Jennifer Engelen
  • Verena Schuster
  • Bruno Dietsche
  • Carsten Konrad
  • Andreas Jansen
  • Udo Dannlowski
  • Tilo Kircher
  • Axel Krug
Translational Neurosciences - Original Article

Abstract

Patients with major depressive disorder (MDD) exhibit gray matter volume (GMV) reductions in limbic regions. Clinical variables—such as the number of depressive episodes—seem to affect volume alterations. It is unclear whether the observed cross-sectional GMV abnormalities in MDD change over time, and whether there is a longitudinal relationship between GMV changes and the course of disorder. We investigated T1 structural MRI images of 54 healthy control (HC) and 37 MDD patients in a 3-Tesla-MRI with a follow-up interval of 3 years. The Cat12 toolbox was used to analyze longitudinal data (p < 0.05, FWE-corrected, whole-brain analysis; flexible factorial design). Interaction effects indicated increasing GMV in MDD in the bilateral amygdala, and decreasing GMV in the right thalamus between T1 and T2. Further analyses comparing patients with a mild course of disorder (MCD; 0–1 depressive episode during the follow-up) to patients with a severe course of disorder (SCD; > 1 depressive episode during the follow-up) revealed increasing amygdalar volume in MCD. Our study confirms structural alterations in limbic regions in MDD patients and an association between these impairments and the course of disorder. Thus, we assume that the reported volumetric alterations in the left amygdala (i.e. volumetric normalization) are reversible and apparently driven by the clinical phenotype. Hence, these results support the assumption that the severity and progression of disease influences amygdalar GMV changes in MDD or vice versa.

Keywords

Gray matter volume Major depressive disorder Amygdala Thalamus Number of depressive episodes Gray matter volume normalization 

Notes

Acknowledgements

This work was supported by Grants from the German Research Foundation (DFG, Grant no. KR 3822/2-1 to AK, DFG, Grant FOR2107 DA1151/5-1 and DA1151/5-2 to UD; SFB-TRR58, Projects C09 and Z02 to UD, the Interdisciplinary Center for Clinical Research (IZKF) of the medical faculty of Münster (Grant Dan3/012/17 to UD), FOR 2107, Grant no. KI 588/14-1, a Grant by the University Medical Center Giessen and Marburg (UKGM, Grant no. 11/2010 MR) and the Von-Behring-Röntgen-Foundation (Grant no. 61-0030).

Compliance with ethical standards

Conflict of interest

All authors report no conflict of interest.

Disclosure

Carsten Konrad received fees for an educational program from Aristo Pharma, Janssen-Cilag, Lilly, MagVenture, Servier, and Trommsdorff as well as travel support and speakers honoraria from Aristo Pharma, Janssen-Cilag, Lundbeck, and Servier.

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Copyright information

© Springer-Verlag GmbH Austria, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of Psychiatry and PsychotherapyPhilipps-University MarburgMarburgGermany
  2. 2.Agaplesion Diakonieklinikum RotenburgCentre for Psychosocial MedicineRotenburg (Wümme)Germany
  3. 3.Department of PsychiatryUniversity of MünsterMünsterGermany

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