Mike M Schmitgen1, Malte S Depping1, Claudia Bach1, Nadine D Wolf1, Katharina M Kubera1, Nenad Vasic2, Dusan Hirjak3, Fabio Sambataro4, Robert C Wolf5. 1. Department of General Psychiatry, Center for Psychosocial Medicine, Heidelberg University, Vosstrasse 4, 69115 Heidelberg, Germany. 2. Department of Psychiatry and Psychotherapy, Clinical Center Christophsbad, Göppingen, Germany. 3. Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University Mannheim, Germany. 4. Department of Experimental and Clinical Medical Sciences (DISM), University of Udine, Italy. 5. Department of General Psychiatry, Center for Psychosocial Medicine, Heidelberg University, Vosstrasse 4, 69115 Heidelberg, Germany. Electronic address: christian.wolf@med.uni-heidelberg.de.
Abstract
BACKGROUND: There is strong neuroimaging evidence that cortical alterations represent a core pathophysiological feature of major depressive disorder (MDD). Differential contributions of cortical features of neurodevelopmental origin, which may distinctly contribute to MDD vulnerability, disease-onset, or symptom expression, are unclear at present. METHODS: We investigated distinct markers of cortical neurodevelopment, i.e. local cortical gyrification (LGI) and thickness (CT) in patients with MDD (n = 38) and healthy controls (HC, n = 22) using 3 T structural magnetic resonance imaging data and surface-based data analysis techniques. CT and LGI were computed using the Computational Anatomy Toolbox (CAT12). Analyses were performed for the entire cortical surface followed by a complementary regions-of-interest approach. RESULTS: MDD patients showed significantly greater LGI in frontal, cingulate, parietal, temporal, and occipital regions compared to HC (FDR-corrected at p < 0.05 using threshold-free cluster enhancement). No significant differences of CT were found. In the MDD-group, correlations were found between duration of illness in years and number of depressive episodes and LGI of frontal, temporal, and parietal regions (p < 0.05). LIMITATIONS: Main limitations are the relatively modest sample size and a cross-sectional study design. We did not control for early environmental factors potentially influencing neurodevelopment, such as childhood trauma. We report associations uncorrected for multiple comparisons. CONCLUSIONS: The data suggest different local trajectories of cortical change in MDD. In addition, our data support the notion that aberrant cortical development may serve as a vulnerability marker of MDD, as well as a potential predictor of disease course.
BACKGROUND: There is strong neuroimaging evidence that cortical alterations represent a core pathophysiological feature of major depressive disorder (MDD). Differential contributions of cortical features of neurodevelopmental origin, which may distinctly contribute to MDD vulnerability, disease-onset, or symptom expression, are unclear at present. METHODS: We investigated distinct markers of cortical neurodevelopment, i.e. local cortical gyrification (LGI) and thickness (CT) in patients with MDD (n = 38) and healthy controls (HC, n = 22) using 3 T structural magnetic resonance imaging data and surface-based data analysis techniques. CT and LGI were computed using the Computational Anatomy Toolbox (CAT12). Analyses were performed for the entire cortical surface followed by a complementary regions-of-interest approach. RESULTS:MDDpatients showed significantly greater LGI in frontal, cingulate, parietal, temporal, and occipital regions compared to HC (FDR-corrected at p < 0.05 using threshold-free cluster enhancement). No significant differences of CT were found. In the MDD-group, correlations were found between duration of illness in years and number of depressive episodes and LGI of frontal, temporal, and parietal regions (p < 0.05). LIMITATIONS: Main limitations are the relatively modest sample size and a cross-sectional study design. We did not control for early environmental factors potentially influencing neurodevelopment, such as childhood trauma. We report associations uncorrected for multiple comparisons. CONCLUSIONS: The data suggest different local trajectories of cortical change in MDD. In addition, our data support the notion that aberrant cortical development may serve as a vulnerability marker of MDD, as well as a potential predictor of disease course.
Authors: Dusan Hirjak; Katharina M Kubera; Georg Northoff; Stefan Fritze; Alina L Bertolino; Cristina E Topor; Mike M Schmitgen; Robert C Wolf Journal: Schizophr Bull Date: 2019-10-24 Impact factor: 9.306
Authors: Mike M Schmitgen; Katharina M Kubera; Malte S Depping; Henrike M Nolte; Dusan Hirjak; Stefan Hofer; Julia H Hasenkamp; Ulrich Seidl; Bram Stieltjes; Klaus H Maier-Hein; Fabio Sambataro; Alexander Sartorius; Philipp A Thomann; Robert C Wolf Journal: Eur Arch Psychiatry Clin Neurosci Date: 2019-07-05 Impact factor: 5.270
Authors: Jessica P Y Hua; Thomas M Piasecki; Yoanna E McDowell; Cassandra L Boness; Constantine J Trela; Anne M Merrill; Kenneth J Sher; John G Kerns Journal: Drug Alcohol Depend Date: 2020-02-15 Impact factor: 4.492