Cortical thickening in remitters compared to non‐remitters with major depressive disorder following 8‐week antidepressant treatment

• Published in: Acta psychiatrica Scandinavica Vol. 140; no. 3; pp. 217 - 226
• Main Authors: Saricicek Aydogan, A., Oztekin, E., Esen, M. E., Dusmez, S., Gelal, F., Besiroğlu, L., Zorlu, N.
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01.09.2019
• Subjects: Antidepressants; brain; Cognition; Cortex (frontal); Cortex (parietal); Cortex (temporal); cortical thickness; depression; Magnetic resonance imaging; Mental depression; Neuroimaging; NMR; Norepinephrine; Nuclear magnetic resonance; remission; Rumination; Serotonin uptake inhibitors; antidepressants; depression; brain; cortical thickness; remission; neuroimaging
• ISSN: 0001-690X; 1600-0447
• DOI: 10.1111/acps.13065

Objective Little is known about the relationship between antidepressant treatment outcomes and underlying neurobiological mechanisms in patients with major depressive disorder (MDD). In this prospective study, we aimed to investigate how cortical thickness and subcortical volumes differed between remitter and non‐remitter patients with MDD. Methods Fifty‐eight patients with MDD with a score of at least 17 on the 17‐item Hamilton Depression Rating Scale and free of medication for at least 2 months and 41 healthy controls underwent structural magnetic resonance imaging. At the baseline, patients with MDD started on either selective serotonin reuptake inhibitors, serotonin‐norepinephrine reuptake inhibitors, or vortioxetine. After 8‐week antidepressant treatment, patients with MDD were scanned using the same MRI protocol. Structural images were analyzed using the FreeSurfer software package (version 6.0). Results Longitudinal analyses showed remitter patients with MDD had significantly greater right cerebral cortex thickening in six significant clusters, including superior temporal cortex, precuneus, rostral middle frontal cortex, pars opercularis (although the cluster extends into the insula), inferior parietal cortex, and supramarginal cortex than in non‐remitter patients with MDD. Conclusion Our results suggest that distinct antidepressant treatment‐related structural alterations in brain regions implicated in cognition, emotion regulation, and rumination might be associated with treatment outcome.