Viljami Salmela, PhD; Lumikukka Socada, MD; John Söderholm, MD; Roope Heikkilä, MA; Jari Lahti, PhD; Jesper Ekelund, MD, PhD; Erkki Isometsä, MD, PhD
Background: Previous studies have suggested that processing of visual contrast information could be altered in major depressive disorder. To clarify the changes at different levels of the visual hierarchy, we behaviourally measured contrast perception in 2 centre-surround conditions, assessing retinal and cortical processing.
Methods: As part of a prospective cohort study, our sample consisted of controls (n = 29; 21 female) and patients with unipolar depression, bipolar disorder and borderline personality disorder who had baseline major depressive episodes (n = 111; 74 female). In a brightness induction test that assessed retinal processing, participants compared the perceived luminance of uniform patches (presented on a computer screen) as the luminance of the backgrounds was varied. In a contrast suppression test that assessed cortical processing, participants compared the perceived contrast of gratings, which were presented with collinearly or orthogonally oriented backgrounds.
Results: Brightness induction was similar for patients with major depressive episodes and controls (p = 0.60, d = 0.115, Bayes factor = 3.9), but contrast suppression was significantly lower for patients than for controls (p < 0.006, d = 0.663, Bayes factor = 35.2). We observed no statistically significant associations between contrast suppression and age, sex, or medication or diagnostic subgroup. At follow-up (n = 74), we observed some normalization of contrast perception.
Limitations: We assessed contrast perception using behavioural tests instead of electrophysiology.
Conclusion: The reduced contrast suppression we observed may have been caused by decreased retinal feedforward or cortical feedback signals. Because we observed intact brightness induction, our results suggest normal retinal but altered cortical processing of visual contrast during a major depressive episode. This alteration is likely to be present in multiple types of depression and to partially normalize upon remission.
Submitted May 14, 2020; Revised Aug. 13, 2020; Accepted Sept. 12, 2020.
Acknowledgments: This study was supported by research grants from the City of Helsinki, the Helsinki and Uusimaa Hospital District, and the Finnish Psychiatric Association.
Affiliations: From the Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland (Salmela, Lahti); and the Department of Psychiatry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland (Socada, Söderholm, Heikkilä, Ekelund, Isometsä).
Competing interests: None declared.
Contributors: V. Salmela, L. Socada, J. Söderholm, J. Ekelund and E. Isometsä designed the study. L. Socada, J. Söderholm and E. Isometsä acquired the data, which V. Salmela, L. Socada, J. Söderholm, R. Heikkilä, J. Lahti and E. Isometsä analyzed. V. Salmela, J. Söderholm, J. Lahti and E. Isometsä wrote the article, which all authors reviewed. All authors approved the final version to be published and can certify that no other individuals not listed as authors have made substantial contributions to the paper.
Content licence: This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY-NC-ND 4.0) licence, which permits use, distribution and reproduction in any medium, provided that the original publication is properly cited, the use is non-commercial (i.e. research or educational use), and no modifications or adaptations are made. See: https://creativecommons.org/licenses/by-nc-nd/4.0/
Correspondence to: V. Salmela, Department of Psychology and Logopedics, Faculty of Medicine, P.O. Box 21 (Haartmaninkatu 3), FI-00014 University of Helsinki, Finland; email@example.com