J Psychiatry Neurosci 2012;37(3):154-69
Andrée M. Cusi, BSc; Anthony Nazarov, BSc; Katherine Holshausen, BSc; Glenda M. MacQueen, MD, PhD; Margaret C. McKinnon, PhD
Cusi, Nazarov, McKinnon — Department of Psychiatry and Behavioural Neurosciences, McMaster University; Cusi, Nazarov, McKinnon — Mood Disorders Program, St. Joseph’s Healthcare Hamilton, Hamilton, Ont.; Holshausen — Department of Psychology, Queen’s University, Kingston, Ont.; MacQueen — Department of Psychiatry, University of Calgary, Calgary, Alta.; McKinnon — Kunin-Lunenfeld Applied and Evaluative Research Unit, Baycrest, Toronto, Ont.
Background: This review integrates neuroimaging studies of 2 domains of social cognition — emotion comprehension and theory of mind (ToM) — in patients with major depressive disorder and bipolar disorder. The influence of key clinical and method variables on patterns of neural activation during social cognitive processing is also examined.
Methods: Studies were identified using PsycINFO and PubMed (January 1967 to May 2011). The search terms were “fMRI,” “emotion comprehension,” “emotion perception,” “affect comprehension,” “affect perception,” “facial expression,” “prosody,” “theory of mind,” “mentalizing” and “empathy” in combination with “major depressive disorder,” “bipolar disorder,” “major depression,” “unipolar depression,” “clinical depression” and “mania.”
Results: Taken together, neuroimaging studies of social cognition in patients with mood disorders reveal enhanced activation in limbic and emotion-related structures and attenuated activity within frontal regions associated with emotion regulation and higher cognitive functions. These results reveal an overall lack of inhibition by higher-order cognitive structures on limbic and emotion-related structures during social cognitive processing in patients with mood disorders. Critically, key variables, including illness burden, symptom severity, comorbidity, medication status and cognitive load may moderate this pattern of neural activation.
Limitations: Studies that did not include control tasks or a comparator group were included in this review.
Conclusion: Further work is needed to examine the contribution of key moderator variables and to further elucidate the neural networks underlying altered social cognition in patients with mood disorders. The neural networks under lying higher-order social cognitive processes, including empathy, remain unexplored in patients with mood disorders.
Submitted Dec. 15, 2010; Revised July 2, Sept. 2, 2011; Accepted Sept. 8, 2011.
Acknowledgements: This article was supported by an Ontario Mental Health Foundation (OMHF) studentship to A.M. Cusi and grants from the Canadian Institutes of Health Research, OMHF and National Alliance for Research on Schizophrenia and Depression to M.C. McKinnon.
Competing interests: None declared for A.M. Cusi, A. Nazarov, K. Holshausen and M.C. McKinnon. G.M. MacQueen declares that her institute has received grant support from AstraZeneca and that she has received speaker fees from AstraZeneca, BMS, Janssen, Lilly and Pfizer and payment for development of educational presentations from the Canadian Psychiatric Association.
Contributors: G.M. MacQueen and M.C. McKinnon designed the review. A.M. Cusi, A. Nazarov, K. Holshausen and M.C. McKinnon acquired the data. A.M. Cusi and M.C. McKinnon analyzed the data. A.M. Cusi, A. Nazarov, K. Holshausen and M.C. McKinnon wrote the article. A.M. Cusi, G.M. MacQueen and M.C. McKinnon reviewed the article. All authors approved its publication.
Correspondence to: M.C. McKinnon, Mood Disorders Program, St. Joseph’s Healthcare, 100 West 5th St., Box 585, Hamilton ON L8N 3K7; email@example.com