J Psychiatry Neurosci 2010; 34(3): 175-180
Jakub Z. Konarski, MSc; Sidney H. Kennedy, MD; Zindel V. Segal, PhD; Mark A. Lau, PhD; Peter J. Bieling, PhD; Roger S. McIntyre, MD; Helen S. Mayberg, MD
Konarski, Kennedy, McIntyre — University Health Network; Konarski, Kennedy — Institute of Medical Science; Kennedy, Segal, Lau, McIntyre, Mayberg — Department of Psychiatry; Segal — Department of Psychology, University of Toronto; Segal, Lau — Centre for Addiction and Mental Health, Toronto; Bieling — St. Joseph’s Healthcare and the Department of Psychiatry, McMaster University, Hamilton, Ont.; Mayberg — Department of Psychiatry and Neurology, Emory University, Atlanta, Ga. and the Rotman Research Institute, Baycrest Centre, Toronto, Ont.
Background: Longitudinal neuroimaging investigations of antidepressant treatment offer the opportunity to identify potential baseline
biomarkers associated with poor outcome.
Methods: To explore the neural correlates of nonresponse to cognitive behavioural therapy (CBT) or venlafaxine (VEN), we compared pretreatment (18)F-fluoro-2-deoxy-D-glucose positron emission tomography scans of participants with major depressive disorder responding to either 16 weeks of CBT (n = 7) or VEN treatment (n = 9) with treatment nonresponders (n = 8).
Results: Nonresponders to CBT or VEN, in contrast to responders, exhibited pretreatment hypermetabolism at the interface of the pregenual and subgenual cingulate cortices.
Limitations: Limitations of our study include the small sample sizes and the absence of both arterial sampling to determine absolute glucose metabolism and high-resolution structural magnetic resonance imaging coregistration for region-of-interest analyses.
Conclusions: Our current findings are consistent with those reported in previous studies of relative hyperactivity in the ventral anterior cingulate cortex in treatment-resistant populations.
Submitted Feb. 28, 2008; Revised Jun. 5, Oct. 14, 2008; Accepted Oct. 15, 2008
Acknowledgements: We thank Doug Hussey, BSc; Alvina Ng, BSc; and Alan A. Wilson, PhD, from the PET Centre, University of Toronto. This study was supported by the Canadian Institutes of Health Research (# 86023 H.S.M., S.H.K., Z.V.S.) and Wyeth Pharmaceuticals (S.H.K., H.S.M., Z.V.S.).
Competing interests: This study was supported by the Canadian Institutes of Health Research and Wyeth Pharmaceuticals. None declared for Mr. Konarski and Drs. Segal, Lau and Bieling. Dr. Kennedy has conducted paid consultancies for Pfizer, Servier and Wyeth; received research support from ANS, AstraZeneca, CIHR, Eli Lilly, GlaxoSmithKline, Lundbeck, NARSAD, OMHF, OPGRS and the Stanley Foundation; and has received speaker fees from ANS, Astra- Zeneca, Biovail, Eli Lilly, Lundbeck, Servier and Wyeth. Dr. McIntyre sits on the advisory boards of AstraZeneca, Bristol-Myers Squibb, France Foundation, GlaxoSmithKline, Janssen-Ortho, Solvay/Wyeth, Eli Lilly, Organon, Lundbeck, Biovail, Pfizer and Shire; he has received speaker fees from Janssen-Ortho, AstraZeneca, Eli Lilly, Lundbeck and Biovail and research support from Eli Lilly. Dr. Mayberg has consulted for Advanced Neuromodulation Systems Inc.
Contributors: Drs. Mayberg, Kennedy and Segal designed the study. Mr. Konarski and Drs. Segal, Lau, Bieling and Mayberg acquired the data. Mr. Konarski and Drs. Kennedy and Mayberg analyzed the data. Mr. Konarski and Drs. Kennedy and McIntyre wrote the paper. Mr. Konarski and Drs. Kennedy, Segal, Lau, Bieling, McIntyre and Mayberg reviewed the article. All authors approved final publication.
Correspondence to: Dr. S.H. Kennedy, University Health Network, Toronto General Hospital, 200 Elizabeth St., Eaton North Wing 8-222, Toronto ON M5G 2C4; fax 416 340-4198; email@example.com