期刊
PSYCHOTHERAPY AND PSYCHOSOMATICS
卷 83, 期 5, 页码 298-307出版社
KARGER
DOI: 10.1159/000361078
关键词
Cognitive-behavioral therapy; Antidepressant; Selective serotonin reuptake inhibitor; gamma-Aminobutyric acid; Glutamine; Glutamate
资金
- Patrick and Catherine Weldon Donaghue Medical Research Foundation
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Mental Health [R01 MH071676-05, K02 MH076222-04, R21 AA018210, R01 DA021785]
- The State of Connecticut Department of Mental Health and Addiction Services (through Connecticut Mental Health Center and Clinical Neuroscience Research Unit)
- Veterans Affairs (VA) National Center for PTSD
- VA Alcohol Research Center
- NIMH [T32 MH19961]
- NIDA [T32-DA022975]
- National Center for Advancing Translational Science (NCATS), components of the National Institutes of Health (NIH) [UL1 TR000142]
- NIH roadmap for Medical Research
Background: Previous studies have demonstrated that antidepressant medication and electroconvulsive therapy increase occipital cortical gamma-anninobutyric acid (GABA) in major depressive disorder (MDD), but a small pilot study failed to show a similar effect of cognitive-behavioral therapy (CBT) on occipital GABA. In light of these findings we sought to determine if baseline GABA levels predict treatment response and to broaden the analysis to other metabolites and neurotransmitters in this larger study. Methods:A total of 40 MDD outpatients received baseline proton magnetic resonance spectroscopy (H-1-MRS), and 30 subjects completed both pre- and post-CBT H-1-MRS; 9 CBT nonresponders completed an open-label medication phase followed by an additional/3rd H-1-MRS. The magnitude of treatment response was correlated with occipital amino acid neurotransmitter levels. Results: Baseline GABA did not predict treatment outcome. Furthermore, there was no significant effect of CBT on GABA levels. However, we found a significant group x time interaction (F-1,(28) = 6.30, p = 0.02), demonstrating reduced glutamate in CBT responders, with no significant glutamate change in CBT nonresponders. Conclusions: These findings corroborate the lack of effect of successful CBT on occipital cortical GABA levels in a larger sample. A reduction in glutamate levels following treatment, on the other hand, correlated with successful CBT and antidepressant medication response. Based on this finding and other reports, decreased occipital glutamate may be an antidepressant response biomarker. Healthy control comparator and nonintervention groups may shed light on the sensitivity and specificity of these results. (C) 2014 S. Karger AG, Basel
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