Differences in brain glucose metabolism between responders to CBT and venlafaxine in a 16-week randomized controlled trial.
OBJECTIVE
Neuroimaging investigations reveal changes in glucose metabolism (fluorine-18-fluorodeoxyglucose positron emission tomography [PET]) associated with response to disparate antidepressant treatment modalities, including cognitive behavior therapy (CBT), antidepressant pharmacotherapies, and deep brain stimulation. Using a nonrandomized design, the authors previously compared changes following CBT or paroxetine in depressed patients. In this study, the authors report changes in fluorine-18-fluorodeoxyglucose PET in responders to CBT or venlafaxine during a randomized controlled trial.


METHODS
Subjects meeting DSM-IV-TR criteria for a major depressive episode and a diagnosis of a major depressive disorder received a fluorine-18-fluorodeoxyglucose PET scan before randomization and after 16 weeks of antidepressant treatment with either CBT (N=12) or venlafaxine (N=12). Modality-specific and modality-independent regional brain metabolic changes associated with response status were analyzed.


RESULTS
Response rates were comparable between the CBT (7/12) and venlafaxine (9/12) groups. Response to either treatment modality was associated with decreased glucose metabolism bilaterally in the orbitofrontal cortex and left medial prefrontal cortex, along with increased metabolism in the right occipital-temporal cortex. Changes in metabolism in the anterior and posterior parts of the subgenual cingulate cortex and the caudate differentiated CBT and venlafaxine responders.


CONCLUSIONS
Responders to either treatment modality demonstrated reduced metabolism in several prefrontal regions. Consistent with earlier reports, response to CBT was associated with a reciprocal modulation of cortical-limbic connectivity, while venlafaxine engaged additional cortical and striatal regions previously unreported in neuroimaging investigations.
Kennedy
Sidney H
SH
University Health Network, Institute of Medical Science, University of Toronto, Department of Psychiatry, and Toronto General Hospital, 200 Elizabeth St., Eaton North Wing 8-222, Toronto, Ontario M5G 2C4, Canada. sidney.kennedy@uhn.on.ca
Konarski
Jakub Z
JZ
Segal
Zindel V
ZV
Lau
Mark A
MA
Bieling
Peter J
PJ
McIntyre
Roger S
RS
Mayberg
Helen S
HS
D000328:Adult; D001921:Brain / Q000000981:diagnostic imaging / Q000187:drug effects / Q000378:metabolism*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D015928:Cognitive Behavioral Therapy; D003131:Combined Modality Therapy; D003511:Cyclohexanols / Q000493:pharmacokinetics / Q000627:therapeutic use*; D003865:Major Depressive Disorder / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism; D007839:Functional Laterality / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008032:Limbic System / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D017367:Selective Serotonin Reuptake Inhibitors / Q000493:pharmacokinetics / Q000627:therapeutic use*; D016896:Treatment Outcome; D000069470:Venlafaxine Hydrochloride
D003511:Cyclohexanols; D019788:Fluorodeoxyglucose F18; D005947:Glucose; D017367:Selective Serotonin Reuptake Inhibitors; D000069470:Venlafaxine Hydrochloride