期刊
NEUROPSYCHOPHARMACOLOGY
卷 27, 期 5, 页码 782-791出版社
NATURE PUBLISHING GROUP
DOI: 10.1016/S0893-133X(02)00351-2
关键词
anxiety; orbitofrontal cortex; positron emission tomography; posterior cingulate cortex; serotonergic reuptake inhibitor; neuroimaging
资金
- NIMH NIH HHS [R01MH50275, R01MH60219] Funding Source: Medline
The purpose of this study was to identify neuroimaging predictors of medication response in contamination-rela led obsessive compulsive disorder (OCD). Prior studies of OCD had indicated that glucose metabolic rates within orbitofrontal cortex (OFC) were inversely correlated with subsequent response to serotonergic reuptake inhibitors (SRIs) and that glucose metabolic rates within posterior cingulate cortex (PCC) were positively correlated with subsequent response to cingulotomy. Nine subjects with contamination-related OCD underwent a 12-week open trial of treatment with the SRI fluvoxamine. Percent change in Yale-Brown Obsessive Compulsive Scale score,from pre- to post-treatment, served as the index of treatment response. Positron emission tomography (PET) measurements of regional cerebral blood flow (rCBF) were obtained prior to treatment, in the context Of a symptom provocation paradigm. Statistical parametric mapping was used to identify brain loci where pre-treatment rCBF was significantly correlated with subsequent treatment response. Consistent with a priori hypotheses, lower rCBF values in OFC and higher rCBF values in PCC predicted better treatment response. This same pattern Of associations was present regardless of whether the imaging data were acquired during a provoked or neutral state. These findings are consistent with prior studies of OCD, indicating that PET indices of brain activity within OFC are inversely correlated with subsequent response to SRIs. In addition, similar to findings regarding cingulotomy for OCD, indices of activity within PCC appear to be positively correlated with response to fluvoxamine as well. Finally, this pattern is sufficiently robust as to be relatively independent Of symptomatic state at the time of tracer uptake. (C) 2002 American College of Neuropsychopharmacology. Published by Elsevier Science Inc.
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