Localized orbitofrontal and subcortical metabolic changes and predictors of response to paroxetine treatment in obsessive-compulsive disorder

Citation
S. Saxena et al., Localized orbitofrontal and subcortical metabolic changes and predictors of response to paroxetine treatment in obsessive-compulsive disorder, NEUROPSYCH, 21(6), 1999, pp. 683-693
Citations number
56
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROPSYCHOPHARMACOLOGY
ISSN journal
0893133X → ACNP
Volume
21
Issue
6
Year of publication
1999
Pages
683 - 693
Database
ISI
SICI code
0893-133X(199912)21:6<683:LOASMC>2.0.ZU;2-K
Abstract
Previous positron emission tomography (PET) studies of patients with obsess ive-compulsive disorder (OCD) have found elevated glucose metabolic rates i n the orbitofrontal cortex (OFC) and caudate nuclei that normalize with res ponse to treatment. Furthermore, OCD symptom provocation differentially act ivates specific subregions of the OFC, which have distinct patterns of conn ectivity and serve different functions. Therefore, we sought to determine t he role of specific subregions of the OFC and associated subcortical struct ures in mediating OCD symptoms, by determining how glucose metabolism in th ese structures changes with paroxetine treatment of OCD patients. We also s ought to determine whether pretreatment OFC metabolism would predict respon se to paroxetine, as it has for other OCD treatments. Twenty subjects wit O CD received [F-18]-fluorodeoxyglucose (FDG)-PET scans before and after 8 to 12 weeks of treatment with paroxetine, 40 mg/day. In patients who responde d to paroxetine, glucose metabolism decreased significantly in right antero lateral OFC and right caudate nucleus. Lower pretreatment metabolism in bot h left and right OFC predicted greater improvement in OCD severity wit trea tment. These results add to evidence indicating that orbitofrontal-subcorti cal circuit function mediates the symptomatic expression of OCD. Specific s ubregions of the OFC may by differentially involved in the pathophysiology of OCD and/or its response to pharmacotherapy. [Neuropsychopharmacology 21: 683-693, 1999] (C) 1999 American College of Neuropsychopharmacology. Publis hed by Elsevier Science Inc.