ORIGINAL ARTICLES Cerebral Metabolic Correlates as Potential Predictors of Response to Anterior Cingulotomy for Obsessive Compulsive Disorder Scott L. Rauch, Darin D. Dougherty, G. Rees Cosgrove, Edwin H. Cassem, Nathaniel M. Alpert, Bruce H. Price, Andrew A. Nierenberg, Helen S. Mayberg, Lee Baer, Michael A. Jenike, and Alan J. Fischman Background: As interventions for severe, treatment-re- fractory obsessive compulsive disorder (OCD), neurosur- gical procedures are associated with only modest efficacy. The purpose of this study was to identify cerebral meta- bolic correlates as potential predictors of treatment re- sponse to anterior cingulotomy for OCD. Methods: Clinical data were analyzed in the context of a retrospective design. Subjects were 11 patients who un- derwent stereotactic anterior cingulotomy for OCD. Symptom severity was measured using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) before and at approximately 6 months postoperative. Preoperative F-18-fluorodeoxyglucose-positron emission tomography (FDG-PET) data were available. Statistical parametric mapping methods were used to identify loci of significant correlation between preoperative regional cerebral me- tabolism and postoperative reduction in Y-BOCS scores. Results: One locus within right posterior cingulate cortex was identified, where preoperative metabolism was signif- icantly correlated with improvement in OCD symptom severity following cingulotomy. Specifically, higher pre- operative rates of metabolism at that locus were associ- ated with better postoperative outcome. Conclusions: A possible predictor of treatment response was identified for patients with OCD undergoing anterior cingulotomy. Further research, utilizing a prospective design, is indicated to determine the validity and reliabil- ity of this finding. If confirmed, an index for noninvasively predicting response to cingulotomy for OCD would be of great value. Biol Psychiatry 2001;50:659 – 667 © 2001 Society of Biological Psychiatry Key Words: Neurosurgery, positron emission tomogra- phy, posterior cingulate cortex, anxiety, neuroimaging, treatment Introduction N euroimaging research has been influential in shaping contemporary models of obsessive compulsive disor- der (OCD) (Rauch 2000; Rauch and Baxter 1998; Saxena et al 1998). Convergent findings have implicated a net- work of brain regions, including orbitofrontal cortex, anterior cingulate cortex, and the striatum, in the patho- physiology of OCD. These areas exhibit hyperactivity at rest that is accentuated during symptom provocation and attenuated following successful psychiatric treatment. Beyond constructing neurobiologic models of disease, one potential clinical application entails the use of neuro- imaging to identify predictors of treatment response. Three prospective studies of OCD patients have already found that pretreatment positron emission tomography (PET) measurements of cerebral metabolic rates within orbito- frontal cortex significantly predict subsequent response to pharmacotherapy with serotonergic reuptake inhibitors (SRIs) (Brody et al 1998; Saxena et al 1999; Swedo et al 1992). Specifically, lower pretreatment rates of orbitofron- tal metabolism have consistently been associated with better subsequent responses to SRIs. Conversely, in one of these reports (Brody et al 1998), higher cerebral metabolic rates within left orbitofrontal cortex were associated with better responses to behavioral therapy. These findings underscore the potential for neuroimaging data to guide treatment decisions in psychiatric practice. In general, most patients with OCD can be managed with a combination of behavioral therapy and/or pharma- cological treatment. Patients with very severe forms of OCD who fail to respond to an exhaustive array of conventional therapies and remain disabled are sometimes considered for surgical intervention; however, neurosurgi- cal treatment for OCD is an invasive procedure with only From the Departments of Psychiatry (SLR, DDD, EHC, AAN, LB, MAJ), Radiology (SLR, DDD, NMA, AJF), Neurosurgery (GRC), and Neurology (BHP), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Department of Neurology (BHP), McLean Hospital, Belmont, Massachusetts; Departments of Psychiatry & Neurology (HSM), Rotman Research Institute, University of Toronto, Ontario. Address reprint requests to Dr. S.L. Rauch, Massachusetts General Hospital-East, Department of Psychiatry, 13 th Street, Building 149, Room 9130, Charlestown, MA 02129. Received October 26, 2000; revised April 17, 2001; accepted April 25, 2001. © 2001 Society of Biological Psychiatry 0006-3223/01/$20.00 PII S0006-3223(01)01188-X