Thalamic Volume in Pediatric Obsessive–Compulsive Disorder Patients before and after Cognitive Behavioral Therapy David R. Rosenberg, Nili R. Benazon, Andrew Gilbert, April Sullivan, and Gregory J. Moore Background: Neurobiologic abnormalities in the thala- mus have been implicated in the pathophysiology of obsessive– compulsive disorder. We recently reported in- creased thalamic volume in treatment-naive pediatric obsessive– compulsive disorder patients versus case- matched healthy comparison subjects that decreased to levels comparable to control subjects after effective par- oxetine therapy. To our knowledge, no prior study has measured neuroanatomic changes in the thalamus of obsessive– compulsive disorder patients near illness onset before and after cognitive behavioral therapy. Methods: Volumetric magnetic resonance imaging stud- ies were conducted in 11 psychotropic drug-naive 8 –17- year-old children with obsessive– compulsive disorder be- fore and after 12 weeks of effective cognitive behavioral therapy monotherapy (30% reduction in obsessive– compulsive disorder symptom severity). Results: No significant change in thalamic volume was observed in obsessive– compulsive disorder patients be- fore and after cognitive behavioral therapy. Conclusions: Our findings suggest that reduction in thalamic volume after paroxetine therapy may be specific to paroxetine treatment and not the result of a general treatment response or spontaneous improvement. These results are preliminary in view of the small sample studied. Biol Psychiatry 2000;48:294 –300 © 2000 So- ciety of Biological Psychiatry Key Words: Obsessive– compulsive disorder, pediatric, thalamus, magnetic resonance imaging, cognitive behav- ioral therapy Introduction O bsessive– compulsive disorder (OCD) is a severe, prevalent (Flament et al 1988; Hanna 1995; Valleni- Basile et al 1994), and often chronically disabling illness with onset in childhood or adolescence in up to 80% of all cases (Pauls et al 1995). Investigation of early-onset OCD is therefore critical, as it can minimize potential confounds of illness duration and treatment intervention (Chakos et al 1994; Keshavan et al 1994). The thalamus is a site of integration and relay and is thought to be involved in the pathophysiology of OCD (Baxter 1992; Insel 1992; Modell et al 1989). Partial thalamotomy, for example, can reduce symptom severity in treatment-refractory OCD patients (Chiocca and Mar- tuza 1990). Metabolic abnormalities in the thalamus of adult OCD patients associated with symptom severity and response to treatment (Baxter 1992; Cottraux et al 1996; Lucey et al 1995; McGuire et al 1994; Perani et al 1995; Rauch et al 1994) provide more direct evidence for involvement of the thalamus in OCD. More recently, Gilbert et al (2000) reported increased thalamic volume in 21 treatment-naive pediatric OCD patients versus 21 case-matched healthy comparison subjects. Pharmacologic treatment studies have repeatedly dem- onstrated the effectiveness of the selective serotonin re- uptake inhibitors (SSRIs) in treating OCD (Grados et al 1999) and have spawned the “serotonin hypothesis” of OCD. Baxter et al (1996) have hypothesized that the preferential response of OCD patients to SSRIs may be a result of thalamocortical alterations in serotonergic neuro- transmission, as the thalamus has a particularly dense serotonergic innervation (Chugani et al 1998; Oke et al 1997). Serotonin has been shown to play a critical role in modulating thalamocortical function (Bennett-Clarke et al 1995, 1996; Chubakov et al 1986; Lebrand et al 1996; Rhoades et al 1994; Salt and Eaton 1996). In adult OCD patients, reduction in metabolic activity has been observed after SSRI treatment (Baxter 1992). Using volumetric magnetic resonance imaging (MRI), Gilbert et al (2000) From the Departments of Psychiatry & Behavioral Neurosciences (DRR, NRB, AS, GJM), Pediatrics (DRR), and Radiology (GJM), Wayne State University School of Medicine, Detroit, Michigan, and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania (AG). Address reprint requests to David R Rosenberg, M.D., Wayne State University School of Medicine, University Health Center, 9B-21, 4201 St. Antoine Boulevard, Detroit MI 48201. Received January 8, 2000; revised March 20, 2000; accepted April 1, 2000. © 2000 Society of Biological Psychiatry 0006-3223/00/$20.00 PII S0006-3223(00)00902-1