Corpus callosal signal intensity in treatment-naive pediatric obsessive compulsive disorders

1. Obsessive compulsive disorder (OCD) is increasingly recognized as a seve re, highly prevalent and chronically disabling disorder, emerging during ch ildhood in as many as 80% of cases. The authors previously found significan t abnormalities in the region of the corpus callosum (CC) connecting ventra l prefrontal cortex and striatum in pediatric OCD patients compared to cont rols that correlated significantly with OCD symptom severity. We speculated that this abnormality might reflect aberrant myelinization in OCD patients . 2. In order to better characterize the abnormality, the authors examined CC signal intensity (SI), believed to be a reliable index of myelinization of the CC. Lower numbers would indicate a greater concentration of white matt er, while higher numbers indicate higher concentrations of gray matter. We compared the SI from midsagittal magnetic resonance images of 21 treatment- naive OCD patients, 7.2-17.7 years, and 21 case-matched healthy controls to examine regional CC signal intensity of the anterior, middle and posterior genu, body, isthmus, and the anterior, middle and the posterior splenii. 3. Mean total genu SI for the patient group (.993+.006) was significantly l ess than the total genu SI of controls (.994+.006) at F(1,37)= 4.73; p =.03 6. This abnormality in SI was localized to the CC region connecting ventral PFC and striatum, the anterior genu for the OCD group (.991+.007) which wa s also less than control (.995+.007) at F(1,37)= 5.47; p =.025., with no ab normality observed in middle or posterior genu regions. Genu SI was also in versely correlated with OCD symptom severity (r = .55, p =.013) but not ill ness duration. Genu SI also correlated positively with genu area (r =.52, p =.020) in OCD patients but not controls. 4. Developmental abnormalities in genu size may arise from abnormalities in myelination in early onset OCD patients. The increased genu myelination ob served in OCD patients may alter signal transduction and function of VPFC-s triatal association circuits.