The parietal cortex was implicated in both adult and pediatric OCD. These results support the hypothesis that the pathophysiology of OCD cannot be solely explained by alterations of the classical CSTC regions and emphasize the importance of parietal regions. Widespread cortical thickness abnormalities were found in medicated adult OCD patients, while more pronounced surface area deficits were found in medicated pediatric OCD patients. Cortical thickness and surface area represent distinct features of the cortex and may be differentially affected by OCD and possibly moderated by medication status. Further work, using longitudinal designs, and incorporating genetic and environmental variables, will be useful in understanding the precise mechanisms underlying the structural abnormalities preceding the onset of the illness and occurring during the course of the illness.
