In this brief review of two of the neurobiologic aspects of OCD, two simplistic models have been suggested. Although these models reflect different perspectives, they may not be independent. For instance, the striatum, which is a focus for the neuroanatomic model, receives a dense serotonergic projection from the dorsal raphé. Similarly, as mentioned previously, combining PET studies and drug treatment demonstrates that the increased metabolic activity seen in the orbital cortex appears to normalize with serotonin uptake inhibitor treatment. Insights into the neurobiology of this syndrome will require combining perspectives as well as developing additional approaches. In addition, the search for neurobiologic abnormalities must be guided by a continuing regard for phenomenology. There is no reason, a priori, to assume that this syndrome subsumes only one disorder. The careful dissection of subgroups--whether based on symptom type, character style, or comorbid diagnoses--will be increasingly vital for understanding the results of neuropharmacologic and functional imaging studies.