Several models seek to explain the psychobiology of obsessive-compulsive disorder (OCD). While none fully explains brain mechanisms responsible for the psychopathology of OCD, such models, based on clinical and experimental studies, elucidate further direction. This article reviews evidence from clinical observations and from electrophysiological and imaging studies on which the models were based A variety of neurological diseases that involve the fronto-striatal and limbic/paralimbic systems are associated with obsessive and compulsive symptoms. Electrophysiological and imaging studies in OCD patients free from demonstrable neurological lesions, strongly suggest that these regions are involved in the pathobiology of obsessive-compulsive disorder. The most consistent findings in imaging studies were increased metabolism and blood flow in orbito-frontal regions at rest and, in addition, regional changes in the striatum and in limbic/paralimbic regions during symptom provocation. Imaging studies indicate predominant prefrontal hyperactivity, particularly on the right. Neuroimaging, electrophysiological and neuropsychological studies suggest that both hemispheres may contribute, perhaps to different degrees, to the pathophysiology of OCD. Since OCD ir a heterogeneous disorder, it if likely that regionally specific pathology in the disorder will be variable.
