Obsessive-compulsive disorder (OCD) has been studied extensively in recent years, with increased emphasis on understanding OCD's biological substrates. There has been significant progress in documenting abnormal brain function in OCD patients, particularly in the orbitofrontal cortex, basal ganglia, and thalamus. Similar progress has broadened our understanding of the cognitive and behavioral manifestations of the disorder, including deficits in set shifting, hyperattention, and visuospatial construction abilities. Unfortunately, these results have not been replicated consistently. This report comprises a review of previous attempts to characterize the neurobiology and neuropsychology of OCD, and a discussion of several factors in OCD research that can help to explain previous inconsistencies.Obsessive-compulsive disorder (OCD) is a relatively common form of psychopathology with a lifetime prevalence of2%-3% (Robins et al., 1984). Although the anatomical and behavioral regularities of the disorder have been studied extensively over the past 20 years, there has been relatively little success in the attempt to establish how the former give rise to the latter. Popular models of OCD have drawn upon a variety of disciplines, including learning theory (Mowrer, 1960), cybernetics (Pitman, 1987) and psychoanalysis (Fenichel, 1945). Often, however, these models have had relatively little to say about the dysfunctional aspects of the OCD brain. This is due in part to the fact that, until recently, the neuroanatomical substrates ofOCD were poorly understood. Although OCD researchers had long suspected the involvement of the frontal cortex and basal ganglia in OCD neuropathology, there was little empirical evidence to support such claims. Only through the use ofmodern neuroimaging techniques have many of these suspicions been confirmed.Neurobiological studies ofOCD have produced a wealth of data, but the inability to consistently replicate results has left many questions unanswered. Neuropsychological studies have similarly generated much information, but with equal uncertainty. An adequate theory ofOCD must integrate the findings from each of these two disciplines, but any such integration would be premature at the moment, given the variability present within each. The goal of this review is therefore not to provide an all-encompassing theory ofOCD expression, but rather to delineate several factors that may explain the discrepancies among previous studies of OCD. Consideration of these factors will help clarify the relevant neurobiological and neuropsycho-