New pathophysiological approaches to obsessive-compulsive disorder. Since the beginning of research in the 1980s, it has been consistently shown that obsessive-compulsive disorder (OCD) is neurobiologically underpinned by the dysfunction of a so-called cortico-striato-thalamo-cortical loop (CSTC). Within this loop, various structures have been identified as being affected, foremost among which are the orbitofrontal and anterior cingulate cortices, as well as the caudate nucleus, one of the structures of the striatum. More recently, a large number of studies have contributed to broadening this classical view of the altered CSTC loop by revealing the involvement of broader cerebral networks involving notably the temporal and parietal cortices. These functional and structural alterations are underpinned by an impairment of certain neurotransmission systems. While serotonin was the first to be incriminated due to the efficacy of serotonergic antidepressants, it turns out that years of research in genetics and neuroimaging have invalidated this hypothesis in favour of a new target: glutamate. Our understanding of the pathophysiology of OCD is thus constantly being refined through the combination of increasingly precise neuroanatomical, neurochemical, and genetic data, and will ultimately contribute to the development of new therapies for this disorder.