Le trouble obsessionnel compulsif (TOC) est une affection fréquente touchant 2 à 3 % de la population générale. Il s’agit d’un trouble anxieux invalidant d’évolution le plus souvent chronique. Les obsessions sont définies par l’irruption intrusive et incessante dans la pensée d’une idée qui entraîne une anxiété importante. Les compulsions sont des comportements, répétitifs ou ritualisés, visant à neutraliser ou à réduire la charge anxieuse provoquée par l’émergence des pensées obsédantes. L’approche phénoménologique du TOC oriente vers l’altération d’un certain nombre de fonctions, détection des erreurs, processus émotionnels, motivationnels et de récompense. Ceci suggère l’implication des circuits cortico-striato-pallido-thalamo-corticaux dans la physiopathologie de cette affection, et notamment ceux mettant en jeu le cortex orbito-frontal et le cortex cingulaire antérieur dans l’étiopathogénie du TOC, à la lumière de nos connaissances actuelles des relations structure-fonction issues des données de la neurophysiologie expérimentale chez l’animal, complétées par les travaux de neuro-imagerie fonctionnelle chez l’homme. C’est précisément cette démarche physiopathologique interrogeant en permanence ce que l’on sait de la clinique du TOC que nous nous proposons d’adopter dans ce travail de revue.

Obsessive-compulsive disorder (OCD), that affects 2 to 3 % of the general population, is characterized by recurrent intrusive thoughts and repetitive, time-consuming behaviors. It is a severely incapacitating mental illness that causes profound impairment in psychosocial functioning and quality of life. Although the physiopathology of OCD is still far from resolved, the existence of a biological basis for OCD is now clearly established and should be interpreted from phenomenological considerations, on the one hand, and in the light of our increasing knowledge of the physiology of cortico-subcortical functional loops, on the other. In a phenomenological view, the heart of the obsessional process is the subject’s underlying impression that « something is wrong ». In other words, obsessions may be thought of as the permanent perception of a mistake and/or error in certain behavioral situations. Compulsions occur as behavioral responses aimed at relieving the tensions or anxiety generated by the situation. If obtained, this relief may be felt to be a form of reward. Nevertheless, it is only transient, thereby creating a feeling of considerable anxiety. This contributes to immediately reproducing the behavior in a cyclic manner, on the basis of an internal motivational state through an expectation of the reward. Therefore, it can be assumed that several malfunctioning processes are altered within the OCD : 1) error recognition ; and, 2) emotion and motivation. This suggests that there is a dysfunction of the brain regions mediating these cognitive and emotional functions. Experimental neurophysiology in laboratory animals indicates the central role of the fronto-subcortical circuits originating in the orbitofrontal and anterior cingulate cortices, respectively. The orbitofrontal cortex (OFC) and ventromedial areas are involved in appraisal of the emotional and motivational values of environmental information, and in integrating the subject’s prior experience, which is crucial in decision-making. The OFC also contributes to the selection, comparison and judgment of stimuli and error detection. The anterior cingulate cortex (ACC) is comprised of 1) a ventral or affective region that could keep attention on the internal emotional and motivational status and regulation of autonomic responses, and 2) a dorsal and cognitive region that serves a wide range of functions including attention, working memory, error detection, conflict monitoring, response selection, and anticipation of incoming information. Ventral striatum, that is intimately connected to the OFC and ACC, participates in the preparation, initiation and execution of behavioral responses oriented toward reward delivery following the cognitive and emotional integration of behaviorally relevant information at the cortical level. Functional imaging research in humans has shown an increased functional activity in the OFC, ACC, head of the caudate nucleus and thalamus in OCD patients. These functional abnormalities have been found in basal conditions and during provocation tests. Moreover, the therapeutic efficacy of antidepressants with preponderant serotonin-reuptake inhibiting properties and cognitive-behavioral therapies seems to be associated with a progressive reduction in activity of the OFC, ACC and the caudate nucleus. Therefore, these observations are suggestive of the responsibility of 5HT neurotransmission in the dysfunction of the frontal-subcortical loops that emanate from the OFC and ACC. However, several lines of research suggest that the dopamine system, with which 5HT interacts, may play a major role in the expression of OC symptoms. In conclusion, it seems that in OCD there is a dysfunction of the brain regions that belong to the orbitofrontal and anterior cingulate loops in view of evidence obtained from separate and complementary approaches.