Abstract
Impairment of the cerebral error detection mechanism is believed to be one of the causes of obsessive-compulsive disorder (OCD) and the anterior cingulate cortex (ACC) is the key element supporting this mechanism. However, neuroimaging data on the functional activity of the ACC in patients with OCD in the state of operational rest* and during activity are extremely diverse. An earlier explanation of this fact was the hypothesis that changes in ACC activity depend on the nature of the OCD present. With the aim of testing this hypothesis experimentally, the present studies performed combined PET-fMRI studies of the functional activity of the ACC in patients with OCD in the state of operational rest and on performance of activity presumptively involving the error detection mechanism. This activity was modeled using a Go/NoGo test with two tasks with different levels of difficulty. The ACC in patients in the state of operational rest showed glucose hypermetabolism, which decreased with increases in disease duration. The functional activity of the ACC during performance of actions was decreased in patients with OCD as compared with a group of healthy subjects. In addition, ACC activity on performance of the simpler task was found to increase with the course of illness; conversely, performance of the more difficult task decreased activity. Thus, the data obtained here support the hypothesis. Glucose hypermetabolism in the state of operational rest at the initial stages of illness was replaced by hypometabolism, probably because the ACC stopped carrying out its normal functions, which were compensated for by redistribution of the function among other relatively intact structures. This may lead to distortion of the functional specialization of the ACC, where the functional activity of the ACC in conditions of enhanced cognitive load decreased with increases in the duration of illness, while activity increased in conditions of relatively simple cognitive loading.
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