OBJECTIVE: Obsessive-compulsive disorder (OCD) is characterized by the dysfunction of control and reward mechanisms. However, only few neuroimaging studies of OCD have examined the reward processing. We examined the neural responses during incentive processing in OCD. METHOD: Twenty unmedicated patients with OCD and 20 age-, sex-, and IQ-matched healthy controls underwent functional magnetic resonance imaging while performing a modified monetary incentive delay task. RESULTS: Compared with controls, patients with OCD showed increased ventral striatal activation in the no-loss minus loss outcome contrast and a significant positive correlation between the ventral striatal activation and compulsion symptom severity. In addition, patients with OCD showed increased activations in the frontostriatal regions in the gain minus no-gain outcomes contrast. During loss anticipation, patients with OCD showed less activations in the lateral prefrontal and inferior parietal cortices. However, during gain anticipation, patients with OCD and healthy controls did not differ in the ventral striatal activation. CONCLUSION: These findings provide neural evidence for altered incentive processing in unmedicated patients with OCD, suggesting an elevated sensitivity to negatively affect stimuli as well as dysfunction of the ventral striatum.
OBJECTIVE:Obsessive-compulsive disorder (OCD) is characterized by the dysfunction of control and reward mechanisms. However, only few neuroimaging studies of OCD have examined the reward processing. We examined the neural responses during incentive processing in OCD. METHOD: Twenty unmedicated patients with OCD and 20 age-, sex-, and IQ-matched healthy controls underwent functional magnetic resonance imaging while performing a modified monetary incentive delay task. RESULTS: Compared with controls, patients with OCD showed increased ventral striatal activation in the no-loss minus loss outcome contrast and a significant positive correlation between the ventral striatal activation and compulsion symptom severity. In addition, patients with OCD showed increased activations in the frontostriatal regions in the gain minus no-gain outcomes contrast. During loss anticipation, patients with OCD showed less activations in the lateral prefrontal and inferior parietal cortices. However, during gain anticipation, patients with OCD and healthy controls did not differ in the ventral striatal activation. CONCLUSION: These findings provide neural evidence for altered incentive processing in unmedicated patients with OCD, suggesting an elevated sensitivity to negatively affect stimuli as well as dysfunction of the ventral striatum.
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