BACKGROUND: Previous studies suggest that obsessive-compulsive disorder (OCD) is associated with moderate cognitive deficits. There is also evidence for altered serotonergic transmission in OCD. The aim of this study was to evaluate the impact of rapid plasma tryptophan depletion on cognitive functioning in OCD. METHODS: A double-blind crossover study was conducted to explore the effects of tryptophan depletion on cognitive functioning, obsessive or compulsive (OC) symptoms and mood in OCD patients treated withselective serotonin reuptake inhibitors. RESULTS: After 5 h of tryptophan depletion, 6 out of 7 patients reported worsening of mood (placebo condition: 3 patients). No effect was found regarding OC symptoms. There was a small and nonsignificant improvement of nonverbal memory and fluency. Problem solving ability and verbal memory, in contrast, were slightly impaired after tryptophan depletion. The results, however, represented only tendencies without reaching significance. CONCLUSION: The results suggest that OC symptoms may not depend on the short-time availability of serotonin. As some critical cognitive functions improved following tryptophan depletion, there is no evidence from our study that neuropsychological impairment in OCD can be reduced to a lowered level of serotonin. Future studies are needed to further clarify these findings by use of larger samples. 2008 S. Karger AG, Basel
RCT Entities:
BACKGROUND: Previous studies suggest that obsessive-compulsive disorder (OCD) is associated with moderate cognitive deficits. There is also evidence for altered serotonergic transmission in OCD. The aim of this study was to evaluate the impact of rapid plasma tryptophan depletion on cognitive functioning in OCD. METHODS: A double-blind crossover study was conducted to explore the effects of tryptophan depletion on cognitive functioning, obsessive or compulsive (OC) symptoms and mood in OCDpatients treated with selective serotonin reuptake inhibitors. RESULTS: After 5 h of tryptophan depletion, 6 out of 7 patients reported worsening of mood (placebo condition: 3 patients). No effect was found regarding OC symptoms. There was a small and nonsignificant improvement of nonverbal memory and fluency. Problem solving ability and verbal memory, in contrast, were slightly impaired after tryptophan depletion. The results, however, represented only tendencies without reaching significance. CONCLUSION: The results suggest that OC symptoms may not depend on the short-time availability of serotonin. As some critical cognitive functions improved following tryptophan depletion, there is no evidence from our study that neuropsychological impairment in OCD can be reduced to a lowered level of serotonin. Future studies are needed to further clarify these findings by use of larger samples. 2008 S. Karger AG, Basel
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