Neuropsychological findings in obsessive-compulsive disorder (OCD) have been explained in terms of reduced cognitive shifting ability as a result of low levels of frontal inhibitory activity. This deficit could be reflected in an abnormal P300 component of the event-related potential. The improvement in cognitive processing due to pharmacological treatment would modify the P300 component, bringing it close to that of normal controls. Nineteen patients suffering from OCD and 19 normal controls were recorded. We used a computerized version of the auditory 'odd-ball paradigm' to obtain the P300 component at the Pz electrode. Patients were tested twice, drug-free and under treatment with clomipramine in 250-300 mg doses. We observed the P300 component to have lower amplitude and longer latency in drug-free OCD patients when compared with controls. P300 amplitude in OCD increased after treatment, although this was supported only by a statistical trend. There was no modification in P300 latency after treatment. It is possible that inhibitory activity improves with treatment and allows patients to answer with more confidence, which results in an increase in P300 amplitude. This study suggests that cognitive dysfunction in OCD fluctuates with changes in the clinical associated with treatment, probably in relationship to central serotoninergic transmission.