mid-central source (245-ms peak latency) that was unique to novel stimuli and was markedly reduced in depressed patients when compared to healthy controls. Again, group differences were less evident for later sources corresponding to P3b. This supports the hypothesis that the novelty P3 reduction in depression is indicative of a deficit in early shifting of attention to novel distracter stimuli, involving a source localizable to the midline frontocentral region. Findings of a recent study by Ruchsow et al. (2008) suggest that impaired control processes involved in inhibiting responses to novel stimuli may also contribute to the P3 reduction at midline central sites. They measured ERPs of 21 patients having a major depression and 21 healthy controls during a Go/Nogo flanker task. The P3 to Go trials has a parietal distribution, whereas the Nogo-P3, like the novelty P3, has a more frontocentral distribution. Depressed patients showed reduced Nogo-P3, but P3b to Go trials did not differ from controls. Further study should be given to the possibility that a common deficit in cognitive control processes may underlie reductions of novelty P3 and Nogo-P3 in depression.
