An alternative explanation is that temporal shifts in P3-processes from trial-to-trial (i.e. “latency jitter” or more generally, a reduction in phase-locking) can also diminish trial-averaged (evoked) voltage (Makeig et al., 2002; Sauseng et al., 2007; Sayers et al., 1974). Specifically, if the same P3-related neuroelectrical activity occurs at the same time on each target trial of the ERP task, this activity should contribute prominently in the trial-averaged evoked target P3. Conversely, if the neuroelectric processes that underpin P3 are not consistent across trials, this would result in weak evoked P3. We posit that the temporal onset and offset of P3-related delta and theta components may be more variable across trials in externalizing-diagnosed individuals relative to controls and that this heightened “ERP arrhythmia” is partly responsible for the evoked P3-reductions seen in externalizing. This unexplored possibility would be characterized by a reduction in inter-trial phase-locking for externalizing individuals.
