These findings were limited to externalizing disorders and do not rule out the possibility that similar effects might also be observed with other clinical diagnoses where P3 amplitude is abnormally low such as schizophrenia (Jeon and Polich, 2003). For instance, Ford et al. (1994) found that the latencies of trial level P3 peaks were more variable for schizophrenia patients relative to controls. When these findings were revisited (Ford et al., 2008), they found that patients exhibited less intertrial delta and theta phase-locking and weaker trial level delta energy (irrespective of phase) during P3. Unlike our study, Ford et al.’s (2008) results indicated that delta measures accounted for evoked P3 amplitude reductions seen in patients. Nonetheless, the present report and the Ford et al. findings converge by showing reduced delta and theta phase-locking for schizophrenia and externalizing groups, a potentially interesting neurobiological similarity that could help explain comorbidity shared across these disorders. Viewing P3 in terms of its time-frequency energy and phase-locking dynamics may prove to be an important tool for future research to compare and contrast pathophysiological factors for a
