There is evidence to suggest that ERPs may originate from an additive, evoked activation of neural assemblies independent of ongoing EEG as well as by the phase resetting of ongoing EEG oscillations in response to sensory input (for review, see Rangaswamy and Porjesz, 2008; Sauseng et al., 2007). Considerable efforts have been made in understanding how these models may potentially explain the generation of human ERPs. For instance, it has been proposed that the P3 component arises from a series of superimposed event-related oscillations (EROs) that are induced by sensory or cognitive processes that influence the dynamics of EEG rhythms (e.g. Demiralp et al., 2001; Karakas et al., 2000; Yordanova and Kolev, 1996). EROs are estimated by performing a decomposition of the EEG signal into phase and magnitude information over a range of frequencies and then the changes in those frequencies are characterized over a millisecond time scale with respect to task events. EROs have been demonstrated to be sensitive measures of both normal and abnormal cognitive functioning in humans (see Basar et al., 1999, 2001; Gevins et al., 1998;
