In electrophysiological research the majority of studies have used this “reverse oddball” paradigm and mainly investigated two time-locked (stimulus) components of the ERP: namely, N2 and P3. Traditionally, N2 and P3 amplitude differences have been suggested to be associated with inhibition of the prepotent response on NoGo trials (Eimer, 1993; Falkenstein et al., 1999; Jodo and Kayama, 1992). N2 and P3 latency effects have also been found, and taken to be critical indicators of active inhibitory processes for the Go/NoGo task, suggesting a pattern of sequential activation rather than altered activity level in key cortical structures that may mediate success in the task (see Roche et al., 2005). While the NoGo N2 has been associated with the subject's recognition of the need for inhibition (e.g., Kok, 1986), the NoGo P3 has been considered a more precise indicator of the effectiveness of motor response inhibition (Smith et al., 2007). While there is abundant literature available on the functional significance and clinical relevance of the Go/NoGo P3, there are relatively fewer studies that have evaluated the N2 component, especially in a clinical
