Figure 2 shows the ERPs elicited by the symmetric (A) and random (B) stimuli, as both standards and deviants, and also the deviant-minus-standard difference potentials. The stimuli elicited a positive–negative–positive (C1–C2–C3) set of pattern-specific exogenous components (Jeffreys & Axford, 1972). Table 1 shows the latency values of the exogenous components, and Fig. 3 shows the scalp distribution of the C1, C2 and C3 components and the difference surface distributions. Figure 2 shows that the deviant and standard symmetric stimuli elicited similar ERPs. In fact, in the t-tests, the difference did not reach the criterion level (deviant-minus-standard amplitude difference is different from zero at at least five subsequent points). However, over the posterior–occipital locations, random deviant and random standards were different in an earlier (112–120 ms) and in a later (284–292 ms) range. In both ranges, the difference was negative. Table 2 shows the amplitudes of the random deviants and standards in the two ranges.
Event-related potential amplitudes elicited by the deviant and standard random stimuli were compared in both latency ranges by the use of anovas with factors probability (deviant and standard), anteriority (parieto-occipital and occipital) and laterality (left, midline, and right). In the 112–120-ms range, only the probability main effect was significant (F1,11 = 6.31, P < 0.05, η2 = 0.36), showing the occipital/parieto-occipital distribution of the early negativity. In a similar analysis of the 284–292-ms range, the main effect of anteriority (F1,11 = 7.13, P < 0.05, η2 = 0.39) and the probability × anteriority interaction (F1,11 = 7.52, P < 0.05, η2 = 0.41) were significant. According to the Tukey HSD tests, the deviant-minus-standard difference was significant only at the occipital locations (P < 0.01 in all cases). As the results show, vMMN appeared in two latency ranges. However, it is possible that, instead of the emergence of vMMN, the earlier effect was an amplitude modulation of the C2 component. Nevertheless, as Fig. 2 shows, the latency of the difference potential was shorter at the occipital locations. To investigate the latency difference (116 vs. 130 ms), we compared the C2 and difference potential latencies at the parieto-occipital and occipital locations (POz and Oz). In an anova, the main effect of anteriority was significant (F1,11 = 6.33, P < 0.05, η2 = 0.36) and the component (difference vs. standard) × anteriority interaction was significant (F1,11 = 4.93, P < 0.05, η2 = 0.30). However, the main effect of component was only marginally significant (F1,11 = 3.46, P < 0.09, η2 = 0.24). To further investigate the relationship between the C2 and the difference potential, we compared the surface distributions. As Fig. 3 indicates, the distribution of the difference potential was wider than the C2 distribution. To investigate the possibility of distribution difference, we added further electrodes to both sides on both rows (P7, P8, PO7, and PO8) to the previous electrode set (PO3, POz, PO4, O1, Oz, and O2), and vector-scaled the data (McCarthy & Wood, 1985). The C2 amplitude was measured as the average of a ± 4-ms point around the peak of the component (130 ms). In an anova with factors component (C2 and difference potential), anteriority and laterality, only the three-way interaction was significant (F4,44 = 3.82, P < 0.05, ε = 0.53, η2 = 0.26). According to the Tukey HSD test, C2 was larger at the anterior row, and C2 amplitude was larger at the midline. We found significant differences in the distribution of early vMMN and C2. Additionally, we compared the vector-scaled amplitude values of the two vMMNs in an anova with factors difference potential (early and late) anteriority (parieto-occipital and occipital), and laterality (left, midline, and right). Owing to the lack of significant effects, we could not conclude that the surface distributions were different.