and NVS were most robust (i.e., at FCz and Cz; cf. Fig. 4), and Fig. 9B depicts novel-minus-nontarget difference waveforms at FCz where novelty MMN (factor 185) was maximal so as to mimic deviant-minus-standard MMN waveforms computed in passive auditory paradigms (e.g., Higuchi et al., 2013; Murphy et al., 2013). As can be seen, the three converters lacked any evidence of MMN, whereas a strong MMN response was observed between 150 and 230 ms (i.e., the typical time interval for measuring MMN) for controls and CHR patients who did not develop psychosis. To better quantify this observation, and for descriptive purposes only, a post-hoc ANOVA was computed for novelty MMN (tPCA factor 185 at midfrontocentral sites; cf. Tab. 3B) with 3 converters, 19 nonconverters and 20 controls as the only between-subjects factor, which revealed a highly significant group × condition interaction (F[2,39] = 6.73, p = .003). As expected, simple effects of condition were present in controls (novels vs. targets, − 1.15 ±1.51 vs. 0.32 ±1.02; F[1,39] = 41.6, p < .0001) and nonconverters (−0.86 ±1.41 vs. 0.42 ±0.82; F[1,39] = 29.5, p < .0001), but were in opposite direction and not significant in converters (1.09 ±1.87 vs. 0.25 ±0.70;
