similar olfactory CSD findings for N1 sink and P2 source, and thus closely replicated the previous findings of Kayser et al., (2010c). In addition, the results showed that three patients who later developed psychosis had poorer odor detection and thresholds, along with marked reductions of N1 and P2 (in the absence of significant group differences between CHR and control subjects), suggesting that olfactory measures may be of utility in predicting the transition from prodromal phase to psychosis among CHR subjects. Furthermore, in a follow-up study using a different task (three-stimulus novelty oddball task) for essentially the same cohort of CHR (prodromal) patients and healthy controls, Kayser et al. (2014) found that, similar to their previous study (Kayser et al., 2013), the same three prodromal individuals who later developed psychosis had marked reductions of novelty MMN whereas prodromal patients as a group did not show this reduction. In addition, CHR patients showed reduced ERO (alpha desynchronization at 9 Hz) over the right posterior regions for the target stimuli (at 610 ms) compared to healthy controls, suggesting a deficit of alpha-mediated cognitive control processes, and these ERO abnormalities were also most pronounced for the three converters. This series of studies confirmed that
