of P3 or late positive complex). These findings are in line with prior evidence linking negative symptoms to P3 reductions in schizophrenia (e.g., Mathalon et al., 2000). Regarding the lack of overall P3 reductions in CHR patients, the reasons for the discordance from prior research are not clear. Apart from ample differences in ERP methodology, prior studies typically employed a standard two-tone oddball paradigm, which differed from the present three-stimulus oddball task, which includes rare, unique events likely to result in increased alertness and processing demands. However, we note that Koh et al. (2011), who used a two-tone oddball task, did not find differences between ultra-high-risk patients and healthy controls in alpha inter-trial coherence, which could be expected to be a main contributor to P3 amplitude. Importantly, the failure to observe reduced P3 amplitude in CHR patients cannot be attributed to employing CSD-PCA methods, which do not obscure or create effects that are not present in the original data (cf. Fig. 3). Clearly, more research is needed to delineate the importance of paradigmatic and other methodological aspects for uncovering electrophysiologic deficits in individuals at risk.
