Specifically, we hypothesized that target and novelty P3, as well as alpha event-related desynchronization following P3, would be reduced in CHR patients. While target and novelty P3 are typically observed with ERPs during a novelty oddball (e.g., Bruder et al., 2009), the CSD transform also reveals a distinct component complex that uniquely characterizes the brain’s response to novel stimuli, which is obscured by volume-conducted surface potentials (Tenke et al., 2010). This sink/source complex consists of a robust vertex-maximum source with an approximate peak latency of 250 ms that we termed novelty vertex source (NVS), which is preceded by a marked negativity that we originally termed novelty N2 sink (180 ms peak latency, FCz maximum). To the extent that the NVS is linked to P3a, we also expected NVS reductions comparable to previous findings of reduced P3a in CHR patients (e.g., Atkinson et al., 2012; Hermens et al., 2010). Likewise, to the extent that the preceding novelty N2 sink is related to MMN, we anticipated deficits in novelty MMN in CHR patients. A secondary focus was whether these electrophysiologic measures may
