Despite evidence of olfactory dysfunction in schizophrenia and suggestions that it may be an endophenotypic marker of this disorder, there have been few studies of olfaction in CHR individuals (e.g., Brewer et al., 2003; Kamath et al., 2011; Woodberry et al., 2010). None of these studies employed direct electrophysiologic measures of olfactory cortical function. The present study sought to fill this gap by measuring olfactory ERPs in CHR patients and age- and gender-matched healthy participants. Among several procedural improvements to our previous study in schizophrenia (Kayser et al., 2010), we: (a) employed an odor detection task with three different concentrations of H2S (strong, medium, weak) and blank air as a control condition; (b) increased the spatial resolution from a 31- to a denser 49-channel EEG montage to further refine the characterization of current generators underlying distinct olfactory ERP components (N1, P2); and (c) used randomization tests of component topographies (cf. Kayser et al., 2007) as a tool to identify regions associated with odorspecific stimulus processing (H2S vs. blank air). Following our previous developments in ERP analysis (e.g., Kayser & Tenke,
