In one of the first neurophysiologic studies of psychosis risk, van der Stelt et al. (2005) employed an auditory target detection (oddball) task and found that CHR patients (n = 10) had reduced P3 amplitudes at parietal, centroparietal and central scalp sites when compared with age- and sex-matched controls. In other cross-sectional studies, Bramon et al. (2008) and Özgürdal et al. (2008) reported moderately reduced P3 in CHR patients (n = 35 and n = 54, respectively) when compared to controls, and Frommann et al. (2008) observed a widespread reduction of P3 in a large sample of CHR patients studied during an early (n = 50) or late (n = 50) initial prodromal state. In a longitudinal design, van Tricht et al. (2010) observed reduced target P3b in 18 CHR patients who later developed psychosis. Although none of these studies reported a reduction of auditory N1 amplitude in CHR patients, several cross-sectional studies observed reductions in MMN, showing that CHR individuals had reduced MMN amplitude to deviant tones differing from standard 1000-Hz tones in stimulus duration (Atkinson et al., 2012;
