“…This suggests that individuals with SAUD may display alterations in the striate cortex, the dorsal extrastriate cortex of the middle occipital gyrus, or the ventral extrastriate cortex of the fusiform gyrus, all these areas being potential P1 generators (Di Russo et al., 2002, 2005; Holder et al., 2010). Delay and changes in the waveform of the N75 (C1) (Cosi et al., 1986; Devetag, 1988; Kelley et al., 1984) and the N145 (N1) (Devetag, 1988), of striate and extrastriate origin (Di Russo et al., 2002, 2005), respectively, have also been reported, whereas other studies did not reveal any change in pattern‐reversal VEP (Bauer & Easton, 1996; Emmerson et al., 1987; Kothari et al., 2018; Meinck et al., 1990). These discrepancies might be due to differences in medication (e.g., use of disulfiram in Kelley et al., 1984), length of abstinence (e.g., a few days/weeks in Cosi et al., 1986; 3 and 6 months in Bauer & Easton, 1996 and Kothari et al., 2018; more than 1 year in Devetag, 1988), or other experimental differences among which potential fluctuations in the locations, sizes, and reversal frequencies of the checkerboards (Holder et al., 2010).…”