Neurophysiologic abnormalities are more common or more pronounced in the auditory than visual modality (Egan et al., 1994; Ford et al., 1994; Kayser et al., 2009; Pfefferbaum, Ford, White, & Roth, 1989), leading Ford wondering whether this may be related “to whatever dysfunction leads to more frequent auditory than visual hallucinations” (Ford, 1999, p. 668). In fact, our sample did not reveal similar N1 sink reductions for patients experiencing other (e.g., visual, olfactory, somatic/tactile) but not auditory hallucinations, which bolsters the notion that impairments in auditory function play a central role in the etiology of schizophrenia. On the other hand, electrophysiological recording conventions, such as using a linked-ears or -mastoids reference that drastically reduces ERP amplitudes at inferior-parietal sites (cf. Kayser et al., 2003, 2009), may have contributed to the notion of modality-specific ERP reductions in schizophrenia. If the underlying generator of the studied ERP phenomena is in close proximity to the EEG reference, as is the case for secondary visual cortex along the ventral processing stream, the surface potentials as measured at nearby sites (e.g., P7/8, P9/10) will be
