dysfunction in schizophrenia, Kayser et al. (2010c) employed a nose-referenced EEG recording in a sensory detection study. This involved 200 ms presentations of olfactory stimuli (hydrogen sulfide) to which participants responded whether they perceived a low or high intensity odor. Given that linked-mastoids or linked-ears are frequently employed as EEG reference for chemosensory ERP studies, these investigators changed the original nose-referenced ERPs to a mastoid reference in order to compare the resulting ERP waveforms to CSDs, which revealed that using a linked-mastoid reference can dramatically mask an olfactory N1 component. Results showed that the N1 sink and P2 source were markedly reduced in schizophrenic patients for high intensity stimuli, thus confirming olfactory dysfunction in schizophrenia. Further, the study demonstrated that similar results were obtained for CSDs derived from different recording montages and systems. In a replication study using the same task, Kayser et al. (2013) investigated clinical high-risk (CHR) subjects at prodromal phase of psychosis and healthy controls and obtained similar olfactory CSD findings for N1 sink and P2 source, and thus closely replicated the previous findings of Kayser et al., (2010c). In addition, the results showed that three patients who later developed psychosis had poorer odor detection and thresholds,
