Few studies, however, have been directed at the neurophysiologic processes underlying olfactory dysfunction in schizophrenia. In the first electrophysiologic study, Turetsky et al. (2003) measured OERPs in 21 patients with schizophrenia and 20 healthy controls to three concentrations of H2S. Patients and controls did not differ significantly in ratings of the perceived intensity of the odors, but, nonetheless, patients had reduced N1 and P2 amplitudes, with the largest difference for the strongest odor intensity. Turetsky, Kohler, Gur, and Moberg (2008) also found similar reductions of N1 and P2 amplitude in first degree relatives of patients with schizophrenia, suggesting that this represents a vulnerability marker for this disorder. Using odorants of different hedonic value (i.e., rose-like phenethyl alcohol and rotten butter-like isobutyraldehyde), Pause, Hellmann, Goder, Aldenhoff, and Ferstl (2008) reported shorter peak latencies across several ERP components in nine schizophrenic compared to nine depressed and nine healthy men, but these effects were evidently most robust for N1 during the presentation of negative odors. Unfortunately, no ERP waveforms were included in this report, making it difficult to evaluate the exact meaning of these findings or to relate them to other studies.
