Abstract

Background: Deficits in odor threshold sensitivity, discrimination and identification are common in schizophrenia, presumably originating from brain structures also linked to their cognitive and emotional disturbances. However, the neurophysiological processes underlying olfactory dysfunction in schizophrenia have only been studied by Turetsky et al (2003) who found reduced N1 and P2 amplitudes.¹ Methods: Nose-referenced 30-channel ERPs were recorded from 32 schizophrenic and 35 healthy adults (18/18 male) during an odor detection task. Hydrogen sulfide (H₂) stimuli (200 ms duration) at concentrations of 50% and 100% were presented to the left or right nostril by a constant-flow olfactometer (variable ISI 15-25 s). Time of odor stimulation was not cued. Subjects indicated whether they perceived a low or high odor intensity. To identify and measure neuronal generator patterns underlying ERPs, unrestricted Varimax-PCA was performed on their reference-free current source densities (spherical splines). Results: Patients’ behavioral performance was on par with that for healthy controls for high (22.5% vs. 23.4% misses) and low (41.1% vs. 44.9%) odor concentrations. Patients showed similar olfactory ERP and CSD waveforms when compared to controls, but their N1 sink (300 ms, bilateral frontotemporal maximum) and P2 source (615 ms, mid-parietal maximum) amplitudes were smaller. However, both groups had greater N1 sinks and P2 sources to high than low odor intensities. Conclusions: OERP amplitude reductions to H₂S stimuli in schizophrenia appear to reflect reduced activity in frontocentral, midline frontopolar, and parietal regions.

Key Words: olfaction, schizophrenia, event-related potential (ERP), current source density (CSD), principal components analysis (PCA), surface Laplacian

References

¹ Turetsky et al 2003. Biol Psychiatry 53(5):403-11.