Olfaction in the psychosis prodrome: electrophysiological and behavioral measures of odor detection.

Mean scores (±SEM) of odor thresholds and odor identification (Sniffin’ Sticks) for HR patients and healthy controls. Dark insert bars reflect nasal chemosensory performance for three converters. Dashed lines indicate published normative values (medians) for healthy controls aged 16 to 35 years (Kobal et al., 2000).

Mean (±SEM) sensitivity (dL) of odor detection as a function of odor intensity, revealing a monotonic increase for both CHR patients and healthy controls. Dark insert bars reflect behavioral performance for three converters.

Grand mean olfactory ERP [µV] waveforms (−100 to 1400 ms, 100 ms pre-stimulus baseline) referenced to linked mastoids of CHR patients and healthy controls for H2S stimuli (pooled across intensity) and blank air at all 49 recording sites. Horizontal and vertical electrooculograms (EOG) are shown before blink correction. Two prominent ERP components identified in previous studies are labeled at sites T7 (N1) and Cz (P2).

Reference-free current source density ( SD) [µV/cm²] waveforms for 21 HR patients comparing weak, medium and strong H2S stimuli and blank air at all 49 recording sites. Two prominent CSD components are labeled at sites T7 (N1 sink) and Pz (P2 source), where they closely corresponded to their ERP counterparts.

CSD waveforms as in Figure 4 for 20 healthy controls.

(A) Factor loadings of the first three PCA factors (with explained variance) extracted from olfactory CSD waveforms (N = 41). (B) CSD factor score topographies corresponding to N1 sink (top) and P2 source (bottom) for 21 CHR patients and 20 healthy controls comparing H2S stimuli of weak, medium, and strong intensity and blank air. (C) Squared univariate (channel-specific) paired samples T statistics thresholded at the 95th quantile (p = 0.05) of the corresponding randomization distribution (maximum of all 49-channel squared univariate paired samples T statistics) of difference between H2S stimuli (pooled across intensity) and blank air (N = 41). To facilitate comparisons of the max(T2) topographies with the underlying sink-source difference topographies, the sign of the difference at each site was applied to the respective T2 value, which is otherwise always positive. Inset topographies show the sites selected for repeated measures ANOVA models performed on CSD factors 345 (N1 sink) and 600 (P2 source) to probe region-specific sink (cyan) or source (orange) activations associated with odor detection, as indicated by colored locations. All topographies are two-dimensional representations of spherical spline interpolations (m = 2; λ = 0) derived from the mean factors scores or T2 statistics available for each recording site.

Mean (±SEM) factor scores of N1 sink at lateral-temporal and medial-frontocentroparietal sites (T7/8, FC5/6, C3/4, CP5/6) and P2 source at mid-frontocentral and mid-parietal sites (FCz, FC1/2, Cz, C3/4, CP1/2, Pz, P3/4, POz) as a function of odor intensity, revealing a monotonic increase for both CSD components in prodromal patients and healthy controls. Please note the inverted ordinate (negativity up), showing increases in N1 sink amplitude upwards and increases in P2 source amplitude downwards.

Scatter plots for odor thresholds (pooled across nostril), odor identification, odor detection sensitivity, N1 sink and P2 source (sites as in Figure 8) comparing CHR patients (three converters marked by dark circles) and healthy controls. Detection sensitivity, N1 sink and P2 source are pooled across odor intensity. Group means are indicated by black horizontal lines.