Auditory Mismatch Negativity and P300a Elicited by the "Optimal" Multi-feature Paradigm in Early Schizophrenia.

The mismatch negativity (MMN) is an EEG-derived event-related potential (ERP) elicited by any violation of a predicted auditory "rule," regardless of whether one is attending to the stimuli and is thought to reflect updating of the stimulus context. Redirection of attention toward a rare, distracting stimulus event, however, can be measured by the subsequent P3a component of the P300. Chronic schizophrenia patients exhibit robust MMN deficits, as well as reductions in P3a amplitude. While, the substantial literature on the MMN in first-episode and early phase schizophrenia in this population reports reduced amplitudes, there also exist several contradictory studies. Conversely, P3a reduction in this population is relatively consistent, although the literature investigating this is small. The primary goal of this study was to contribute to our understanding of whether auditory change detection mechanisms are altered in early phase schizophrenia and, if so, under what conditions. Event-related potentials elicited by duration, frequency, gap, intensity, and location deviants (as elicited by the "optimal" multi-feature paradigm) were recorded in 14 early phase schizophrenia (EP) patients and 17 healthy controls (HCs). Electrical activity was recorded from 15 scalp electrodes. MMN/P3a amplitudes and latencies for each deviant were compared between groups and were correlated with clinical measures in EPs. There were no significant group differences for MMN amplitudes or latencies, though EPs did exhibit reduced P3a amplitudes to gap and duration deviants. Furthermore, PANSS (Positive and Negative Syndrome Scale) positive symptom scores were correlated with intensity MMN latencies and duration P3a amplitudes in EPs. These findings suggest that MMNs may not be as robustly reduced in early phase schizophrenia (relative to chronic illness), but that alterations may be more likely in patients with increased positive symptomatology. Furthermore, these findings offer further support to previous work suggesting that the understudied P3a may have good complementary utility as a marker of early cortical dysfunction in psychosis.