The role of atypical semantic activation and stress in odd speech: Implications for individuals with psychometrically defined schizotypy

BackgroundOdd speech is a cardinal symptom of schizophrenia; however, little is known about the mechanisms that lead to this construct in schizophrenia or schizotypy, the estimated 10% of the population who exhibit traits presumed to reflect genetic liability to schizophrenia. The lack of research concerning specific mechanisms of odd speech represents an important knowledge gap. Here, our primary aim was to examine how atypical semantic activation (ASA) and stress are related to odd speech in individuals with psychometrically-defined schizotypy.MethodsWe employed highly sensitive laboratory procedures to test whether significant differences in ASA exist between psychometric schizotypy (n = 45) and non-psychometric schizotypy (n = 26) groups. We also examined odd speech across four conditions that varied according to valence (pleasant, unpleasant) and arousal (high, low) and analyzed whether ASA mediates odd speech in schizotypy.ResultsThe psychometric schizotypy group demonstrated significantly increased ASA, in the large effect size range. They also demonstrated a significant increase in one odd speech condition and a trend level group by arousal interaction was observed. Our hypothesis that ASA mediates odd speech in schizotypy was not supported.ConclusionsIndividuals with psychometric schizotypy exhibit semantic activation that is similar to patients with schizophrenia, albeit in a milder form. This study also provides evidence that ASA is a potential endophenotype of schizophrenia. Future studies should further explore properties of odd speech and ASA. Suggested avenues include cognitive deficits, particularly working memory, exploring underlying mechanisms, and examining how these constructs affect individuals across the schizophrenia-spectrum.