Auditory cortex responsiveness during talking and listening: early illness schizophrenia and patients at clinical high-risk for psychosis.

OBJECTIVE

The corollary discharge mechanism is theorized to dampen sensations resulting from our own actions and distinguish them from environmental events. Deficits in this mechanism in schizophrenia may contribute to misperceptions of self-generated sensations as originating from external stimuli. We previously found attenuated speech-related suppression of auditory cortex in chronic patients, consistent with such deficits. Whether this abnormality precedes psychosis onset, emerges early in the illness, and/or progressively worsens with illness chronicity, is unknown.

METHODS

Event-related potentials (ERPs) were recorded from schizophrenia patients (SZ; n = 75) and age-matched healthy controls (HC; n = 77). A subsample of early illness schizophrenia patients (ESZ; n = 39) was compared with patients at clinical high-risk for psychosis (CHR; n = 35) and to a subgroup of age-matched HC (n = 36) during a Talk-Listen paradigm. The N1 ERP component was elicited by vocalizations as subjects talked (Talk) and heard them played back (Listen).

RESULTS

As shown previously, SZ showed attenuated speech-related N1 suppression relative to HC. This was also observed in ESZ. N1 suppression values in CHR were intermediate to HC and ESZ and not statistically distinguishable from either comparison group. Age-corrected N1 Talk-Listen difference z scores were not correlated with illness duration in the full SZ sample.

CONCLUSIONS

Putative dysfunction of the corollary discharge mechanism during speech is evident early in the illness and is stable over its course. The intermediate effects in CHR patients may reflect the heterogeneity of this group, requiring longitudinal follow-up data to address if speech-related N1 suppression abnormalities are a risk marker for conversion to psychosis.