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Impaired Corollary Discharge Mechanisms in Schizophrenia: Evidence From Readiness Potential and Auditory N1
Antonio Arjona-Valladares1, Luis Sobrino-Conde2, Rosa M Beño-Ruiz-de-la-Sierra1
1Psychiatry Department, School of Medicine, University of Valladolid, 47005 Valladolid, Spain.
Background And Hypothesis:
Altered brain activity preceding behavior may reflect a reduced ability to suppress the sensory consequences of self-generated actions in schizophrenia. The corollary discharge (CD) mechanism has been proposed to underlie this process. In the present study, we investigated CD by analyzing the readiness potential (RP) and its relationship to auditory N1 suppression in patients with schizophrenia compared to healthy controls (HCs). We also examined the association between RP activity and anomalous self-experiences (ASEs).
Study Design:
Event-related potentials were recorded from 48 patients with schizophrenia and 55 HCs during a vocalization paradigm including talk and listen conditions. RP amplitude and N1 suppression were quantified as the amplitude difference between listen and talk conditions. Regression analyses assessed the relationship between these components within each group and examined associations between RP and N1 amplitudes and ASEs, measured using the Inventory of Psychotic-Like Anomalous Self-Experiences (IPASE) scale, in the schizophrenia group.
Study Results:
In the talk condition, HCs showed greater RP amplitude compared with the listen condition, a difference that was absent in the schizophrenia group. In HCs, this RP increase was followed by suppression of the N1 component. A significant correlation between RP amplitude and N1 suppression was observed in HCs but not in patients. Importantly, reduced N1 suppression in patients with schizophrenia was associated with higher IPASE scores.
Conclusions:
These findings suggest that schizophrenia involves impairments in early cortical processes related to efference copy and corollary discharge mechanisms, reflected in reduced RP amplitude and the lack of coupling with N1 suppression. Such alterations may contribute to deficits in sensory prediction and to anomalous self-experiences in schizophrenia.
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