Sensory attenuation deficit and auditory hallucinations in schizophrenia: a causal mechanism or a risk factor? Evidence from meta-analyses on N1 ERP component

Background: Sensory attenuation (SA), the dampened perception of self-generated sensory information, is typically associated with reduced ERP signals, like for the N1 component of auditory ERPs. SA, together with efficient monitoring of intentions and actions, should facilitate the distinction between self-generated and externally-generated sensory events, optimizing the interaction with the world. According to many, SA is deficient in schizophrenia. The question arises whether altered SA reflects a sufficient mechanism to explain positive symptoms like auditory hallucinations. A systematic association of reduced SA in hallucinating patients would support this hypothesis. Methods: We conducted a series of meta-analyses on 15 studies on auditory SA in which the N1 component of ERP-EEG signals was measured during talking (self-generated sensory signals condition) or when listening to pre-recorded vocalizations (externally-generated sensory signals condition). Results: We found that schizophrenic individuals do show some auditory SA, as their N1 signal is significantly attenuated in talking conditions with respect to listening conditions. Yet, the magnitude of such attenuation is reduced with respect to healthy controls. This phenomenon generalizes independently from the stage of the disease, from the severity of positive symptoms, and regardless of whether patients have auditory hallucinations or not. Conclusions: These findings suggest that a reduced SA cannot be a sufficient mechanism for explaining positive symptoms like auditory hallucinations in schizophrenia. As a reduced SA was also present in subjects at risk of schizophrenia, reduced SA may represent a risk factor for the disorder. We discuss the implications of these results for clinical-cognitive models of schizophrenia.