Disentangling early sensory information processing deficits in schizophrenia

ObjectiveThe disentangling of early sensory information processing deficits and examination of their relationships to demographic and clinical factors are important steps for the validation of potential biomarkers and/or endophenotypes of schizophrenia. The aims of the present study were to characterize commonly used sensory event-related potential deficits, to determine whether they are (1) distinct from one another and (2) independently associated with important clinical characteristics.MethodsMMN, P3a and RON event-related potentials (ERP) were recorded from schizophrenia patients (SZ; n = 429) and nonpsychiatric comparison subjects (NCS; n = 286). Subgroup analyses on demographic and clinical variables were performed.ResultsSchizophrenia patients exhibited robust ERP deficits at frontocentral electrodes (MMN: d = 1.10; P3a: d = 0.87; RON: d = 0.77), consistent with previous studies. Each ERP component uniquely accounted for variance in amplitude and schizophrenia deficits. Amplitude reductions occurred with increasing age in both NCS and SZ patients. A small subset of patients prescribed combinations of 1st and 2nd generation antipsychotics exhibited significantly reduced MMN amplitude relative to other medication-defined subgroups.ConclusionsMMN, P3a, and RON are dissociable deficits with distinct relationships to age and medication status in schizophrenia patients, potentially reflecting divergent pathophysiological processes. Reduced MMN in patients taking multiple antipsychotic medications appear to be attributable to greater severity of symptoms and functional impairments, rather than a medication effect.SignificanceIndependent information processing deficits in schizophrenia patients may differentially contribute to the commonly observed deficits in neurocognitive and psychosocial functioning.

► MMN, P3a and RON ERP components each uniquely accounted for variance in amplitude and schizophrenia deficits. ► This study is the largest investigation of auditory MMN, P3a, and RON published to date in schizophrenia and therefore may serve as a definitive characterization of sensory processing abnormalities in schizophrenia. ► Deficits in MMN, P3a and RON may be associated with (or perhaps influenced by) clinical and demographic variables including antipsychotic medication type or status and age and therefore may result from divergent underlying functional, anatomical and genomic sources.