Abstract
It has been surprisingly difficult to find associations between neural signatures of schizophrenia and the symptoms that define it. That is, many of the legacy components of the event-related potential (ERP)— P50, N100, P200, P300—are reduced in patients with schizophrenia, in first-degree relatives of patients with schizophrenia, in schizophrenia patients early in their illness, and even in people at clinical high risk for schizophrenia. Nevertheless, these ERP components tend to be relatively insensitive to symptoms. This might be due to a number of reasons. First, this could reflect a lack of relationship, a failure to report disappointing findings, or a failure to test for relationships. Second, many ERP studies were not designed to be sensitive to symptoms or to the mechanisms that might underlie them. Third, assessing symptoms is sometimes dependent on the patients’ ability to describe unfathomable experiences and the clinicians’ ability to understand and interpret them. Fourth, medications and comorbidities may decouple the symptoms from the neurobiology. Finally, we must also consider the possibility that the schizophrenia diagnosis breeds truer than the symptoms it comprises.
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