Impaired deviance detection as the core psychopathological mechanism of schizophrenia

Understanding the core psychopathological mechanism of schizophrenia is crucial for its diagnosis and treatment. In this article, we update the evidence for our previous proposal that the core of neurocognitive dysfunctions in schizophrenia is the impairment of deviance detection. We discuss the dysfunction of the N-methyl-d-aspartate (NMDA) receptors in schizophrenia, which resembles that induced by ketamine and leads to a reduced mismatch negativity in electroencephalography (EEG), and we demonstrate that the genetic findings and structural changes in the brain associated with schizophrenia correspond to impaired deviance detection as the core cognitive impairment. In a broader psychopathological perspective, this impairment disrupts the interaction between predictive and evidence-based mechanisms of speech processing in the brain, which may help elucidate the emergence of core symptoms such as delusions and hallucinations. Furthermore, we discuss how disruptions in deviance detection contribute to negative symptoms and significantly hinder everyday functioning and autonomy in individuals with schizophrenia. Integration of numerous findings into this model provides compelling evidence that impaired deviance detection is a prominent contributor to the manifestation of symptoms and the pathological progression of this psychiatric condition. We suggest that targeting the core cognitive deficiency, that of deviance detection may enhance psychological and pharmacological approaches to diagnose and rehabilitate schizophrenia.