Parallel distributed processing and the emergence of schizophrenic symptoms.
Schizophrenia bulletin January 1, 1993 DOI: 10.1093/schbul/19.1.119 via PubMed
Summary
AI-generated from the abstractSchizophrenia may involve a breakdown in communication between different cortical areas of the brain. Evidence from psychotic states induced by phencyclidine, the adult form of metachromatic leukodystrophy, and neurometabolic studies supports this idea. A computer simulation of such brain pathology suggests two consequences: some cortical circuits become functionally autonomous, and a subset of these produce "parasitic foci" that repetitively reproduce the same cognitive output. These parasitic foci, located at different levels of language processing, are proposed to underlie symptoms such as delusions of control, paranoid delusions of the idee fixe type, thought broadcasting, auditory hallucinations, and certain deficit symptoms. A neurodevelopmental model of impaired corticocortical communication is described.
Study at a glance
| Characteristics | Review Peer reviewed |
|---|---|
| Key finding | Schizophrenia may reflect a breakdown in communication between cortical areas, leading to functionally autonomous circuits and parasitic foci that produce specific symptoms. |
Abstract
Computer simulations of parallel distributed processing (PDP) neural networks have increased our understanding of brain functioning. This article reviews how PDP concepts can contribute to our understanding of schizophrenic symptoms. Psychotic states induced by phencyclidine and the adult form of metachromatic leukodystrophy, as well as neurometabolic studies, suggest that schizophrenia reflects a breakdown in communication between cortical areas. A computer simulation of this type of brain pathology has suggested two neurocognitive consequences: some cortical circuits will become functionally autonomous, and a subset of these circuits will yield "parasitic foci" that slavishly reproduce the same cognitive output. Delusions of control, paranoid delusions of the idee fixe type, thought broadcasting, "voices," and certain deficit symptoms are postulated outcomes of parasitic foci located at different levels of language processing. A neurodevelopmental model of impaired corticocortical communication is described, and this model's implications for further study are outlined.