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A Neural Model of Delusions and Hallucinations in Schizophrenia

Neural Information Processing Systems

We implement and study a computational model of Stevens' [19921 theory of the pathogenesis of schizophrenia. This theory hypothesizes that the onset of schizophrenia is associated with reactive synaptic regeneration occurring in brain regions receiving degenerating temporal lobe projections. Concentrating on one such area, the frontal cortex, we model a frontal module as an associative memory neural network whose input synapses represent incoming temporal projections. We analyze how, in the face of weakened external input projections, compensatory strengthening of internal synaptic connections and increased noise levels can maintain memory capacities (which are generally preserved in schizophrenia). However, These compensatory changes adversely lead to spontaneous, biased retrieval of stored memories, which corresponds to the occurrence of schizophrenic delusions and hallucinations without any apparent external trigger, and for their tendency to concentrate on just few central themes. Our results explain why these symptoms tend to wane as schizophrenia progresses, and why delayed therapeutical intervention leads to a much slower response.


A Neural Model of Delusions and Hallucinations in Schizophrenia

Neural Information Processing Systems

We implement and study a computational model of Stevens' [19921 theory of the pathogenesis of schizophrenia. This theory hypothesizes that the onset of schizophrenia is associated with reactive synaptic regeneration occurring in brain regions receiving degenerating temporal lobe projections. Concentrating on one such area, the frontal cortex, we model a frontal module as an associative memory neural network whose input synapses represent incoming temporal projections. We analyze how, in the face of weakened external input projections, compensatory strengthening of internal synaptic connections and increased noise levels can maintain memory capacities (which are generally preserved in schizophrenia). However, These compensatory changes adversely lead to spontaneous, biased retrieval of stored memories, which corresponds to the occurrence of schizophrenic delusions and hallucinations without any apparent external trigger, and for their tendency to concentrate on just few central themes. Our results explain why these symptoms tend to wane as schizophrenia progresses, and why delayed therapeutical intervention leads to a much slower response.


A Neural Model of Delusions and Hallucinations in Schizophrenia

Neural Information Processing Systems

We implement and study a computational model of Stevens' [19921 theory of the pathogenesis of schizophrenia. This theory hypothesizes thatthe onset of schizophrenia is associated with reactive synaptic regeneration occurring in brain regions receiving degenerating temporallobe projections. Concentrating on one such area, the frontal cortex, we model a frontal module as an associative memory neural network whose input synapses represent incoming temporal projections. We analyze how, in the face of weakened external input projections, compensatory strengthening of internal synaptic connections and increased noise levels can maintain memory capacities(which are generally preserved in schizophrenia). However, These compensatory changes adversely lead to spontaneous, biasedretrieval of stored memories, which corresponds to the occurrence of schizophrenic delusions and hallucinations without anyapparent external trigger, and for their tendency to concentrate onjust few central themes. Our results explain why these symptoms tend to wane as schizophrenia progresses, and why delayed therapeuticalintervention leads to a much slower response.