Ruppin E, Reggia J A, Horn D
School of Mathematics, Tel Aviv University, Israel.
Schizophr Bull. 1996;22(1):105-23. doi: 10.1093/schbul/22.1.105.
We implement and study a computational model of Stevens' theory of the pathogenesis of schizophrenia. This theory hypothesizes that the onset of schizophrenia is associated with reactive synaptic regeneration in brain regions that receive 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. Modeling Stevens' hypothesized pathological synaptic changes in this framework results in adverse side effects similar to hallucinations and delusions seen in schizophrenia: spontaneous, stimulus-independent retrieval of stored memories focused on just a few of the stored patterns. These could account for the delusions and hallucinations that occur in schizophrenia without any apparent external trigger and for their tendency to concentrate on a few central cognitive and perceptual themes. The model explains why the positive symptoms of schizophrenia tend to wane as the disease progresses, why delayed therapeutic intervention leads to a much slower response, and why delusions and hallucinations may persist for a long time when they do occur.
我们实施并研究了史蒂文斯（Stevens）关于精神分裂症发病机制理论的计算模型。该理论假设，精神分裂症的发作与接收颞叶退化投射的脑区中的反应性突触再生有关。聚焦于其中一个这样的区域，即额叶皮质，我们将额叶模块建模为一个联想记忆神经网络，其输入突触代表传入的颞叶投射。在这个框架中对史蒂文斯假设的病理性突触变化进行建模，会产生类似于精神分裂症中出现的幻觉和妄想等不良副作用：自发地、与刺激无关地检索存储的记忆，且仅聚焦于少数存储模式。这些可以解释精神分裂症中在没有任何明显外部触发因素的情况下出现的妄想和幻觉，以及它们倾向于集中在一些核心认知和感知主题上的现象。该模型解释了为什么精神分裂症的阳性症状会随着疾病进展而趋于减弱，为什么延迟的治疗干预会导致反应慢得多，以及为什么妄想和幻觉一旦出现可能会持续很长时间。
