Eytan Ruppin, James Reggia, David Horn
We implement and study a computational model of Stevens' [19921 theory of the pathogenesis of schizophrenia. This theory hypoth(cid:173) esizes that the onset of schizophrenia is associated with reactive synaptic regeneration occurring in brain regions receiving degener(cid:173) ating 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 mem(cid:173) ory capacities (which are generally preserved in schizophrenia) . However, These compensatory changes adversely lead to sponta(cid:173) neous, biased retrieval of stored memories, which corresponds to the occurrence of schizophrenic delusions and hallucinations with(cid:173) out any apparent external trigger, and for their tendency to con(cid:173) centrate on just few central themes. Our results explain why these symptoms tend to wane as schizophrenia progresses, and why de(cid:173) layed therapeutical intervention leads to a much slower response.
Eytan Ruppin, James A. Reggia, David Hom