This paper presents the first functional evaluation of spontaneous, uncued retrieval from long-term memory in a cognitive architecture. The key insight is that current deliberate cued retrieval mechanisms require the agent to have knowledge of when and what to retrieve --- knowledge that may be missing or incorrect. Spontaneous uncued retrieval eliminates these requirements through automatic retrievals that use the agent's problem solving context as a heuristic for relevance, thus supplementing deliberate cued retrieval. Using constraints derived from this insight, we sketch the space of spontaneous retrieval mechanisms and describe an implementation of spontaneous retrieval in Soar together with an agent that takes advantage of that mechanism. Empirical evidence is provided in the Missing Link word-puzzle domain, where agents using spontaneous retrieval out-perform agents without that capability, leading us to conclude that spontaneous retrieval can be a useful mechanism and is worth further exploration.

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.

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.

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.