Abstract

One of the most pervasive findings in studies of schizophrenics with thought disorders is their peculiar pattern of semantic priming, which presumably reflects abnormal associative processes in the semantic system of these patients. Semantic priming is manifested by faster and more accurate recognition of a word-target when preceded by a semantically related prime, relative to an unrelated prime condition. Compared to control, semantic priming in schizophrenics is characterized by reduced priming effects at long prime-target Stimulus Onset Asynchrony (SOA) and, sometimes, augmented priming at short SOA. In addition, unlike controls, schizophrenics consistently show indirect (mediated) priming (such as from the prime ‘wedding’ to the target ‘finger’, mediated by ‘ring’). In a previous study, we developed a novel attractor neural network model with synaptic adaptation mechanisms that could account for semantic priming patterns in healthy individuals. Here, we examine the consequences of introducing attractor instability to this network, which is hypothesized to arise from dysfunctional synaptic transmission known to occur in schizophrenia. In two simulated experiments, we demonstrate how such instability speeds up the network’s dynamics and, consequently, produces the full spectrum of priming effects previously reported in patients. The model also explains the inconsistency of augmented priming results at short SOAs using directly related pairs relative to the consistency of indirect priming. Further, we discuss how the same mechanism could account for other symptoms of the disease, such as derailment (‘loose associations’) or the commonly seen difficulty of patients in utilizing context. Finally, we show how the model can statistically implement the overly-broad wave of spreading activation previously presumed to characterize thought-disorders in schizophrenia.

Highlights

  • Schizophrenia, one of the most debilitating mental illnesses, is frequently accompanied by thought disorders

  • Simulation 1: short stimulus onset asynchrony. In this simulation we examined whether the acceleration of latching as hypothesized in the schizophrenic semantic network can account for the schizophrenic priming results at short Stimulus Onset Asynchrony (SOA)

  • Replicating our previous results with healthy subjects [17], the current simulations yielded reduced Reaction Time (RT) for targets following related primes compared to unrelated primes at both short and long SOAs, demonstrating a robust semantic priming effect

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Summary

Introduction

Schizophrenia, one of the most debilitating mental illnesses, is frequently accompanied by thought disorders. Among the many subtypes of thought-disorders that have been identified, one of the most common is loosening control on associative thinking, often termed derailment or ‘loose associations’ [1]. During discourse, such patients are often unable to maintain the relevant topic of conversation and repeatedly switch ideas, one after the other, sometimes based on a sporadic word from the previous sentence. The basic finding in such studies is that reaction time is faster and accuracy is higher when the target is preceded by a semantically or associatively related prime compared to an unrelated prime. Many factors have been found to modulate this effect, including the lag between the onsets of the prime and target (termed ‘Stimulus Onset Asynchrony’ or ‘SOA’; e.g., short SOA of around 200 ms or long SOA of 500 ms or more), as well as the exact type of relations between them (e.g., direct relatedness like table-chair compared to indirect relatedness like lion-stripes, mediated by tiger)

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