Abstract
BackgroundPrevious research has yielded evidence for enhanced semantic priming in formal thought-disordered schizophrenia patients, a result that fits well with the hypothesis of disinhibited processes of spreading activation in this population. ObjectiveThe current study examined whether hyper priming among schizophrenia patients is an outcome of further spreading of activation of a node or a result of farther activation of nodes in the semantic network. We also try to shed light on the fate of this activation. MethodsThe present study tested this hypothesis by using semantic and identical priming in two different experiments. SOA (stimulus onset asynchrony) was manipulated (240 ms vs. 740 ms) within block. It is assumed that among healthy individuals, performance relies on a balance between activation and inhibition processes, contrary to in schizophrenic individuals. In order to examine this hypothesis, we compared formal thought-disordered schizophrenia patients, non thought-disordered schizophrenia patients, and healthy controls. ResultsFor thought-disordered schizophrenia patients, we found a large positive semantic effect and identical priming effect (129 ms and 154 ms, respectively) only with short SOA. SOA and type of priming did not modulate priming effects in the control groups. ConclusionsThis result supports the claim that there is a lack of inhibitory processes among thought-disordered patients. Hyper priming in the thought-disorder group may be an outcome of hyper activation followed by rapid decay below baseline threshold.
Highlights
One of the major positive cognitive symptoms characteristic of schizophrenia is formal thought disorder [1,2], which includes loss of abstraction ability, tangentiality, loss of word associations, derailment, thought blocking, deficits in abstract thinking and over-inclusive thinking [1,3]
Vinogradov et al.’s [30] conclusion was that the priming effect with the control groups and the hyper priming at short stimulus onset asynchrony (SOA) among thought disorder (TD) participants demonstrate intact semantic networks
These findings are comparable to those of Manschreck et al [4], who examined short SOAs and found hyper priming in the TD group
Summary
One of the major positive cognitive symptoms characteristic of schizophrenia is formal thought disorder [1,2], which includes loss of abstraction ability, tangentiality, loss of word associations, derailment, thought blocking, deficits in abstract thinking and over-inclusive thinking [1,3]. It was suggested that this effect relies on two types of processes: automatic spreading of activation (ASA) and control The latter encompasses inhibitory processes, which allow inhibiting semantically unrelated information [12,13]. With stimulus onset asynchrony (SOA) shorter than about 250 ms between prime and target, the priming effect is thought to be the outcome of automatic spreading of activation in the semantic network. Previous research has yielded evidence for enhanced semantic priming in formal thought-disordered schizophrenia patients, a result that fits well with the hypothesis of disinhibited processes of spreading activation in this population. Results: For thought-disordered schizophrenia patients, we found a large positive semantic effect and identical priming effect (129 ms and 154 ms, respectively) only with short SOA. Hyper priming in the thought-disorder group may be an outcome of hyper activation followed by rapid decay below baseline threshold
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