Abstract

ObjectiveIt has been suggested that positive psychotic symptoms reflect ‘aberrant salience’. Previously we provided support for this hypothesis in first-episode schizophrenia patients, demonstrating that delusional symptoms were associated with aberrant reward processing, indexed by the Salience Attribution Test (SAT). Here we tested whether salience processing is abnormal in schizophrenia patients with long-standing treatment-refractory persistent delusions (TRS). MethodEighteen medicated TRS patients and 31 healthy volunteers completed the SAT, on which participants made a speeded response to earn money in the presence of cues. Each cue comprised two visual dimensions, colour and form. Reinforcement probability varied over one of these dimensions (task-relevant), but not the other (task-irrelevant). ResultsParticipants responded significantly faster on high-probability relative to low-probability trials, representing implicit adaptive salience; this effect was intact in TRS patients. By contrast, TRS patients were impaired on the explicit adaptive salience measure, rating high-probability stimuli less likely to be associated with reward than controls. There was little evidence for elevated aberrant salience in the TRS group. ConclusionThese findings do not support the hypothesis that persistent delusions are related to aberrant motivational salience processing in TRS patients. However, they do support the view that patients with schizophrenia have impaired reward learning.

Highlights

  • Advances in understanding the role of dopamine in reward learning support the hypothesis that psychotic symptoms reflect the formation of abnormal stimulus-reinforcement associations (Kapur, 2003)

  • Stimuli that are repeatedly paired with a reward, termed conditioned stimuli (CS+), are able to elicit phasic dopamine firing in the midbrain when presented alone, while unconditioned stimuli (CS −) that do not predict reward do not elicit such a response (Schultz et al, 1997)

  • At alpha = 0.05, this study had 80% power to detect a large effect size (d = 0.85), which is of comparable magnitude to the increase in explicit aberrant salience we previously identified in individuals in an at-risk mental state for psychosis, not all of whom had delusion-like thoughts, relative to healthy volunteers (d = 0.93: Roiser et al, 2013)

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Summary

Introduction

Advances in understanding the role of dopamine in reward learning support the hypothesis that psychotic symptoms reflect the formation of abnormal stimulus-reinforcement associations (Kapur, 2003). Stimuli that are repeatedly paired with a reward, termed conditioned stimuli (CS+), are able to elicit phasic dopamine firing in the midbrain when presented alone, while unconditioned stimuli (CS −) that do not predict reward do not elicit such a response (Schultz et al, 1997) It has been shown, in humans and in animals, that presentation of a CS + leads to increased response vigour compared to the presentation of a CS − (Cools et al, 2008; Roiser et al, 2006; Talmi et al, 2008; Wyvell and Berridge, 2000), an effect that is modulated by ventral striatal dopamine (Wyvell and Berridge, 2000). A necessary corollary of this is that antipsychotic medication will necessarily attenuate adaptive (appropriate) motivational salience which may result in negative sideeffects related to loss of motivation, such as apathy and anhedonia

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