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Cortical salience network activation precedes the development of delusion severity

Published online by Cambridge University Press:  18 July 2016

T. T. Raij*
Affiliation:
Department of Psychiatry, Helsinki University and Helsinki University Hospital, Helsinki, Finland Department of Neuroscience and Biomedical Engineering and Aalto NeuroImaging, Aalto University School of Science, Espoo, Finland
T. Mäntylä
Affiliation:
Department of Neuroscience and Biomedical Engineering and Aalto NeuroImaging, Aalto University School of Science, Espoo, Finland Mental Health Unit, National Institute for Health and Welfare, Helsinki, Finland Institute of Behavioral Sciences, University of Helsinki, Helsinki, Finland
O. Mantere
Affiliation:
Department of Psychiatry, Helsinki University and Helsinki University Hospital, Helsinki, Finland
T. Kieseppä
Affiliation:
Department of Psychiatry, Helsinki University and Helsinki University Hospital, Helsinki, Finland Mental Health Unit, National Institute for Health and Welfare, Helsinki, Finland
J. Suvisaari
Affiliation:
Mental Health Unit, National Institute for Health and Welfare, Helsinki, Finland
*
*Address for correspondence: Dr T. T. Raij, Advanced Magnetic Imaging Centre, PO Box 13000, FI-00076 Aalto, Finland. (Email: raijtu@neuro.hut.fi)

Abstract

Background

Delusion is the most characteristic symptom of psychosis. While researchers suggested an association between changes of the cortical salience network (CSN) and delusion, whether these CSN findings are a cause or a consequence of delusion remains unknown.

Method

To assess the effect of CSN functioning to forthcoming changes in delusion scores, we measured brain activation with 3-T functional magnetic resonance imaging in two independent samples of first-episode psychosis patients (total of 27 patients and 23 healthy controls). During scanning, the patients evaluated statements about whether an individual's psychosis-related experiences should be described as a mental illness, and control statements that were also evaluated by healthy controls. Symptoms were assessed at the baseline and at 2 months follow-up with Brief Psychiatric Rating Scale.

Results

Both tasks activated the CSN in comparison with rest. Activation of CSN (‘illness evaluation v. control task’ contrast) in patients positively correlated with worsening of or less improvement in delusions at the 2-month follow-up assessment. This finding was independent of delusion and clinical insight scores at the baseline evaluation.

Conclusions

Our findings link symptom-evaluation-related CSN functioning to severity of delusion and, importantly, add a new layer of evidence for the contribution of CSN functioning to the longitudinal course of delusions.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2016 

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