Background
Referential delusions are the most common symptom of schizophrenia and offer an opportunity
to examine the neural correlates of delusions because they occur in discrete episodes
that can be studied in the scanner. The cortical midline structures (CMS) and subcortical
regions, including the amygdala and striatum, are linked with self-reference in healthy
adults. Less is known about the neural substrates of altered self-reference in schizophrenia.
Methods
In this study, patients with schizophrenia experiencing prominent referential delusions
(n = 18) and healthy control subjects (n = 17) were presented with ambiguous sentences while in the magnetic resonance imaging
scanner and asked to rate whether they felt the sentences had been written specifically
about them. The sentences were either generic (nonpersonalized) or individually tailored
personalized sentences, designed to induce referential ideation. We hypothesized that
both groups would show activity in the CMS, limbic, and striatal regions and that
induced referential ideation would be associated with greater activity in striatal
areas in patients with schizophrenia.
Results
A robust main effect of endorsement (endorsed vs. nonendorsed) was observed in the
CMS, as well as subcortical regions, including the nucleus accumbens/ventral striatum,
amygdala, insula, and midbrain dopamine regions. A group-by-endorsement interaction
was seen in the medial prefrontal cortex, insula and nucleus accumbens/ventral striatum.
Activity in insula and ventral striatum also correlated with the strength of the delusions
of reference.
Conclusions
Referential ideation in persons with delusions is associated with heightened CMS,
limbic and striatal activity and reduced differentiation between self- and non-self-relevant
information.
Key Words
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Article info
Publication history
Published online: August 11, 2011
Accepted:
May 31,
2011
Received in revised form:
May 27,
2011
Received:
January 27,
2011
Identification
Copyright
© 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.