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A systematic review of the structural neuroimaging correlates of thought disorder
•Temporal, frontal and subcortical regions are implicated in thought disorder.•Implicated regions may point to attentional mechanisms underlying thought disorder.•More hypothesis-driven thought disorder research is needed.•Inadequate thought disorder measurement may account for null findings. One cl...
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Published in: | Neuroscience and biobehavioral reviews 2018-01, Vol.84, p.299-315 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •Temporal, frontal and subcortical regions are implicated in thought disorder.•Implicated regions may point to attentional mechanisms underlying thought disorder.•More hypothesis-driven thought disorder research is needed.•Inadequate thought disorder measurement may account for null findings.
One clinical dimension often cited as a hallmark of schizophrenia is thought disorder (TD). The aim of the current systematic review was to summarise our current understanding of the neurobiology of TD that has been investigated with structural neuroimaging techniques. Ninety-seven relevant studies were identified from January 1990 to August 2016, 26 of which had TD-motivated research questions or hypotheses. The remaining 71 studies conducted exploratory clinical analyses that included TD amongst a number of psychotic symptoms. These studies implicate the left superior temporal gyrus in TD. There was also evidence to suggest associations between TD and structural measures within the orbitofrontal cortex, cerebellum, nucleus accumbens, and amygdala-hippocampal region. However, there is a dearth of structural neuroimaging research driven by TD-motivated hypotheses. Furthermore, few studies have explored specific TD symptoms or subgroups, or surface-based morphometric measures of cortical structure, despite theoretical and practical reasons for doing so. It is hoped that the current review will assist in the augmentation of diverse hypothesis-driven research into the aetiology of TD. |
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ISSN: | 0149-7634 1873-7528 |
DOI: | 10.1016/j.neubiorev.2017.08.017 |