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Positive symptoms are a useful predictor of aggression in schizophrenia. Although a similar pattern of abnormal brain structures related to both positive symptoms and aggression has been reported, this observation has not yet been confirmed in a single sample.
To study the association between positive symptoms and aggression in schizophrenia on a neurobiological level, a prospective meta-analytic approach was employed to analyze harmonized structural neuroimaging data from 10 research centers worldwide. We analyzed brain MRI scans from 902 individuals with a primary diagnosis of schizophrenia and 952 healthy controls.
The result identified a widespread cortical thickness reduction in schizophrenia compared to their controls. Two separate meta-regression analyses revealed that a common pattern of reduced cortical gray matter thickness within the left lateral temporal lobe and right midcingulate cortex was significantly associated with both positive symptoms and aggression.
These findings suggested that positive symptoms such as formal thought disorder and auditory misperception, combined with cognitive impairments reflecting difficulties in deploying an adaptive control toward perceived threats, could escalate the likelihood of aggression in schizophrenia.
Delusional disorder has been the subject of very little investigation
using brain imaging.
To examine potential structural and/or functional brain abnormalities in
We used structural imaging (voxel-based morphometry, VBM) and functional
imaging (during performance of the n-back task and
whole-brain resting connectivity analysis) to examine 22 patients meeting
DSM-IV criteria for delusional disorder and 44 matched healthy
The patients showed grey matter reductions in the medial frontal/anterior
cingulate cortex and bilateral insula on unmodulated (but not on
modulated) VBM analysis, failure of de-activation in the medial
frontal/anterior cingulate cortex during performance of the
n-back task, and decreased resting-state connectivity
in the bilateral insula.
The findings provide evidence of brain abnormality in the medial
frontal/anterior cingulate cortex and insula in delusional disorder. A
role for the former region in the pathogenesis of delusions is consistent
with several other lines of evidence.
The pathological basis of tardive dyskinesia is unknown. Although its clinical features implicate the basal ganglia, imaging studies have not found clear evidence that it is associated with volume changes in these or other brain structures.
To determine, using voxel-based structural imaging, whether there are regions of grey matter volume change in people with schizophrenia who also have tardive dyskinesia compared with those without tardive dyskinesia.
A total of 81 people with chronic schizophrenia, 32 with tardive dyskinesia and 49 without, were examined using magnetic resonance imaging (MRI) and whole-brain, optimised voxel-based morphometry. A comparison group of 61 healthy controls was also examined.
Compared with those without tardive dyskinesia, patients with tardive dyskinesia showed a pattern of volume reductions in predominantly subcortical regions, including the basal ganglia and the thalamus. Within the basal ganglia, volume reductions were seen in the caudate nucleus, to a lesser extent in the putamen, and only marginally in the globus pallidus. The patients with tardive dyskinesia, but not those without, showed significant volume reductions in the basal ganglia compared with the healthy controls but both groups had smaller volumes than controls in other affected areas.
The pathological process or processes that underlie the development of tardive dyskinesia are not just neurochemical in nature, but affect brain structure.
Cognitive impairment is an established feature of schizophrenia. However,
little is known about its relationship to the structural and functional
brain abnormalities that characterise the disorder.
To identify structural and/or functional brain abnormalities associated
with schizophrenic cognitive impairment.
We carried out structural magnetic resonance imaging (MRI) and
voxel-based morphometry in 26 participants who were cognitively impaired
and 23 who were cognitively preserved, all with schizophrenia, plus 39
matched controls. Nineteen of those who were cognitively impaired and 18
of those who were cognitively preserved plus 34 controls also underwent
functional MRI during performance of a working memory task.
No differences were found between the participants who were cognitively
intact and those who were cognitively impaired in lateral ventricular
volume or whole brain volume. Voxel-based morphometry also failed to
reveal clusters of significant difference in grey and white matter volume
between these two groups. However, during performance of the n-back task,
the participants who were cognitively impaired showed hypoactivation
compared with those who were cognitively intact in the dorsolateral
prefrontal cortex among other brain regions.
Cognitive impairment in schizophrenia is not a function of the structural
brain abnormality that accompanies the disorder but has correlates in
altered brain function.
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