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Although executive impairment has been reported in mania, its brain functional correlates have been relatively little studied. This study examined goal management, believed to be more closely related to executive impairment in daily life than other executive tasks, using a novel functional magnetic resonance imaging (fMRI) paradigm in patients in this illness phase.
Twenty-one currently manic patients with bipolar disorder and 30 matched healthy controls were scanned while performing the Computerized Multiple Elements Test (CMET). This requires participants to sequentially play four simple games, with transition between games being made either voluntarily (executive condition) or automatically (control condition).
CMET performance was impaired in the manic patients compared to the healthy controls. Manic patients failed to increase activation in the lateral frontal, cingulate and inferior parietal cortex when the executive demands of the task increased, while this increase was observed in the healthy controls. Activity in these regions was associated with task performance.
Manic patients show evidence of impaired goal management, which is associated with a pattern of reduced medial and lateral frontal and parietal activity.
The brain functional correlates of autobiographical recall are well established, but have been little studied in schizophrenia. Additionally, autobiographical memory is one of a small number of cognitive tasks that activates rather than de-activates the default mode network, which has been found to be dysfunctional in this disorder.
Twenty-seven schizophrenic patients and 30 healthy controls underwent functional magnetic resonance imaging while viewing cue words that evoked autobiographical memories. Control conditions included both non-memory-evoking cues and a low level baseline (cross fixation).
Compared to both non-memory evoking cues and low level baseline, autobiographical recall was associated with activation in default mode network regions in the controls including the medial frontal cortex, the posterior cingulate cortex and the hippocampus, as well as other areas. Clusters of de-activation were seen outside the default mode network. There were no activation differences between the schizophrenic patients and the controls, but the patients showed clusters of failure of de-activation in non-default mode network regions.
According to this study, patients with schizophrenia show intact activation of the default mode network and other regions associated with recall of autobiographical memories. The finding of failure of de-activation outside the network suggests that schizophrenia may be associated with a general difficulty in de-activation rather than dysfunction of the default mode network per se.
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.
Although executive and other cognitive deficits have been found in patients with borderline personality disorder (BPD), whether these have brain functional correlates has been little studied. This study aimed to examine patterns of task-related activation and de-activation during the performance of a working memory task in patients with the disorder.
Sixty-seven DSM-IV BPD patients and 67 healthy controls underwent fMRI during the performance of the n-back task. Linear models were used to obtain maps of within-group activations and areas of differential activation between the groups.
On corrected whole-brain analysis, there were no activation differences between the BPD patients and the healthy controls during the main 2-back v. baseline contrast, but reduced activation was seen in the precentral cortex bilaterally and the left inferior parietal cortex in the 2-back v. 1-back contrast. The patients showed failure of de-activation affecting the medial frontal cortex and the precuneus, plus in other areas. The changes did not appear to be attributable to previous history of depression, which was present in nearly half the sample.
In this study, there was some, though limited, evidence for lateral frontal hypoactivation in BPD during the performance of an executive task. BPD also appears to be associated with failure of de-activation in key regions of the default mode network.
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.
Little is known about how functional imaging changes in bipolar disorder
relate to different phases of the illness.
To compare cognitive task activation in participants with bipolar
disorder examined in different phases of illness.
Participants with bipolar disorder in mania (n = 38),
depression (n = 38) and euthymia (n =
38), as well as healthy controls (n = 38), underwent
functional magnetic resonance imaging during performance of the n-back
working memory task. Activations and de-activations were compared between
the bipolar subgroups and the controls, and among the bipolar subgroups.
All participants were also entered into a linear mixed-effects model.
Compared with the controls, the mania and depression subgroups, but not
the euthymia subgroup, showed reduced activation in the dorsolateral
prefrontal cortex, the parietal cortex and other areas. Compared with the
euthymia subgroup, the mania and depression subgroups showed
hypoactivation in the parietal cortex. All three bipolar subgroups showed
failure of de-activation in the ventromedial frontal cortex. Linear
mixed-effects modelling revealed a further cluster of reduced activation
in the left dorsolateral prefrontal cortex in the patients; this was
significantly more marked in the mania than in the euthymia subgroup.
Bipolar disorder is characterised by mood state-dependent hypoactivation
in the parietal cortex. Reduced dorsolateral prefrontal activation is a
further feature of mania and depression, which may improve partially in
euthymia. Failure of de-activation in the medial frontal cortex shows
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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