Neurobiological Correlates of Delusion: Beyond the Salience Attribution Hypothesis

Pankow, Anne; Knobel, Astrid; Voss, Martin; Heinz, Andreas

doi:10.1159/000337132

Cited by 45 publications

(32 citation statements)

References 139 publications

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“…Dopamine dysfunction is one of the core theories that aim to explain the neurobiological correlates of schizophrenia and specific symptoms (Pankow et al, 2012). Specifically increased, chaotic firing of dopaminergic neurons in the ventral striatum may lead to incentive salience to irrelevant stimuli, which is supposed to be involved in the generation of delusional mood and delusions of reference and may thereby lead to suspiciousness, aggressiveness and delusions of persecution (Heinz, 1999; Heinz and Schlagenhauf, 2010; Heinz et al, 1998; Kapur, 2003; Laruelle and Abi-Dargham, 1999; Morrison and Murray, 2009).…”

Section: Discussionmentioning

confidence: 99%

Ventral striatum gray matter density reduction in patients with schizophrenia and psychotic emotional dysregulation

Stegmayer

Horn

Federspiel

et al. 2014

NeuroImage: Clinical

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IntroductionSubstantial heterogeneity remains across studies investigating changes in gray matter in schizophrenia. Differences in methodology, heterogeneous symptom patterns and symptom trajectories may contribute to inconsistent findings. To address this problem, we recently proposed to group patients by symptom dimensions, which map on the language, the limbic and the motor systems. The aim of the present study was to investigate whether patients with prevalent symptoms of emotional dysregulation would show structural neuronal abnormalities in the limbic system.Method43 right-handed medicated patients with schizophrenia were assessed with the Bern Psychopathology Scale (BPS). The patients and a control group of 34 healthy individuals underwent structural imaging at a 3T MRI scanner. Whole brain voxel-based morphometry (VBM) was compared between patient subgroups with different severity of emotional dysregulation. Group comparisons (comparison between patients with severe emotional dysregulation, patients with mild emotional dysregulation, patients with no emotional dysregulation and healthy controls) were performed using a one way ANOVA and ANCOVA respectively.ResultsPatients with severe emotional dysregulation had significantly decreased gray matter density in a large cluster including the right ventral striatum and the head of the caudate compared to patients without emotional dysregulation. Comparing patients with severe emotional dysregulation and healthy controls, several clusters of significant decreased GM density were detected in patients, including the right ventral striatum, head of the caudate, left hippocampus, bilateral thalamus, dorsolateral prefrontal and orbitofrontal cortex. The significant effect in the ventral striatum was lost when patients with and without emotional dysregulation were pooled and compared with controls.DiscussionDecreased gray matter density in a large cluster including the right ventral striatum was associated with severe symptoms of emotional dysregulation in patients with schizophrenia. The ventral striatum is an important part of the limbic system, and was indicated to be involved in the generation of incentive salience and psychotic symptoms. Only patients with severe emotional dysregulation had decreased gray matter in several brain structures associated with emotion and reward processing compared to healthy controls. The results support the hypothesis that grouping patients according to specific clinical symptoms matched to the limbic system allows identifying patient subgroups with structural abnormalities in the limbic network.

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Section: Discussionmentioning

confidence: 99%

Ventral striatum gray matter density reduction in patients with schizophrenia and psychotic emotional dysregulation

Stegmayer

Horn

Federspiel

et al. 2014

NeuroImage: Clinical

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“…The FTLD-TDP subtyping followed the current “harmonized” nomenclature. 22 All cases were also screened for p62-positive/TDP-43-negative intraneuronal inclusions, pathognomonic markers of C9ORF72 expansion in amygdala, 10,23 a brain area involved in different kind of delusions. Finally, the presence of additional overlapping neurodegenerative disorders was compared between the 2 groups.…”

Section: Methodsmentioning

confidence: 99%

Clinicopathological Study of Patients With C9ORF72-Associated Frontotemporal Dementia Presenting With Delusions

Shinagawa

Naasan

Karydas

et al. 2014

J Geriatr Psychiatry Neurol

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Background Several clinical studies point to a high prevalence of psychotic symptoms in frontotemporal dementia associated with C9ORF72 mutations, but clinicopathological studies addressing the association between C9ORF72 mutations and delusions are lacking. Method Seventeen patients with pathologically proven frontotemporal lobar degeneration (FTLD) associated with C9ORF72 mutations were identified from Neurodegenerative Disease Brain Bank. Of the 17 cases with C9ORF72 mutation, 4 exhibited well-defined delusions. The clinical history, neurological examination, neuropsychological testing, neuroimaging analysis, and postmortem assessment of the patients with delusions were evaluated and compared with the other cases. Result The content of the delusions was mixed including persecution, infidelity, and grandiosity. All cases showed parkinsonism; voxel-based morphometry analysis showed greater precuneus atrophy in patients with delusions than those without delusions. All 4 had unclassifiable FTLD with TAR DNA-binding protein inclusions, with characteristics of both type A and type B. Three cases had additional τ pathology and another had α-synuclein pathology. Conclusion C9ORF72 carriers with well-defined delusions likely associated with additional pathologies and parietal atrophy in neuroimaging. Patients presenting with middle-aged onset of delusions should be screened for C9ORF72 mutations, especially if family history and parkinsonism are present.

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“…These findings may be attributed to the fact that while negative symptomatology is believed to result from decreased dopaminergic activity in the prefrontal cortex directly involved in WM (Okubo et al, 1997;Heckers et al, 1999;Monteleone et al, 2002). Positive and general symptoms as well as apathy are associated with possibly altered activity in the areas less crucial to WM performance, such as the hippocampus (Krieckhaus et al, 1992;Tamminga et al, 2010) and the basal ganglia (Pankow et al, 2012;Khadka et al, 2013;Sorg et al, 2013).…”

Section: Cognitive Performance Of Sz Patients With Respect To Clinicamentioning

confidence: 99%

Impairments of Working Memory in Schizophrenia and Bipolar Disorder: the Effect of History of Psychotic Symptoms and Different Aspects of Cognitive Task Demands

Hewedi

Frydecka

Moustafa

2015

European Psychiatry

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Comparisons of cognitive impairments between schizophrenia (SZ) and bipolar disorder (BPD) have produced mixed results. We applied different working memory (WM) measures (Digit Span Forward and Backward, Short-delay and Long-delay CPT-AX, N-back) to patients with SZ (n = 23), psychotic BPD (n = 19) and non-psychotic BPD (n = 24), as well as to healthy controls (HC) (n = 18) in order to compare the level of WM impairments across the groups. With respect to the less demanding WM measures (Digit Span Forward and Backward, Short-delay CPT-AX), there were no between group differences in cognitive performance; however, with respect to the more demanding WM measures (Long-delay CPT-AX, N-back), we observed that the groups with psychosis (SZ, psychotic BPD) did not differ from one another, but performed poorer than the group without a history of psychosis (non-psychotic BPD). A history of psychotic symptoms may influence cognitive performance with respect to WM delay and load effects as measured by Long-delay CPT-AX and N-back tests, respectively. We observed a positive correlation of WM performance with antipsychotic treatment and a negative correlation with depressive symptoms in BPD and with negative symptoms in SZ subgroup. Our study suggests that WM dysfunctions are more closely related to a history of psychosis than to the diagnostic categories of SZ and BPD described by psychiatric classification systems.

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Neurobiological Correlates of Delusion: Beyond the Salience Attribution Hypothesis

Cited by 45 publications

References 139 publications

Ventral striatum gray matter density reduction in patients with schizophrenia and psychotic emotional dysregulation

Ventral striatum gray matter density reduction in patients with schizophrenia and psychotic emotional dysregulation

Clinicopathological Study of Patients With C9ORF72-Associated Frontotemporal Dementia Presenting With Delusions

Impairments of Working Memory in Schizophrenia and Bipolar Disorder: the Effect of History of Psychotic Symptoms and Different Aspects of Cognitive Task Demands

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