Regional gray matter volume and structural network strength in somatic vs. non-somatic delusional disorders

Huber, Markus; Lepping, Peter; Kirchler, Erwin; Kärner, Martin; Sambataro, Fabio; Herrnberger, Bärbel; Corlett, Philip R.; Freudenmann, Roland W.

doi:10.1016/j.pnpbp.2017.11.022

Cited by 16 publications

(18 citation statements)

References 59 publications

(53 reference statements)

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“…Another structural imaging study of patients with SZ and somatic delusions has also shown structural abnormalities in frontal, insular and thalamic regions [35]. As discussed previously, alterations in those regions support the notion of impaired neural networks related to somatosensory perception and top-down regulation of sensory input, i. e. prediction processing [34]. Thus, impaired somatosensory networks could mediate somatic delusions as opposed to delusions without somatic content.…”

Section: Introductionsupporting

confidence: 53%

“…To elucidate possible neural substrates of somatic delusions, we previously investigated structural brain alterations in patients with DI, using magnetic resonance imaging (MRI) and voxel-based as well as source-based morphometry techniques. In two studies, we compared patients with DI to healthy controls (HC) [32,33], and recently, we compared patients with DI to HC and to patients presenting with non-somatic DD (NS-DD) [34].…”

Section: Introductionmentioning

confidence: 99%

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Abnormal cerebellar volume in somatic vs. non-somatic delusional disorders

et al. 2020

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Background: There is abundant evidence for cerebellar involvement in schizophrenia, where the cerebellum has been suggested to contribute to cognitive, affective and motor dysfunction. More recently, specific cerebellar regions have also been associated with psychotic symptoms, particularly with auditory verbal hallucinations. In contrast, little is known about cerebellar contributions to delusions, and even less is known about whether cerebellar involvement differs by delusional content. Methods: Using structural magnetic resonance imaging at 1.0 T together with cerebellum-optimized segmentation techniques, we investigated gray matter volume (GMV) in 14 patients with somatic-type delusional disorder (S-DD), 18 patients with non-somatic delusional disorder (NS-DD) and 18 patients with schizophrenia (SZ) with persistent non-somatic delusions. A total of 32 healthy controls (HC) were included. Between-group comparisons were adjusted for age, gender, chlorpromazine equivalents and illness duration. Results: Compared to HC, S-DD patients showed decreased GMV in left lobule VIIIa. In addition, S-DD patients showed decreased GMV in lobule V and increased GMV in bilateral lobule VIIa/crus II compared to NS-DD. Patients with SZ showed increased GMV in right lobule VI and VIIa/crus I compared to HC. Significant differences between HC and NS-DD were not found. Conclusions: The data support the notion of cerebellar dysfunction in psychotic disorders. Distinct cerebellar deficits, predominantly linked to sensorimotor processing, may be detected in delusional disorders presenting with predominantly somatic content.

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Section: Introductionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Abnormal cerebellar volume in somatic vs. non-somatic delusional disorders

et al. 2020

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“…Moreover, a deficit of integrative visual areas, particularly the retrosplenial cortex, was suspected in delusional misidentification [27]. In support of a content-specific neural signature of delusional belief, we have previously shown abnormal brain structure of cortical and subcortical sensorimotor regions in patients with somatic type delusions [23,24,32].…”

Section: Introductionmentioning

confidence: 75%

“…A model proposed by Palaniyappan and Liddle [28] suggests disrupted reciprocal connectivity of the PFC to the insula to precisely distribute representations of goal-directed and planned behavior. Of note, abnormal insula volume has been also observed in patients with somatic type DD [23,100]; thus, this particular brain area is not among the regions that specifically mediate delusional content.…”

Section: Discussionmentioning

confidence: 96%

“…In previous neuroimaging studies, structural and functional abnormalities in distinct frontotemporal regions, anterior cingulate cortex and insula were frequently observed [20,21]. In somatictype DD, gray matter volume (GMV) decreases in the frontal portion of the left insula [22] were described along with GMV abnormalities in prefrontal, insular, striatal and thalamic regions [23,24]. Prefrontal cortex [25,26] and insula have been suggested to play a key role in delusion formation, irrespective of delusional content.…”

Section: Introductionmentioning

confidence: 98%

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Aberrant Gray Matter Volume and Cortical Surface in Paranoid-Type Delusional Disorder

et al. 2020

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Introduction: Delusions are core symptoms of schizophrenia-spectrum and related disorders. Despite their clinical relevance, the neural correlates underlying such phenomena are unclear. Recent research suggests that specific delusional content may be associated with distinct neural substrates. Objective: Here, we used structural magnetic resonance imaging to investigate multiple parameters of brain morphology in patients presenting with paranoid type delusional disorder (pt-DD, n = 14) compared to those of healthy controls (HC, n = 25). Methods: Voxel-and surface-based morphometry for structural data was used to investigate gray matter volume (GMV), cortical thickness (CT) and gyrification. Re-sults: Compared to HC, patients with pt-DD showed reduced GMV in bilateral amygdala and right inferior frontal gyrus. Higher GMV in patients was found in bilateral orbitofrontal and in left superior frontal cortices. Patients also had lower CT in frontal and temporal regions. Abnormal gyrification in patients was evident in frontal and temporal areas, as well as in bilateral insula. Conclusions: The data suggest the presence of aberrant GMV in a right prefrontal region associated with belief evaluation, as well as distinct structural abnormalities in areas that essentially subserve processing of fear, anxiety and threat in patients with pt-DD. It is possible that cortical features of distinct evolutionary and genetic origin, i.e. CT and gyrification, contribute differently to the pathogenesis of pt-DD.

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