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Clinical Focus: Neurological & Psychiatric Disorders - Original Research

Frontal and subcortical contribution to visual hallucinations in dementia with Lewy bodies and Parkinson’s disease

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Pages 509-522 | Received 14 Jun 2019, Accepted 13 Aug 2019, Published online: 28 Aug 2019
 

ABSTRACT

Objectives: Visual hallucinations (VH) are common in Lewy body disease (LBD), and have been associated with cognitive and structural brain alterations. Evidence so far concerns mainly Parkinson’s disease (PD), but little is known about symptom-specific pathophysiological mechanisms across the LBD spectrum, especially related to the presence of dementia. The aim of the present pilot study was to investigate the neuroanatomical, and neuropsychological characteristics related to VH in two forms of LBD, namely dementia with Lewy bodies (DLB) and PD without dementia.

Methods: Whole brain voxel-based morphometry (VBM) analyses on 3D MRI acquired structural brain scans, and neuropsychological testing were performed on 28 clinically diagnosed DLB (11 with VH, 17 NVH), and 24 PD (9 with VH, and 15 NVH) patients. In order to assess differences in gray matter (GM) regional volumes, and cognitive performance, hallucinating patients for each group were compared with corresponding non-hallucinating ones.

Results: DLB patients with VH presented significantly worse visual attention deficits compared to those without, which persisted even when controlling for visual perception. Whole brain VBM analysis revealed decreased GM volume in DLB with VH in the right superior and medial frontal gyri, putamen, caudate nucleus and insula. Subcortical regional volumes were also significantly associated with visual attention performance. Hallucinating PD patients, instead, presented more severe executive dysfunction, but VBM showed no volumetric differences between the two PD subgroups. Post hoc region of interest analyses revealed striatal GM loss in PD with VH.

Conclusion: Frontal and striatal GM atrophy may contribute to the emergence of VH in DLB, which may be fostered by the more severe attention deficits. Striatal GM loss and executive dysfunction, instead, appeared to underlie VH in PD without dementia.

Acknowledgments

This is a summary of independent research carried out at the NIHR Sheffield Biomedical Research Center (Translational Neuroscience). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.

Declaration of interest

The authors report no conflicts of interest. Peer reviewers on this manuscript have received an honorarium from Postgraduate Medicine for their review work but have no other relevant financial relationships to disclose.

Supplemental material

Supplemental data for this article can be accessed here.

Correction Statement

This article has been republished with minor changes. These changes do not impact the academic content of the article.

Notes

1. Data for the PD sample were collected while Angelo Antonini was employed by the IRCCS Fondazione Ospedale San Camillo, Venice, Italy.

Additional information

Funding

This paper was written independently; no company or institution supported the authors financially or by providing a professional writer.

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