Quantitative Susceptibility Mapping in Lewy Body Dementia

Poster No:

271 

Submission Type:

Abstract Submission 

Authors:

Rohan Bhome1,2, George Thomas1, Karin Shmueli3, James Cole1,2, Rimona Weil1,4,5

Institutions:

1Dementia Research Centre, UCL, London, United Kingdom, 2Centre for Medical Image Computing, UCL, London, United Kingdom, 3Department of Medical Physics and Biomedical Engineering, UCL, London, United Kingdom, 4Wellcome Centre for Human Neuroimaging, UCL, London, United Kingdom, 5Movement Disorders Consortium, National Hospital for Neurology and Neurosurgery, London, United Kingdom

First Author:

Rohan Bhome  
Dementia Research Centre, UCL|Centre for Medical Image Computing, UCL
London, United Kingdom|London, United Kingdom

Co-Author(s):

George Thomas, Dr  
Dementia Research Centre, UCL
London, United Kingdom
Karin Shmueli, Prof  
Department of Medical Physics and Biomedical Engineering, UCL
London, United Kingdom
James Cole, PhD  
Dementia Research Centre, UCL|Centre for Medical Image Computing, UCL
London, United Kingdom|London, United Kingdom
Rimona Weil  
Dementia Research Centre, UCL|Wellcome Centre for Human Neuroimaging, UCL|Movement Disorders Consortium, National Hospital for Neurology and Neurosurgery
London, United Kingdom|London, United Kingdom|London, United Kingdom

Introduction:

Lewy body dementia (LBD) encompasses both Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). It is common and causes significant morbidity [1].

What drives selective vulnerability of particular brain regions in LBD is poorly understood. Iron dyshomeostasis may be relevant because excessive iron interacts with α-synuclein to cause neurodegeneration in Lewy body diseases [2]. Therefore, Quantitative Susceptibility Mapping (QSM), which reflects regional differences in iron content, particularly in deep grey matter [3], may have utility in LBD.

One previous study used QSM to investigate magnetic susceptibility in the substantia nigra in DLB [4]. However, it has never been used to evaluate iron deposition in other brain regions. Here, we present a whole brain QSM analysis comparing LBD with both Parkinson's disease without demenita (PD) and controls.

Methods:

We included 54 participants with LBD (39 DLB; 15 PDD), 55 with PD and 34 healthy controls. We only included PD participants classed as high visual performers because this group is less likely to progress to dementia than poor visual performers [5], thereby providing an enriched PD comparator group.

All participants underwent susceptibility- and T1-weighted 3T MRI scans. For QSM pre-processing, we used ROMEO [6] to unwrap phase images and brain masks were calculated from magnitude images using Brain Extraction Tool (BET2). Background field removal was performed using Laplacian boundary value extraction [7] and Multi-Scale Dipole Inversion was used to calculate susceptibility maps [8]. A study-wise template was created from all participants' T1-weighted images and QSM images were transformed into this space [9]. QSM images were spatially smoothed using a 3D Gaussian kernel (3-mm standard deviation).

Voxel-wise, whole brain statistical analyses were performed using absolute QSM values as this is required for statistical conditioning. FSL Randomise was used to perform permutation analyses with threshold-free cluster enhancement. 10,000 permutations were performed to identify significant clusters which were reported at family-wise error (FWE)-corrected P<0.05. Regression analyses, adjusting for age and sex, were performed to compare group differences in voxel-wise magnetic susceptibility and test associations between magnetic susceptibility and clinical measures (composite cognitive score, MoCA, Hooper Visual Organisation Test, and the Movement Disorder Society Unified PD Rating Scale (UPDRS).

Results:

In DLB compared to controls, there were increases in absolute susceptibility in left precentral, bilateral postcentral, left middle temporal and right supramarginal cortical regions (FWE-corrected p<0.05). In LBD compared to controls, there were increases in the bilateral superior and middle frontal regions, and the left superior and middle temporal regions (FWE-corrected p<0.05). LBD showed significant increases in absolute susceptibility in the right inferior frontal, temporal and insula regions (FWE-corrected p<0.05) compared to PD.

The only significant association between a clinical measure and absolute susceptibility was for UPDRS in DLB where significant clusters of increased susceptibility were identified in the right middle frontal and superior temporal lobes (FWE-corrected p<0.05).

Conclusions:

Our work is the first to investigate magnetic susceptibility throughout the brain in LBD. We found absolute susceptibility increases in several cortical regions in LBD relative to PD and controls. This could imply cortical iron dyshomeostasis in LBD and is consistent with the existing understanding of LBD being associated with cortical neuropathology [10]. Our findings highlight the relevance of QSM in LBD. Future work should utilise a region-of-interest approach to test the association between clinical measures and regional susceptibilities in LBD more precisely. This could shed further light on the potential of QSM as a clinically relevant neuroimaging measure of LBD severity.

Disorders of the Nervous System:

Neurodegenerative/ Late Life (eg. Parkinson’s, Alzheimer’s) 1

Modeling and Analysis Methods:

Methods Development
Segmentation and Parcellation
Other Methods

Novel Imaging Acquisition Methods:

Imaging Methods Other 2

Keywords:

Aging
Data analysis
Degenerative Disease
MRI
Neurological

1|2Indicates the priority used for review

Provide references using author date format

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