Brain network reorganisation and spatial lesion distribution in systemic lupus erythematosus

Valdés Hernández, Maria del C. and Smith, Keith and Bastin, Mark E. and Nicole Amft, E. and Ralston, Stuart H. and Wardlaw, Joanna M. and Wiseman, Stewart J. (2021) Brain network reorganisation and spatial lesion distribution in systemic lupus erythematosus. Lupus, 30 (2). pp. 285-298. ISSN 1477-0962 (https://doi.org/10.1177/0961203320979045)

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Abstract

Objective This work investigates network organisation of brain structural connectivity in systemic lupus erythematosus (SLE) relative to healthy controls and its putative association with lesion distribution and disease indicators. Methods White matter hyperintensity (WMH) segmentation and connectomics were performed in 47 patients with SLE and 47 healthy age-matched controls from structural and diffusion MRI data. Network nodes were divided into hierarchical tiers based on numbers of connections. Results were compared between patients and controls to assess for differences in brain network organisation. Voxel-based analyses of the spatial distribution of WMH in relation to network measures and SLE disease indicators were conducted. Results Despite inter-individual differences in brain network organization observed across the study sample, the connectome networks of SLE patients had larger proportion of connections in the peripheral nodes. SLE patients had statistically larger numbers of links in their networks with generally larger fractional anisotropy weights (i.e. a measure of white matter integrity) and less tendency to aggregate than those of healthy controls. The voxels exhibiting connectomic differences were coincident with WMH clusters, particularly the left hemisphere’s intersection between the anterior limb of the internal and external capsules. Moreover, these voxels also associated more strongly with disease indicators. Conclusion Our results indicate network differences reflective of compensatory reorganization of the neural circuits, reflecting adaptive or extended neuroplasticity in SLE.

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