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To detect the abnormal cortical thickness and disrupted brain resting-state functional connectivity (RSFC) in patients with systemic lupus erythematosus (SLE) without neuropsychiatric symptoms (non-NPSLE). Using T1-weighted 3D brain structural data, we first determined the regions with abnormal cortical thickness in a cohort of 33 adult female non-NPSLE patients. By taking brain regions with significantly reduced cortical thickness as the seeds, we calculated their RSFC based on the resting-fMRI data and detected the relationship between the RSFC and cortical thickness in the non-NPSLE patients. Compared to the controls, the non-NPSLE patients showed significantly cortical thinning in the left fusiform gyrus (FUS.L), left lingual gyrus (LING.L), right lingual gyrus (LING.R) and left superior frontal cortex (SFC.L). As for the RSFC, statistical analyses indicated that the abnormal cortical thickness in LING.L is associated with increased RSFC in the left posterior cingulate cortex (PCC.L), and cortical thinning in SFC.L associated with decreased RSFC in left cerebellum 6 (CRBL 6.L) in non-NPSLE patients. In addition, in non-NPSLE patients, the decreased cortical thickness in LING.L was correlated to the increased RSFC in PCC.L, and decreased cortical thickness in SFC.L was correlated to the decreased RSFC in CRBL 6.L. Our findings suggest that the cortical abnormalities may affect brain intrinsic connectivity in non-NPSLE patients.

Previous neuroimaging studies have revealed cognitive dysfunction in patients with systemic lupus erythematosus (SLE) and suggested that it may be related to disrupted brain white matter (WM) connectivity. However, no study has examined the topological properties of brain WM structural networks in SLE patients, especially in patients with non-neuropsychiatric SLE (non-NPSLE). In this study, we acquired DTI datasets from 28 non-NPSLE patients and 24 healthy controls, constructed their brain WM structural networks by using a deterministic fiber tracking approach, estimated the topological parameters of their structural networks, and compared their group differences. We reached the following results: 1) At the global level, the non-NPSLE patients showed significantly increased characteristic path length, normalized clustering coefficient and small-worldness, but significantly decreased global efficiency and local efficiency compared to the controls; 2) At the nodal level, the non-NPSLE patients had significantly decreased nodal efficiency in regions related to movement control, executive control, and working memory (bilateral precentral gyri, bilateral middle frontal gyri, bilateral inferior parietal lobes, left median cingulate gyrus and paracingulate gyrus, and right middle temporal gyrus). In addition, to pinpointing the injured WM fiber tracts in the non-NPSLE patients, we reconstructed the major brain WM pathways connecting the abnormal regions at the nodal level with the corticospinal tract (CST), superior longitudinal fasciculus-parietal terminations (SLFP), and superior longitudinal fasciculus-temporal terminations (SLFT). By analyzing the diffusion parameters along these WM fiber pathways, we detected abnormal diffusion parameters in the bilateral CST and right SLFT in the non-NPSLE patients. These results seem to indicate that injured brain WM connectivity exists in SLE patients even in the absence of neuropsychiatric symptoms.