Abstract

BackgroundThe purpose of this study was to investigate whether white matter microstructure is altered in patients suffering from systemic lupus erythematosus (SLE), and if so, whether such alterations differed between patients with and without neuropsychiatric symptoms.MethodsStructural MRI and diffusion tensor imaging (DTI) were performed in 64 female SLE patients (mean age 36.9 years, range 18.2–52.2 years) and 21 healthy controls (mean age 36.7 years, range 23.3–51.2 years) in conjunction with clinical examination, laboratory tests, cognitive evaluation, and self-assessment questionnaires. The patients were subgrouped according to the American College of Rheumatology Neuropsychiatric Systemic Lupus Erythematosus case definitions into non-neuropsychiatric SLE (nonNPSLE) and neuropsychiatric SLE (NPSLE).ResultsComparisons between the SLE group and healthy controls showed that the mean fractional anisotropy (FA) was significantly reduced in the right rostral cingulum (p = 0.038), the mid-sagittal corpus callosum (CC) (p = 0.050), and the forceps minor of the CC (p = 0.015). The mean diffusivity (MD) was significantly increased in the left hippocampal cingulum (p = 0.017). No significant differences in MD or FA values were identified between NPSLE and nonNPSLE patients. Disease duration among all SLE patients correlated significantly with reduced FA in the CC (p < 0.05). No correlations were found between DTI parameters and white matter hyperintensities, SLE Disease Activity Index-2000, Systemic Lupus International Collaborating Clinical/ACR Organ Damage Index, or Montgomery Asberg Depression Rate Score Self-report.ConclusionsWe found alterations of white matter microstructure in SLE patients that were related to disease duration and fatigue. Our results indicate that cerebral involvement in SLE is not isolated to the NPSLE subgroup.

Highlights

  • The purpose of this study was to investigate whether white matter microstructure is altered in patients suffering from systemic lupus erythematosus (SLE), and if so, whether such alterations differed between patients with and without neuropsychiatric symptoms

  • Considering our previous findings from resting state functional Magnetic resonance imaging (MRI), where we demonstrated hypoconnectivity and hyperconnectivity in several crucial resting-state networks in both nonNPSLE and neuropsychiatric SLE (NPSLE) patients and that some of these alterations showed a significant correlation to disease duration, we hypothesized that the cerebral microstructure would be altered in NPSLE as well as in nonNPSLE patients and that these alterations would correlate to the disease duration rather than whether they belonged to the NPSLE subgroup or not

  • The scores for SLE were lower on average on all domains of the Central Nervous System Vital Signs (CNS-VS) test compared to the HC group, but only psychomotor speed was significantly lower (p = 0.001), which indicates some degree of cognitive decline in SLE patients per se (Table 1)

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Summary

Introduction

The purpose of this study was to investigate whether white matter microstructure is altered in patients suffering from systemic lupus erythematosus (SLE), and if so, whether such alterations differed between patients with and without neuropsychiatric symptoms. Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease that affects many organ systems including the central nervous system [1, 2]. The distinction between non-neuropsychiatric SLE (nonNPSLE) and neuropsychiatric SLE (NPSLE) is not always clear and accurate diagnosis remains challenging as patients with nonNPSLE as well as HC might experience neuropsychiatric symptoms, such as headache or cognitive decline [8,9,10]. Symptoms range from mild ones such as headache, fatigue, cognitive decline, and mood disorders, to more severe conditions such as epilepsy, stroke, dementia, and psychosis [3, 8]. Possible mechanisms include autoneuronal antibodies [11, 12], intrathecal production of proinflammatory cytokines that might disintegrate the blood–brain barrier [13], vascular involvement through microangiopathy, chronic diffuse ischemia, thromboembolism, and atherosclerosis [3, 14]

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