Abstract
Diffusion-based magnetic resonance imaging (MRI) studies, namely diffusion-weighted imaging (DWI) and diffusion-tensor imaging (DTI), have been performed in the context of systemic lupus erythematosus (SLE), either with or without neuropsychiatric (NP) involvement, to deepen cerebral microstructure alterations. These techniques permit the measurement of the variations in random movement of water molecules in tissues, enabling their microarchitecture analysis. While DWI is recommended as part of the initial MRI assessment of SLE patients suspected for NP involvement, DTI is not routinely part of the instrumental evaluation for clinical purposes, and it has been mainly used for research. DWI and DTI studies revealed less restricted movement of water molecules inside cerebral white matter (WM), expression of a global loss of WM density, occurring in the context of SLE, prevalently, but not exclusively, in case of NP involvement. More advanced studies have combined DTI with other quantitative MRI techniques, to further characterize disease pathogenesis, while brain connectomes analysis revealed structural WM network disruption. In this narrative review, the authors provide a summary of the evidence regarding cerebral microstructure analysis by DWI and DTI studies in SLE, focusing on lessons learned and future research perspectives.
Highlights
Neuropsychiatric (NP) involvement in systemic lupus erythematosus (SLE) is one of the most protean and challenging features of the disease, targeting both the central (CNS) and, to a lesser extent, the peripheral (PNS) nervous system
A CNS biochemical profile can be explored by proton magnetic resonance spectroscopy (H1-Magnetic Resonance Spectroscopy (MRS)) [23,24]; nervous tissue microstructure integrity can be evaluated by diffusion-tensor imaging (DTI) [25,26] and magnetization transfer imaging (MTI) [27–29]; regional and whole brain perfusion can be assessed by perfusion weighted imaging (PWI) with or without contrast administration [30]
Lower mean Apparent Diffusion Coefficient (ADC) values at amygdala level in SLE and Neuropsychiatric Lupus Erythematosus (NPSLE) compared to healthy controls (HCs), in particular for N-methyl-D-aspartate receptor (NMDAR)-Ab positive patients
Summary
Neuropsychiatric (NP) involvement in systemic lupus erythematosus (SLE) is one of the most protean and challenging features of the disease, targeting both the central (CNS) and, to a lesser extent, the peripheral (PNS) nervous system. NP manifestations may be focal or diffuse, spanning from mild to severe clinical pictures able to heavily impact patient’s quality of life [1], and contributing to increased mortality compared to the general population and SLE patients without NP involvement [2,3]. The second mechanism, mainly associated with diffuse NP clinical pictures, is driven by autoimmune-mediated neuroinflammation, and involves complement activation, increased permeability of the blood–brain barrier (BBB), intrathecal migration of neuronal autoantibodies, local production of immune complexes, proinflammatory cytokines, and other inflammatory mediators [5–10]. The expert clinical judgement in the context of a multidisciplinary team, along with a tight follow up of individual cases, remains the “gold standard” for diagnosis and management of NPSLE [13–16]
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