Changes in White Matter Microstructure Suggest an Inflammatory Origin of Neuropsychiatric Systemic Lupus Erythematosus. Issue 8 (27th July 2016)

• Record Type: Journal Article
• Authors: Magro‐Checa, César; Ercan, Ece; Wolterbeek, Ron; Emmer, Bart; van der Wee, Nic J.; Middelkoop, Huub A.; Kruyt, Nyika D.; Ronen, Itamar; van Buchem, Mark A.; Huizinga, Tom W.; Steup‐Beekman, Gerda M.
• Is Part Of: Arthritis & rheumatology. Volume 68:Issue 8(2016)
• Page Start: 1945
• Page End: 1954
• Publication Date: 2016-07-27
• Subjects: Arthritis -- Periodicals; Rheumatism -- Periodicals; 616.72
• DOI: 10.1002/art.39653
• Languages: English
• ISSNs: 2326-5191

Abstract

Abstract : Objective: To assess white matter (WM) and gray matter (GM) magnetization transfer ratio histogram peak heights (MTR‐HPHs) in different subsets of patients with neuropsychiatric systemic lupus erythematosus (NPSLE) who have unremarkable findings on 3T magnetic resonance imaging of the brain and to evaluate whether these values could be used to highlight different clinically suspected underlying pathogenic processes or identify the clinical NPSLE status or whether they could be associated with a specific NPSLE syndrome. Methods: Sixty‐four SLE patients with neuropsychiatric symptoms were included. The initial NPSLE diagnosis and suspected underlying pathogenic process were established by multidisciplinary evaluation. The final diagnosis was made after also considering the disease course 6–18 months later. Thirty‐three patients with central nervous system (CNS) NPSLE and 31 SLE patients with neuropsychiatric symptoms unrelated to SLE (non–SLE‐related NP) were included. Twenty SLE patients without neuropsychiatric symptoms and 36 healthy control subjects were included for comparison. Differences in the WM and GM mean MTR‐HPHs and between the different NPSLE subgroups (CNS NPSLE diagnosis, NPSLE phenotype [inflammatory or ischemic], and clinical changes after treatment) and the relationship to NPSLE syndromes were evaluated. Results: Patients with inflammatory NPSLE had significantly lower WM MTR‐HPHs than did the healthy controls, the SLE patients, and the non–SLE‐related NP patients. Cognitive disorder, mood disorder, and psychosis were related to lower WM MTR‐HPH values and cerebrovascular symptoms to higher values. Furthermore, the mean MTR‐HPHs in the WM increased when the clinical status of the NPSLE patients improved. Conclusion: Measurement of MTR‐HPH of the WM has the potential to identify inflammatory NPSLE with CNS involvement. This finding underscores the usefulness of this technique for the detection of cerebral changes in NPSLE patients and for the assessment of clinical changes after treatment.