Brain Magnetic Resonance Imaging in Newly Diagnosed Systemic Lupus Erythematosus

Abstract

Objective We wished to determine the prevalence of cerebral atrophy and focal lesions in a cohort of patients with newly diagnosed systemic lupus erythematosus (SLE) and the association of these brain abnormalities with clinical characteristics. Methods A total of 97 patients with SLE, within 9 months of diagnosis, with 4 or more American College of Rheumatology classification criteria, were enrolled. Brain magnetic resonance imaging was performed. Results The patients were 97% female, mean age 38.1 (SD 12.2) years, education 15.1 (2.8) years; 59 Caucasian, 11 African American, 19 Hispanic, 5 Asian, and 3 other ethnicity. Cerebral atrophy was prevalent in 18% (95% CI 11%–27%): mild in 12%, moderate in 5%. Focal lesions were prevalent in 8% (95% CI 4%–16%): mild in 2%, moderate in 5%, severe in 1%. Patients with cerebral atrophy were more likely to have anxiety disorder (p = 0.04). Patients with focal lesions were more likely to be African American (p = 0.045) and had higher Safety of Estrogens in Lupus Erythematosus National Assessment SLEDAI scores (p = 0.02) and anti-dsDNA (p = 0.05). Conclusion In this population with newly diagnosed SLE, brain abnormalities were prevalent in 25% of patients. These findings suggest that the brain may be affected extremely early in the course of SLE, even before the clinical diagnosis of SLE is made. Followup of these patients is planned, to determine the reversibility or progression of these abnormalities and their association with and potential predictive value for subsequent neuropsychiatric SLE manifestations.

Magnetic Resonance Imaging in Neuropsychiatric Lupus

“…In a quantitative cerebral MRI assessment, Appenzeller et al 34 showed that age, duration of neuropsychiatric manifestations and total corticosteroid dosage were independent predictors for WMH in SLE. In a recent study in patients with newly diagnosed SLE, WMH were found in 8% of the patients 38 . Nevertheless, these lesions were observed more frequently in NPSLE when compared with SLE without neuropsychiatric manifestations, with average ranges from 40 to 60% 8, 11, 19, 34, 36, 38, 39 .…”

“…In a recent study in patients with newly diagnosed SLE, WMH were found in 8% of the patients 38 . Nevertheless, these lesions were observed more frequently in NPSLE when compared with SLE without neuropsychiatric manifestations, with average ranges from 40 to 60% 8, 11, 19, 34, 36, 38, 39 . WMH were associated with cerebrovascular disease, cognitive dysfunction, seizures, antiphospholipid antibodies, low complements (C3, C4, CH50), age, disease duration, and total corticosteroid dose 8, 34 .…”

“…WMH were associated with cerebrovascular disease, cognitive dysfunction, seizures, antiphospholipid antibodies, low complements (C3, C4, CH50), age, disease duration, and total corticosteroid dose 8, 34 . Previous reports demonstrated a significant association between both NPSLE activity (Neuro-SLEDAI) and injury (Neuro-SLICC) scores with the number of WMH (high lesion burden) 11, 34, 36, 38, 40 . Furthermore, new lesions were noticed during onset of new neuropsychiatric manifestations, and resolution of lesions was found with clinical improvement 25, 41, 42 .…”

“…Furthermore, new lesions were noticed during onset of new neuropsychiatric manifestations, and resolution of lesions was found with clinical improvement 25, 41, 42 . Quantitative methods are increasingly proposed for the quantification and follow-up of the WMH in NPSLE, as they can function as an independent predictor for the NPSLE activity and injury, holding promise to open a new line of follow-up of NPSLE patients and their response to therapy, similar to the monitoring of multiple sclerosis 32, 34, 38 .…”

“…Brain atrophy was also correlated with lupus anticoagulant, low complement, longer disease duration, cognitive dysfunction and cerebrovascular disease 22, 36 . Many authors suggested that the atrophy might be the result of the prednisone use 36, 49 , while others found no association 30, 38, 50, 51 , which suggests that additional mechanisms, probably related to NPSLE itself, seem to be involved 52– 55 .…”