Abnormality in hippocampal signal intensity predicts atrophy in patients with systemic lupus erythematosus

Abstract

Objectives To quantify signal abnormalities in the hippocampus (Hsig) of patients with systemic lupus erythematosus (SLE) and to determine if Hsig predict hippocampal atrophy (HA) in SLE. Methods We included all SLE patients and healthy age- and sex-matched individuals with two magnetic resonance imaging (MRI) scans performed with a minimum of 1 year interval. All individuals underwent a standardized neuropsychological evaluation. Individual results were converted into standard scores and compared to normative data. SLE patients were additionally assessed for disease activity (SLE Disease Activity Index (SLEDAI)), damage (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI)), and the presence of antiphospholipid antibodies. MRI was performed on an Elscint 2 T scanner and T1 inversion recovery and T2 coronal images were used for analysis. Volumetric (HV) and signal quantification (Hsig) were determined by standardized protocols. Results We included 54 SLE patients (48 women; mean age 32.2 ± 10.56 years). Hsig were found at study entry in 15 (45.5%) patients. Hsig in the body and tail of non-atrophic hippocampi correlated with progression of volume loss during the follow-up period ( r = 0.8, p < 0.001). The presence of Hsig in the head of atrophic hippocampi correlated with progression of HA ( r = 0.73, p = 0.005) during the same period. No correlation of Hsig and disease activity or prednisone dose was observed. Conclusion HA is frequently observed in SLE patients and volume loss is progressive in a subgroup of patients. The evaluation of Hsig is an easy tool to determine patients that may have progressive hippocampal volume loss and should be followed more closely with MRI and cognitive evaluation.

Reduced volumes of the CA1 and CA4-dentate gyrus hippocampal subfields in systemic lupus erythematosus

“…Recent results confirmed that hippocampal volume reduction is indeed frequently diagnosed in SLE, 11 and the alteration of hippocampal signal intensity is a useful marker to determine patients with further progressive hippocampal atrophy. 12 However, in SLE patients without neuropsychiatric manifestations not all studies reported hippocampal atrophy even though the patients showed a generalized cognitive deficit. 24 A possible explanation is that less severely affected SLE patients are characterized by hippocampal subfield-specific volume reductions (CA1 and CA4-DG) as shown in the present study.…”

“…5,6 There is structural neuroimaging evidence for reduced volumes of the hippocampal formation, corpus callosum, cerebellum, cerebral cortex, and amygdala in SLE. [7][8][9][10][11][12] Functional neuroimaging studies demonstrated altered metabolism and functional connectivity in the prefrontal cortex, inferior parietal cortex, hippocampus, and anterior cingulate cortex of patients with SLE. 5,13,14 The hippocampal formation is not a homogeneous structure: It consists of several histologically distinguishable modules, such as Cornu Ammonis (CA) regions, dentate gyrus (DG), presubiculum, and subiculum.…”