General and specific factors associated with severity of cognitive impairment in systemic lupus erythematosus

Abstract

Objective. To determine factors affecting the severity of cognitive impairment in systemic lupus erythematosus (SLE) and to analyze its anatomic location. Methods. Fifteen cognitive functions grouped into 8 domains were evaluated in 52 patients with SLE and 20 with rheumatoid arthritis. Patients were classified according to severity of impairment as normal, mild, or moderate/severe. Multivariate analysis was performed to identify the main factors affecting severity of cognitive deficits. The most likely anatomic site of damage according to neuropsychological performance was compared with the lesion's location on magnetic resonance imaging (MRI). Results. In SLE patients, a stepwise regression analysis showed that the number of impaired functions (dependent variable) was associated with antiphospholipid antibody positivity (aPL؉; P ‫؍‬ 0.04), the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI; P ‫؍‬ 0.001), hypertension (P ‫؍‬ 0.032), and was inversely related to educational level (P ‫؍‬ 0.021). Including MRI, the number of impaired functions was associated with severity of MRI (P < 0.001), the SDI (P ‫؍‬ 0.013), and the presence of Raynaud's phenomenon (P ‫؍‬ 0.04). The contemporary presence of aPL؉ and Raynaud's phenomenon resulted in a higher probability to develop moderate/severe cognitive deficits (P ‫؍‬ 0.015). Two logistic multiple regression analyses identified hypertension (P < 0.05), the SDI (P < 0.01), and moderate/severe MRI findings as main predictors of moderate/severe impairment (dependent variable). The damage site hypothesized through neuropsychological testing corresponded with MRI findings in 71.7% of SLE patients K ‫؍‬ 0.42, P ‫؍‬ 0.005). Conclusion. Hypertension, aPL؉, accumulated damage, and MRI lesions are the main factors affecting severity of cognitive impairment in SLE. The hypothesized sites of central nervous system involvement according to neuropsychological testing correlated with MRI findings in most patients.

Neurocognitive Impairment in Corticosteroid-naive Patients with Active Systemic Lupus Erythematosus: A Prospective Study

“…The prevalence rate of NCI observed here (28%) was lower than that of studies 33,34,35,36,37 using similar neuropsychological test batteries 1 . We speculate that this reflects nonuse of corticosteroids and shorter disease durations, which were characteristic of the patients in our study.…”

Factors and comorbidities associated with central nervous system involvement in systemic lupus erythematosus: a retrospective cross-sectional case–control study from a single center

“…A pivotal role of aPL in NPSLE and their predictive value for NP damage progression are well known [22][23][24][25][26][27][28][29][30][31][32] and substantially confirmed also by the present study. Other factors deemed as related to NP involvement have been previously proposed including high disease activity, caucasian ethnicity, presence of anti-Ro/SSA antibodies [20,21], vasculitis, nephritis, anti-dsDNA, LA and anti-Sm [23][24][25][26][27][28].…”

“…In particular, aPL and use of GC, diabetes, depression, low levels of education have been related with cognitive dysfunction [30], which improved after prolonged use of aspirin, thus supporting the hypothesis of an impaired vascular supply in the pathogenesis of this complication. Other authors, also, found a correlation between cognitive dysfunctions and the presence of aPL, hypertension, Raynaud's phenomenon, disease-related cumulative damage [31,33].…”

Putative Mechanisms of Cognitive Dysfunction in Chemotherapy-Naïve Diffuse Large B-Cell Lymphoma: A Case Report and Review of the Literature

“…In rheumatoid arthritis (RA), IL-6 and TNF-a are elevated (Rosengren, Firestein, & Boyle, 2003) in serum as well as synovial fluid (Grom et al, 1996). Patients with RA show mild deficits of motor and processing speed, executive functions, and less often, learning and memory (Appenzeller, Bertolo, & Costallat, 2004), although others argue that those deficits may be attributable to nonspecific sources (Tomietto et al, 2007). Collectively, systemic inflammation associated with variable degrees of cognitive dysfunction across disease entities raises the question as to what factors determine cognitive expression of elevated proinflammatory cytokines levels.…”