Background Up to 50% of systemic lupus erythematosus (SLE) patients experience neuropsychiatric manifestations (NP) during the disease course but many might have subclinical neuropsychiatric lupus (NPL), causing significant increase in morbidity and mortality. The pathogenesis of NPL is multifactorial and involves various inflammatory cytokines, autoantibodies and immune complexes1.
Objectives To examine for the presence of subclinical NPL, cerebral atherosclerosis and their correlation - if any to brain magnetic resonance imaging (MRI/MRA) findings and SLE disease activity.
Methods This is a cross sectional observational study that included thirty adult female SLE patients fulfilling the updated ACR classification criteria for SLE2. All were subjected to: detailed history taking, thorough clinical examination, assessment of SLE disease activity using Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score, psychometric evaluations using the Modified Mini-Mental State Examination (MMSE) to assess for cognitive dysfunction, Hamilton Depression Rating Scale (HAM-D) and Hamilton Anxiety Scale (HAM-A) to assess for the presence of depression and anxiety respectively. CBC, ESR, full blood chemistry, urine analysis, protein/creatinine ratio, brain MRI/MRA.
Results The mean age was 31.7 years (22 to 40 years). 12 patients (40%) had positive antiphospholipid (APL) antibodies with or without clinically evident antiphospholipid syndrome (APS). 22/30 (73.33%) had different NP manifestations, 13 had depression (43.3%), 15 had anxiety (50%) and 16 had cognitive impairment (53.3%). All patients with depression and anxiety, 87.5% of patients with dementia had MRI abnormalities. All SLE patients with positive aPL were found to have MRI abnormalities, while MRI abnormalities were found in only 8 SLE patients with negative aPL (100% vs. 44.4%) (p<0.001). There was a statistically significant correlation between SLE disease activity and both NP manifestations and MRI/MRA abnormalities. aPL antibodies also had a significant correlation with NP manifestations. MRI abnormalities included discrete white matter lesions (60%), cortical atrophy (25%) and gross infarctions (15%). MRA revealed atherosclerotic changes of one or more of the large intracranial vessels in (27.27%) of NPSL patients.
Conclusions Significant number of SLE patients without overt neuropsychiatric manifestations were found to have subclinical cerebrovascular and cognitive dysfunctions, depression and anxiety by simple bedside questionnaires. SLE disease activity positively correlates with neuropsychiatric manifestations. The presence of APL antibodies is a strong risk factor for developing NPSL. Several distinct brain MRI patterns were observed in patients with active NPSL, suggestive of different pathogenetic mechanisms.
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Disclosure of Interest None declared