Clinical Characteristics and Risk Factors Associated with Seizures in Neuropsychiatric Systemic Lupus Erythematosus
Andrea Nuñez de Caceres Garcia1, David Medina Julio2, Ximena García-Velazquez2, Osmar Albores3, Alvaro Calderon-Cantu2, Rogelio Dominguez-Moreno4, Michelle Coutiño Díaz5, Carlos Cantu3
1Tec de Monterrey / Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, 2Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, 3Neurology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, 4Neurology, Danish Headache Center, 5Tec de Monterrey
Objective:
To describe clinical characteristics and risk factors associated with seizures caused by Neuropsychiatric Systemic Lupus Erythematosus (NPSLE) compared to non-NPSLE seizures in SLE.
Background:
Seizures are among the most common of the 19 NPSLE syndromes and are associated with an increased risk of death. However not all seizures in SLE patients are due to lupus activity, all other causes of seizures must first be excluded.
Design/Methods:
A retrospective case-control study conducted at a referral center in Mexico City using medical records of 85 patients diagnosed with SLE and seizures between 2005-2024.
Results:
The case group included 37 patients with NPSLE associated seizures, 32 females (86.5%), 5 males (13.5%); mean age of 26.2±9 years. Control group encompassed 48 patients with SLE and seizures from other causes, 40 females (83.3%), 8 (16.7%) males; mean age 28.2±11.5 years. The etiology of NPSLE seizures remained unknown in 12 cases (32.4%) after excluding all other causes, while 13 (35.1%) were associated with CSF Ribosomal P antibodies, 5 (13.5%) with thrombosis from antiphospholipid syndrome, and 7 (18.9%) with vasculitis. Most common etiologies in control group were posterior reversible encephalopathy syndrome 18 (37.5%) and hypertensive crisis 7 (14.5%), followed by structural 5 (10.4%) and metabolic causes 5 (10.4%). Generalized seizure onset was the most frequent in both groups, occurring in 20 (54%) cases and 34 (70.8%) controls. Borderline positive associations between cases of NPSLE seizures and a low C3 (OR = 4.2, 95% CI 1.1-16.1, p = 0.05), plus a low C4 (OR = 5.2, 95% CI 1.1-25.2, p = 0.05) were found. NPSLE cases had a higher mean SLEDAI-2K score (21.9 vs 15.8) p=0.05 at SLE diagnosis compared to controls.
Conclusions:
Other etiologies of seizures must first be considered before attributing them to NPSLE. Determining seizure etiology in patients with SLE is essential in guiding management and treatment.
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