Background The attribution of neuropsychiatric manifestations to systemic lupus erythematosus (SLE) or unrelated causes is often obscure.

Objectives The attribution of neuropsychiatric events to lupus (SLE related) or other causes (non-SLE related) in a large SLE cohort.

Methods Retrospective study of 707 SLE patients from “Attikon” lupus cohort ^[1,2]. Neuropsychiatric manifestations were classified as either primary neuropsychiatric SLE (SLE related; attributed to SLE using a combination of multidisciplinary physician judgment with attribution models ^[3]) or secondary NPSLE (non-SLE related; neuropsychiatric manifestations not attributed to SLE) or manifestations of uncertain attribution.

Results 258 patients developed 345 NP events in total. Among them, 140 (40.6%) were attributed to SLE, while 148 (42.9%) were classified as secondary NPSLE. In 57 NP events, the attribution remained uncertain. Among primary NP manifestations, cerebrovascular events (n=34, 24.3%), seizures (n=25, 17.8%) and cranial neuropathies (n=18, 5.2%) were the most common, while mood disorders (n=69, 46.6%) and headache (n=22, 14.9%) were the most common secondary NPSLE. The extra-CNS clinical and serological phenotype do not differ between primary and secondary NPSLE. Patients with primary NPSLE as compared to secondary NPSLE, were more likely to accrue irreversible damage (SLICC damage index > 0) (OR=2.88, 95%CI 1.67-4.96) and develop additional neuropsychiatric manifestations (OR=3.74, 95%CI 1.98-7.09).

Conclusion A significant proportion of NP events cannot classified as primary or secondary NPSLE. Cerebrovascular eventσ and seizures are the most common primary NP manifestations in SLE. The primary NPSLE is associated with accrual of irreversible damage and increased risk of developing additional NP manifestations.

References

1. Nikolopoulos D, Kostopoulou M, Pieta A, Karageorgas T, Tseronis D, Chavatza K. Evolving phenotype of systemic lupus erythematosus in Caucasians: low incidence of lupus nephritis, high burden of neuropsychiatric disease and increased rates of late-onset lupus in the ‘ Attikon ’ cohort. Lupus. 2020:1-9. doi:10.1177/0961203320908932
2. Nikolopoulos D, Kitsos D, Papathanasiou M, et al. Demyelinating Syndromes in Systemic Lupus Erythematosus: Data From the “Attikon” Lupus Cohort. Front Neurol. 2022;13. doi:10.3389/FNEUR.2022.889613
3. Bortoluzzi A, Scirè CA, Bombardieri S, et al. Development and validation of a new algorithm for attribution of neuropsychiatric events in systemic lupus erythematosus. Rheumatology. 2014;54(5):891-898. doi:10.1093/rheumatology/keu384

Acknowledgements: NIL.

Disclosure of Interests None Declared.

Keywords: Registries

DOI: 10.1136/annrheumdis-2023-eular.5996