Abstract Neuropsychiatric systemic lupus erythematosus (NPSLE) encompasses a heterogeneous spectrum of central nervous system manifestations. Its diagnosis remains clinical and by exclusion, as neuroimaging, cerebrospinal fluid (CSF) analysis, and serologic markers lack sensitivity and specificity 1,2. We present a rare case of an elderly woman with end-stage renal disease due to lupus nephritis and new-onset status epilepticus whose course highlights the difficulty of distinguishing post-ictal encephalopathy and infection from lupus cerebritis. An 85-year-old woman with history of hypersensitivity pneumonitis, end stage renal disease due to lupus nephritis , on dialysis presented with acute altered mental status and two episodes of generalized tonic-clonic seizures, necessitating admission to the Intensive care unit for seizure management. Continuous EEG demonstrated left fronto-central focal status epilepticus. Initial MRI and CSF studies for infectious etiologies were unrevealing; C3 was mildly decreased but C4 and anti-dsDNA were normal. Given concern for neuropsychiatric lupus, she received high dose methylprednisolone for three days followed by a slow taper over the next ten days, without significant neurological improvement. Repeat MRI revealed a left anterior temporal FLAIR hyperintensity with mild enhancement, thought to represent post-ictal changes versus lupus cerebritis. A second Lumbar puncture remained non-inflammatory but demonstrated a positive CSF antineuronal antibody. Despite this finding, complements and dsDNA remained normal, and CRP was markedly elevated, suggesting infection rather than an immune mediated pathology. Through multidisciplinary consensus, it was determined that the presentation was most consistent with prolonged post-ictal encephalopathy and critical illness, and further immunosuppression or plasmapheresis was not recommended. Through antiepileptic therapy, the seizures were controlled, with slow but incomplete return to baseline. This case illustrates several atypical features that challenge the diagnosis of neuropsychiatric SLE 3,4. First, NPSLE rarely presents de novo in advanced age. Second, the absence of pleocytosis or elevated protein on serial CSF examinations, stable complement levels, negative anti-dsDNA, and lack of clinical response to high-dose steroids argue against active lupus cerebritis 5. Third, the isolated CSF antineuronal antibody, while highly specific in selected cohorts, can be detected in up to 10% of patients without NPSLE and should not be interpreted in isolation. This case emphasizes the importance of a comprehensive, multidisciplinary evaluation and caution against over-diagnosing neuropsychiatric lupus based solely on antibody positivity or nonspecific MRI findings, especially in elderly patients with competing infectious and metabolic processes. This abstract is funded by: None
Rodriguez et al. (Fri,) studied this question.