SLE and autoimmune neuropsychiatry — structured clinical viva

Reject false dichotomies. Neither "antipsychotics only" nor reflexive same-night cyclophosphamide without infection work-up is correct. Frame as possible inflammatory NPSLE psychosis with active SLE serology pending full attribution.[1][2]

Nomenclature. Use ACR 1999 case definitions (19 syndromes). Psychosis is listed; listing is not automatic causality.[1]

Differential. Primary psychosis coincidence; infection/opportunistic CNS infection; steroid toxicity if recent high-dose exposure; metabolic; APS cerebrovascular disease if focal signs; primary autoimmune encephalitis if multistage hard neurologic course.[2][3]

Mechanisms for the viva. Inflammatory autoantibodies (anti-ribosomal P association; NR2 cross-reactive anti-DNA — DeGiorgio) versus ischaemic aPL injury. Branch treatment accordingly.[4][5][2]

Work-up. Activity labs, aPL, infection screen, MRI, EEG/LP as indicated, consider anti-P. Normal MRI does not exclude diffuse disease.[3][6]

Treatment. After infection exclusion, severe inflammatory NP events: high-dose glucocorticoids ± immunosuppression (cyclophosphamide classically for severe CNS) under rheumatology. Symptomatic lowest-effective antipsychotic as bridge. aPL vascular phenotype → antithrombotic track.[2][3]

Answer the team. "We will not depot-and-forget, and we will not cytotoxic-blind. Attribute, exclude infection, co-manage mechanism-based disease therapy, use psychotropics supportively."[2][6]