Posterior reversible encephalopathy syndrome (PRES) is observed in <1% of patients with systemic lupus erythematosus (SLE). ^1-3 Distinguishing PRES from lupus cerebritis has important therapeutic implications for treatment, however distinguishing the two can be a diagnostic dilemma. ^{2-5, 7, 8} Here we present a case and suggest a potential clinical approach. 

CASE REPORT 

A 21-year-old female with poorly controlled SLE complicated by prior CNS lupus vasculitis and uncontrolled hypertension presented to the emergency department with two days of worsening frontal headache, blurry vision, vomiting and abdominal pain. On admission, systolic blood pressures were in the 220’s and she developed worsening confusion without focal deficits. Her creatinine was 2.14 mg/dL, platelets 36/µL, and rheumatologic markers consistent with a lupus flare. MRI brain showed T2/FLAIR hyperintensities diffusely throughout the pons, midbrain, bilateral parietal, occipital and bilateral frontal lobes, as well as foci of diffusion restriction in bilateral pons suggestive of acute microinfarction. These features were concerning for PRES and possible lupus cerebritis. Improved mentation occurred as blood pressure was controlled. Management with intravenous nicardipine, solumedrol, rituximab, and oral cyclophosphamide yielded further improvement in mentation, headache, and blurry vision.

Lupus cerebritis and PRES have overlapping clinical features, radiographic findings, and CSF profiles.^4-9  The finding of FLAIR hyperintense lesions in bilateral occipital and parietal areas on brain MRI, in the setting of uncontrolled hypertension and encephalopathy, is a classic radiographic pattern of PRES; however,  other areas may also be involved radiographically.^5,9 Microinfarctions and inflammatory CSF findings, such as pleocytosis and elevated protein,  may be present in either condition.⁶ These overlapping features highlight a need for appropriate interpretation considering the clinical context. Our patient’s history of prior CNS lupus, encephalopathy in the setting of an active lupus flare and concurrent uncontrolled hypertension prompted initiation of treatment of both potential etiologies with subsequent improvement.