Article Text
Abstract
Description Manifestations of neuropsychiatric lupus are highly variable. Neuroimage such as magnetic resonance imaging (MRI) has been used extensively for evaluating neuropsychiatric lupus. Here we reported a patient with neuropsychiatric lupus and positive anti-ribosomal P antibody in acute confusion status underwent MRI evaluation, which revealed bilateral pallidal lesions.
Case Report This 24-year-old woman was diagnosed with systemic lupus erythematosus ( joint pain, positive ANA, low complement, anti-dsDNA, and anti-ribosomal P antibody) and had regular follow-ups at our rheumatology clinic. According to her mother, the patient had consciousness disturbance with anxiety and bad dreams ten days before ER visit. Three days before ER visit, incoherent speech and unstable gait were noted. She was brought to our clinic and then referred to ER. At ER, a fever up to 38.9 degree Celsius and tachycardia of 111 per minute with Glasgow coma scale E4M6V5 were recorded. Blood pressure was 132/76 mmHg, and SpO2 was 97%. Chest roentgenography or urine analysis showed no evidence of infection. EKG was normal. Methylprednisolone 20 mg every 12 hours was given. The brain MRI data showed symmetric T2 hyperintensity without diffusion restriction in bilateral globus pallidi (figure 1). Differential diagnoses such as CO toxification or serotonin syndrome were carefully ruled out by history taking. In this case, the MRI image revealed bilateral pallidal necrosis. Bilateral pallidal necrosis may present in CO toxification or serotonin syndrome. However, CO toxification usually presents with dizziness, and drowsiness followed by coma while serotonin syndrome is characterized by fever, drowsiness, and involuntary movement. Our patient presented with fever, involuntary movement, and hallucination, which is compatible with neuropsychiatric lupus manifestation but may be pathogenically related to basal ganglia system disorder as suggested by MRI.
Conclusions The neuroimage of bilateral pallidal necrosis in the patient with SLE provides a direction for elucidating the pathogenesis of neuropsychiatric lupus.
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