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SLE Chorea — SCE Rheumatology MCQ

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HardSLE & Antiphospholipid SyndromeSLE ChoreaSCE Rheumatology

A 35-year-old woman with established systemic lupus erythematosus develops subacute generalised chorea. She has no family history of a movement disorder and has not taken a dopamine-receptor-blocking drug. There is no cognitive or psychiatric change, seizure activity or autonomic instability. Cerebrospinal fluid is acellular, and brain MRI, including diffusion-weighted imaging, shows no infarction. Lupus anticoagulant, anticardiolipin and anti-β2-glycoprotein I antibodies are persistently positive. Which pathophysiological mechanism best explains her chorea?

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Correct answer: A — Antiphospholipid-antibody-mediated striatal neuronal dysfunction and neuroinflammation

The best answer is A. Chorea is a recognised antiphospholipid-antibody-associated neuropsychiatric manifestation of SLE. Although basal-ganglia microthrombosis was historically proposed, overt infarction is not required: most reported patients do not have basal-ganglia lesions on conventional MRI, and current models favour antibody-mediated disruption of striatal neuronal function with neuroinflammatory effects, potentially alongside microvascular mechanisms. Anti-NMDA-receptor encephalitis would usually produce encephalopathy, psychiatric symptoms, seizures or autonomic disturbance. Huntington disease is a progressive inherited disorder rather than a subacute aPL-associated syndrome. Tardive dyskinesia requires relevant dopamine-receptor-blocking exposure. Parkinson disease results from nigrostriatal dopaminergic loss and principally causes bradykinesia and rigidity, not acute generalised chorea.

Reference: Zhang S et al. Dancing with disorder: chorea—an unusual and neglected manifestation of antiphospholipid syndrome. Lupus Science & Medicine. 2024. https://pubmed.ncbi.nlm.nih.gov/39353714/