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Objectives Neuropsychiatric systemic lupus erythematosus (NPSLE) encompasses a broad range of central and peripheral nervous system manifestations, including cerebrovascular events, seizures, and cognitive or mood disorders. Movement disorders such as chorea or ballismus are uncommon presentations, usually attributed to immune-mediated basal ganglia dysfunction or vascular mechanisms related to antiphospholipid antibodies (aPL). Recognizing these hyperkinetic manifestations is crucial, as they may indicate active neuroimmune involvement early in the disease course.Methods We will present a case of a patient who has been followed for 6 years with diagnoses of SLE and APS and who developed ischemic stroke and movement disorder.Results A 40-year-old woman with a six-year history of SLE and APS presented with right arm weakness, gait disturbance, and dysarthria. Her SLE diagnosis was based on Raynaud’s phenomenon, digital ulcers, photosensitivity, arthritis, and positive ANA (1:640, homogeneous), anti-dsDNA (135 IU/mL), anti-RNP, and anti-SSA antibodies. APS was supported by repeated positivity for anticardiolipin IgM. Comorbidities included diabetes, hypertension, hypothyroidism, and avascular necrosis of both femoral heads. Current medications included mycophenolate mofetil, methylprednisolone, nifedipine, bosentan, and aspirin, along with intermittent iloprost and hyperbaric oxygen therapy for digital ulcers. A brain MRI showed a left middle cerebral artery (MCA) infarction without basal ganglia involvement. During hospitalization, she developed involuntary movements of the right arm consistent with hemichorea/ballismus. Warfarin anticoagulation and rituximab were initiated. One month later, her motor function improved, and involuntary movements regressed significantly.Conclusions This case illustrates hemichorea/ballismus in a patient with SLE and APS following an MCA infarct, occurring without radiologic basal ganglia involvement, suggesting a clinicoradiologic dissociation within NPSLE. The pathophysiology may involve immune-mediated disruption of the striato-thalamo-cortical network, microvascular injury beyond MRI resolution, or circulating autoantibody effects on dopaminergic signaling. The patient’s recurrent anticardiolipin IgM positivity supports a thrombotic mechanism, while the favorable response to anticoagulation and rituximab highlights the dual need to address both vascular and inflammatory pathways. Recognition of such cases is critical for early intervention, as combined immunomodulatory and antithrombotic therapy can lead to substantial neurological recovery.