Case Report: New Onset Hyperkinetic Movement Disorder in IgA Lambda Myeloma
Recommended Citation
Agarwal U, Fu S, Albanna AJ, Qureshi MA, Bulica B, Newman DS. Case Report: New Onset Hyperkinetic Movement Disorder in IgA Lambda Myeloma. Parkinsonism Relat Disord 2025; 134.
Document Type
Conference Proceeding
Publication Date
5-1-2025
Publication Title
Parkinsonism Relat Disord
Abstract
Introduction: We report a case of new-onset movement disorder and encephalopathy in a 57-year-old female with IgA lambda multiple myeloma. Case Description: The patient was evaluated for persistent encephalopathy and hyperkinetic movements. Previously, she was hospitalized for hypercalcemia and diagnosed with IgA lambda myeloma (IgA >6000 mg/dL, positive bone marrow biopsy). Her hospital course included sepsis, respiratory failure requiring intubation, and fluctuating mentation. She exhibited persistent upper extremity hyperkinetic movements. A hyperviscosity panel showed elevated plasma viscosity of 1.91 (normal <1.6), prompting transfer for plasmapheresis. At our institution, examination revealed encephalopathy with frequent hyperkinetic movements in bilateral upper extremities, including abduction, choreiform, and near-ballistic patterns. MRI brain showed microbleeds at the gray-white junction without other abnormalities. EEG indicated mild-to-moderate encephalopathy. Lumbar puncture revealed elevated lactate (3.1 mmol/L), with unremarkable autoimmune and viral studies. Lab work showed anemia (Hb 7.4 g/dL) and elevated IgA (5525 mg/dL). The patient underwent plasmapheresis to reduce IgA below 2000 mg/dL, followed by three cycles of bortezomib and dexamethasone. Over three weeks, her mentation improved, and she regained the ability to follow commands and answer yes/no questions. Her hyperkinetic movements resolved. Unfortunately, her hospital stay was prolonged by complications, and she expired two months later. Discussion: This case highlights hyperviscosity-associated encephalopathy and hyperkinetic movement disorder in IgA lambda myeloma, managed effectively with plasmapheresis and chemotherapy. It also highlights the importance of CSF lactate as a surrogate marker for microvascular hypoxia leading to encephalopathy and chorea. The existing literature lacks reports of choreiform or other hyperkinetic movement disorders linked to IgA myeloma or other monoclonal gammopathies. Hyperviscosity-induced movement disorders, however, are documented in polycythemia vera. It has been hypothesized that similar hyperviscosity-driven mechanisms underlie diabetic striatopathy via cytotoxic edema affecting basal nuclei. This case underscores the importance of early recognition and treatment of hyperviscosity to address neurological complications in myeloma.
Volume
134
