A 63-year-old Pakistani woman with history of hypertension and recent immigration to the U.S., presented with several months of progressive multifocal extremity weakness and numbness. She was initially treated with high-dose steroids for presumed inflammatory or autoimmune polyradiculopathy and incidentally diagnosed with hepatocellular carcinoma, which was treated with microablation therapy. She improved and was discharged on a steroid taper.
Several months later, she developed new right arm and worsening bilateral leg weakness and numbness. Symptoms were now refractory to high-dose steroids. Examination revealed right arm and bilateral leg areflexia. NCS/EMG revealed subacute severe right brachial plexopathy, and acute on chronic lumbosacral plexopathy without demyelinating features. MRI revealed enhancement of right cervical and bilateral lumbosacral nerve roots. She underwent three lumbar punctures, which revealed lymphocytic pleocytosis, hypoglycorrhachia, markedly elevated protein, and elevated adenosine deaminase. Cytology, flow cytometry, and other infectious studies were negative. Based on CSF findings and history of living in an endemic area, she was presumptively diagnosed with CNS tuberculosis and initiated on RIPE therapy and dexamethasone.
Despite treatment, she continued to decline. To improve diagnostic yield, steroids were discontinued prior to a fourth lumbar puncture, which revealed a minute clonal B-cell population. Lumbar dural biopsy confirmed diffuse large B-cell lymphoma.