Case presentationA 38-year-old woman with MS receiving natalizumab presented to the neurology clinic with the complaint of a new neurologic symptom. Clinical courseThe patient had a 6-year history of clinically stable MS, albeit exhibiting radiographic progression despite strict adherence to daily subcutaneous glatiramer acetate (GA).Furthermore, on switching first to weekly IM interferon beta (IFN-β)1a, she experienced clinical relapses and subsequently developed recalcitrant transaminitis while using three times weekly, subcutaneous IFN-β 1b (figure 1).Owing to continued disease activity and side effects from GA and IFN, she was switched to monthly IV natalizumab despite John Cunningham Polyomavirus antibody positivity (JCV Ab+) with an Ab index 3.37-3.83.She remained clinically and radiographically stable from the inception of natalizumab with surveillance MRIs performed quarterly.However, after her 47th natalizumab infusion, she developed a coarse action and position tremor involving her right distal upper extremity.Brain MRI revealed a nonenhancing left thalamic T2 hyperintensity (figure 2, A and B).Natalizumab was suspended while her physicians investigated the underlying etiology for her new clinical symptom and corresponding imaging abnormality.CSF analyses was noninflammatory and JCV DNA was undetectable by PCR.The initial diagnostic supposition was that the lesion was potentially on the basis of inflammatory demyelination, even in the absence *National Multiple Sclerosis Society Case Conference Proceedings Faculty.
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