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A 51-year-old woman with relapsing–remitting multiple sclerosis (RRMS) and 3-year history of natalizumab use developed expressive aphasia. A brain magnetic resonance image (MRI) showed left frontotemporal and right parietal lesion with mild contrast enhancement and cerebrospinal fluid (CSF) was positive for John Cunningham virus (JCV) by polymerase chain reaction (PCR). The patient received five cycles of plasmapheresis followed by intravenous immunoglobulin. Despite this intervention, her speech deteriorated and she developed right hemiparesis. Upon referral to our institution, CSF quantitative JCV PCR was notable for 834 copies/ml. The patient was given an initial dose of 50,000 units of interleukin-2 (IL-2) subcutaneously (SQ) followed by 1 million units IL-2 SQ daily. Due to concern for immune reconstitution inflammatory syndrome (IRIS), the patient also received intravenous methylprednisone weekly. The regimen was tolerated well by the patient with no severe adverse effects. Clinically, the patient showed some improvement, and became more responsive and regained right lower extremity antigravity strength. After 12 weeks of IL-2 therapy, JCV quantitative PCR was notable for 31 copies/ml and the patient was more responsive. Due to persistence of JCV, IL-2 therapy was changed to mefloquine. At follow up after 6 months, the patient showed no clinical deterioration.

Optical coherence tomography (OCT) is a noninvasive tool used for measuring tissue at micrometer resolution. It has been extensively applied to ocular pathologies and is now being studied as a biomarker in various neurologic conditions. The retina represents a unique environment for study, with unmyelinated axons that directly synapse into the central nervous system. When trying to quantify axonal degradation in neurologic disease, the currently used imaging modalities are limited in sensitivity and specificity. Early data suggest that several neurologic conditions have pathologic changes in the retinal nerve fiber layer of the eye, creating a potential surrogate marker for neurodegeneration. OCT has the potential to become a noninvasive, reproducible test for axonal degeneration that could become an invaluable tool for measuring the efficacy of potential neuroprotective agents. If the natural history of neurodegeneration, as measured by OCT, can be documented in diseases such as Alzheimer’s, Parkinson’s and multiple sclerosis, then OCT can be used to measure alterations in the rate of degeneration when treatment is applied. Thus, OCT represents a new, promising technology for documenting outcomes in neuroprotection trials.