Fulminant CNS Demyelination After Discontinuation of TNF-Inhibitor(TNFi) therapy
NEUROLOGY(2020)
Abstract
Objective: Review a rare case of TNFi induced central nervous system (CNS) demyelination after TNFi discontinuation. Background: U.S. Food and Drug Administration issued warning labels exist on all TNFi for “rare cases of new onset or exacerbation of CNS demyelinating disorders”. Typically, these demyelinating conditions improve or resolve with discontinuation of TNFi therapy. We present a case of CNS demyelination onset during TNFi therapy, with continued progression 9 months following TNFi discontinuation. Design/Methods: NA Results: A 54 year-old gentleman with history of psoriatic arthritis, treated with TNFi therapy x 8 months, presented with gait instability, blurry vision and tonic spasms of the left hand. On exam, direction-changing nystagmus, ocular misalignment, and left hemiparesis/hemiataxia were noted. Magnetic resonance imaging (MRI) demonstrated numerous enhancing and non-enhancing lesions within the cerebrum, brainstem and spinal cord. Cerebral spinal fluid analysis demonstrated lymphocytic pleocytosis, elevated protein and 5 unpaired oligoclonal bands, without infectious or neoplastic findings. Histopathology from a brain biopsy was consistent with demyelination. TNFi therapy was discontinued. Six weeks later, decreased monocular visual acuity with associated red desaturation was noted. Repeat MRI exhibited enhancement of the optic nerve and new enhancing lesions within the CNS. Treatment with an additional course of intravenous steroids, plasmapheresis and Rituximab was initiated. The patient has remained clinically stable, but continues to have enhancing lesions 9 months after initial presentation. Conclusions: CNS demyelination in association with TNFi therapy has been well reported; however, the natural history and response to treatment remains largely uncharacterized [7]. We present a case of CNS demyelination with continued progression following TNFi discontinuation, necessitating treatment with high dose steroids and steroid-sparing immunomodulation. It is crucial for neurologists to recognize the potential of TNF blockade leading to demyelination of the CNS even after discontinuation of therapy and order repeat imaging if symptoms are persistent. Disclosure: Dr. Beeler has nothing to disclose. Dr. Baker has nothing to disclose.
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Key words
fulminant cns demyelination,tnf-inhibitor
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