Abstract
Tumor necrosis factor-a (TNF-a) inhibition, used in the treatment of rheumatoid arthritis (RA), is associated with central nervous system (CNS) events including new onset and/or exacerbations of pre-existing demyelinating neurological diseases. We describe a patient with refractory RA where adalimumab, a fully humanized IgG1 monoclonal antibody against TNF-a, may have contributed to the development of meningoencephalitis, with brain biopsy suggestive of hypertrophic pachymeningitis, a rare complication of this disease. The patient had recurrence of neurological symptoms upon repeated administration of adalimumab, and resolution of symptoms after withdrawal.
