Abstract
Fingolimod is a structural analog to sphingosine and acts as a functional antagonist for the sphingosine-1-phosphate receptor, exerting disease-modifying effects in MS by trapping lymphocytes in lymph nodes.1 Patients with MS have been rarely reported to develop tumefactive demyelinating lesions (TDLs) during fingolimod therapy, especially within the early period following the initiation of treatment.1 It has been speculated that alterations in the population of immune cells during fingolimod therapy may lead to TDLs.2
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