Fingolimod is an oral sphingosine 1-phosphate receptor modulator that prevents recirculation of lymphocyte subsets from lymph nodes. It decreases the number of relapses, slows the progression of disability, and improves MRI endpoints in patients with relapsing-remitting multiple sclerosis (RRMS).1 Infrequent but specific side effects are bradycardia, leukopenia, and macular edema.Case report. In November 2010, a 23-year-old woman with RRMS since September 2007 started fingolimod 0.5 mg per day in the setting of the openlabel FTY720D2316 trial. Interferon-␤ treatment was initiated in 2008, but discontinued mid-2010 because of side effects. Her disease course was relatively mild with low frequency and complete recovery of relapses. In March 2011, she presented with a left-sided hemiparesis, headache, and nausea that had gradually developed over 2 weeks. Because she had no clinical signs of infection, an exacerbation of multiple sclerosis (MS) was considered initially and she was admitted for IV methylprednisolone treatment. During the administration of the first dosage, the hemiparesis progressed and she had 2 partial epileptic seizures with jerks of the left leg, 1 of which generalized. We discontinued methylprednisolone and fingolimod and started valproic acid and acyclovir. New demyelinating lesions, infection (herpes or varicella encephalitis, toxoplasmosis, or brain abscess), and neoplasm (lymphoma, glioma) were considered to be possible causes of her symptoms.Cranial MRI showed 2 large white matter lesions in the right hemisphere with surrounding vasogenic edema, mass effect, and open ring enhancement after gadolinium administration (figure, A). This suggested multifocal tumefactive demyelination, which was supported by magnetic resonance spectroscopy ( figure, B-D). A pyogenic abscess was unlikely because of absence of diffusion restriction.Serologic studies were negative for syphilis, Borrelia, HIV, and toxoplasmosis; and cytomegalovirus (CMV), herpes simplex virus (HSV), varicella-zoster virus (VZV), and Epstein-Barr virus (EBV) were all immunoglobulin G positive and immunoglobulin M negative. In the CSF we found 7 leukocytes/L (0-4), glucose 3.5 mmol/L (serum glucose 6.4 mmol/L), protein 1,065 mg/L (0 -500). No pathologic cells were found in the CSF. CSF cultures for bacteria, mycobacteria, yeast, and fungus were negative. CSF PCR for mycobacteria, CMV, EBV, HSV-1, HSV-2, VZV, and JCV was negative.We discontinued treatment with acyclovir after viral PCRs returned negative. The patient recovered within 1 week and was discharged with a slight residual left-sided hemiparesis.In the weeks after discharge she recovered completely. We performed serial follow-up MRI, showing gradual regression and remyelination of the lesions. Discrete areas of focal demyelination remained. One month after discharge, small new gadolinium-enhancing lesions were seen, indicating new inflammatory MS activity ( figure, A). This led us to start glatiramer acetate.Discussion. Tumefactive demyelination refers to demyelinating brain le...

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Glossary CI = confidence interval; IQR = interquartile range; LED = levodopa equivalent dose; OLVG = Onze Lieve Vrouwe Gasthuis; PD = Parkinson disease; VIPD-Q = Visual Impairment in Parkinson's Disease Questionnaire.