Clinical Ophthalmology Open Access Full Text Article Dovepress open access to scientific and medical research C A s E R E P O R T Hemianopia and visual loss due to progressive multifocal leukoencephalopathy in natalizumab-treated multiple sclerosis Tina Rike Herold1 Veronika Jakl3 Anno Graser4 Kirsten Eibl-Lindner1,2 1Department of Ophthalmology, 2Department of Ophthalmology, Campus Innenstadt, 3Department of Neurology, 4Department of Clinical Radiology, Campus Grosshadern, University of Munich, Ludwig- Maximilians University, Munich, Germany Correspondence: Kirsten Eibl-Lindner Department of Ophthalmology, Ludwig-Maximilians University, University of Munich, Campus Innenstadt, Mathildenstrasse 8, Munich 80336, Germany Tel +49 89 5160 3811 Fax +49 89 5160 5160 Email kirsten.eibl@med.uni-muenchen.de submit your manuscript | www.dovepress.com Dovepress http://dx.doi.org/10.2147/OPTH.S30636 Abstract: This case describes typical ophthalmic findings as a key feature for diagnosis of progressive multifocal leukoencephalopathy (PML) and its possible differential diagnosis. A 58-year-old female patient with relapsing-remitting multiple sclerosis on immunotherapy with natalizumab developed visual disturbance, reading problems, and visual field defects due to PML. PML is a reactivation of latent infection with the John Cunningham virus, which is a type of polyomavirus acquired in childhood or adolescence and is quite common in the general population. PML so far has been mostly associated with other immunodeficiency disorders, such as acquired immunodeficiency syndrome, but is also gaining importance in association with the increasing use and duration of treatment with natalizumab in patients suffering from multiple sclerosis. Natalizumab is a highly specific α4-integrin antagonist approved for treat- ment of patients with active relapsing-remitting multiple sclerosis. Keywords: progressive multifocal leukoencephalopathy, natalizumab, multiple sclerosis, hemianopia Case report A 58-year-old female patient with relapse-remitting multiple sclerosis since 1992 had been treated from 1999 until 2007 with interferon beta-1a at two different doses. Because of leukopenia and increasing relapses, immunomodulatory therapy was switched to natalizumab (Tysabri®) in 2007. After only one relapse while on this treatment, she presented to an external neurological department in August 2010 with a reading disorder, deterioration in visual acuity, and weakness and spasm in her right leg. After intravenous treatment with methylprednisolone 1000 mg per day for 5 days, her clinical neurological symptoms partly recovered, but an ophthalmological deficit characterized by visual loss and visual field defects was unresponsive to this treatment (see Figure 1). Although ataxia and weakness on the right side increased, a lumbar puncture was negative for John Cunningham virus (by polymerase chain reaction [PCR]) at that time. In October 2010, the patient was referred to the neurological department of the Ludwig-Maximilians University in Munich with suspicion of progressive multifocal leukoencephalopathy (PML) because the John Cunningham virus PCR was now posi- tive in the cerebrospinal fluid (468 copies/mL). The ophthalmologic examination at our clinic in October 2010 showed a best corrected visual acuity of 20/100 Snellen equivalent in the right eye and in the left eye. The anterior segment was unremarkable in both eyes, as was the pupillary reaction. Examination of the fundus showed slight paleness of the optic nerve head bilaterally. The macular region and retinal periphery Clinical Ophthalmology 2012:6 1131–1133 1131 © 2012 Herold et al, publisher and licensee Dove Medical Press Ltd. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.