Herold et al Figure 1 Cranial T1-weighted magnetic resonance imaging at the end of september 2010 revealed nodular contrast enhancement with subcortical diffuse restriction in the right parieto-occipital region which is not typical for multiple sclerosis. Note: Also, the left side already showed a small subcortical lesion with diffusion restriction. were normal. The visual field (Octopus 101, 30°, Haag Streit, Germany) displayed a homonymous hemianopia on the left side (Figure 2). Cranial T1-weighted magnetic resonance imaging revealed a nodular contrast enhancement with sub- cortical diffuse restriction in the right parieto-occipital region, consistent with the diagnosis of PML, in addition to white matter lesions typical of multiple sclerosis (Figure 1). Lumbar puncture showed normal white blood cell count, glucose of 52 mg/dL and protein of 60 mg/dL in the spinal fluid. A PCR for John Cunningham virus was positive (431 copies/mL) and confirmed the diagnosis of PML. Within one month, general ataxia, reduction of free walk- ing distance to 165 m, and weakness in the left leg worsened (Expanded Disability Score 5.5), whereas the findings on visual field testing remained stable. Follow-up magnetic reso- nance imaging revealed new subcortical temporo-occipital Dovepress lesions with hyperintense signals in native T1-weighted images with diffuse restriction and contract enhancement at a size of 1.3 cm. The left side showed a small subcortical lesion with diffusion restriction. The patient then underwent combination therapy of immu- noadsorption (five times), mirtazapine 45 mg/day, mefloquine 250 mg for 7 days, and immunoglobulins 25 mg/day on two consecutive days, starting in October 2010. Cyclosporin 150 mg/day was added in order to suppress potential immune reconstitution inflammatory syndrome, which has been described in almost all patients with natalizumab-associated PML so far. Immune reconstitution inflammatory syndrome refers to clinical worsening in patients with opportunistic infections due to recovery of the immune system. Despite one month of therapy and repeat high-dose methylpredniso- lone, the patients’ clinical and neurological status steadily worsened. As a result, the ophthalmological parameters, including visual acuity and visual field, were not evaluable due to the poor clinical condition of the patient. According to the patients’ subjective symptoms and enlarging PML lesions on magnetic resonance imaging, it can be assumed that these parameters were further deteriorating. A biopsy was performed demonstrating that the PML was the leading pathological finding in this patient and not immune recon- stitution inflammatory syndrome.1 Comment This case demonstrates the difficulty in diagnosis and treat- ment of natalizumab-associated PML due to the subtle clinical Figure 2 Visual field testing in October 2010 demonstrated a homonymous hemianopia to the left (Octopus 101, 30°, Haag Streit, Germany). Note: Follow-up visual field testing during natalizumab cessation and PML treatment did not show any change in these findings. 1132 submit your manuscript | www.dovepress.com Dovepress Clinical Ophthalmology 2012:6