Information has been received from the authors of the literature report as stated below, regarding a 66 year old woman with progressive relapsing multiple sclerosis (MS) who developed varicella-zoster virus (VZV) encephalitis while on fingolimod despite vaccination. She presented with a stuttering course over several weeks. Five months after starting fingolimod, she was treated for a presumed MS flare with a 5-day course of high-dose IV methylprednisolone (manufacturer unknown). A brain MRI showed stable chronic white matter lesions. She presented 18 days later with transient word-finding difficulty, was diagnosed with a TIA, and started on aspirin and a statin. She presented 9 days later after a generalized tonic clonic seizure; she had no history of prior seizures. Levetiracetam was started, and dalfampridine was stopped, with control of her seizures. During this admission, MRI showed restricted diffusion and T2 hyperintensity in the left caudate head. CSF had glucose of 50, protein of 74, 13 erythrocytes, 133 leukocytes (61% lymphocytes); VZV was detected by PCR (other viral studies were negative; CSF VZV immunoglobulin M and immunoglobulin G [IgG] were not assessed). In the interval preceding this admission, uveitis was diagnosed in the right eye; while there were no skin vesicular lesions, in retrospect the authors consider the uveitis a likely manifestation of VZV infection. Fingolimod was stopped, and she was treated with 11 days with IV acyclovir, but her mental status worsened 5 days after stopped acyclovir. A subsequent MRI showed progression of the caudate lesion thought to be caused by direct parenchymal infection, so she was restarted on IV acyclovir and steroids with clinical improvement and eventual discharge to a rehabilitation facility. Two months later, the patient was readmitted with new ischemic infarctions in 2 vessel territories, including the left globus pallidus and the left occipital lobe (subacute, not shown). CT angiography showed stenosis only in the right PCA, which was not associated with an ischemic lesion. Her CSF was retested and found to be negative for VZV, but the ischemic events were attributed to delayed VZV vasculitis. She subsequently stabilized with no further seizures or ischemic events over an 8-month follow-up period. VZV encephalitis was unexpected in this patient since she had had the chicken pox as a child and had received ZOSTAVAX 11 months prior to her seizure. Her serum IgG titers against VZV were > 100 ER/mL before initiation of fingolimod and at the time of VZV infection. Her MS regimen included both natalizumab and fingolimod in the previous year and 3 years on copaxone prior to that. After receiving high-dose methylprednisolone (manufacturer unknown) but before the diagnosis of VZV infection, the lymphocyte count dropped to 580 without substantial change in total leukocyte count. The case reported suggested that prior immunization did not eliminate the risk of serious VZV infection in the context of fingolimod therapy. It should be noted that this patient was not severely immunosuppressed and had a higher CD4 + count than is typical for patients on fingolimod. However, this patient's VZV infection developed (or worsened) after receiving high-dose steroids. These cases suggest that high-dose steroids should be used with caution in patients on fingolimod. Equally importantly, the case highlights several atypical manifestations of CNS VZV infections that might be found in immunosuppressed patients, including uveitis, direct infection of brain parenchyma, and vasculitis-induced cerebral ischemia. Upon internal review, the event of Varicella zoster encephalitis was considered to be serious due to other important medically event. Additional information has been requested.