Herpes Zoster Optic Neuropathy: Comment

Letters to the Editor be-determined role of other influencing factors. Or, optic atrophy could be considered a manifestation of a progressive leukoencephalopathy (2) as seen in patients with the progressive form of multiple sclerosis (3). However, this hypothesis does not explain findings obtained in some adult patients with severe leukoencephalopathies who remain free of significant thinning of the RNFL, or with young adult patients such as ours, with optic atrophy early in the clinical course. Third, is optic atrophy in VWM/CACH an expression of factors associated with the environment, metabolism, or genetics? This is a challenging and unsolved question. Factors including the role of oxidation stress impacting optic nerve function (4) and the presence of susceptibility genes could explain, at least partly, the variability of optic atrophy in leukoencephalopathy. The presence of optic atrophy in VWM/CACH patients requires further study. It is unclear if it is a specific phenotype of the disease, a nonspecific marker of the progression of brain involvement, or due to environmental or genetic susceptibility factors. Simon Samaan, MD Department of Medical Genetics, UF Molecular Genetics, Robert Debre University Hospital, Paris, France INSERM UMR-S1141, DHU PROTECT, Paris Diderot University, Robert Debre University Hospital, Paris, France Pierre Labauge, MD, PhD Neurology Unit, University Hospital Guy de Chauliac, Montpellier, France The authors report no conflicts of interest. Damien Biotti, MD Neurology Unit, Pierre Paul Riquet/Purpan University Hospital, Toulouse, France Jeanne Lajoie, MD Ophthalmology Unit, Purpan University Hospital, Toulouse, France Fabrice Bonneville, MD, PhD Radiology Unit, Purpan University Hospital, Toulouse, France Herpes Zoster Optic Neuropathy: Comment I read with great interest the retrospective case series by Kaufman et al (1) describing the presentation, management, and visual outcomes of 6 patients with herpes zoster optic neuropathy (HZON). HZON is a rare presentation of herpes zoster ophthalmicus. This optic neuropathy may be difficult to diagnose and the consensus on management is lacking. As the authors have pointed out, nonarteritic ischemic optic neuropathy, giant cell arteritis, and other infectious or inflammatory etiologies can affect a similar age group, and it is important to differentiate between these entities. I have seen 2 cases of HZON where viral polymerase chain reaction (PCR) of aqueous fluid obtained by anterior chamber paracentesis was helpful in confirming 572 REFERENCES 1. Barros SR, Parreira SCR, Miranda AFB, Pereira AMB, Campos NMP. New insights in vanishing white matter disease: Isolated bilateral optic neuropathy in adult onset disease. J Neuroophthalmol. 2018;38:42-46. 2. Pfueller CF, Brandt AU, Schubert F, Bock M, Walaszek B, Waiczies H, Schwenteck T, Dorr J, Bellmann-Strobl J, Mohr C, Weinges-Evers N, Ittermann B, Wuerfel JT, Paul F. Metabolic changes in the visual cortex are linked to retinal nerve fiber layer thinning in multiple sclerosis. PLoS One. 2011;6:e18019. 3. Saidha S, Al-Louzi O, Ratchford JN, Bhargava P, Oh J, Newsome SD, Prince JL, Pham D, Roy S, van Zijl P, Balcer LJ, Frohman EM, Reich DS, Crainiceanu C, Calabresi PA. Optical coherence tomography reflects brain atrophy in multiple sclerosis: a fouryear study. Ann Neurol. 2015;78:801-813. 4. Kimura A, Namekata K, Guo X, Noro T, Harada C, Harada T. Targeting oxidative stress for treatment of glaucoma and optic neuritis. Oxid Med Cell Longev. 2017;2017:2817252. the diagnosis of HZON. The first patient was a 73-yearold man who developed V1 distribution rash and was placed on an unknown medication for 2 weeks (patient was managed out of the country at the time). On discontinuing the medication, he developed acute vision loss on the affected side. We evaluated him 6 weeks later and he was found to have a pale nerve with visual acuity 20/150. MRI was unable to be performed due to the patient's pacemaker. Computed tomography scan of the brain and orbits and an extensive infectious and inflammatory serum panel were negative. Aqueous fluid was positive for varicella zoster virus (VZV). The patient was started on antiviral therapy with subsequent improvement of visual acuity to 20/80 in the involved eye. Our second patient was a 65-year-old man who presented with unilateral stromal keratitis and iritis. Initially, there was limited view to the fundus due to the anterior segment Letters to the Editor: J Neuro-Ophthalmol 2018; 38: 566-574 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Letters to the Editor findings, and he was treated for ocular herpes simplex and started on oral acyclovir (400 mg · 5 per day) and topical steroid drops. Two weeks later, the keratitis and uveitis resolved without improvement of vision, and the patient was found to have optic disc edema. He was referred to our service, and an MRI of the brain and orbits and a comprehensive inflammatory and infectious serum panel were negative, but viral PCR of the aqueous fluid was positive for VZV, and of note, negative for herpes simplex virus. The patient's acyclovir dose was increased to 800 mg · 5 per day along with a 2-week course of oral prednisone. At 2-week follow-up, the patient had resolution of optic disc swelling and visual acuity improved from 20/60 to 20/30. Kaufman et al described the work-up of HZON in their case series to include brain MRI, and erythrocyte sedimentation rate, C-reactive protein, and serum studies to rule out other infectious and inflammatory etiologies. Cerebrospinal fluid analysis was not diagnostic in their case series; however, I believe that aqueous PCR can be helpful in confirming the diagnosis of HZON. Fulminant Intracranial Hypertension Managed With Temporary Lumbar Drain 20/50 bilaterally. Visual field mean deviation was 5.08 dB, right eye, and 6.07 dB, left eye, and retinal nerve fiber layer thickness was 87 mm, right eye and 86 mm, left eye. The patient was maintained on acetazolamide 2 g/day. To avoid severe vision loss, patients with FIH may require urgent surgical intervention. One study of patients with FIH indicated that better visual recovery occurred when surgery was undertaken within 4 days of initial evaluation (2). There are several aspects of our patient's case that are worthy of mention. First, in other reports, lumbar drains were left in place from 3 to 10 days (1,3). In our patient, the lumbar drain was in place for only 48 hours, yet she still experienced significant improvement in visual function. Our patient's drainage rate was initially titrated to 20 cc of CSF every 2 hours and then reduced, while Jiramongkolchai et al (1) set a rate of 10-15 cc every hour per the institutional protocol of their medical center. Finally, lumbar drains previously have been used as a temporizing measure before definitive surgery in patients with FIH. Yet, the few studies that have been reported raise the possibility that lumbar drains may have an important role to play in re-establishing normal intracranial pressure and possibly reduce the need for a surgical procedure. In addition to the lumbar drain, administering acetazolamide, methylprednisolone, or furosemide likely contributed to our patient's recovery. Yet, it was only after placement of a lumbar drain that our patient's clinical course began to show improvement. Further research is needed to determine the optimal duration and drainage rate required for a lumbar drain in the treatment of FIH. I n the Journal of Neuro-Ophthalmology, Jiramongkolchai et al (1) reported 2 patients with fulminant intracranial hypertension (FIH) who were managed with temporary lumbar drains in the setting of severe visual loss. We also cared for a pediatric patient with FIH because of minocycline and used a lumbar drain as part of the therapeutic regimen. A 15-year-old girl with a body mass index of 30 kg/m2 was evaluated for FIH. Visual acuity was hand motions, right eye, and 20/400, left eye. Automated visual fields (Humphrey 24-2) revealed mean deviations of 235.0 dB in both eyes with foveal sensitivities of 23 dB, right eye, and 13 dB, left eye. There was Frisen Grade 5 papilledema bilaterally, and optical coherence tomography showed peripapillary retinal nerve fiber layer thickening in both eyes (325 mm, right eye; 362 mm, left eye). Opening pressure on lumbar puncture was 50 cm of H2O with normal cerebrospinal fluid (CSF) constituents. The patient was initially managed with intravenous medications: acetazolamide 4 g/day, methylprednisolone 1 g/day, and furosemide 80 mg/day. Because of failure to improve, a temporary lumbar drain was placed on hospital Day 4 and titrated to drain 20 cc of CSF every 2 hours. On postlumbar drain Day 1, the drain was titrated to 12 cc of CSF every 2 hours, but on postlumbar drain Day 2, the patient developed lowerextremity paresthesias concerning for over drainage and the drain was removed. Over the next several weeks, the patient's vision began to gradually improve and at her 4-month visit, acuity was Letters to the Editor: J Neuro-Ophthalmol 2018; 38: 566-574 Cindy Lam, MD, FRCSC Department of Ophthalmology and Vision Sciences, Kensington Vision and Research Centre, University of Toronto, Toronto, Canada The author reports no conflicts of interest. REFERENCE 1. Kaufman AR, Myers EM, Moster ML, Stanley J, Kline LB, Golnik KC. Herpes zoster optic neuropathy. J Neuroophthalmol. 2018;38:179-189. Yandong Bian, BA Dan Gong, MD 573 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.