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BACKGROUND: Folic acid supplementation in patients with folic acid deficiency has been associated with increased clearance of phenytoin to its cytochrome P450 (CYP) 2C9-mediated metabolite, 5-(4'-hydroxyphenyl)-5-phenylhydantoin. OBJECTIVE: The aim of this study was to determine whether folic acid supplementation increases the dosage requirement of the CYP2C9 substrate warfarin, and the formation clearance of the CYP2C9-mediated product, (S)-7-hydroxywarfarin. METHODS: Patients aged >or=18 years with folic acid deficiency who were receiving long-term treatment with a stable dosage of warfarin were studied prospectively, before and 30 to 60 days after the initiation of supplementation with folic acid. Warfarin dosage and international normalized ratio (INR) were documented, and the formation clearance of (S)- and (R)-7-hydroxywarfarin and the oral clearance of (S)- and (R)-warfarin were determined. RESULTS: Twenty-four white patients (14 males; mean (SD) age, 55.0 [19.7] years; body mass index, 30.64 [6.8] kg/m(2)) were enrolled. Treatment with folic acid was associated with a significantly increased mean (SD) formation clearance of (S)-7-hydroxywarfarin (1.096 [0.816] vs 1.608 [1.302] mL/min; P = 0.048). Before folic acid supplementation, the mean (SD) warfarin dosage was 5.98 (2.12) mg/d, and the INR was 2.51 (0.55). During supplementation, the warfarin dosage was 6.17 (2.31) mg/d and the INR was 2.63 (0.65) (both, P = NS vs before supplementation). CONCLUSIONS: Folic acid supplementation was associated with significantly increased formation clearance of (S)-7-hydroxywarfarin. Changes in warfarin dosage requirements and INR were nonsignificant. [ABSTRACT FROM AUTHOR]

Objective: The first international consensus criteria for optic neuritis (ICON) were published in 2022. We applied these criteria to a prospective, global observational study of acute optic neuritis (ON)., Methods: We included 160 patients with a first-ever acute ON suggestive of a demyelinating CNS disease from the Acute Optic Neuritis Network (ACON). We applied the 2022 ICON to all participants and subsequently adjusted the ICON by replacing a missing relative afferent pupillary defect (RAPD) or dyschromatopsia if magnetic resonance imaging pathology of the optical nerve plus optical coherence tomography abnormalities or certain biomarkers are present., Results: According to the 2022 ICON, 80 (50%) patients were classified as definite ON, 12 (7%) patients were classified as possible ON, and 68 (43%) as not ON (NON). The main reasons for classification as NON were absent RAPD (52 patients, 76%) or dyschromatopsia (49 patients, 72%). Distribution of underlying ON etiologies was as follows: 78 (49%) patients had a single isolated ON, 41 (26%) patients were diagnosed with multiple sclerosis, 25 (16%) patients with myelin oligodendrocyte glycoprotein antibody-associated disease, and 15 (9%) with neuromyelitis optica spectrum disorder. The application of the adjusted ON criteria yielded a higher proportion of patients classified as ON (126 patients, 79%)., Interpretation: According to the 2022 ICON, almost half of the included patients in ACON did not fulfill the requirements for classification of definite or possible ON, particularly due to missing RAPD and dyschromatopsia. Thorough RAPD examination and formal color vision testing are critical to the application of the 2022 ICON., (© 2024 The Author(s). Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.)

Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare autoimmune demyelinating disorder of the central nervous system. Optic neuritis (ON) is the most common clinical manifestation of MOGAD in adults. In 2023, new MOGAD diagnostic criteria were proposed, highlighting the importance of supplemental criteria when MOG-immunoglobulin G (IgG) titers are unavailable., Objectives: To investigate the applicability of the 2023 MOGAD criteria in patients diagnosed with MOGAD and treated before the availability of MOG-IgG titers., Methods: We conducted a retrospective chart review of patients classified as MOGAD between 2010 and 2023 at Rabin Medical Center. Patient demographics as well as clinical and imaging data were collected, including visual acuity, expanded disability status score, core demyelinating events, antibody status, and brain and optic nerve magnetic resonance imaging data. Patients fulfilling the 2023 MOGAD criteria were reported as definite MOGAD., Results: Fifteen patients met the 2023 MOGAD diagnostic criteria despite lack of MOG-IgG titer. The most common supplemental criterion meeting the 2023 MOGAD criteria was optic disc edema (n=12, 80%), followed by longitudinal optic nerve involvement (53%), bilateral ON (40%), and perineural optic sheath enhancement (33%)., Conclusions: All patients with a clinical diagnosis of MOG-ON in our cohort fulfilled the 2023 MOGAD criteria despite the lack of antibody titers. The 2023 MOGAD criteria can be reliably applied to Israeli cohorts, prior to availability of MOGAD IgG titers, with particular attention to additional supplemental criteria. Since the 2023 MOGAD criteria were published, MOGAD IgG titers have been added to routine testing at our facility.

Background: Patients with genetic optic atrophies must navigate all stages of life with their visual impairment, including the important milestone of family planning. Advances in genetic testing now allows physicians and affected families to consider medical help with the aim of preventing blindness through preconception, preimplantation, and perinatal methods., Methods: This case series presents 4 patients with different genetic optic atrophies (Leber hereditary optic neuropathy [LHON], autosomal dominant optic atrophy, Wolfram syndrome, and papillorenal syndrome) who were followed by the Neuro-Ophthalmology Unit at a tertiary medical center between 2010 and 2023 and were of child-bearing age. The aim of this study was to increase understanding in family planning options for patients with optic atrophies, raise awareness of the solutions available, and provide guidance for clinicians to support their patients., Results: Advances in medicine, genetics, and medical technology allow multidisciplinary teams to assist patients in fulfilling their desire for a genetically healthy offspring. Customized solutions can be designed to meet the specific challenges posed by each type of genetic optic atrophy. The solutions proposed in this series are based on genetic testing done in the parents, which then allows to plan medical and genetic intervention individually. The solutions opted for in this series range from the decision to not have another child until PGD (Preimplantation genetic diagnosis)., Conclusion: We describe how genetic advancements have made it possible for patients with the 4 most common hereditary optic atrophies to fulfill their wish to have children without visually threatening genetic mutations. We also review the recent literature on the penetrance of optic atrophy in OA-mutation carriers and raise 2 significant ethical considerations: the reduction of a future life to a non-life-threatening impairment and that of public expenditure for non-life-threatening conditions., Competing Interests: The authors report no conflicts of interest., (Copyright © 2024 by North American Neuro-Ophthalmology Society.)

Acute optic neuritis treatment lacks standardized protocols. The value of oral prednisone taper (OPT) following intravenous methylprednisolone (IVMP) on visual outcome parameters in optic neuritis (ON) has never been explored. In the present retrospective study, we investigated whether OPT after IVMP affects the structural and functional visual outcomes of inaugural clinically isolated syndrome (CIS)- or multiple sclerosis (MS)-ON. Adult patients with acute, inaugural, unilateral CIS- or MS-ON, treated with IVMP in Germany and Israel were stratified into patients treated with IVMP alone-versus IVMP and OPT. Inclusion criteria were age ≥18, CIS or MS diagnosis according to McDonald criteria 2017, available visual acuity (VA) at nadir before treatment initiation and at follow-up ≥5 months, as well as a spectral domain optic coherence tomography (OCT) data scan at follow-up. Exclusion criteria included recurrent ON, concomitant ophthalmological comorbidities, optical coherence tomography (OCT) of insufficient quality and ON-related escalation therapy after IVMP. The structural outcome was defined as the average retinal nerve fiber layer (RNFL) difference between the ON-affected and the unaffected eye, while the functional outcome was defined as the final high-contrast best-corrected VA (HC-BCVA) at follow-up compared to nadir. The comparative analysis was performed using linear regression analysis, adjusted for sex, age, and days-to-treatment. Fifty-one patients met the inclusion criteria (25% male). The mean age was 33.9 (±10.23) years. Twenty-six patients (51%) received OPT following IVMP. There was no difference in nadir HC-BCVA between the groups (0.39 No OPT; 0.49 With OPT, P = 0.36). Adjusted linear regression analysis did not indicate an influence of OPT on RNFL thickness or on HC-BCVA (beta coefficient for RNFL difference in percentages: 0.51, 95%-CI: [-4.58, 5.59], beta coefficient for logMAR: 0.11, 95%; CI [-0.12, 0.35] at follow-up. In conclusion, the addition of OPT to IVMP did not affect RNFL thickness or the final VA in a retrospective cohort of 51 patients with inaugural acute CIS- or MS-ON. The results of this exploratory study are currently being re-examined in a large-scale, demographically diverse, prospective study., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Wilf-Yarkoni et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Optic neuritis (ON) often occurs at the presentation of multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), and myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD). The recommended treatment of high-dose corticosteroids for ON is based on a North American study population, which did not address treatment timing or antibody serostatus. The Acute Optic Neuritis Network (ACON) presents a global, prospective, observational study protocol primarily designed to investigate the effect of time to high-dose corticosteroid treatment on 6-month visual outcomes in ON. Patients presenting within 30 days of the inaugural ON will be enrolled. For the primary analysis, patients will subsequently be assigned into the MS-ON group, the aquapotin-4-IgG positive ON (AQP4-IgG+ON) group or the MOG-IgG positive ON (MOG-IgG+ON) group and then further sub-stratified according to the number of days from the onset of visual loss to high-dose corticosteroids ( days-to-Rx ). The primary outcome measure will be high-contrast best-corrected visual acuity (HC-BCVA) at 6 months. In addition, multimodal data will be collected in subjects with any ON (CIS-ON, MS-ON, AQP4-IgG+ON or MOG-IgG+ON, and seronegative non-MS-ON), excluding infectious and granulomatous ON. Secondary outcomes include low-contrast best-corrected visual acuity (LC-BCVA), optical coherence tomography (OCT), magnetic resonance imaging (MRI) measurements, serum and cerebrospinal fluid (CSF) biomarkers (AQP4-IgG and MOG-IgG levels, neurofilament, and glial fibrillary protein), and patient reported outcome measures (headache, visual function in daily routine, depression, and quality of life questionnaires) at presentation at 6-month and 12-month follow-up visits. Data will be collected from 28 academic hospitals from Africa, Asia, the Middle East, Europe, North America, South America, and Australia. Planned recruitment consists of 100 MS-ON, 50 AQP4-IgG+ON, and 50 MOG-IgG+ON. This prospective, multimodal data collection will assess the potential value of early high-dose corticosteroid treatment, investigate the interrelations between functional impairments and structural changes, and evaluate the diagnostic yield of laboratory biomarkers. This analysis has the ability to substantially improve treatment strategies and the accuracy of diagnostic stratification in acute demyelinating ON., Trial Registration: ClinicalTrials.gov, identifier: NCT05605951., Competing Interests: SA has received speaker honoraria from Alexion, Bayer, and Roche. JB reports payment for consultation from Horizon Therapeutics, Alexion, Antigenomycs, BeiGene, Chugai, Clene Nanomedicine, Genentech, Reistone Bio, Roche, Imcyse, and TG; grants from Alexion, Novartis, and the National Institutes of Health. In addition, JB has a patent on Compositions and methods for the treatment of neuromyelitis optica. YB has received speaker honoraria from Novartis, Roche, Genzyme-Sanofi, Merck, and Biogen. EC has received reimbursement for developing educational presentations, educational and research grants, consultation fees, and/or travel stipends from Biogen Argentina, Genzyme Argentina, Merck Argentina and LATAM, Roche Argentina and LATAM, Raffo, Novartis Argentina, LACTRIMS, and The Guthy-Jackson Charitable Foundation. JC has served on advisory boards for Horizon, Roche, and UCB. CC has received honoraria for speaking from Bayer and research funding from Novartis. JD has received royalties from Wolters Kluwer, Neurology—UpToDate and from Medlink Neurology as contributing author, from Athena Diagnostics for the use of Ma2 as an autoantibody test, and from Euroimmun for the use of NMDA-receptor, GABA(B)-receptor, GABA(A)-receptor, DPPX, and IgLON5 as autoantibody tests and has received research support from Advance Medical (allosteric modulation of NMDAR) SAGE Therapeutics, Instituto Carlos III/FEDER (FIS PI20/00197, CIBERER CB15/00010, Proyectos Integrados de Excelencia, PIE 16/00014 and AC18/00009), Agencia de Gestio d'Ajuts Universitaris i de Recerca (AGAUR), CERCA Programme Generalitat de Catalunya, ERA-NET NEURON, La Caixa Foundation Health Research Award, Pablove Foundation Childhood Cancer Grant, Safra Foundation, Sage therapeutics, Cellex Foundation, and La Caixa Health Foundation. EF has served on advisory boards for Alexion, Genentech, Horizon Therapeutics, and UCB. He has received speaker honoraria from Pharmacy Times. He received royalties from up-to-date. EF was a site primary investigator in a randomized clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics. EF has received funding from the NIH (R01NS113828). EF is a member of the medical advisory board of the MOG project. EF is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports. A patent has been submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity. CF participates in a regional medical board advisory of Alexion. CG-A has received grants from Biogen Colombia. JH reports grants for OCT research from the Friedrich-Baur-Stiftung and Merck, personal fees, and non-financial support from Celgene, Janssen, Bayer, Merck, Alexion, Horizon, Novartis, Roche, Biogen, and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work. JH was partially funded by the German Federal Ministry of Education and Research [(DIFUTURE), Grant Numbers 01ZZ1603[A-D] and 01ZZ1804[A-H]]. HK has received a grant from the National Research Foundation of Korea; consultancy/speaker fees or research support from Alexion, Aprilbio, Altos Biologics, Biogen, Celltrion, Daewoong, Eisai, GC Pharma, HanAll BioPharma, Handok, Horizon Therapeutics (formerly Viela Bio), Kolon Life Science, MDimune, Mitsubishi Tanabe Pharma, Merck Serono, Novartis, Roche, Sanofi Genzyme, Teva-Handok, and UCB; and is a coeditor for the Multiple Sclerosis Journal and an associated editor for the Journal of Clinical Neurology. CLM reports consultancy fees for Chiesi Farmaceutici, Regulatory PharmaNet, and Thenewway Srl and received speaker honoraria and/or travel support for meetings from Santhera Pharmaceuticals, Chiesi Farmaceutici, Regulatory Pharma Net, Thenewway Srl, First Class Srl, and Biologix. ML-P has received funding for travel and speaker honoraria from Novartis, Biogen, and Roche. MLei was funded by NHS (Myasthenia and Related Disorders Service and National Specialized Commissioning Group for Neuromyelitis Optica, UK) and by the University of Oxford, UK. She has been awarded research grants from the UK association for patients with myasthenia—Myaware and the University of Oxford. She has received speaker honoraria or travel grants from Biogen Idec, Novartis, Argenx, UCB, and the Guthy–Jackson Charitable Foundation. MLei serves on scientific or educational advisory boards for UCB Pharma, Argenx, and Viela/Horizon. SL has received consulting fees and speaker honoraria from Biogen, Novartis, TEVA, Genzyme, Sanofy, and Merck. PL has received reimbursement for developing educational presentations, educational and research grants, consultation fees, and/or travel stipends from Biogen Argentina and LATAM, Genzyme Argentina, Merck Argentina, Roche Argentina, Novartis Argentina, and LACTRIMS. AL has served as a Biogen, Bristol Myers Squibb, Merck Serono, Novartis, Roche, Sanofi/Genzyme, and Teva Advisory Board Member, has received congress and travel/accommodation expense compensations, or speaker honoraria from Biogen, Merck Serono, Mylan, Novartis, Roche, Sanofi/Genzyme, Teva, and Fondazione Italiana Sclerosi Multipla (FISM), her institutions received research grants from Novartis and Sanofi/Genzyme. SMo reports consultancy fees (Invex Therapeutics); advisory board fees (Invex therapeutics, Gensight); and speaker fees (Heidelberg engineering, Chugai-Roche Ltd., Allergan, Santen, Chiesi, and Santhera), all outside the submitted work. RM serves on scientific advisory boards for Alexion, Horizon Therapeutics, Roche, and UCB has received speaker honoraria from Alexion, Biogen, Horizon Therapeutics, Novartis, Roche, and Sanofi Genzyme, has received support for attending scientific meetings by Merck and Euroimmun, has received speaker honoraria from Biogen and Novartis. SMa received speaker honoraria for presenting at scientific meetings by Novartis and Biogen. SMo reports consultancy fees (Invex Therapeutics); advisory board fees (Invex therapeutics, Gensight); and speaker fees (Heidelberg engineering, Chugai-Roche Ltd., Allergan, Santen, Chiesi, and Santhera). All outside the submitted work. FC receives ongoing research support from the National Multiple Sclerosis Society (NMSS), the American Academy of Neurology (AAN), and Deutsche Gesellschaft für Neurologie (DGN). JPa has received support for scientific meetings and honorariums for advisory work from Merck Serono, Novartis, Chugai, Alexion, Roche, Medimmune, Argenx, UCB, Mitsubishi, Amplo, Janssen, and Sanofi. Grants from Alexion, Roche, Medimmune, UCB, and Amplo biotechnology. Patent ref P37347WO and license agreement Numares multimarker MS diagnostics Shares in AstraZeneca. Acknowledges Partial funding by Highly specialized services NHS England. SP is a named inventor on filed patents that relate to functional AQP4/NMO-IgG assays and NMO-IgG as a cancer marker, was consulted for Alexion and MedImmune, has received research support from Grifols, MedImmune, and Alexion, all compensation for consulting activities is paid directly to Mayo Clinic. SR has received research funding from the National Health and Medical Research Council (Australia), the Petre Foundation, the Brain Foundation (Australia), the Royal Australasian College of Physicians, and the University of Sydney. She was supported by an NHMRC Investigator Grant (GNT2008339). She serves as a consultant on an advisory board for UCB and Limbic Neurology and has been an invited speaker for Biogen, Excemed, and Limbic Neurology. AS received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Merck-Serono, Sanofi, Biogen, Roche, Novartis, Alexion, Janssen, and Horizon Therapeutics. DS received a grant from the National Multiple Sclerosis Society and serves on several advisory committees for the Multiple Sclerosis International Federation in unpaid roles. MS received speaker honoraria from Teva Pharmaceuticals and has received funding from the German Research Foundation, Federal Ministry of Education and Research and Federal Ministry for Economic Affairs and Energy, Volkswagen Stiftung, and Berlin Institute of Health. He is holding patents for the 3D printing of computed tomography models and is a shareholder of PhantomX and MSC3D. All unrelated to this work. PSu has served on advisory boards for Horizon Therapeutics, Viridian Therapeutics, Invex Therapeutics, Kriya Therapeutics, and GenSight Biologics. He receives research support from the NIH, DOD, Horizon, Invex, and Viridian. AM has received a grant for Biopas Laboratories and reports speaking fees from Chiesi. HZ received research grants from Novartis and speaking fees from Bayer Healthcare, unrelated to this project. FP served on the scientific advisory boards of Novartis and MedImmune; received travel funding and/or speaker honoraria from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an associate editor of Neurology: Neuroimmunology & Neuroinflammation; is an academic editor of PLoS ONE; consulted for Sanofi Genzyme, Biogen, MedImmune, Shire, and Alexion; received research support from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Geynzme, Alexion, and Merck Serono; and received research support from the German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy-Jackson Charitable Foundation, and NMSS. HS-K received speaker honoraria from Roche. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Asseyer, Asgari, Bennett, Bialer, Blanco, Bosello, Camos-Carreras, Carnero Contentti, Carta, Chen, Chien, Chomba, Dale, Dalmau, Feldmann, Flanagan, Froment Tilikete, Garcia-Alfonso, Havla, Hellmann, Kim, Klyscz, Konietschke, La Morgia, Lana-Peixoto, Leite, Levin, Levy, Llufriu, Lopez, Lotan, Lugaresi, Marignier, Mariotto, Mollan, Ocampo, Cosima Oertel, Olszewska, Palace, Pandit, Peralta Uribe, Pittock, Ramanathan, Rattanathamsakul, Saiz, Samadzadeh, Sanchez-Dalmau, Saylor, Scheel, Schmitz-Hübsch, Shifa, Siritho, Sperber, Subramanian, Tiosano, Vaknin-Dembinsky, Mejia Vergara, Wilf-Yarkoni, Zarco, Zimmermann, Paul and Stiebel-Kalish.)

Optic neuritis (ON) is a frequent presentation at onset of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). The pathophysiology underlying these diseases, especially MOGAD, is still being elucidated. While obesity has been reported to potentially be a risk factor for MS, this has not been explored in NMOSD or MOGAD. We aimed to investigate a possible association between obesity (body mass index [BMI] > 30 kg/m 2 ) in patients with MOGAD, aquaporin 4-IgG positive NMOSD (AQP4-IgG+ NMOSD) or MS. In this multicenter non-interventional retrospective study, data was collected from patients with a first ever demyelinating attack of ON subsequently diagnosed with MOGAD (n = 44), AQP4-IgG+ NMOSD (n = 49) or MS (n = 90) between 2005 and 2020. The following data was collected: age, sex, ethnicity, BMI (documented before corticosteroid treatment), and the ON etiology after diagnostic work-up. A mixed model analysis was performed to assess the potential of obesity or BMI to predict MOGAD-ON, and to distinguish MOGAD-ON from AQP4-IgG+ NMOSD-ON and MS-ON. Main outcome measures included BMI in patients with acute ON and subsequent diagnosis of MOGAD, AQP4-IgG+ NMOSD or MS. A higher BMI was significantly associated with a diagnosis of MOGAD-ON (p < 0.001); in MOGAD patients the mean BMI was 31.6 kg/m 2 (standard deviation (SD) 7.2), while the mean BMI was 24.7 kg/m 2 (SD 5.3) in AQP4-IgG+ NMOSD patients, and 26.9 kg/m 2 (SD 6.2) in MS patients. Mixed-effects multinomial logistic regression, adjusted for age and sex, with obesity as a binary variable, revealed that obesity was associated with a higher odds ratio (OR) of a subsequent MOGAD diagnosis (OR 5.466, 95% CI [2.039, 14.650], p = 0.001) in contradistinction with AQP4-IgG+ NMOSD. This study suggests an association between obesity and MOGAD. Our findings require further exploration, but could have significant pathophysiologic implications if confirmed in larger prospective studies., (© 2022. The Author(s).)

Background: A multitude of terms have been used to describe automated visual field abnormalities. To date, there is no universally accepted system of definitions or guidelines. Variability among clinicians creates the risk of miscommunication and the compromise of patient care. The purposes of this study were to 1) assess the degree of consistency among a group of neuro-ophthalmologists in the description of visual field abnormalities and 2) to create a consensus statement with standardized terminology and definitions., Methods: In phase one of the study, all neuro-ophthalmologists in Israel were asked to complete a survey in which they described the abnormalities in 10 selected automated visual field tests. In phase 2 of the study, the authors created a national consensus statement on the terminology and definitions for visual field abnormalities using a modified Delphi method. In phase 3, the neuro-ophthalmologists were asked to repeat the initial survey of the 10 visual fields using the consensus statement to formulate their answers., Results: Twenty-six neuro-ophthalmologists participated in the initial survey. On average, there were 7.5 unique descriptions for each of the visual fields (SD 3.17), a description of only the location in 24.6% (SD 0.19), and an undecided response in 6.15% (SD 4.13). Twenty-two neuro-ophthalmologists participated in the creation of a consensus statement which included 24 types of abnormalities with specific definitions. Twenty-three neuro-ophthalmologists repeated the survey using the consensus statement. On average, in the repeated survey, there were 5.9 unique descriptions for each of the visual fields (SD 1.79), a description of only the location in 0.004% (SD 0.01), and an undecided response in 3.07% (SD 2.11%). Relative to the first survey, there was a significant improvement in the use of specific and decisive terminology., Conclusions: The study confirmed a great degree of variability in the use of terminology to describe automated visual field abnormalities. The creation of a consensus statement was associated with improved use of specific terminology. Future efforts may be warranted to further standardize terminology and definitions., Competing Interests: The authors report no conflicts of interest., (Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the North American Neuro-Opthalmology Society.)

Objective: To investigate whether visual disability which is known to accumulate by poor recovery from optic neuritis (ON) attacks can be lessened by early treatment, we investigated whether the time from symptom onset to high-dose IV methylprednisolone (IVMP) affected visual recovery., Methods: A retrospective study was performed in a consecutive cohort of patients following their first aquaporin-4 (AQP4)-IgG or myelin oligodendrocyte glycoprotein (MOG)-IgG-ON. Best-corrected visual acuity (BCVA) in ON eyes at 3 months (BCVA3mo) was correlated with time to IVMP (days). In cases of bilateral ON, 1 eye was randomly selected., Results: A total of 29 of 37 patients had ON (27 AQP4-seropositive neuromyelitis optica spectrum disorder [NMOSD] and 9 MOG-IgG-ON), 2 of whom refused treatment. Of the 27 patients included, 10 presented later than 7 days from onset. The median BCVA3mo of patients treated >7 days was 20/100 (interquartile range 20/100-20/200). Patients treated >7 days had an OR of 5.50 (95% CI 0.88-34.46, p = 0.051) of failure to regain 0.0 logMAR vision (20/20) and an OR of 10.0 (95% CI 1.39-71.9) of failure to regain 0.2 logMAR vision (20/30) ( p = 0.01) compared with patients treated within 7 days. ROC analysis revealed that the optimal criterion of delay in IVMP initiation was ≤4 days, with a sensitivity and specificity of 71.4% and 76.9%, respectively., Conclusions: In this retrospective study of ON with AQP4 and MOG-IgG, even a 7-day delay in IVMP initiation was detrimental to vision. These results highlight the importance of early treatment for the long-term visual recovery in this group of patients. A prospective, multicenter study of the effects of timing of IVMP is currently underway., Classification of Evidence: This study provides Class IV evidence that hyperacute treatment of AQP4 and MOG-ON with IVMP increases the chance for good visual recovery (20/20 vision) and that even a greater than 7-day delay in treatment is associated with a higher risk for poor visual recovery.

Optic neuritis (ON) is a common clinical manifestation in myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease. Other clinical manifestations include acute demyelinating encephalomyelitis, transverse myelitis and neuromyelitis optica spectrum disorders. Uncommon presentations of MOG-positive disease have recently been reported. ON in MOG-positive disease commonly involves the anterior portion of both optic nerves, leading to bilateral disc swelling. During the early stages of ON, in the setting of bilateral disc swelling and pain, patients may initially be suspected as pseudotumor cerebri (PTC). In this study, we report five cases presenting early in the course of MOG-IgG-related ON, which were misdiagnosed as PTC in the emergency department. MOG-IgG-positive ON requires timely treatment to prevent RNFL and vision loss secondary to the high relapse rate associated with these antibodies. Our aim is to increase the awareness of the unique findings of MOG-IgG-positive ON, which may initially mimic PTC, thereby delaying treatment.

Background: Optic neuritis (ON) in patients with anti-myelin oligodendrocyte glycoprotein (MOG)-IgG antibodies has been associated with a better clinical outcome than anti-aquaporin 4 (AQP4)- IgG ON. Average retinal nerve fiber layer thickness (RNFL) correlates with visual outcome after ON., Objectives: The aim of this study was to examine whether anti-MOG-IgG ON is associated with better average RNFL compared to anti-AQP4-IgG ON, and whether this corresponds with a better visual outcome., Methods: A retrospective study was done in a consecutive cohort of patients following anti-AQP4-IgG and anti-MOG-IgG ON. A generalized estimating equation (GEE) models analysis was used to compare average RNFL outcomes in ON eyes of patients with MOG-IgG to AQP4-IgG-positive patients, after adjusting for the number of ON events. The final mean visual field defect and visual acuity were compared between ON eyes of MOG-IgG and AQP4-IgG-positive patients. A correlation between average RNFL and visual function was performed in all study eyes., Results: Sixteen patients were analyzed; ten AQP4-IgG-positive and six MOG-IgG-positive. The six patients with MOG-IgG had ten ON events with disc edema, five of which were bilateral. In the AQP4-IgG-positive ON events, 1/10 patients had disc edema. Final average RNFL was significantly better in eyes following MOG-IgG-ON (75.33μm), compared to 63.63μm in AQP4-IgG-ON, after adjusting for the number of ON attacks (GEE, p = 0.023). Mean visual field defects were significantly smaller (GEE, p = 0.046) among MOG-IgG positive ON eyes compared to AQP-IgG positive ON eyes, but last visual acuity did not differ between the groups (GEE, p = 0.153). Among all eyes, average RNFL positively correlated with mean visual field defect (GEE, p = 0.00015) and negatively correlated with final visual acuity (GEE, p = 0.00005)., Conclusions: Following ON, RNFL is better preserved in eyes of patients with MOG-IgG antibodies compared to those with AQP4-IgG antibodies, correlating with better visual outcomes., Competing Interests: Dr. Marignier serves on the scientific advisory board for MedImmune and has received honoraria from Biogen Idec, MerckSerono, Novartis, and Sanofi-Genzyme. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

One of the most important steps during Descemet stripping automated endothelial keratoplasty (DSAEK) is attaching the donor Descemet lenticule to the host's cornea. This is usually carried out by injecting air into the anterior chamber with a syringe and needle. We present an alternative technique using an air fluid exchange system connected to an anterior chamber maintainer used in 22 cases in our institute. This technique has proven to be simple and fast, thus facilitating the successful performance of DSAEK surgery., (Copyright © 2011 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved.)