Myelin oligodendrocyte glycoprotein-related optic neuritis/Bilateral optic neuritis; Myelin oligodendrocyte glycoprotein-related optic neuritis; bilateral painful, progressive vision loss that was worse in the left eye and with eye movements; bilateral painful eye movement; epithelial defect; left relative afferent pupillary defect; Frisen grade-1 disc edema; Perineuritis; optic atrophy; This case was reported in a literature article and described the occurrence of optic neuritis in a 51-year-old female patient who received Herpes zoster (Shingrix) for prophylaxis.   The patient's past medical history included keratomileusis (Laser-assisted in situ keratomileusis). Concurrent medical conditions included hypertension and alcohol use (consumed alcohol occasionally). Concomitant products included valsartan, glucosamine, estradiol (Estradiol Topical) and progesterone.   On an unknown date, the patient received Shingrix. On an unknown date, 11 days after receiving Shingrix, the patient experienced optic neuritis (serious criteria hospitalization and medically significant), myelin oligodendrocyte glycoprotein antibody-associated disease (serious criteria hospitalization and medically significant), loss of vision (serious criteria hospitalization and medically significant), painful eye movement (serious criteria hospitalization), persistent corneal epithelial defect (serious criteria hospitalization), relative afferent pupillary defect (serious criteria hospitalization), disc edema in ocular fundus (serious criteria hospitalization and medically significant), optic perineuritis (serious criteria hospitalization and medically significant) and optic atrophy (serious criteria hospitalization and medically significant). The patient was treated with medical devices nos (Bandage Contact Lens), corticosteroid nos (Corticosteroids (Drug Name Unknown)), methylprednisolone (Methylprednisolone Intravenous) and prednisone (Prednisone (Oral)). On an unknown date, the outcome of the optic neuritis, myelin oligodendrocyte glycoprotein antibody-associated disease, loss of vision, painful eye movement, persistent corneal epithelial defect, relative afferent pupillary defect, disc edema in ocular fundus, optic perineuritis and optic atrophy were recovered/resolved.   The reporter considered the optic neuritis, myelin oligodendrocyte glycoprotein antibody-associated disease, loss of vision, painful eye movement, persistent corneal epithelial defect, relative afferent pupillary defect, disc edema in ocular fundus, optic perineuritis and optic atrophy to be related to Shingrix.  Additional details were reported as follows: This case was reported in a literature article and described the occurrence of Myelin oligodendrocyte glycoprotein-related optic neuritis, in a 51 years old female patient, who was vaccinated with Shingrix vaccine (GlaxoSmithKline) for prophylaxis.  The patient was Caucasian. The patient past medical history was significant for hypertension and Laser-assisted in situ keratomileusis (LASIK). The patient had no prior neurologic signs or symptoms or any family history of demyelinating disease. Medications included valsartan, glucosamine, vitamin D, topical estradiol, and progesterone. The patient consumed alcohol occasionally.  On an unspecified date, the patient received Shingrix (Herpes zoster subunit vaccine) vaccine (Route and site of administration unspecified; batch number not provided, dosage unknown). The age at vaccination was not provided. On an unspecified date, an unknown period after vaccination the patient was presented to hospital with 11 days of bilateral painful, progressive vision loss that was worse in the left eye and with eye movements. The patient was evaluated at an outside facility and treated with corticosteroids and a bandage contact lens for a presumed epithelial defect before the presentation. Three weeks prior to presentation to hospital the patient received the herpes zoster vaccination. 11 days after the vaccination, the patient developed Myelin oligodendrocyte glycoprotein-related optic neuritis (MOG-related optic neuritis). On presentation to the hospital, visual acuity was 20/50 oculus dextrus (OD) and count fingers was at 3 feet oculus sinister (OS). The patient's pupils were isochoric and there was a left relative afferent pupillary defect. External and slit lamp examinations were normal oculus uterque (OU) and the previously noted corneal disease had resolved. On dilated fundus exam, bilateral Frisen grade-1 disc edema was noted. Optical coherence tomography revealed average retinal nerve fiber layer thickness of 98 micrometre OD and 135 micrometre OS (normal range 100 micrometre±10). Laboratory testing for infectious, inflammatory and metabolic etiologies was initially negative except for antinuclear antibody, which was positive with a titer of 1:80. Magnetic resonance imaging (MRI) of the brain revealed bilateral anterior optic nerve and nerve sheath enhancement extending 1.75 cm OS and 0.75 cm OD on the T1 fat-suppressed post contrast sequences, suggestive of bilateral optic neuritis and perineuritis. There was no enhancement of the optic chiasm. The brain, cervical and thoracic MRI were normal. Lumbar puncture showed elevated myelin-binding protein level (16.10; normal 0-5.5 ng/mL) and white blood cell count (4; normal 0-5 cells per cubic millimeter). Biochemistry and opening pressure were normal, and no oligoclonal bands were seen. The patient was treated with 3 days of intravenous methylprednisolone then 11 days of oral prednisone 60 mg daily (approximate 1 mg/kg), and then 2 days of 20 mg and 2 days of 10 mg, similar to the Optic Neuritis treatment trial. It was patient's first episode of optic neuritis and the patient was without demyelinating lesions on MRI, prolonged immunosuppression was not considered necessary and the patient was closely monitored for relapse. MOG antibody was tested with a fluorescence activated cell sorting assay. This testing returned positive at a titer of 1:100 (normal: negative), consistent with MOG-related optic neuritis. The patient was reevaluated after 10 months. The patient had no new symptoms. The visual acuity was 20/40 OD and 20/20 OS, dilated fundus examination revealed temporal pallor OU, and the remainder of the exam was unremarkable. Average retinal nerve fiber layer thickness on Ocular coherence tomography (OCT) was 68 micrometre and 70 micrometre, consistent with optic atrophy. Repeat MOG testing was negative, possibly consistent with a monophasic presentation in the setting of herpes zoster subunit vaccination. Repeat MRI of the brain, orbits, cervical and thoracic spine 12 months after the initial presentation showed resolution of the bilateral optic neuritis/perineuritis. There were no demyelinating lesions or other pathologies. This case has been considered as serious due to hospitalization The authors commented, "Herpes zoster subunit vaccine SHINGRIX is a nonlive recombinant adjuvant vaccine that contains varicella zoster virus glycoprotein E (gE) and AS01B, an adjuvant suspension that induces a greater gE-specific cell-mediated immune response. Though generally safe, the vaccine can trigger a reaction such as fever, headache, or myalgias. Vaccine reactions can also involve recrudescence of previous symptoms, especially in people with known neurological deficits such as multiple sclerosis. The vaccine may also trigger an acute autoimmune event such as acute disseminated encephalomyelitis or antibody mediated optic neuritis. There are 71 reported cases of postvaccination CNS disorders, with acute demyelinating encephalomyelitis and optic neuritis comprising most of these CNS clinical manifestations. In these cases, clinical symptoms had a mean onset of 14.2 days after vaccination, similar to the time course of our patient. Overall, these CNS events are rare. Though the specific mechanism of disease is unconfirmed, hypotheses have been raised about molecular mimicry, enhanced antigen presentation, or a similar mechanism whereby infection and the immune response to infection can trigger demyelination.  Given the known immune activity of the herpes zoster subunit vaccine and the known elevated Cerebrospinal fluid (CSF) myelinbinding protein in our patient, we may hypothesize that this mechanism triggered an acute demyelinating process. There have been few reports of post-vaccination MOG antibody-positive disease in the literature. One case involved a patient having multiple vaccinations (tetanus, measles, mumps, rubella, varicella) before pregnancy and an MOG titer of 1:20 discovered after a presentation with acute disseminated encephalomyelitis-like disease without encephalopathy 2-3 weeks after vaccination. Subsequent MOG testing after recovery was negative. Two other cases were reported to have their first demyelinating episode 2 weeks post-vaccination (diphtheria, tetanus, pertussis, polio, and influenza in the first case and diphtheria, tetanus, and pertussis in the second case). They went on to subsequently have numerous relapses, requiring intravenous methylprednisolone, plasma exchange, and immunosuppressive therapy. Vaccination was suggested to have unmasked the underlying demyelinating disease in these patients. In general, MOG antibody testing and the herpes zoster subunit vaccine (Shingrix) are both fairly new and were both first approved for use in 2017. Thus, we may continue to see new data emerge regarding an association between the two. TMhe herpes zoster subunit vaccine has been implicated in 2 of the 71 reported post-vaccination demyelination cases, though neither of which were MOG antibody related. Given the temporal relationship between these vaccines and symptom onset, it is difficult to associate any of the individual vaccines with the development of anti-MOG-associated demyelination. To our knowledge, this is the first reported case of MOG related optic neuritis after administration of the herpes zoster subunit vaccine (Shingrix). This patient had a clinical presentation consistent with MOG-related optic neuritis, with bilateral painful vision loss and extensive bilateral optic nerve involvement and anterior nerve involvement and disc swelling that was steroid responsive and with anti-MOG antibody positivity in the serum. Clinicians should consider antibody-mediated optic neuritis after vaccination, including MOG-related optic neuritis. If an individual is positive for anti-MOG antibody at presentation, we recommend retesting patients after their initial illness to risk stratify the patient's likelihood of having a monophasic illness or relapsing disease. If antibodies continue to be negative after 6 months, this supports a low likelihood of recurrence and suggests probable monophasic disease. Additionally, monitoring for and counseling about prior post-vaccine adverse outcomes will be relevant in clinical discussions regarding vaccination as the novel coronavirus (2019-nCoV) vaccines become available to the public."