Initial unsolicited report received from the literature on 07-Apr-2018. The following is the abstract from the article: The existence of vaccine-associated optic neuritis is essentially based on the temporal relationship between the administration of a vaccine and the development of optic neuritis in patients with no other known aetiologies for infectious or non-infectious inflammation that could account for the optic neuritis. Influenza vaccine (inactivated or live attenuated) is considered to be one of vaccines that could be related to optic neuritis. The authors describe a rare case of bilateral asymmetric optic neuritis with leptomeningeal enhancement on magnetic resonance imaging (MRI) in a previously healthy young woman who received inactivated influenza vaccination 2 weeks before the onset of symptoms. This case involves female patient (Age not reported) who was vaccinated with dose of INFLUENZA VACCINE (INACTIVATED INFLUENZA VACCINE) (batch number, expiry date, route and site of administration were not reported) on an unspecified date. The patient's medical history and concomitant medication were not reported. On an unspecified date, two weeks following the vaccination, patient had bilateral asymmetric optic neuritis. Laboratory investigation includes leptomeningeal enhancement on magnetic resonance imaging (MRI). Corrective treatment was not reported. Outcome of event was unknown. Upon internal review the case was considered as serious because of important medical event: bilateral asymmetric optic neuritis. Follow-up report received from a literature on 10-Apr-2018. On an unknown date, two weeks after the vaccination, patient had right frontal headache and blurred vision and pain on eye movement of the right eye. Patient had no other constitutional symptoms such as skin rash, fever, and muscle aches and no recent history of febrile illness or tick exposure. Initial ophthalmologic examination of the right eye showed reduced visual acuity (20/40), dyschromatopsia (4/10 on Hardy-Rand-Rittler [HRR] test), a visual field defect (constriction of peripheral visual field) on Humphrey automated perimetry, a relative afferent pupillary defect, and optic disc swelling suggestive of optic neuritis. The left eye was normal on examination, and neurologic examination was otherwise unremarkable. MRI of the brain and orbits with and without gadolinium showed enhancement of the right retrobulbar optic nerve and right hemispheric leptomeninges. Given the atypical presentation of optic neuritis, further evaluation was performed. Serologic studies showed increased erythrocyte sedimentation rate (37mm/h) and C-reactive protein (1.7mg/L),mildly elevated immunoglobulin G4 (IgG4) (112.7 mg/dL) and low vitamin D; however, antinuclear antibody, antineutrophil cytoplasmic antibody, anti-Ro/La, C3/4, aquaporin 4 (AQ4) antibody, angiotensin-converting enzyme (ACE), Lyme, syphilis, human immunodeficiency virus (HIV), Bartonella, Brucella, and quantiferon gold were negative. Vitamins B1, B6, B12, and E levels were normal. Opening pressure on lumbar puncture was 23 cm H2O, and cerebrospinal fluid (CSF) showed leukocytosis (45/micoL; mononuclear dominant), normal protein and glucose levels, no oligoclonal IgG, negative tests for cytomegalovirus, Epstein-Bar virus, herpes simplex virus, and varicella-zoster virus, and negative cultures for Mycobacteriumand other fungi. Chest computed tomography was normal except for a small thyroid nodule. Positron emission tomography (PET) scan showed no lesion outside the brain and orbit. Her vision of the right eye started improving, and she deferred treatment and did not receive corticosteroid. About 3 weeks after the initial visit, the patient developed mild pain and blurred vision in the fellow (left) eye. Repeat brain MRI with and without gadolinium showed new abnormal enhancement of the left optic nerve. Given the atypical presentation of the inflammatory optic neuritis and the involvement of fellow eye, she underwent meningeal and brain biopsies with craniotomy from the right frontal lobe, which showed reactive astrogliosis with lymphocytic infiltration without evidence of neoplasm, granulomas, or vasculitis. Her vision started improving at hospital day 4 and had improved to 20/20 in both eyes by the time of discharge. She deferred intravenous corticosteroid therapy but received oral corticosteroid for 14 days with tapering. A week after completing the course of oral corticosteroids, she experienced worsening of the vision in her right eye (counting fingers at 3 ft). Repeat brain and spinal MRI showed enhancement of the right optic nerve. Repeated rheumatologic work-up, infectious disease work-up, CSF analysis, and paraneoplastic antibody assay, including repeated AQ4 antibody, were unremarkable or negative. She received a 3-day course of intravenous corticosteroid, with minimal improvement of her vision, and then received 5-day plasmapheresis. Patient's other lab data and other corrective treatment was not reported. Patient did not recover from bilateral asymmetric optic neuritis. Also did not recover from blurred vision (also reported as patient's vision of the right eye recovered to 20/25 in 2 weeks after the completion of the treatment and in 3 weeks after recurrence of vision loss). Outcome of other events were not reported. List of documents held by sender: none.; Sender's Comments: Follow-up received on 10-Apr-2018 changes the assessment as follows: The patient experienced bilateral asymmetric optic neuritis post vaccination with inactivated influenza vaccine. Time to onset was compatible. There is a possibility that the event might have alternate underlying infectious etiology. Most cases of optic neuritis are associated with MS, even though optic neuritis can occur in isolation. Lab tests confirming the cause of event or ruling out infectious etiology must be requested. Based upon reported information the role of the vaccine cannot be assessed.