Acetylcholine Nicotinic Receptors

His pain with vision movement was immediately relieved after starting steroid pulse therapy, and his visual acuity subsequently improved to a level of 0

His pain with vision movement was immediately relieved after starting steroid pulse therapy, and his visual acuity subsequently improved to a level of 0. 1 around the decimal level on the day of discharge, which was the tenth day after admission. 0.1 on the day of discharge. Outpatient follow-up 2?weeks later revealed left a decimal vision of 1 1.2, and a complete resolution of the left eye pain. Lessons: Our case indicated that COVID-19 might trigger an autoimmune response that leads to MOG antibody-associated ON, much like other pathogens that were reported in the past. The treatment response to steroid pulse therapy was preferable following a common course of MOG antibody-positive ON. Keywords: case statement, coronavirus disease 2019, myelin oligodendrocyte glycoprotein antibody, optic neuritis 1.?Introduction Currently, the worldwide prevalence of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a great concern for most countries. SARS-CoV2, which was first reported in December 2019 by Wu et al in Wuhan, China, causes coronavirus disease 2019 (COVID-19).[1] As the disease rapidly spreads worldwide, many clinical features of COVID-19, including respiratory,[2] cardiac,[3] neurological,[4C6] and ophthalmic[7C9] illness, has been reported. Recently, myelin Vanin-1-IN-1 oligodendrocyte glycoprotein (MOG) antibodies have been reported to encompass patients with varied pathologies involving the central nervous system, including optic neuritis (ON), acute disseminated encephalomyelitis, and encephalitis.[10C13] Here, we describe a case of acute ON associated with MOG antibody possibly induced by COVID-19 infection. 2.?Case statement A 47-year-old Japanese man presented to our clinic with left eye pain and an upper visual field defect. Two days before the onset of left eye pain, his son tested positive for COVID-19 by polymerase chain reaction (PCR) screening, and he was isolated at home as a close contact. He had a medical history of right adrenal resection due to main aldosteronism and recurrent paranasal sinusitis. He denied any history of immunological or neurological disease. He also did not have any family history of auto-immune diseases. He had no respiratory symptoms, fever, or loss of taste. He denied recent travel or contact with crowding. Our examination revealed a decimal visual acuity of 0.2 in the left eye, with a left relative afferent pupillary defect. The average critical flicker frequency value was 42?Hz Vanin-1-IN-1 in the right vision and 20?Hz in the left eye. Eye movement was normal, although left vision pain worsened when moving the eyes. Fundus examination with pupil dilation revealed no disc edema, disc redness, retinal hemorrhage, or switch in retinal vessels. Intraocular pressure was 14/14?mm Hg using a Goldmann applanation tonometer. He had symptoms of paranasal sinusitis, a stuffy nose, and flowing mucus. He tested positive for COVID-19 by nasopharyngeal PCR screening. To rule out nasal ON, we conducted magnetic resonance imaging (MRI) of the brain and orbits with gadolinium contrast. Postcontrast T1-weighted fat-suppressed MRI revealed the bilateral (but left-dominant) uniform enhancement along with optic nerve sheaths (Fig. ?(Fig.1).1). No sign of inflammation or accumulation Vanin-1-IN-1 CALCA of pus in the paranasal sinus was detected on MRI. Brain MRI revealed no sign of abnormal intensity, which is usually observed in multiple sclerosis. There was no abnormal sign on chest x-ray and computed tomography. Open in a separate window Physique 1 Postcontrast T1-weighted fat-suppressed magnetic resonance imaging (MRI) of the orbits. (A) Coronal MRI of the orbits reveals bilateral (but left dominant) uniform enhancement of the optic nerve. (B) Sagittal MRI of the right orbit reveals a slightly ill-defined appearance of the optic nerve and slight enhancement of optic nerve sheaths. (C) Sagittal MRI of the left orbit reveals uniform enhancement along with optic nerve sheaths. We also conducted blood and cerebrospinal fluid (CSF) testing. There were no abnormal blood count or biochemical profile results. The C-reactive protein level was 0.10?mg/dL and the erythrocyte sedimentation rate was 2?mm (1?mm/h). Serum test results for antinuclear antibody, QuantiFERON-TB, cytoplasmic-antineutrophil cytoplasmic antibody, perinuclear-cytoplasmic-antineutrophil cytoplasmic antibody, and aquaporin-4 were all unfavorable. Lumbar puncture revealed no elevation of white blood cells or proteins with a normal opening pressure of 160?cmH2O. PCR screening of SARS-CoV-2 RNA in the CSF was unfavorable. MOG-immunoglobulin G (MOG-IgG) screening in blood was positive with a titer of 1 1:128, whereas that in the CSF was unfavorable. After optic and systemic examination, the patient was diagnosed with MOG antibody-positive ON possibly induced by COVID-19 and.