Citation: Journal of Neurology. 268(8):2690-2696, 2021 Aug.; .Journal: Journal of neurology.Published: 2021; ; ; ISSN: 0340-5354.Full author list: Daimee M; Kataria S; Sriwastava S; Sultan S; Tandon M.UI/PMID: 33047223.Subject(s): *COVID-19 | *Myasthenia Gravis | Aged | China | Female | Humans | Myasthenia Gravis/co [Complications] | Receptors, Cholinergic | SARS-CoV-2Institution(s): MedStar Washington Hospital CenterDepartment(s): NeurologyActivity type: Journal Article.Medline article type(s): Journal ArticleOnline resources: Click here to access onlineDigital Object Identifier: https://dx.doi.org/10.1007/s00415-020-10263-1 (Click here)Abbreviated citation: J Neurol. 268(8):2690-2696, 2021 Aug; .Abstract: The novel coronavirus outbreak of SARS-CoV-2 first began in Wuhan, China, in December 2019. The most striking manifestation of SARS-CoV-2 is atypical pneumonia and respiratory complications; however, various neurological manifestations are now well recognized. Currently, there have been very few case reports regarding COVID-19 in patients with a known history of myasthenia gravis. Myasthenia gravis (MG) causes muscle weakness, especially respiratory muscles, in high-risk COVID-19 patients, which can lead to severe respiratory compromise. There are few reported cases of severe myasthenia crisis following COVID-19, likely due to the involvement of the respiratory apparatus and the use of immunosuppressive medication. We report the first case of ocular MG developing secondary to COVID-19 infection in a 65-year-old woman. Two weeks prior to hospitalization, the patient suffered from cough, fever, and diarrhea and was found to be positive for COVID-19 via a nasopharyngeal RT-PCR swab test. The electrodiagnostic test showed decremental response over more than 10% on repetitive nerve stimulation test of orbicularis oculi. She tested positive for antibodies against acetylcholine receptor. COVID-19 is known to cause the release of inflammatory cytokines, leading to immune-mediated damage. MG is an immune-mediated disorder caused by molecular mimicry and autoantibodies against the neuromuscular junction.