New onset of ocular myasthenia gravis in a patient with COVID-19: a novel case report and literature review. [Review]
Citation: Journal of Neurology. 268(8):2690-2696, 2021 Aug.PMID: 33047223Institution: MedStar Washington Hospital CenterDepartment: NeurologyForm of publication: Journal ArticleMedline article type(s): Journal ArticleSubject headings: *COVID-19 | *Myasthenia Gravis | Aged | China | Female | Humans | Myasthenia Gravis/co [Complications] | Receptors, Cholinergic | SARS-CoV-2Year: 2021ISSN:- 0340-5354
Item type | Current library | Collection | Call number | Status | Date due | Barcode |
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Journal Article | MedStar Authors Catalog | Article | 33047223 | Available | 33047223 |
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.
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