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Neurology ; 98(18 SUPPL), 2022.
Article in English | EMBASE | ID: covidwho-1925347

ABSTRACT

Objective: NA Background: A 32 year-old man with no medical history and no prior documented SARS-CoV2 infection developed malaise, dyspnea, and exercise intolerance in the days following first dose SARS-CoV2 vaccine administration (Pzifer-BioNTECH mRNA). Dysarthria and dysphagia manifested within hours of the second vaccine dose administration, and progressed to severe bifacial weakness with reduced eyelid and mouth closures within one week's time. Design/Methods: NA Results: Severe dysphagia prompted hospitalization and neurology consultation. At an outside hospital, IVIG (2 gm/kg) and pyridostigmine were initiated for empiric treatment of suspected myasthenia gravis. The patient's facial strength, dysphagia and dysarthria improved. Anti-AChR and anti-MuSK serologic studies were non-reactive. A thymoma was not identified. MR brain, cerebrospinal fluid, and ganglioside antibody serologic studies were without explanatory pathological findings. A nerve conduction study, obtained in the outpatient setting, demonstrated decrement in facial nerve-nasalis CMAPs with low frequency repetitive stimulation, consistent with a post-synaptic neuromuscular disorder. Monthly IVIG infusions and pyridostigmine were prescribed. The patient's symptoms worsened and he was rehospitalized. A repeat nerve conduction study revealed post-exercise and repetitive stimulation-induced decrements in median-abductor policus brevis and spinal accessorytrapezius CMAPs, confirming a systemic post-synaptic neuromuscular disorder. AChR binding and blocking antibodies were ultimately detected through repeat serologic testing, consistent with autoimmune myasthenia gravis. Plasma exchange and prednisone therapies engendered near full symptom resolution. Conclusions: While myasthenia gravis symptom exacerbation and crisis in the setting of vaccination are well described, no cases of new-onset myasthenia gravis following vaccination are reported to date. Further, the patient's bifacial weakness with impaired eyelid closure was atypical in contrast to ptosis and diploia typically observed in oculo-bulbar forms of myasthenia gravis. The immune-mediated mechanism and clinical phenotype of SARS-CoV2 vaccinationassociated myasthenia gravis require further investigation.

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