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Abstract Details

COVID-19?associated myositis with severe proximal and bulbar weakness
Infectious Disease
P9 - Poster Session 9 (5:30 PM-6:30 PM)

Here we report a patient with COVID-19 associated inflammatory myopathy, presenting with facial, bulbar and proximal limb weakness. A 58-year-old woman presented with cough, dyspnea, and myalgia. Vital signs and her physical exam was unremarkable. Initial PCR testing for SARSCoV-2 was negative and the patient was discharged home. She returned three weeks later with more severe dyspnea, cough, dysarthria, dysphagia, odynophagia and severe generalized weakness with inability to ambulate. She had no sensory symptoms or bowel or bladder dysfunction. Physical examination was significant for tachycardia and oxygen saturation of 88% on room air. She had bilateral ptosis, facial weakness, hypernasal dysarthria and profound symmetric proximal limb weakness. Reflexes were symmetrically diminished. Repeated SARS-CoV-2 PCR was positive. MRI of the entire neuroaxis showed no central or peripheral nervous system involvement, but demonstrated diffuse muscle edema and enhancement, with a region of myonecrosis Motor nerve conduction studies were unremarkable, needle electromyography revealed sparse fibrillation potentials; On admission, CK was elevated to 700 U/L. Anti-Sjögren's-syndrome-related antigen and anti-small ubiquitin-like modifier-1 activating enzyme antibodies were both strongly positive and Ku antibody was weakly positive. Muscle biopsy showed perivascular inflammatory infiltration with endomysial extension, regenerating fibers and upregulation of HLA Class ABC expression on non-necrotic fibers. Our presumptive diagnosis was COVID-19 associated myositis and a five-day course of 1000 mg intravenous methylprednisolone was administered. Over two weeks, her CK levels normalized and she recovered the ability to raise her arms and legs from the bed and showed slow improvement in bulbar function.


Viral infection is a well-known cause of myositis. The severe immune activation known to occur in COVID-19 patients likely plays a major pathophysiologic role. The finding of multiple serologic autoimmune antibodies is intriguing suggesting an epiphenomenon rather than activation or unmasking of a specific immune response directed to the muscles.

Hui Zhang, MD
Dr. Zhang has nothing to disclose.
Zeinab Charmchi, MD Dr. Charmchi has nothing to disclose.
Roberta J. Seidman, MD (Department of Pathology) Dr. Seidman has nothing to disclose.
Yaacov Anziska, MD (SUNY-Downstate Medical Center) Dr. Anziska has nothing to disclose.
No disclosure on file
Jonathan Perk, MD, PhD, FAAN (Suny Downstate University) Dr. Perk has nothing to disclose.