ABSTRACT
Background and aims: Although various reports indicated the presence of myalgia in 44–70% and “skeletal muscle injury” (increased CK and myalgia) in 23% of hospitalized patients with SARS-CoV-2 infection, the characterization of neuromuscular involvement is still unsatisfactory, and electrophysiologic studies have rarely been performed. Methods: We describe a case of acute myopathy at onset of SARS-CoV-2 infection. Results: A 73-year-old woman, with post-infarct ischemic heart disease in her medical history, presented with progressive weakness in the lower limbs and pain, without fever. On admission, neurological examination showed proximal tetraparesis, prevalent in the lower limbs, and reflexes were diminished. CK in the serum was to >6000 U/L (normal value 10–145 U/L), hepatic enzymes were elevated (GOT 814 U/L, n.v.1–31), urin Hb > 1 (n.v. absent).Polymerase chain reaction (PCR) testing for SARS-COV-2 was positive. Chest X-ray showed right lower patchy opacities, but oxygen saturation was 94% on room air. Motor nerve conduction studies (NCS) showed mild sensory polyneuropathy;the needle electromyography (EMG) demonstrated myopathic abnormalities with fibrillation potentials in the lower limbs, rapid recruitment on interference pattern and reduced compound muscle action potential amplitude. The therapy with high dose of steroids induced significative clinical improvement. In two weeks, CK levels almost normalized and the patient recovered the ability to walk with assistance. Conclusions: The severe immune activation known to occur in COVID-19 patients probably plays an important pathophysiological role for onset of rhabdomyolysis, but further studies are needed to elucidate the mechanisms, appropriate treatment, and long-term clinical outcomes of muscular manifestations associated with COVID-19 disease. [Formula presented]