It is well known that the spectrum of SARS-CoV-2 infection ranges from asymptomatic or mildly symptomatic patients to rapidly progressive, acute respiratory distress syndrome (ARDS) and death. Although various reports indicated the presence of myalgia in 44%–70% and increased creatine kinase (CK) in about 33% of hospitalized patients,1 or skeletal muscle injury (increased CK and myalgia) in 23%,2 the characterization of neuromuscular involvement is still unsatisfactory, and no electrophysiologic studies have been performed. Very recently, patients who developed the Guillain-Barre syndrome (GBS) in the course of coronavirus disease 2019 (COVID-19) have been described.3 In the past literature, there were a few reports of neuromuscular involvement in association with other beta-coronavirus, including critical illness myopathy (CIM) or polyneuropathy.1,4 Moreover, myopathic changes, as fiber atrophy or necrosis, have been reported in postmortem muscle samples of 8 patients who died of SARS (severe acute respiratory syndrome) due to SARS-CoV infection.4.
ASJC Scopus subject areas
- Clinical Neurology