Neuromuscular comorbidity of COVID-19

Abstract

Backgraund. The outbreak of the novel and highly infectious COVID-19 has resulted in hundreds of millions of infections and millions of deaths globally. Infected individuals experience upper and lower respiratory complications that range in severity and may lead to wide-spread inflammation and generalized hypoxia or hypoxemia that impacts multiple organ systems, including the central and peripheral nervous systems. According to the data available today, the neurological symptoms associated with COVID-19 infection are described in detail. Based on these studies, it can be assumed that SARS-Cov-2 may be neurotropic and / or contribute to or create conditions conducive to direct or indirect damage to the nervous system. Aim: The aim of the study was to identify complications of COVID-19 infection in patients with neuromuscular diseases (myasthenia gravis, chronic polyneuropathy, myopathy).
Material and Methods: The study included 20 patients infected with COVID-19 with generalized myasthenia gravis, 8 with chronic polyneuropathy and 5 with progressive dystrophy. Among patients with myasthenia gravis, there were 15 women and 17 men aged 50 to 69 years. Among 8 patients with chronic polyneuropathy, there were 3 women and 5 men aged 25 to 74 years, and among patients with progressive dystrophy - 3 women and 2 men aged 36 to 62 years. Patients were examined approximately at intervals of 3 weeks to 2 months after infection with COVID-19. Patients underwent CT scan of the chest, ENMG, titers of antibodies to AChE, MuSk, Titin, LIA-ANA profile were determined, blood tests were performed, CPK and C-reactive proteins were determined in the blood. Results. In 15 patients out of 20 with myasthenia gravis, an exacerbation of the condition was noted, mainly with respiratory symptoms, of which Lambert-Eaton syndrome was diagnosed in one patient after infection with COVID-19 and in 3 had motor-sensory polyneuropathy with a predominant lesion of sensory fibers; the condition of 5 patients did not change, the infection was asymptomatic. In 8 patients with chronic polyneuropathy in remission after infection with COVID-19, an exacerbation of the condition was noted, namely, a deepening of the degree of axon damage, expressed in the lower extremities and sensory fibers, in one patient EMG study revealed changes characteristic of polymyositis. Of the 5 patients with progressive dystrophy, 2 had motor-sensory polyneuropathy against the background of myalgia, in 2 patients an increase in muscle damage was detected electrophysiologically, in one case EMG revealed changes characteristic of polymyositis. Conclusion. Based on the results obtained, it can be assumed that not only comorbid pathology occurs as a result of infection with COVID-19, but the COVID-19 virus can also be considered as a modifying factor in the course of the disease.