We appreciated to read the review article by Galassi et al. about neuromuscular implications of infections with SARS-CoV-2 (COVID-19) [1]. The authors collected 13 cases with polyradiculitis affecting the peripheral nerves, cranial nerves, or both [1]. It was concluded that Guillain-Barre syndrome (GBS) is the only neuromuscular disorder (NMD) triggered by SARS-CoV-2 [1]. We have the following comments and concerns.

The first shortcoming of the study is that GBS is not the only NMD triggered by SARS-CoV-2. In addition to polyradiculitis, myositis [2,3], myalgia [4], rhabdomyolysis [5-7], mononeuropathy of the facial nerve [8,9], myasthenia, and polyneuropathy [10] have been reported as neuromuscular manifestations of COVID-19. The low prevalence of NMD caused by SARS-CoV-2 may be due to the dominance of pulmonary compromise in COVID-19 patients, which may give rise to missing manifestations of the peripheral nervous system (PNS). A further reason could be that NMD in severely ill, intubated, and artificially ventilated patients may be missed, particularly if it the NMD is transient and present only at the intensive care unit. 

Another shortcoming is that it was not differentiated between primary and secondary NMD triggered by SARS-CoV-2. Primary NMD may be due to the viral attack. Secondary NMD may be due to the immunological response against the virus or due to side effects of the treatment applied for COVID-19. 

Secondary myopathy may be the consequence of a side effect of anti-viral agents (lopinavir/ritonavir), of chloroquine, or of steroids, frequently given for COVID-19. Secondary myopathy may be also due to critical ill myopathy in patients on the intensive care unit. Secondary neuropathy includes GBS and critical-ill neuropathy. Chloroquine has been also reported to trigger myasthenic syndrome [11].

Immunological disorders affecting the PNS may be GBS, myasthenia, or myositis. Neuromuscular complications of treatment include critical ill neuropathy/myopathy, or myopathy due to steroids, anti-viral agents, or chloroquine.

A recently reported complication of COVID-19 may be myasthenia gravis. The first cases of myasthenia triggered by SARS-CoV-2 were reported by Restivo et al. [12]. Myasthenia triggered by SARS- CoV-2 has been also reported in a Turkish patient [13].

Whether hypogeusia/hyposomia is due to affection of the cranial nerves or due to other causes, remains speculative.

A third point that should be considered in COVID-19 patients is that the infection may worsen already pre-existing NMD, such as myasthenia [14]. In several patients with myasthenia, SARS-CoV-2 led to exacerbation of myasthenia [14] or even myasthenic crisis [15]. 

Overall, SARS-CoV-2 may cause direct damage of muscle/nerve by the virus or the immune reaction against the virus, there may be muscle/nerve damage due to side effects of the anti-viral treatment, and SARS-CoV-2 may worsen a pre-existing NMD. The spectrum of NMDs due to infection with SARS-CoV-2 is more variegated than anticipated. Primary and secondary NMD due to SARS-CoV-2 infection should be delineated as treatment may vary between these entities, and it is helpful to differentiate between NMD caused by direct attack of the virus and a NMD caused by the secondary immune response.