LAUSR

We read with great interest the case reports about patients with COVID-19 with Miller Fisher syndrome and polyneuritis cranialis by Gutiérrez-Ortiz et al.,1 which provided a link between these diseases and the symptom spectrum of SARS-CoV-2 infection. As we know, the Miller Fisher syndrome and polyneuritis cranialis are an autoimmune neuropathy triggered by autoantibodies specific for the polysialogangliosides GQ1b and GT1a in axonal terminals and causes the inflammation and demyelination of the peripheral and cranial nerves.2 A recent article also proposed that autoimmune injury may be involved in the mechanisms of nervous system symptoms of COVID-19.3 In addition, Zika virus—another coronavirus—is also associated with autoimmune peripheral neuropathy.4,5 These thus support the connection of Miller Fisher syndrome and polyneuritis cranialis with SARS-CoV-2 infection. We wonder whether the authors examined the presence of SARS-CoV-2 RNA and antibodies for SARS-CoV-2 in CSF and ruled out the infection by other common viruses in 2 patients with COVID-19? This will provide more convincing evidence to support SARS-CoV-2 infection-induced autoimmune injury on peripheral nerves, and immunoglobulin therapy may be considered for some patients with COVID-19.