Reader response: Miller Fisher Syndrome and polyneuritis cranialis in COVID-19
JianqiangNi, Neurologist, Department of Neurology, the First Affiliated Hospital of Soochow University (Suzhou City, China)
XingshunXu, Neurologist, Department of Neurology, the First Affiliated Hospital of Soochow University (Suzhou City, China)
Submitted May 18, 2020
We read with great interest the case reports about COVID-19 patients 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, 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 cerebrospinal fluid (CSF) and ruled out the infection by other common viruses in two COVID-19 patients? 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 COVID-19 patients.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References
Gutiérrez-Ortiz C, Méndez A, Rodrigo-Rey S, et al. Miller Fisher Syndrome and polyneuritis cranialis in COVID-19. Neurology 2020 Epub Apr 17.
Rodella U, Scorzeto M, Duregotti E, et al. An animal model of Miller Fisher syndrome: Mitochondrial hydrogen peroxide is produced by the autoimmune attack of nerve terminals and activates Schwann cells. Neurobiol Dis 2016;96:95–104.
Li H, Xue Q, Xu X. Involvement of the Nervous System in SARS-CoV-2 Infection. Neurotox Res 2020 Epub May 13.
Parra B, Lizarazo J, Jimenez-Arango JA, et al. Guillain-Barre syndrome associated with Zika virus infection in Colombia. N Engl J Med 2016;375:1513–1523.
Brasil P, Sequeira PC, Freitas AD, et al. Guillain-Barre syndrome associated with Zika virus infection. Lancet 2016;387:1482.
We read with great interest the case reports about COVID-19 patients 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, 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 cerebrospinal fluid (CSF) and ruled out the infection by other common viruses in two COVID-19 patients? 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 COVID-19 patients.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References