Editors' note: Miller Fisher syndrome and polyneuritis cranialis in COVID-19.

Abstract

In an effort to grow our understanding of the neurologic complications of the novel human coronavirus, SARS-CoV-2, Drs. Gutiérrez-Ortiz et al. reported a patient with the Miller Fisher syndrome and another patient with polyneuritis cranialis. Several days earlier, both patients manifested respiratory and systemic symptoms consistent with the coronavirus disease 2019 (COVID-19) and confirmed by oropharyngeal swab. Drs. Ni and Xu found this report of autoimmune-related peripheral neuropathy consistent with known complications of the Zika virus—a single-stranded RNA virus similar to coronavirus but actually a member of the genus Flavivirus. They inquired whether the authors tested the patients for other common viruses and evaluated for the presence of antibodies to SARS-CoV-2 in the CSF. In response, the authors indicated they did not test the CSF for antibodies to SARS-CoV-2 because of the lack of validity for the assay. Owing to healthcare limitations during the pandemic, only the first patient had their CSF tested for other CNS pathogens (negative for enterovirus, herpes simplex virus type 1 and 2, varicella zoster virus, and neurosyphilis). This patient also had a negative PCR test for SARS-CoV2 in the CSF. The temporal relationship between symptom onset of COVID-19 in these patients and the development of neurologic manifestations—within 3–5 days—argue for a strong association of SARS CoV-2 and autoimmune-related peripheral neuropathy. In an effort to grow our understanding of the neurologic complications of the novel human coronavirus, SARS-CoV-2, Drs. Gutiérrez-Ortiz et al. reported a patient with the Miller Fisher syndrome and another patient with polyneuritis cranialis. Several days earlier, both patients manifested respiratory and systemic symptoms consistent with the coronavirus disease 2019 (COVID-19) and confirmed by oropharyngeal swab. Drs. Ni and Xu found this report of autoimmune-related peripheral neuropathy consistent with known complications of the Zika virus—a single-stranded RNA virus similar to coronavirus but actually a member of the genus Flavivirus. They inquired whether the authors tested the patients for other common viruses and evaluated for the presence of antibodies to SARS-CoV-2 in the CSF. In response, the authors indicated they did not test the CSF for antibodies to SARS-CoV-2 because of the lack of validity for the assay. Owing to healthcare limitations during the pandemic, only the first patient had their CSF tested for other CNS pathogens (negative for enterovirus, herpes simplex virus type 1 and 2, varicella zoster virus, and neurosyphilis). This patient also had a negative PCR test for SARS-CoV2 in the CSF. The temporal relationship between symptom onset of COVID-19 in these patients and the development of neurologic manifestations—within 3–5 days—argue for a strong association of SARS CoV-2 and autoimmune-related peripheral neuropathy.