Editors' Note: CSF Biomarkers in Patients With COVID-19 and Neurologic Symptoms: A Case Series

Abstract

In “CSF Biomarkers in Patients With COVID-19 and Neurologic Symptoms: A Case Series,” Edén et al. describe CSF results in 6 patients with neurologic symptoms in the setting of COVID-19 infection. Three patients had a positive CSF SARS-CoV-2 PCR initially, although the cycle threshold was elevated (>35), indicating a low viral load. It is important that SARS-CoV-2 RNA was undetectable in all 3 samples when reanalyzed. All patients had elevated CSF neopterin and β2-microglobulin. Kumar and Lall comment that these findings are consistent with nonspecific inflammation and emphasize the fact that neuropathogenesis in COVID-19 is multifactorial because of systemic inflammation, hypoxemia, hypercoagulability, and potentially unidentifiable mechanisms. Brenner agrees that these findings suggest COVID-19 does not directly invade the CNS, but that it can cause an autoimmune or immune-mediated meningoencephalitis. He proposes that treatment with steroids, IVIG, and/or plasmapheresis may be considered. Edén agrees that a number of different mechanisms may contribute to the development of neurologic symptoms in patients with COVID-19 and reinforces the need for ongoing research to evaluate potential interventions. In “CSF Biomarkers in Patients With COVID-19 and Neurologic Symptoms: A Case Series,” Edén et al. describe CSF results in 6 patients with neurologic symptoms in the setting of COVID-19 infection. Three patients had a positive CSF SARS-CoV-2 PCR initially, although the cycle threshold was elevated (>35), indicating a low viral load. It is important that SARS-CoV-2 RNA was undetectable in all 3 samples when reanalyzed. All patients had elevated CSF neopterin and β2-microglobulin. Kumar and Lall comment that these findings are consistent with nonspecific inflammation and emphasize the fact that neuropathogenesis in COVID-19 is multifactorial because of systemic inflammation, hypoxemia, hypercoagulability, and potentially unidentifiable mechanisms. Brenner agrees that these findings suggest COVID-19 does not directly invade the CNS, but that it can cause an autoimmune or immune-mediated meningoencephalitis. He proposes that treatment with steroids, IVIG, and/or plasmapheresis may be considered. Edén agrees that a number of different mechanisms may contribute to the development of neurologic symptoms in patients with COVID-19 and reinforces the need for ongoing research to evaluate potential interventions.