A case series of patients with COVID-19 published in Neurology shows neurochemical evidence of neuronal injury and glial activation in patients with moderate and severe disease.
Forty-seven patients with confirmed COVID-19 were divided into severity groups, mild (n=20), moderate (n=9) and severe (n=18). Biomarker findings were compared to age-matched controls. Blood samples were collected at a mean of 13.0 days (SD 7.37) from symptom onset and at follow-up 11.4 days (SD 5.06) after the first sample.
Patients with severe COVID-19 had higher plasma concentrations of glial fibrillary acidic protein (GFAp) and neurofilament light protein (NfL) than controls, while GFAp was also increased in patients with moderate disease. An early peak in GFAp in severe patients had decreased upon follow-up, while NfL showed a sustained increase. This may reflect a sequence of early astrocyte response and more delayed axonal injury.
There are two theories of how SARS-CoV-2 is able to infect the CNS; spread across the cribriform plate of the ethmoid bone in proximity to the olfactory bulb, resulting in the common loss of smell; or later occurring haematogenous spread with accompanying hypoxia, respiratory and metabolic acidosis.
Further studies are required on the nature of the neuronal injury.