Chronic long-COVID syndrome: A protracted COVID-19 illness with neurological dysfunctions

Abstract

After almost a year of COVID-19, the chronic long-COVID syndrome has been recognized as an entity in 2021. The patients with the long-COVID are presenting with ominous neurological deficits that with time are becoming persistent and are causing disabilities in the affected individuals. The mechanisms underlying the neurological syndrome in long-COVID have remained obscure and need to be actively researched to find a resolution for the patients with long-COVID. Here, the factors like site of viral load, the differential immune response, neurodegenerative changes, and inflammation as possible causative factors are debated to understand and investigate the pathogenesis of neuro-COVID in long-COVID syndrome.

Keywords: COVID-19; SARS-CoV-2; long-COVID; neurological deficits.

FIGURE 1

Long‐COVID: CNS Access and NeuroCOVID syndrome. SARS‐CoV‐2 viral loads can follow anatomical pathways from the nasal cavity to the brain (A‐A1) via the cribriform plate of the ethmoid bone (A1) and the lungs via respiratory passages (B). Patients in long‐COVID report diverse neurological signs and symptoms (C‐list) that can be due to slow neuronal damage (C1) (neurodegeneration) or due to low‐grade inflammation and cytokine‐mediated damage (C2). SARS‐CoV‐2 has been isolated from beneath the cribriform plate and the neurons of the frontal lobe in COVID‐19 patients