Infections caused by SARS‐CoV‐2 have not only resulted in a gigantic number of morbidities and mortalities worldwide in COVID‐19, but its ability to cause a protracted illness in form of long‐COVID is now becoming increasingly evident. The syndromic manifestation in long‐COVID has shown to become chronic and the affected individuals are seen to be predominately exhibiting neurological deficits which are worrying. The most daunting task in long‐COVID is to understand the mechanisms underlying mechanism in general and the pathogenesis of neurological signs and symptoms in particular. Debated here are local routes and systemic mechanisms by which SARS‐CoV‐2 can involve the nervous system to evoke a low‐grade smoldering neuronal injury that possibly contributes to the neurological deficits reported.

One of the possible reasons for the observation of neurological deficits in long‐COVID is a possibly a slowly progressive degenerative effect of the SARS‐CoV‐2 following the neuronal entry. Such finding has been reported recently to affected patients and it should be no surprise to see the degenerative processes, reflecting as neurological deficits. Though the underlying mechanisms leading to neuronal damage are yet to be completely understood, neuronal atrophy, hypometabolism, and defects induced in synaptic transmission can be the covert pathways induced by SARS‐CoV‐2 in long‐COVID to inflict neuronal damage.