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. 2020 Jun;15(2):167-173.
doi: 10.1007/s11481-020-09924-9. Epub 2020 May 23.

SARS-CoV-2 Infection Leads to Neurological Dysfunction

Arpan Acharya  1 , Bhavesh D Kevadiya  1   2 , Howard E Gendelman  3 , Siddappa N Byrareddy  4
Affiliations

SARS-CoV-2 Infection Leads to Neurological Dysfunction

Arpan Acharya et al. J Neuroimmune Pharmacol. 2020 Jun.

Abstract

A number of neurological disease complications have been seen following infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While most person with COVID-19 respiratory disease demonstrate headache, nausea and vomiting, up to 40% present also experience dizziness, confusion, cerebrovascular disease, muscle pain, ataxia and seizures. Loss of taste and smell, defects in visual acuity and pain occur in parallel. Such central nervous system (CNS) signs and symptoms linked to laboratory-confirmed SARS-CoV-2 infection is often life threatening. Health care providers currently evaluating patients with neurologic symptoms need consider COVID-19 in any differential diagnosis. These considerations will facilitate prompt testing, isolation and prevention of viral transmission speeding best clinical outcomes. Graphical Abstract.

Keywords: Animal models; CNS; COVID-19; Guillain-Barré syndrome; Neurologic manifestations; SARS-CoV-2; Therapeutics.

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Figures

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Graphical Abstract
Fig. 1
Fig. 1
The neurovirulence of SARS-CoV-2. Increasing data has now provided evidence that SARS-C0V-2 is both neurotropic and neurovirulent. The virus invades the CNS soon after infection and gains access into the CSF and to brain subregions that include the brain stem and cortex. After crossing the blood-brain barrier (BBB) virus can replicate in microglia and neurons with collateral damage to the barrier. An inflammatory cascade is set into motion that includes ongoing collateral damage and secondary seizures, delirium and stroke. A key finding that is the requirements of the ACE2 cell entry receptor. The CoV spike glycoprotein, by which SARS-CoV-2 binds to cell membranes. The expression of this receptor in neurons and endothelial cells outlines the virus neuroinvasive potential. It is possible that both respiratory and neural failures are linked to brain stem damage and as such both direct infection and indirect inflammatory mechanisms are likely both operative. Differential host immune-mediated responses may determine outcomes. Disease models are surely needed to investigate potential neurological complications and to explore mechanisms of alternative immune-mediated pathogenicity and developmental therapies
Fig. 2
Fig. 2
Neurological signs and symptoms occur as a result of SARS-COV-2 infection. These are in addition to life threatening ARDS. These include, but are not limited to, headache, dizziness, myalgia and fatigue, ARDS (a primary part of the disease complex, brain stem (respiratory and cardiac) impairments, primary cardiac disease, anosmia, an inflammatory encephalitis, delirium and cognitive impairments, stroke, seizures, spinal cord injuries and the Guillain-Barre syndrome. All are associated with SARS-CoV-2 infections
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