Acute Ischemic Stroke in Covid 19

Abstract

Corona virus disease (Covid 19) is an infectious disease caused by Sars-cov2 virus. It mostly affects the respiratory system, resulting in fever, coughing, and shortness of breath. However, the central nervous system may also be affected.  Some COVID-19 patients have exhibited widespread neurological manifestations including stroke. Several mechanisms related to immune-mediated thrombosis and the effect of SARS-CoV-2 in brain tissue may contribute to the pathogenesis of ischemic stroke in patients with COVID-19. Recent studies suggest that the internalization of SARS-CoV-2 is mediated by the binding of the spike glycoprotein of the virus to the angiotensin-converting enzyme 2 (ACE2) on cellular membranes. ACE2 is expressed in several tissues including lung alveolar cells, gastrointestinal tissue, and brain. The aim of this case report is to provide insights into the clinical manifestations and pathophysiological mechanisms of stroke in COVID-19 patients. SARS-CoV-2 can down-regulate ACE2 and, in turn, overactivate the classical renin-angiotensin system (RAS) axis and decrease the activation of the alternative RAS pathway in the brain. The consequent imbalance in vasodilation, neuroinflammation, oxidative stress, and thrombotic response may contribute to the pathophysiology of stroke during SARS-CoV-2 infection. The neuropilin (NRP-1) which is a co-receptor for the vascular endothelial growth factor (VEGF), integrins, and plexins, is involved in the pathogenesis of Acute Ischemic Stroke. When examining a patient who has neurological manifestations, clinicians must use a rigorous approach. To lessen post-covid neurological sequelae, the neurological disease of COVID 19 must be diagnosed and treated early.