Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 ) is a novel beta-coronavirus that causes a variety of neurologic symptoms including anosmia, ageusia, seizures, stroke, confusion, encephalopathy and quadriplegia. Up to 20% of COVID-19 patients who require intensive care unit admission are due to their neurological deficits [3]. SARS-CoV-2 virus have a high similarity to SARS-Cov1 and MERS, appears to have the capacity to injure the central and peripheral nervous systems through direct and indirect ways [4,5]. The binding of SARS-CoV-2 to angiotensin converting enzyme 2 (ACE2) receptor is a critical step in the pathophysiology [6]. The function of ACE2 in normal human physiology is to regulate blood pressure via inhibition of the angiotensin- renin-aldosterone pathways. ACE2 facilitates conversion of angiotensin II to angiotensin (1-7). Higher levels of angiotensin II are associated with vasoconstriction, kidney failure, heart disease, apoptosis, and oxidative processes [8]. This enzyme protein in the cell membranes of multiple organs to serve as the receptor for SARS-CoV-2