Although the respiratory system is the primary target of the coronavirus, studies have demonstrated a strong tropism to the central nervous system (CNS).1,2 The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects cells by binding to the angiotensin-converting enzyme 2 (ACE2) receptor. This receptor is also found in the CNS and plays a crucial role in autoregulating cerebral perfusion pressure.3,4 Additionally, epidemiological data demonstrated increased mortality due to cardiovascular and cerebrovascular diseases during flu pandemics due to a hypercoagulable state.5,6 The triad of neuroinvasion of SARS-CoV-2, induction of hypercoagulable state,5-9 and the inhibition of ACE2 blocking the formation of Angiotensin (1-7) serve as the pathophysiology for neurovascular insults.3,4 We present a case series of coronavirus disease 2019 (COVID-19) patients from 2 health systems developing cerebrovascular insult
