Globally, stroke is a primary reason for death and lasting disability (Benjamin et al., 2019). Inflammation is critical in the course of a stroke and is closely linked to prognosis (Anrather & Iadecola, 2016).The inflammatory response following stroke involves immune cell infiltration, glial cell activation, and the emission of diverse neurotoxic molecules, such as pro-inflammatory cytokines, matrix metalloproteinases, and nitric oxide synthase, which further exacerbates neurological damage by causing endothelial cell damage, bloodbrain barrier (BBB) disruption, and neuronal apoptosis (Jayaraj et al., 2019). Therefore, immunotherapy targeting the post-stroke

Since the Corona Virus Disease 2019 (COVID-19) pandemic, there has been increasing evidence that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with acute cerebrovascular events such as cerebral infarction, cerebral hemorrhage, and cerebral venous thrombosis. Although the mechanism of cerebrovascular complications among COVID-19 patients has not been adequately elucidated, the hypercoagulable state, excessive inflammation and ACE-2-associated alterations in the renin-angiotensin-aldosterone system after SARS-CoV-2 infection probably play an essential role. In this overview, we discuss the possible mechanisms underlying the SARS-CoV-2 infection leading to acute cerebrovascular events and review the characteristics of COVID-19-related acute cerebrovascular events cases and treatment options available worldwide.