Decline in Stroke Presentations During COVID-19 Surge.

BACKGROUND AND PURPOSE: We aimed to investigate the acute stroke presentations during the coronavirus disease 2019 (COVID-19) pandemic. METHODS: The data were obtained from a health system with 19 emergency departments in northeast Ohio in the United States. Baseline period from January 1 to March 8, 2020, was compared with the COVID period from March 9, to April 2, 2020. The variables included were total daily stroke alerts across the hospital emergency departments, thrombolysis, time to presentation, stroke severity, time from door-to-imaging, time from door-to-needle in thrombolysis, and time from door-to-puncture in thrombectomy. The 2 time periods were compared using nonparametric statistics and Poisson regression. RESULTS: Nine hundred two stroke alerts during the period across the emergency departments were analyzed. Total daily stroke alerts decreased from median, 10 (interquartile range, 8-13) during baseline period to median, 8 (interquartile range, 4-10, P=0.001) during COVID period. Time to presentation, stroke severity, and time to treatment were unchanged. COVID period was associated with decrease in stroke alerts with rate ratio of 0.70 (95% CI, 0.60-0.28). Thrombolysis also decreased with rate ratio, 0.52 (95% CI, 0.28-0.97) but thrombectomy remained unchanged rate ratio, 0.93 (95% CI, 0.52-1.62) Conclusions: We observed a significant decrease in acute stroke presentations by ≈30% across emergency departments at the time of surge of COVID-19 cases. This observation could be attributed to true decline in stroke incidence or patients not seeking medical attention for emergencies during the pandemic.

Coronavirus Disease 2019 and Stroke: Clinical Manifestations and Pathophysiological Insights.

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a global health threat. Some COVID-19 patients have exhibited widespread neurological manifestations including stroke. Acute ischemic stroke, intracerebral hemorrhage, and cerebral venous sinus thrombosis have been reported in patients with COVID-19. COVID-19-associated coagulopathy is increasingly recognized as a result of acute infection and is likely caused by inflammation, including inflammatory cytokine storm. Recent studies suggest that axonal transport of SARS-CoV-2 to the brain can occur via the cribriform plate adjacent to the olfactory bulb that may lead to symptomatic anosmia. 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 review 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.