SARS-CoV-2, the virus responsible for novel Coronavirus (COVID-19) infection, has recently been associated with a myriad of hematologic derangements; in particular, an unusually high incidence of venous thromboembolism has been reported in patients with COVID-19 infection. It is postulated that either the cytokine storm induced by the viral infection or endothelial damage caused by viral binding to the ACE-2 receptor may activate a cascade leading to a hypercoaguable state. Although pulmonary embolism and deep venous thrombosis have been well described in patients with COVID-19 infection, there is a paucity of literature on cerebral venous sinus thrombosis (cVST) associated with COVID-19 infection. cVST is an uncommon etiology of stroke and has a higher occurrence in women and young people. We report a series of three patients at our institution with confirmed COVID-19 infection and venous sinus thrombosis, two of whom were male and one female. These cases fall outside the typical demographic of patients with cVST, potentially attributable to COVID-19 induced hypercoaguability. This illustrates the importance of maintaining a high index of suspicion for cVST in patients with COVID-19 infection, particularly those with unexplained cerebral hemorrhage, or infarcts with an atypical pattern for arterial occlusive disease.

BACKGROUND AND PURPOSE: Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infection is associated with hypercoagulability. We sought to evaluate the demographic and clinical characteristics of cerebral venous thrombosis among patients hospitalized for coronavirus disease 2019 (COVID-19) at 6 tertiary care centers in the New York City metropolitan area. MATERIALS AND METHODS:We conducted a retrospective multicenter cohort study of 13,500 consecutive patients with COVID-19 who were hospitalized between March 1 and May 30, 2020. RESULTS: Of 13,500 patients with COVID-19, twelve had imaging-proved cerebral venous thrombosis with an incidence of 8.8 per 10,000 during 3 months, which is considerably higher than the reported incidence of cerebral venous thrombosis in the general population of 5 per million annually. There was a male preponderance (8 men, 4 women) and an average age of 49 years (95% CI, 36-62 years; range, 17-95 years). Only 1 patient (8%) had a history of thromboembolic disease. Neurologic symptoms secondary to cerebral venous thrombosis occurred within 24 hours of the onset of the respiratory and constitutional symptoms in 58% of cases, and 75% had venous infarction, hemorrhage, or both on brain imaging. Management consisted of anticoagulation, endovascular thrombectomy, and surgical hematoma evacuation. The mortality rate was 25%. CONCLUSIONS:Early evidence suggests a higher-than-expected frequency of cerebral venous thrombosis among patients hospitalized for COVID-19. Cerebral venous thrombosis should be included in the differential diagnosis of neurologic syndromes associated with SARS-CoV-2 infection. ABBREVIATIONS: COVID-19 ¼ coronavirus disease 2019; CVST ¼ cerebral venous sinus thrombosis; CVT ¼ cerebral venous thrombosis; SARS-CoV-2 ¼ Severe Acute Respiratory Syndrome coronavirus 2 C oronavirus disease 2019 (COVID-19) is predominantly an acute respiratory disease caused by a single-stranded RNA virus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which originated in Wuhan, China. 1 The virus possesses a spike protein that binds to angiotensin-converting enzyme receptors, expressed on respiratory epithelium, facilitating entry into the host cell. [2][3][4] Susceptibility of organ systems to this virus may depend on the extent of expression of angiotensin-converting enzyme receptors on cell surfaces. These receptors are expressed on endothelial cells, pericytes, macrophages, glial cells, and cardiac myocytes. [2][3][4] Viral entry into these cells can lead to diverse manifestations such as acute respiratory distress syndrome, acute kidney injury, transaminitis, cardiac injury, and neurologic complications. [3][4][5][6] Neurologic symptoms include headache, confusion, hypogeusia, hyposmia, myalgias, and delirium, while neurologic complications include acute ischemic stroke, encephalitis, and Guillain-Barre syndrome. 3,[6][7][8] Postmortem data have revealed cerebral edema and partial neuronal degeneration in some patients as well. 9 Early evidence suggests an inc...

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Carotid atherosclerosis is implicated in 20-30 % of strokes. However, the annual risk of stroke in patients with asymptomatic carotid stenosis is less than 5 %. Symptomatic carotid stenosis poses a greater risk for recurrent stroke with estimates as high as 15 % per year. This paper aims to raise awareness of populations at risk for carotid stenosis, the role of carotid screening and the sensitivity and specificity of various diagnostic modalities. The results of previous trials that support current guidelines for management of symptomatic and asymptomatic carotid stenosis will also be reviewed.