Table 2 Cerebrovascular disease among different COVID-19 reports
From: Comparing COVID-19-linked neurological complications with other viral infections
Acute cerebrovascular disease | New York USA case report (n = 5) [9] | London UK case report (n = 6) [3] | Philadelphia USA Case report (n = 2) [15] | Wuhan China case series (n = 6) [1] |
|---|---|---|---|---|
Onset age | Younger than 50 years (ranged from 33 to 49); 4 of them were male | Ranged from 53–85 years old; 5 of them were male | Ranged from 31 and 62 years old; 1 of them were male | Patients with severe infection were older (58.2 ± 15.0)and had more acute CVD |
Stroke type | Large-vessel ischemic stroke | All had large vessel occlusion with markedly elevated D-dimer levels. 3 had multi-territory infarcts; 2 had concurrent venous thrombosi | One is subarachnoid haemorrhage from a ruptured aneurysm; another is ischaemic stroke with massive haemorrhagic conversion | Five patients with ischemic stroke and 1 with cerebral hemorrhage |
Comorbidity | One patient had history of stroke; 2 had diabetes; 1 had hyperlipidemia | Majority 5/6 had multiple comorbidities including cardiopathy, hypertension, diabetes, cancer and previous stroke history | No | Patients with severe infection had more underlying disorders, especially hypertension, and showed fewer typical symptoms of COVID-19, such as fever and cough |
Prognosis | One out of five was sent to intensive care unit | Two out of 6 required intensive care unit support | Zero out of two required intensive care unit | One out of six deceased |
Potential mechanism | Possible due to Coagulopathy and vascular endothelial dysfunction | Coagulation activation and thrombin generation due to proinflammatory cytokines which induce endothelial and mononuclear cell activation | Underlying inflammatory and hypercoagulable state may incite cerebrovascular disease without disruption of the blood–brain barrier | ACE2 and immune injury may play a role |