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Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, is associated with coagulopathy causing venous and arterial thrombosis.1 2 Recent data from the pandemic epicentre in Wuhan, China, reported neurological complications in 36% of 214 patients with COVID-19; acute cerebrovascular disease (mainly ischaemic stroke) was more common among 88 patients with severe COVID-19 than those with non-severe disease (5.7% vs 0.8%).3 However, the mechanisms, phenotype and optimal management of ischaemic stroke associated with COVID-19 remain uncertain. We describe the demographic, clinical, radiological and laboratory characteristics of six consecutive patients assessed between 1st and 16th April 2020 at the National Hospital for Neurology and Neurosurgery, Queen Square, London, UK, with acute ischaemic stroke and COVID-19 (confirmed by reverse-transcriptase PCR (RT-PCR)) (table 1). All six patients had large vessel occlusion with markedly elevated D-dimer levels (≥1000μg/L). Three patients had multiterritory infarcts, two had concurrent venous thrombosis, and, in two, ischaemic strokes occurred despite therapeutic anticoagulation.
A 64-year-old man presented 10 days after COVID-19 symptom onset (cough, breathlessness, fever, myalgia and poor appetite), with respiratory failure warranting intensive care unit admission. Mycoplasma pneumoniae infection was treated with clarithromycin. On day 15, he developed mild left arm weakness and incoordination. MRI confirmed intradural left vertebral artery occlusion and acute left posterior inferior cerebellar artery territory infarction with petechial haemorrhage (online supplementary figure S1A). D-dimer was >80 000 µg/L. He received aspirin and clopidogrel. On day 19, he developed bilateral pulmonary embolism, treated with therapeutic low molecular weight heparin (LMWH). On day 22, he developed acute bilateral …
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