COVID-19 and Stroke: An Emerging Association

Dear editor, We have read with interest the letter of Finsterer and Scorza [1], which commented on our article, regarding a case of stroke and thromboses at different sites in a CO VID19 positive patient. We want to answer the observa tions that have been raised. Carotid US was not done since the patient underwent angio CT scan that studied not only intracranial vessels, but also carotid and vertebral arteries since their origin, including aortic arch. Multimodal MRI was not done. However, this patient underwent 4 CT scans: the second one showed the appearance of the acute ischemic lesion (not present at the first CT scan), the third showed the hemorrhagic transformation of the lesion and the fourth its stability, so that the acuity and the dynamics of the pa thology had been adequately investigated. The patient underwent a 72 h ECG continuous record ing and transthoracic echocardiogram that did not show elements which could support a cardioembolic genesis of stroke. There was no clinical, ECG, or US evidence for Tsakotsubo syndrome. Our investigations did not support a cardioembolic pathogenesis. Consequently we consid ered, until proven otherwise, the atherothrombotic patho genesis as the more likely. During the hospital period the patient underwent 2 tho rax CT scans, which did not reveal signs of suspicion for a neoplasm; however, given the multiple thromboses at dif ferent sites, a paraneoplastic syndrome could have been suspected; actually, after the discharge the patient under went a total body CT scan that did not show neoplastic le sions. We reported 2 different ways through which SARS CoV2 may penetrate the central nervous system: it may be either through the olfactory nervous terminations or alter natively through the hematogenous route. Our study was not focused on the genesis of dysgeusia in SARSCoV2, and we agree that a cytokine storm could contribute to the neurologic involvement of SARSCoV2 [1]. Our aim was to show how even milder cases of COVID19 could be re lated with stroke, and that these patients for the first time could arrive to physiscian’s attention due to a cerebrovas cular accident. We agree that among the patients with SARSCoV2, those with higher vascular risk factors are more likely af fected by stroke. As well as other viruses, SARSCoV2 may represent a trigger that can favor stroke in patients with high vascular risk. However, further recent evidence sup ported the role of SARSCoV2 in endothelial disfunction and induction of a procoagulative state [2, 3]. We specu lated how COVID19 may be related with stroke; however, we are conscious that at the moment, it is not possible to sustain a certain and direct contribution of SARSCoV2 in stroke pathogenesis and that further evidence is needed.