The outbreak of a novel coronavirus since December 12, 2019 become an emergency of major international concern, and is a great challenge for clinicians. The typical symptoms are fever, sore throat, fatigue, cough or dyspnea coupled with recent exposure. The SARS-CoV-2 infection is of clustering onset, which is more likely to affect older males with comorbidities [
10]. The elderly always have higher risk factors associated with acute ischemic stroke or embolization vascular events. Considering that this patient is 79 years old and the immune response is not as strong as that in young men, typical symptoms of SARS-CoV-2 infection were not observed. After he visited friends, 10 days later, he began to cough slightly. The mean incubation period of COVID-19 is 6.4 days, ranging from 2.1 to 11.1 days (2.5th to 97.5th percentile) [
11]. We suspect that he was exposed to the viral environment, in which some aerosols may carry SARS-CoV-2. This patient was hospitalized with right limb weakness and disfluent speech, and chest CT examination later found typical images of COVID-19, suggesting that neurologists ought to inquire more information about the contact history. In addition, chest CT and laboratory examinations, including swab tests, should be prescribed for the diagnosis of COVID-19.
In this case, to explain right limb weakness as the initial symptom, it has been hypothesized that SARS-CoV-2 infection caused hypoxemia and excessive secretion of inflammatory cytokines, which induced acute ischemic stroke. Hypoxemia significantly reduces the energy required by cell metabolism, increases anaerobic fermentation, and causes intracellular acidosis and oxygen free radicals. With the continuation of hypoxia, intracellular calcium ion concentration increases significantly, inducing a series of cell damage, including apoptosis. Moreover, hypoxia can also induce inflammatory responses, including inflammatory cell infiltration and cytokine release, leading to further tissue ischemia [
12]. Inflammation plays an important role in the occurrence, development and prognosis of cardiovascular and cerebrovascular diseases. Compared with non-ICU patients, ICU patients with a SARS-CoV-2 infection had higher plasma cytokine levels, including IL-2, IL-7, IL-10, GSCF, IP10, MCP1, MIP1A, and TNFα [
2]. Inflammation contributes to atherosclerosis and affects plaque stability [
13]. Additionally, the SARS-CoV-2 virus binds to angiotensin-converting enzyme 2 (ACE2) present on brain endothelial and smooth muscle cells. Depletion of ACE2 by SARS-CoV-2 may tip the balance in favor of the “harmful” ACE1/angiotensin II axis and promote tissue injury including stroke [
14]. Following these ideas, we presume that SARS-CoV-2 infection pneumonia is one of the pathogeneses of ischemic stroke. The latest full-length genome sequences obtained revealed that SARS-CoV-2 uses the cell entry receptor ACE2 [
15]. Structural analysis suggests that ACE2 can bind to B
0AT1 (SLC6A19), which is a neutral amino acid transporter, providing important clues to the molecular basis for coronavirus recognition and infection [
16]. Due to the combination of SARS-CoV-2 with the ACE2 receptor, some hypertensive patients with SARS-CoV-2 infection may experience abnormally elevated blood pressure, which increases the risk of intracerebral hemorrhage. In a familial cluster of pneumonia associated with SARS-CoV-2, older patients (aged > 60 years) have more systemic symptoms, such as thrombocytopenia, which enhances the chances of acute cerebrovascular events [
5]. In the clinic, some COVID-19 patients have intracranial infection symptoms, including headache, epilepsy, and consciousness disorders; some COVID-19 patients have acute cerebrovascular disease symptoms, including paralysis of limbs; and a few have neuralgia and paresthesia.
Early diagnosis, quarantine, and supportive treatments are essential to cure patients. As SARS-CoV-2 is an emerging virus, no antiviral agents have been recommended for coronavirus infection [
17]. In this case, low doses of dexamethasone therapy were used to avoid inflammatory storms. Corticosteroids suppress lung inflammation but also inhibit immune responses and pathogen clearance. The clinical outcomes of coronavirus and similar outbreaks do not support the use of corticosteroids [
18‐
20]. Current interim guidance from the WHO on the clinical management of severe acute respiratory infection when SARS-CoV-2 infection is suspected (released January 28, 2020) advises against the use of corticosteroids unless indicated for another reason. For the treatment of hypertension, blockers of the AT1 receptor (ARBs), such as losartan, may be protective in stroke. While there has been some concern that ARBs and ACE inhibitors may be harmful in COVID-19 patients by increasing expression of ACE2 and SARS-CoV-2 binding, a joint statement from the American Heart Association. Under this controversial issue, amlodipine besylate tablets were given to lower blood pressure.