Dear Editor, We are grateful to Hooshmandi et al. [1] (ENE-20204-59) for the interest shown in our article and for their comments. At the time of writing, Piacenza was the second most heavily hit Italian city by COVID-19 pandemic (1.415%) [2], providing an exceptional perspective of the current situation in the neurological field. We previously emphasized how the main limit of our comments was the brief observation period, that is, 1 month, that is when the outbreak of SARS-CoV-2 peaked. In the following period, only few small case series of COVID-19 stroke patients have been reported [3–8]. Therefore, little information is available on stroke in this unknown pathological scenario. Despite the lack of current scientific literature on the topic, which is limited to anecdotal reports, numerous hypotheses have been put forward as to the role of the thrombophilic state induced by 2019-nCoV and the likely increased risk of stroke in infected patients [9–11]. From February 21 to April 28, 2020, 854 COVID-19 patients were admitted to our facility, 17 of whom with concomitant ischemic stroke symptoms (mean age 76.1 ± 8.8). No young adult stroke patient was observed. There was no rare stroke etiology or unforeseen high incidence in stroke subtypes. Severity of stroke evaluated by the NIHSS seems to correlate with extension of interstitial pneumonia documented with chest CT scan (personal data, in press). However, anecdotal evidence is collected in a casual or informal manner and relies entirely on personal testimony. Therefore, it is generally considered to have a limited value, due to a number of potential weaknesses. For this reason, we agree with Hooshmandi et al. that it is too early to consider a direct “cause-effect” relationship between 2019-nCoV infection and stroke occurrence so that further prospective and large-volume studies are warranted. The occurrence of different types of cerebrovascular diseases during the 2019-nCoV pandemic can be documented only by international multicenter studies. Indeed, the prevalence of COVID-19 is so high in pandemic hotspots that an incidental association between infection and neurological manifestations cannot be excluded. During a pandemic, when science and medicine are asked to provide answers, neurologists should strive to keep high scientific research standards and place trust in their clinical methods, starting with an accurate patient interview and then moving through standard neurological examination. The clinical path is then completed by

中文翻译：

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COVID-19 相关中风：吠错树？

尊敬的编辑，我们感谢 Hooshmandi 等人。[1] (ENE-20204-59) 表示对我们文章的关注和他们的评论。在撰写本文时，皮亚琴察是受 COVID-19 大流行影响第二重的意大利城市 (1.415%) [2]，为神经病学领域的现状提供了独特的视角。我们之前强调了我们评论的主要限制是短暂的观察期，即 1 个月，也就是 SARS-CoV-2 爆发的高峰期。在接下来的时间里，只有少数 COVID-19 卒中患者的小病例系列报道[3-8]。因此，在这种未知的病理情况下，关于中风的信息很少。尽管目前缺乏关于该主题的科学文献，仅限于轶事报告，关于 2019-nCoV 诱发的血栓形成倾向和感染患者中风风险可能增加的作用，已经提出了许多假设 [9-11]。从 2020 年 2 月 21 日至 4 月 28 日，我们的设施收治了 854 名 COVID-19 患者，其中 17 名伴有缺血性中风症状（平均年龄 76.1 ± 8.8 岁）。没有观察到年轻的成年中风患者。在中风亚型中没有罕见的中风病因或不可预见的高发病率。NIHSS 评估的中风严重程度似乎与胸部 CT 扫描（个人数据，印刷中）记录的间质性肺炎的扩展相关。然而，轶事证据是以随意或非正式的方式收集的，完全依赖于个人证词。因此，由于许多潜在的弱点，它通常被认为具有有限的价值。出于这个原因，我们同意 Hooshmandi 等人的观点。现在考虑 2019-nCoV 感染与中风发生之间的直接“因果关系”还为时过早，因此有必要进行进一步的前瞻性和大容量研究。2019-nCoV 大流行期间不同类型脑血管疾病的发生只能通过国际多中心研究来记录。事实上，COVID-19 在大流行热点地区的流行率如此之高，以至于不能排除感染与神经系统表现之间的偶然关联。在大流行期间，当要求科学和医学提供答案时，神经科医生应努力保持高科学研究标准并信任他们的临床方法，从准确的患者访谈开始，然后通过标准的神经系统检查。