Department of Clinical Neurosciences, Division of Neurology, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Division of Neuroradiology, Geneva University Hospitals and University of Geneva, Geneva, Switzerland.
J Med Virol. 2021 Jul;93(7):4374-4381. doi: 10.1002/jmv.26973. Epub 2021 Apr 23.
Severe acute respiratory coronavirus 2 (SARS-CoV-2) has been associated with neurological complications, including acute encephalopathy. To better understand the neuropathogenesis of this acute encephalopathy, we describe a series of patients with coronavirus disease 2019 (COVID-19) encephalopathy, highlighting its phenomenology and its neurobiological features. On May 10, 2020, 707 patients infected by SARS-CoV-2 were hospitalized at the Geneva University Hospitals; 31 (4.4%) consecutive patients with an acute encephalopathy (64.6 ± 12.1 years; 6.5% female) were included in this series, after exclusion of comorbid neurological conditions, such as stroke or meningitis. The severity of the COVID-19 encephalopathy was divided into severe and mild based on the Richmond Agitation Sedation Scale (RASS): severe cases (n = 14, 45.2%) were defined on a RASS < -3 at worst presentation. The severe form of this so-called COVID-19 encephalopathy presented more often a headache. The severity of the pneumonia was not associated with the severity of the COVID-19 encephalopathy: 28 of 31 (90%) patients did develop an acute respiratory distress syndrome, without any difference between groups (p = .665). Magnetic resonance imaging abnormalities were found in 92.0% (23 of 25 patients) with an intracranial vessel gadolinium enhancement in 85.0% (17 of 20 patients), while an increased cerebrospinal fluid/serum quotient of albumin suggestive of blood-brain barrier disruption was reported in 85.7% (6 of 7 patients). Reverse transcription-polymerase chain reaction for SARS-CoV-2 was negative for all patients in the cerebrospinal fluid. Although different pathophysiological mechanisms may contribute to this acute encephalopathy, our findings suggest the hypothesis of disturbed brain homeostasis and vascular dysfunction consistent with a SARS-CoV-2-induced endotheliitis.
严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）与神经系统并发症有关，包括急性脑病。为了更好地了解这种急性脑病的神经发病机制，我们描述了一系列 2019 年冠状病毒病（COVID-19）脑病患者，强调了其表型及其神经生物学特征。2020 年 5 月 10 日，日内瓦大学附属医院收治了 707 名感染 SARS-CoV-2 的患者；在排除了中风或脑膜炎等合并神经系统疾病后，本系列纳入了 31 名（4.4%）急性脑病患者（64.6±12.1 岁；6.5%为女性）。根据 Richmond 激动镇静量表（RASS），将 COVID-19 脑病的严重程度分为严重和轻度：严重病例（n=14，45.2%）定义为最严重时 RASS＜-3。这种所谓的 COVID-19 脑病的严重形式更常出现头痛。肺炎的严重程度与 COVID-19 脑病的严重程度无关：31 名患者中有 28 名（90%）出现急性呼吸窘迫综合征，但两组之间没有差异（p=0.665）。25 名患者中有 92.0%（23 名）磁共振成像异常，20 名患者中有 85.0%（17 名）颅内血管钆增强，而 85.7%（6 名）患者报告脑脊液/血清白蛋白比值升高提示血脑屏障破坏。所有患者的脑脊液中均未检测到 SARS-CoV-2 的逆转录-聚合酶链反应。尽管不同的病理生理机制可能导致这种急性脑病，但我们的研究结果表明，假设是大脑内环境平衡紊乱和血管功能障碍，这与 SARS-CoV-2 诱导的内皮炎症一致。
