Department of Neurology, University Hospital Zurich, Zurich, Switzerland.
Institute of Medical Virology, University of Zurich, Zurich, Switzerland.
BMC Infect Dis. 2021 Mar 24;21(1):298. doi: 10.1186/s12879-021-05987-y.
Severe acute respiratory syndrome virus 2 (SARS-CoV-2) is spreading globally and causes most frequently fever and respiratory symptoms, i.e. Coronavirus disease 2019 (COVID-19), however, distinct neurological syndromes associated with SARS-CoV-2 infection have been described. Among SARS-CoV-2-infections-associated neurological symptoms fatigue, headache, dizziness, impaired consciousness and anosmia/ageusia are most frequent, but less frequent neurological deficits such as seizures, Guillain-Barré syndrome or ataxia may also occur.
Herein we present a case of a 62-year-old man who developed a subacute cerebellar syndrome with limb-, truncal- and gait ataxia and scanning speech 1 day after clinical resolution of symptomatic SARS-CoV-2 infection of the upper airways. Apart from ataxia, there were no signs indicative of opsoclonus myoclonus ataxia syndrome or Miller Fisher syndrome. Cerebral magnetic resonance imaging showed mild cerebellar atrophy. SARS-CoV-2 infection of the cerebellum was excluded by normal cerebrospinal fluid cell counts and, most importantly, absence of SARS-CoV-2 RNA or intrathecal SARS-CoV-2-specific antibody production. Other causes of ataxia such as other viral infections, other autoimmune and/or paraneoplastic diseases or intoxication were ruled out. The neurological deficits improved rapidly after high-dose methylprednisolone therapy.
The laboratory and clinical findings as well as the marked improvement after high-dose methylprednisolone therapy suggest a post-infectious, immune-mediated cause of ataxia. This report should make clinicians aware to consider SARS-CoV-2 infection as a potential cause of post-infectious neurological deficits with an atypical clinical presentation and to consider high-dose corticosteroid treatment in case that a post-infectious immune-mediated mechanism is assumed.
严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）正在全球范围内传播，主要引起发热和呼吸道症状，即 2019 年冠状病毒病（COVID-19），然而，与 SARS-CoV-2 感染相关的明确神经系统综合征已被描述。在 SARS-CoV-2 感染相关的神经系统症状中，疲劳、头痛、头晕、意识障碍和嗅觉/味觉丧失最为常见，但也可能出现较少见的神经系统缺陷，如癫痫发作、吉兰-巴雷综合征或共济失调。
本文报告了一例 62 岁男性病例，他在症状性上呼吸道 SARS-CoV-2 感染临床缓解后 1 天出现亚急性小脑综合征，表现为肢体、躯干和步态共济失调以及扫视性言语障碍。除了共济失调外，没有眼球震颤-肌阵挛共济失调或米勒费舍尔综合征的迹象。小脑磁共振成像显示轻度小脑萎缩。正常的脑脊液细胞计数以及最重要的是缺乏 SARS-CoV-2 RNA 或鞘内 SARS-CoV-2 特异性抗体产生排除了小脑的 SARS-CoV-2 感染。其他导致共济失调的原因，如其他病毒感染、其他自身免疫和/或副肿瘤性疾病或中毒，也已排除。高剂量甲基强的松龙治疗后，神经功能缺损迅速改善。
实验室和临床发现以及高剂量甲基强的松龙治疗后的明显改善提示，该患者的共济失调是感染后免疫介导的原因。本报告应使临床医生意识到，应将 SARS-CoV-2 感染视为具有非典型临床表现的感染后神经功能缺损的潜在原因，并在假设存在感染后免疫介导机制时考虑使用大剂量皮质类固醇治疗。
