Subacute cerebellar ataxia following respiratory symptoms of COVID-19: a case report

被引:22
|
作者
Werner, Jana [1 ]
Reichen, Ina [1 ]
Huber, Michael [2 ]
Abela, Irene A. [2 ,3 ]
Weller, Michael [1 ]
Jelcic, Ilijas [1 ,4 ]
机构
[1] Univ Hosp Zurich, Dept Neurol, Zurich, Switzerland
[2] Univ Zurich, Inst Med Virol, Zurich, Switzerland
[3] Univ Hosp Zurich, Dept Infect Dis & Hosp Epidemiol, Zurich, Switzerland
[4] Univ Hosp Zurich, Neuroimmunol & Multiple Sclerosis Res Sect, Dept Neurol, Zurich, Switzerland
基金
瑞士国家科学基金会;
关键词
Post-infectious neurological disease; Post-infectious cerebellar ataxia; SARS-CoV-2; infection; COVID-19; Case report; CYTOTOXIC LESIONS;
D O I
10.1186/s12879-021-05987-y
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
BackgroundSevere 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-Barre syndrome or ataxia may also occur.Case presentationHerein 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.ConclusionsThe 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.
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页数:7
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