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저자정보
Martins-Filho Paulo Ricardo (Investigative Pathology Laboratory, Federal University of Sergipe, Aracaju, Brazil) Pereira de Andrade Ana Luiza (Investigative Pathology Laboratory, Federal University of Sergipe, Aracaju, Brazil) Pereira de Andrade Ana Júlia (Investigative Pathology Laboratory, Federal University of Sergipe, Aracaju, Brazil) Moura da Silva Maria Daniella (Investigative Pathology Laboratory, Federal University of Sergipe, Aracaju, Brazil) de Souza Araújo Adriano Antunes (Laboratory of Pharmaceutical Assays and Toxicity Federal University of Sergipe São Cristóvão Brazil) Nunes Paula Santos (Laboratory of Pharmaceutical Assays and Toxicity, Federal University of Sergipe, Sao Cristovao, Bra) Santos Victor Santana (Centre for Epidemiology and Public Health, Federal University of Alagoas, Arapiraca, Brazil) Ferreira Lis Campos (Neuroimmunology Clinic, Federal University of Sergipe, Aracaju, Brazil) de Aquino Neves Eduardo Luis (Division of Neurology, Department of Medicine, Federal University of Sergipe, Aracaju, Brazil) Quintans-Júnior Lucindo José (Laboratory of Neuroscience and Pharmacological Assays, Federal University of Sergipe, Sao Cristovao)
저널정보
대한신경과학회 Journal of Clinical Neurology Journal of Clinical Neurology 제17권 제4호
발행연도
2021.10
수록면
541 - 545 (5page)
DOI
10.3988/jcn.2021.17.4.541

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Background and Purpose Miller Fisher syndrome (MFS) is a subtype of Guillain-Barre syndrome characterized by the triad of ophthalmoparesis, areflexia, and ataxia. Although cases of MFS have been associated with severe acute respiratory syndrome coronavirus 2 (SARSCoV- 2) infection, no studies have synthesized the clinical characteristics of patients with this condition. Methods In this rapid systematic review, we searched the PubMed database to identify studies on MFS associated with SARS-CoV-2 infection. Results This review identified 11 cases, of whom 3 were hospitalized with motor and/or sensory polyneuropathy as the first sign of SARS-CoV-2 infection. SARS-CoV-2 RNA was not detected in analyses of cerebrospinal fluid, suggesting a mechanism of immune-mediated injury rather than direct viral neurotropism. However, antiganglioside antibodies were found in only two of the nine patients tested. It is possible that target antigens other than gangliosides are involved in MFS associated with SARS-CoV-2 infection. Conclusions The present patients exhibited clinical improvement after being treated with intravenous immunoglobulin. Although rare, patients with SARS-CoV-2 infection may present neurological symptoms suggestive of MFS. Early recognition of the MFS clinical triad is essential for the timely initiation of treatment.

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