Miller Fisher Syndrome in Patients With Severe Acute Respiratory Syndrome Coronavirus 2 Infection: A Systematic Review
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Background and Purpose Miller Fisher syndrome (MFS) is a subtype of Guillain-Barré 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.
Abstract
Background and Purpose Miller Fisher syndrome (MFS) is a subtype of Guillain-Barré 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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