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J Emerg Med ; 61(6): e141-e145, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1428149


BACKGROUND: Guillain-Barré Syndrome (GBS) is a rapidly progressive immune-mediated polyneuropathy often associated with an antecedent infectious illness or vaccination. The classic presentation of GBS is characterized by ascending limb weakness and numbness with loss of reflexes. However, atypical variants involving the face and arms or with purely sensory symptoms also exist. In up to 30% of cases, GBS progresses to respiratory failure, with patients requiring mechanical ventilation. CASE REPORT: We report a case of atypical GBS occurring after Coronavirus disease 2019 (COVID-19) vaccination in an otherwise healthy 38-year-old man. The patient's clinical presentation was characterized by bilateral hand and foot paresthesias, dysarthria, bilateral facial weakness, and an absence of classic ascending limb weakness. Albuminocytological dissociation within the cerebrospinal fluid was suggestive of GBS. The patient received intravenous immunoglobulin therapy, with modest improvement in his symptoms at the time of his discharge from the hospital. Why Should an Emergency PhysicianBe Aware of This? Patients with GBS are at risk for life-threatening complications, including respiratory failure requiring mechanical ventilation. It is critical for emergency physicians to be aware of the manifold presentations of GBS for early recognition and treatment. This may be of particular importance in the context of a worldwide vaccination campaign in response to the COVID-19 pandemic.

COVID-19 , Guillain-Barre Syndrome , Adult , COVID-19 Vaccines , Guillain-Barre Syndrome/diagnosis , Guillain-Barre Syndrome/etiology , Humans , Male , Pandemics , SARS-CoV-2 , Vaccination/adverse effects
Brain Behav Immun ; 89: 601-603, 2020 10.
Article in English | MEDLINE | ID: covidwho-651618


We describe a man whose first manifestations of Creutzfeldt-Jakob disease occurred in tandem with symptomatic onset of coronavirus disease 2019 (COVID-19). Drawing from recent data on prion disease pathogenesis and immune responses to SARS-CoV-2, we hypothesize that the cascade of systemic inflammatory mediators in response to the virus accelerated the pathogenesis of our patient's prion disease. This hypothesis introduces the potential relationship between immune responses to the novel coronavirus and the hastening of preclinical or manifest neurodegenerative disorders. The global prevalence of both COVID-19 and neurodegenerative disorders adds urgency to the study of this potential relationship.

Brain/diagnostic imaging , Coronavirus Infections/complications , Creutzfeldt-Jakob Syndrome/complications , Pneumonia, Viral/complications , Aged , Betacoronavirus , Brain/physiopathology , COVID-19 , Coronavirus Infections/immunology , Creutzfeldt-Jakob Syndrome/diagnosis , Creutzfeldt-Jakob Syndrome/immunology , Creutzfeldt-Jakob Syndrome/physiopathology , Disease Progression , Electroencephalography , Fluorodeoxyglucose F18 , Humans , Magnetic Resonance Imaging , Male , Pandemics , Pneumonia, Viral/immunology , Positron-Emission Tomography , Radiopharmaceuticals , SARS-CoV-2