SARS‐CoV‐2 and Guillain–Barré syndrome: AIDP variant with a favourable outcome

European Journal of Neurology - Tập 27 Số 9 - Trang 1751-1753 - 2020
Agustina M. Lascano1, Jean Benoît Epiney2, Matteo Coen3, Jacques Serratrice3, Raphaël Bernard‐Valnet2, Patrice H. Lalive1, Thierry Küntzer2, Annemarie Hübers1
1Division of Neurology, Department of Clinical Neurosciences, Faculty of Medicine, Geneva University Hospitals and University of Geneva, Geneva, Switzerland
2Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital (Centre Hospitalier Universitaire Vaudois) and University of Lausanne, Lausanne, Switzerland
3Service of Internal Medicine, Department of Medicine, Geneva University Hospitals and Unit of Development and Research in Medical Education (UDREM), Faculty of Medicine, University of Geneva, Geneva, Switzerland

Tóm tắt

Background and purposeThe spectrum of COVID‐19, caused by severe acute respiratory syndrome coronavirus 2 infection (SARS‐CoV‐2), includes different neurologic manifestations of the central and peripheral nervous system.MethodsFrom March through April 2020, in two university hospitals located in western Switzerland, we examined three patients with Guillain–Barré syndrome (GBS) following SARS‐CoV‐2.ResultsThese cases were characterized by a primary demyelinating electrophysiological pattern (Acute inflammatory demyelinating polyneuropathy or AIDP) and a less severe disease course compared to recently published case series. Clinical improvement was observed in all patients at week five. One patient was discharged from hospital after full recovery with persistence of minor neurological signs (areflexia). Two of the three patients remained hospitalized: one was able to walk and the other could stand up with assistance.ConclusionsWe report three cases of typical GBS (AIDP) occurring after SARS‐CoV‐2 infection and presenting with a favourable clinical course. Given the interval between COVID‐19‐related symptoms and neurological manifestations (mean of 15 days) we postulate a secondary immune‐mediated mechanism rather than direct viral damage.

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European Journal of Neurology

Tập 27 Số 9

1751-1753

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