Guillain-Barré syndrome in SARS-CoV-2 infection: an instant systematic review of the first six months of pandemic

• Published in: Journal of neurology, neurosurgery and psychiatry Vol. 91; no. 10; pp. 1105 - 1110
• Main Authors: Uncini, Antonino, Vallat, Jean-Michel, Jacobs, Bart C
• Format: Journal Article
• Language: English
• Published: England BMJ Publishing Group LTD 01.10.2020
• Subjects: Adult; Aged; Ataxia; Betacoronavirus; Coronavirus Infections - complications; Coronavirus Infections - diagnosis; Coronavirus Infections - therapy; Coronaviruses; COVID-19; Cytomegalovirus; Disease transmission; Encephalitis; Female; Fever; Guillain-Barre syndrome; Guillain-Barre Syndrome - diagnosis; Guillain-Barre Syndrome - therapy; Guillain-Barre Syndrome - virology; Humans; Infections; Laboratories; Male; Middle Aged; Pandemics; Patients; Pneumonia; Pneumonia, Viral - complications; Pneumonia, Viral - diagnosis; Pneumonia, Viral - therapy; SARS-CoV-2; Serology; Severe acute respiratory syndrome coronavirus 2; Systematic review; Ventilators; Young Adult; Italy; China; Guillain-Barre syndrome; neurovirology; systematic reviews
• ISSN: 0022-3050; 1468-330X
• DOI: 10.1136/jnnp-2020-324491

A systematic review from 1 January to 30 June 2020 revealed 42 patients with Guillain-Barré syndrome (GBS) associated with SARS-CoV-2 infection. Single cases and small series were reported from 13 countries, the majority from Europe (79.4%) and especially from Italy (30.9%). SARS-CoV-2 infection was demonstrated by nasopharyngeal swab (85.7%) and serology (14.3%). Median time between COVID-19 and GBS onset in 36 patients was 11.5 days (IQR: 7.7–16). The most common clinical features were: limb weakness (76.2%), hypoareflexia (80.9 %), sensory disturbances (66.7 %) and facial palsy (38.1%). Dysautonomia occurred in 19%, respiratory failure in 33.3% and 40.5% of patients were admitted in intensive care unit. Most patients (71.4%) had the classical clinical presentation but virtually all GBS variants and subtypes were reported. Cerebrospinal fluid (CSF) albumin-cytological dissociation was found in 28/36 (77.8%) and PCR for SARS-CoV-2 was negative in 25/25 patients. Electrodiagnosis was demyelinating in 80.5% and levels 1 and 2 of Brighton criteria of diagnostic certainty, when applicable, were fulfilled in 94.5% patients. Antiganglioside antibodies were positive in only 1/22 patients. Treatments were intravenous immunoglobulin and/or plasma exchange (92.8%) with, at short-time follow-up, definite improvement or recovery in 62.1% of patients. One patient died. In conclusion, the most frequent phenotype of GBS in SARS-CoV-2 infection is the classical sensorimotor demyelinating GBS responding to the usual treatments. The time interval between infectious and neuropathic symptoms, absence of CSF pleocytosis and negative PCR support a postinfectious mechanism. The abundance of reports suggests a pathogenic link between SARS-CoV-2 infection and GBS but a case-control study is greatly needed.