Guillain-Barré syndrome in SARS-CoV-2 infection: an instant systematic review of the first six months of pandemic.
Identifieur interne : 000450 ( Main/Corpus ); précédent : 000449; suivant : 000451Guillain-Barré syndrome in SARS-CoV-2 infection: an instant systematic review of the first six months of pandemic.
Auteurs : Antonino Uncini ; Jean-Michel Vallat ; Bart C. JacobsSource :
- Journal of neurology, neurosurgery, and psychiatry [ 1468-330X ] ; 2020.
English descriptors
- KwdEn :
- Adult (MeSH), Aged (MeSH), Betacoronavirus (MeSH), Coronavirus Infections (complications), Coronavirus Infections (diagnosis), Coronavirus Infections (therapy), Female (MeSH), Guillain-Barre Syndrome (diagnosis), Guillain-Barre Syndrome (therapy), Guillain-Barre Syndrome (virology), Humans (MeSH), Male (MeSH), Middle Aged (MeSH), Pandemics (MeSH), Pneumonia, Viral (complications), Pneumonia, Viral (diagnosis), Pneumonia, Viral (therapy), Young Adult (MeSH).
- MESH :
- complications : Coronavirus Infections, Pneumonia, Viral.
- diagnosis : Coronavirus Infections, Guillain-Barre Syndrome, Pneumonia, Viral.
- therapy : Coronavirus Infections, Guillain-Barre Syndrome, Pneumonia, Viral.
- virology : Guillain-Barre Syndrome.
- Adult, Aged, Betacoronavirus, Female, Humans, Male, Middle Aged, Pandemics, Young Adult.
Abstract
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.
DOI: 10.1136/jnnp-2020-324491
PubMed: 32855289
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pubmed:32855289Le document en format XML
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<author><name sortKey="Uncini, Antonino" sort="Uncini, Antonino" uniqKey="Uncini A" first="Antonino" last="Uncini">Antonino Uncini</name>
<affiliation><nlm:affiliation>Department of Neuroscience, Imaging and Clinical Sciences, University "G. d'Annunzio" Chieti-Pescara, Chieti, Italy uncini@unich.it.</nlm:affiliation>
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<author><name sortKey="Vallat, Jean Michel" sort="Vallat, Jean Michel" uniqKey="Vallat J" first="Jean-Michel" last="Vallat">Jean-Michel Vallat</name>
<affiliation><nlm:affiliation>Department of Neurology, National Reference Center for "Rare Peripheral Neuropathies", CHU Dupuytren, Limoges, France.</nlm:affiliation>
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<author><name sortKey="Jacobs, Bart C" sort="Jacobs, Bart C" uniqKey="Jacobs B" first="Bart C" last="Jacobs">Bart C. Jacobs</name>
<affiliation><nlm:affiliation>Departments of Neurology and Immunology, Erasmus MC, Rotterdam, The Netherlands.</nlm:affiliation>
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<term>Aged (MeSH)</term>
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<term>Coronavirus Infections (complications)</term>
<term>Coronavirus Infections (diagnosis)</term>
<term>Coronavirus Infections (therapy)</term>
<term>Female (MeSH)</term>
<term>Guillain-Barre Syndrome (diagnosis)</term>
<term>Guillain-Barre Syndrome (therapy)</term>
<term>Guillain-Barre Syndrome (virology)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Middle Aged (MeSH)</term>
<term>Pandemics (MeSH)</term>
<term>Pneumonia, Viral (complications)</term>
<term>Pneumonia, Viral (diagnosis)</term>
<term>Pneumonia, Viral (therapy)</term>
<term>Young Adult (MeSH)</term>
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<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia, Viral</term>
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<term>Guillain-Barre Syndrome</term>
<term>Pneumonia, Viral</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
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<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.</CopyrightInformation>
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<CoiStatement>Competing interests: None declared.</CoiStatement>
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