Neurological

No affiliation between COVID-19 and Guillain-Barré syndrome

Neuroscientists at UCL have not found a significant link between COVID-19 and the potentially debilitating and sometimes fatal neurological condition of Guillain-Barré syndrome.

The researchers say the results, published in the journal Brain *, along with an associated scientific comment ** from UCL and other international experts, should reassure the public when the UK’s national coronavirus vaccination program is rolled out.

Guillain-Barré syndrome (GBS) is a rare but serious autoimmune disease that attacks the peripheral nervous system and typically affects the feet, hands, and limbs, causing numbness, weakness, and pain. Although the exact cause is unknown, GBS often occurs after a gastroenteritis infection called Camplylobacter, where the immune system mistakenly attacks nerves rather than germs.

GBS is usually reversible, but in severe cases it can lead to prolonged respiratory muscle paralysis, require ventilatory support, and sometimes leave permanent neurological deficits. Early detection by experienced neurologists is the key to proper treatment.

Historical context of virus and vaccine associated GBS

In Latin America (2016 and 2020), more cases of GBS have been linked to Zika virus outbreaks than were expected by chance alone. GBS research reports have raised concerns that there may be a similar link between COVID-19 infection and GBS.

The researchers also say fears of a global surge in GBS after mass vaccination may persist due to a historically small surge in GBS related to the 1976 US swine flu vaccination campaign. This vaccination campaign was discontinued because the risk of developing GBS against the background was statistically higher, although subsequent statistical analysis showed that the risk of an association is lower than originally assumed. In any flu vaccination campaign, the risk of GBS as a result of flu vaccination is estimated to be around one per million doses.

This study

In this epidemiological study and cohort study, UCL researchers attempted to investigate a causal link between COVID-19 infection and GBS.

The team evaluated the number of GBS treatments reported to the NHS England National Immunoglobulin Database between 2016 and 2019. This has been compared to the number of cases reported during the COVID-19 pandemic in the first half of 2020.

The annual incidence of GBS treated in UK hospitals between 2016 and 2019 was 1.65 to 1.88 per 100,000 people. The incidence of GBS decreased by 40-50% between March and May 2020 compared to the same months of 2016-2019. This new finding contradicts other smaller and less extensive international studies.

The possibility that SARS-CoV-2 is causing a global surge in GBS has been diligently monitored, with a number of published small case series already claiming a causal link. However, an increase in GBS cases after the SARS-CoV-2 pandemic was not noted as was the case with the Zika virus pandemic. Our epidemiological study shows that there was no increased incidence of GBS during the first wave of COVID-19; Rather, there was a decrease and therefore no causal link between COVID-19 and GBS can be established.

First author Dr. Stephen Keddie (UCL Queen Square Institute of Neurology)

Separately in this study, the research team also tried to determine whether SARS-CoV-2, the virus that causes COVID-19, has a genetic or protein structure that could trigger an immune response that causes GBS. In contrast to Camplylobacter, which contains human-like antigens that trigger an autoimmune reaction, no credible association has been found with SARS-CoV-2.

Most COVID-19 vaccinations are based on the SARS-CoV-2 spike protein, which triggers a complex immune response and creates antibodies to fight infections. Our analysis shows that SARS-CoV-2 does not contain any additional immunogenic material that is known or proven to drive GBS. Concerns that a COVID vaccination could cause GBS in significant numbers are therefore almost certainly unfounded.

Dr. Keddie

There are around 1,500 cases of GBS in the UK each year (two per 100,000 population). History suggests that researchers say that mass vaccination could be blamed for cases of GBS if they happen accidentally, especially in billions of people who are expected to be vaccinated worldwide.

If we immunize the population against COVID-19, GBS (and other neurological diseases) will just happen to be the window for a normal response to the vaccine in the weeks following immunization alone. These cases can be of concern and concern about vaccination among patients, politicians and regulators, although it is likely that most, if not all, cases are linked to vaccination by chance alone. Such a serious illness can lead to the vaccination being suspended or canceled as a “knee jerk” safety reaction. However, this may only be done if a statistically proven connection has been proven through careful monitoring. With any vaccination program of this magnitude, we need to take small risks that are far less than the risk of COVID infection.

Corresponding Author, Professor Michael Lunn (UCL Queen Square Institute of Neurology)

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Notes for editors

To speak to the researchers or get a copy of the paper, please contact Henry Killworth, UCL Media Relations: T +44 (0) 7881 833274 or E: [email protected] Research Paper, Stephen Keddie , Julia Pakpoor, Christina Mousele, Ainsling Carr, Michael Lunn, “Epidemiological and cohort study finds no connection between Covid-19 and Guillain-Barre syndrome”, will be published on Monday, December 14, 2020 / 7:01 pm (00:01 am (UK time)) published in Brain. Easter time).

* The DOI for this Brain research paper is: https://doi.org/10.1093/brain/awaa433

The scientific commentary, Michael Lunn, David Cornblath, Richard Hughes, Bart Jacobs, Pieetr Van Doorn, Hugh Willisson, “COVID-19 Vaccine and Guillain-Barre Syndrome: Let’s Not Jump To Associations” will be published in Brain at 00: 01 (UK Time) Monday, December 14, 2020 / 7:01 PM (Eastern Time).

** The DOI for the linked scientific commentary also published in Brain is: https://doi.org/10.1093/brain/awaa444

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