Natural influenza infection is a stronger risk factor for the development of GBS than is influenza vaccination and the vaccination reduced the risk of GBS overall by lowering the risk of catching influenza.In the United States, GBS after seasonal influenza vaccination is listed on the federal governments vaccine injury table. On March 24, 2021, after reviewing several post-marketing observational studies, where an increased risk of Guillain–Barré syndrome was observed after 42 days following vaccination with the Zoster vaccine Shingrix, the FDA required safety label changes from the manufacturer GlaxoSmithKline to include warnings for risk of Guillain–Barré syndrome. COVID-19 infection or vaccine related
GBS has been reported in association with COVID-19, and may be a potential neurological complication of the disease. GBS has been reported as a very rare side effect of the Janssen and the Oxford–AstraZeneca COVID-19 vaccine for COVID-19 and European Medicines Agency (EMA) had issued warning to the patients and healthcare providers. The incidence of GBS following the vaccination with the Oxford-AstraZeneca vaccine was originally reported as being lower than the incidence of GBS following a COVID-19 infection. More recent studies, however, found no measurable link between COVID-19 infection and GBS, while correlations with a first dose of AstraZeneca or Janssen vaccines were still positive.COVID-19 has been reported as causing peripheral neuropathy and more recently some evidence of aggravation of autoimmune disorders including GBS. Some studies are now finding Parkinsons Disease is more common in infection survivors.
The key four gangliosides against which antibodies have been described are GM1, GD1a, GT1a, and GQ1b, with different antiganglioside antibodies being associated with particular features; for instance, GQ1b antibodies have been linked with Miller Fisher variant GBS and related forms including Bickerstaff encephalitis. The production of these antibodies after an infection probably is the result of molecular mimicry, where the immune system is reacting to microbial substances, but the resultant antibodies also react with substances occurring naturally in the body. After a Campylobacter infection, the body produces antibodies of the IgA class; only a small proportion of people also produce IgG antibodies against bacterial substance cell wall substances (e.g. lipooligosaccharides) that cross react with human nerve cell gangliosides. It is not currently known how this process escapes central tolerance to gangliosides, which is meant to suppress the production of antibodies against the bodys own substances. Not all antiganglioside antibodies cause disease, and it has recently been suggested that some antibodies bind to more than one type of epitope simultaneously (heterodimeric binding) and that this determines the response. Furthermore, the development of pathogenic antibodies may depend on the presence of other strains of bacteria in the bowel.It has been suggested that a poor injection technique may also cause a direct injury to the axillary nerves adjacent to the injection site in deltoid muscle that may lead to peripheral neuropathy.