• Anti-ganglioside antibody
• ganglioside
• Guillain–Barré syndrome
• rabies vaccine
• Bickerstaff s brainstem encephalitis
• peripheral neuropathy
• Miller Fisher syndrome
• CIDP
• channels
• neurophysiology
• neuromuscular
• motor neuron disease
• neuropathy
• EMG (single fibre)
• HMSN (Charcot-Marie-tooth)
• immunology
• Lambert Eaton syndrome

Guillain–Barré syndrome (GBS) is an autoimmune-mediated peripheral neuropathy typically occurring after microbial infections such as Campylobacter jejuni enteritis. It can also occur following vaccinations such as the 1976 swine flu vaccine in the USA.1 GBS is divided into demyelinating and axonal subtypes. There is now good evidence that gangliosides or similar components trigger the development of axonal GBS.2 Axonal GBS associated with IgG anti-GM1 or anti-GD1a antibodies after bovine brain ganglioside administration have been recorded in several patients. Sensitisation of rabbits with bovine brain gangliosides or isolated GM1 produced a replica of axonal GBS. Based on these findings, it has been suggested that C jejuni components mimic human gangliosides GM1 and GD1a, and C jejuni infection induces the production of autoantibodies against the gangliosides that are expressed in the peripheral nerves, resulting in the limb weakness seen in GBS. By contrast, the mechanism by which certain vaccines elicit the development of GBS remains unresolved, although there have been studies to suggest that the 1976 swine flu vaccine could elicit anti-GM1 antibodies in mice and that the GM1 epitope was present in the influenza haemagglutinin.3

It is important to understand the pathogenesis of postvaccination GBS to allow safer vaccines to be developed. A number of cases …