Discussion:
Guillain-Barré syndrome (GBS) encompasses a variety of demyelinating conditions which include acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy, acute motor-sensory axonal neuropathy and Miller Fisher syndrome6. The annual incidence of GBS in the United States has been estimated as 1.65-1.79 case per 100,0007. The incidence of GBS seems to increase with advancing age and is higher in males than females with a ratio of 1.5:1. GBS has become one of the leading non-traumatic causes of acute flaccid paralysis (AFP), especially in developed countries. The classical presentation of GBS is bilateral symmetric weakness and decreased deep tendon reflexes with or without accompanying sensory symptoms such as numbness or tingling. The most helpful investigations include a lumbar puncture with CSF analysis demonstrating albuminocytological dissociation and electrophysiological studies showing peripheral neuropathy which is either demyelinating or axonal in origin8. The post-infectious occurrence of GBS led to the reinforcement of the molecular mimicry theory as the underlying pathophysiology. It was postulated that certain infectious agents such as Campylobacter jejuni can lead to the formation of cross-reactive antibodies that target gangliosides which constitute a part of the myelin sheath encircling the peripheral nerves9. The axonal neuropathy observed in rabbits following their injection with ganglioside-like structures extracted from the bacterial cell wall of C.jejuni further support this theory10.
The immunological pathogenesis of GBS was further reinforced by the reported cases following vaccination against multiple pathogens. The influenza vaccine was the most notorious, however others such as hepatitis A and tetanus were also on the list of possibly associated vaccines11,12. Despite a relatively large number of reported cases of post-vaccination GBS, a definite causal association was not strongly confirmed. The increased cases of GBS following the administration of the swine influenza vaccine between 1967 and 1977 did point towards a possible causality, however this was negated in further studies conducted in the years after. The same applied for the oral polio and tetanus vaccines. Earlier studies suggested possible causality; however, the results were contradicted by large multicenter epidemiological studies performed later13.
The first case of GBS following COVID-19 vaccination was reported in February 2021 in the USA in an elderly female who presented 2 weeks after the first dose of the vaccine. The patient presented with fatigue and bilateral symmetric weakness of the lower limbs. CSF analysis showed albuminocytological dissociation and she was started on IVIG which led to improvement in the weakness. The patient recovered successfully and was discharged to a rehabilitation institute thereafter14.
Considering the uncertainty of the causal relation between vaccines and GBS, a temporal association is a possibility. However further studies are required before establishing a conclusion. We would like to express our opinion that the reduction in morbidity and mortality achieved by vaccination outweighs the risks of the reported adverse events and extensive research is required before asserting or ruling out a causal relation between COVID-19 vaccine and GBS.