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.