Guillian Barre syndrome is an acute paralytic polyneuropathy
Acute inflammatory demyelinating polyneuropathy is the most common form of GBS
It is usually triggered by an infection - associated with Campylobacter Jejuni, cytomegalovirus and Epstein-Barr virus
Guilllian Barre Syndrome presents as:
Acute ascending weakness
Bilateral
Sensory symptoms - painful pins and needles
Paralysis can ascend to the respiratory muscles and cause respiratory failure
Examination of Guillian Barre syndrome:
Full neurological exam - absent deep tendon reflexes and changes in sensation
Nerve conduction test will show slow velocity
Lumbar puncture - raised protein and normal white cell count
Spirometry to monitor for respiratory muscle involvement - forced vital capacity
Treatment of Guillian Barre Syndrome:
Plasma exchange - to remove antibodies
IV immunoglobulins (first line)
Supportive care - mechanical ventilation
VTE prophylaxis - PE is leading cause of death in GBS
Molecular mimicry occurs in Guillian Barre syndrome. B cells produce antibodies against the invading pathogen but these antibodies also match proteins on the peripheral nerves. They can attack the myelin sheath or the axon itself
The characteristic findings on a LP during acute GBS:
Albuminocytologic dissociation =
Elevation in protein
Normal WCC
Corticosteroids, often used for other classical autoimmune conditions, have shown no clinical benefit in GBS.
The diagnosis of GBS is made clinically using the Brighton criteria