Overview
Pathophysiology
Molecular mimicry after a Campylobacter, influenza, or other respiratory/gastrointestinal infection provokes anti‑ganglioside antibodies that bind myelin‑associated gangliosides.
Molecular mimicry after a Campylobacter, influenza, or other respiratory/gastrointestinal infection provokes anti‑ganglioside antibodies that bind myelin‑associated gangliosides. Complement activation damages Schwann cells, producing segmental demyelination or, in axonal variants, direct axolemmal injury. Loss of myelin interrupts saltatory conduction, creating the characteristic ascending, symmetric weakness and areflexia. Autonomic fibres are equally vulnerable, explaining the frequent labile blood pressure, tachyarrhythmias, and ileus.