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The translation of the pathological findings described in humans to experimental models of acute motor axonal neuropathy

Our mechanistic understanding of the Guillain‐Barre' syndromes (GBS) was greatly enhanced by the human pathological studies of Jack Griffin and colleagues conducted in the mid‐1990s. Subsequently, many of the pathological findings in human GBS were confirmed and extended in animal models. This brief account of GBS pathogenesis focuses on the studies that provided the mechanistic evidence for the role of anti‐ganglioside antibodies and complement in injuring the motor axon in Campylobacter‐associated GBS, thereby supporting the earlier seminal pathological observations.