Wakerley and Yuki1 report the wide heterogeneity of the clinical spectrum of Guillain–Barré syndrome (GBS), highlighting atypical presentations and reviewing the differential diagnoses. The approach is practical and their intent is to facilitate early diagnosis and treatment without relying on laboratory and electrophysiological findings. It is nearly 100 years since the description of GBS, the recognition of its numerous variants and subtypes is just part of its continuously evolving and fascinating history.

GBS has long been considered synonymous with acute inflammatory demyelinating polyradiculoneuropathy (AIDP); the characteristic electrophysiological correlates of demyelination were described from the 1960s. For years, the electrodiagnosis of GBS was considered relatively easy but with time it has become increasingly complicated. In the 1990s, GBS was recognised to include two primary axonal subtypes: acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN), both associated with antecedent Campylobacter jejuni infection and autoantibodies to gangliosides.

AIDP, AMAN and AMSAN are difficult …