Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy triggered by molecular mimicry: antibodies generated against microbial antigens cross-react with gangliosides and glycolipids on peripheral nerve myelin or axons. In acute inflammatory demyelinating polyneuropathy (AIDP — most common subtype, 90% in Western countries), T cells and macrophages attack Schwann cell myelin, causing segmental demyelination and conduction block. In acute motor axonal neuropathy (AMAN), anti-GM1 and anti-GD1a antibodies directly attack axonal membranes at nodes of Ranvier, causing primary axonal degeneration (more common in Asia, associated with Campylobacter jejuni). The ascending weakness pattern reflects immune attack starting at nerve roots (proximal) and motor nerve terminals (distal), progressing centrally. Respiratory failure occurs in 20-30% when the immune attack involves phrenic nerves (C3-5) and intercostal motor nerves. Autonomic involvement (dysautonomia) affects 60-70% and is a major cause of mortality through cardiac arrhythmias, labile blood pressure, and urinary retention.