Traditionally, acquired demyelinating polyneuropathies have been classified as Guillian-Barre syndrome (GBS) if they were acute, or as chronic inflammatory demyelinating polyneuropathy (CIDP) if they were chronic or progressive. Both conditions were thought to be immune-mediated because they are associated with inflammatory infiltrates in the affected nerves, or they respond to immunosuppressive medications. There is increasing evidence, however, that both GBS and CIDP are comprised of several distinct disease entities which differ in their pathophysiology and clinical manifestations, and in their response to specific immunotherapies. An unexpected development is the relatively frequent involvement of oligosaccharide determinants as target antigens in both the acute and chronic demyelinating polyneuropathies. In the acute polyneuropathies the antibodies are typically IgGs, whereas in the chronic polyneuropathies they are usually IgMs. In the acute polyneuropathies, antibodies to GQ1b ganglioside are associated with the Miller-Fisher syndrome, and antibodies to GM1 ganglioside are associated with the acute motor axonal variant of GBS. In the chronic polyneuropathies, antibodies to MAG are associated with demyelinating sensorimotor neuropathy, antibodies to GD1b or sulfatide are associated with sensory neuropathy, and antibodies to GM1 ganglioside are associated with motor neuropathy. Other minor gangliosides have also been implicated in some polyneuropathies. Clues to the mechanisms responsible for development of these disorders come from studies of patients with acute motor axonal neuropathy which is associated with anti-GM1 antibodies. This disease sometimes follows infection with strains of Campylobacter jejuni that bear GM1-like oligosaccharides, suggesting a role for molecular mimickry. In other cases, the disease can follow vaccination or other bacterial or viral infections. However, little is known about the mechanisms which trigger or regulate the immune response to oligosaccharide antigens.