The Guillain-Barré syndrome: no longer a simple concept.

Acute inflammatory demyelinating polyneuropathy or the Guillain-Barré syndrome (GBS) has come to be accepted as a clinical entity, although the boundary between it and chronic inflammatory demyelinating polyneuropathy has given rise to discussion. Recent observations have suggested that the GBS may represent the consequence of more than one pathogenetic mechanism. In most cases the salient pathological change is demyelination. In some this may be mediated predominantly by lymphocytes; in others, where the demyelination is produced primarily by macrophages, the process may be antibody-mediated. Both electrophysiological and pathological evidence indicates that occasional patients with the GBS show extensive axonal degeneration. Although this could represent a "bystander effect" secondary to inflammatory infiltration, at times it may reflect a direct attack on axons. Elucidation of the nature of the pathogenetic mechanisms is essential before rational therapy can be devised.