Guillain-Barré syndrome (GBS), the acute inflammatory neuropathy prototype and its heterogeneous variants, represents the most common cause of acute neuromuscular weakness and paralysis worldwide. An immune-mediated attack, directed against myelin, axons, or both, is presumed to be triggered by molecular mimicry, with both cell- and humoral-dependent mechanisms driving the pathogenic damage. Axonal degeneration in GBS may be primary or secondary to inflammatory demyelination in nerve trunks, and this process could be closely associated with current and future treatment approaches. Considerable progress has been made in recent years; new immunological concepts and treatments are only partly known, but some etiopathological mechanisms of inflammatory neuropathies remain poorly understood.
Guillain-Barrè Syndrome and Axonal Degeneration
Gallo C.;Vecchio D.;Comi C.
2024-01-01
Abstract
Guillain-Barré syndrome (GBS), the acute inflammatory neuropathy prototype and its heterogeneous variants, represents the most common cause of acute neuromuscular weakness and paralysis worldwide. An immune-mediated attack, directed against myelin, axons, or both, is presumed to be triggered by molecular mimicry, with both cell- and humoral-dependent mechanisms driving the pathogenic damage. Axonal degeneration in GBS may be primary or secondary to inflammatory demyelination in nerve trunks, and this process could be closely associated with current and future treatment approaches. Considerable progress has been made in recent years; new immunological concepts and treatments are only partly known, but some etiopathological mechanisms of inflammatory neuropathies remain poorly understood.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
