Pathogenesis of Guillain-Barré syndrome.

摘要: Recent neurophysiological and pathological studies have led to a reclassification of the diseases that underlie Guillain-Barre syndrome (GBS) into acute inflammatory demyelinating polyradiculoneuropathy (AIDP), motor sensory axonal neuropathy (AMSAN) (AMAN). The Fisher ophthalmoplegia, ataxia areflexia is most striking several related conditions. Significant antecedent events include Campylobacter jejuni (4–66%), cytomegalovirus (5–15%), Epstein-Barr virus (2–10%), Mycoplasma pneumoniae (1–5%) infections. These infections are not uniquely associated with any clinical subtype but severe degeneration more common following C. impairment cytomegalovirus. Strong evidence supports an important role for antibodies gangliosides in pathogenesis. In particular ganglioside GM1 present 14–50% patients GBS, cases subtype. Antibodies GQ1b very closely syndrome, its formes frustes syndromes. Ganglioside-like epitopes exist bacterial wall jejuni. Infection by this other organisms triggers antibody response GBS those uncomplicated enteritis. development likely be consequence special properties infecting organism, since some strains such as Penner O:19 O:41 particularly It also immunogenetic background patient few develop after infection even one these strains. Attempts match subtypes fine specificity anti-ganglioside functional effects experimental models continue yet fully explained T cells involved pathogenesis or perhaps all forms GBS. cell responses three myelin proteins, P2, PO PMP22, sufficient induce autoimmune neuritis. Activated circulation stage, up-regulate matrix metalloproteinases, cross blood-nerve barrier encounter their cognate antigens. Identification still at preliminary stage. invasion intact sheaths activated macrophages difficult explain according purely mediated mechanism. different patterns probably due diverse interplay between differing specificities.