Griffin D E
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Res Publ Assoc Res Nerv Ment Dis. 1990;68:91-104.
Post-rabies vaccine encephalomyelitis, postinfectious encephalomyelitis, and acute inflammatory demyelinating polyneuropathy are all monophasic, inflammatory, demyelinating diseases that appear to be autoimmune in pathogenesis and induced by prior antigenic stimulation or infection. The primary encephalitogen for rabies vaccine and postinfectious encephalomyelitis appears to be MBP, with a possible augmenting role for the myelin glycolipids. The primary neuritogen in AIDP may be a glycolipid, but this has not been clearly established. The mechanism by which a prior, apparently unrelated, stimulus leads to postinfectious encephalomyelitis or AIDP is unclear, but abnormalities of immune regulation, possible molecular mimicry between infectious agents and neural constituents, and genetic susceptibility may each play important roles (Table 1).
狂犬病疫苗接种后脑脊髓炎、感染后脊髓炎和急性炎症性脱髓鞘性多发性神经病均为单相性、炎症性、脱髓鞘性疾病，其发病机制似乎为自身免疫性，由先前的抗原刺激或感染诱发。狂犬病疫苗和感染后脊髓炎的主要脑髓炎原似乎是髓磷脂碱性蛋白（MBP），髓磷脂糖脂可能起增强作用。急性炎症性脱髓鞘性多发性神经病（AIDP）的主要神经炎原可能是一种糖脂，但尚未明确证实。先前一种明显无关的刺激导致感染后脊髓炎或AIDP的机制尚不清楚，但免疫调节异常、感染因子与神经成分之间可能存在的分子模拟以及遗传易感性可能均起重要作用（表1）。
