PDF(Pubmed)
Abstract：
Guillain-Barré syndrome occurs via molecular mimicry when a trigger sets off an immune response on peripheral nerve epitopes. Patients typically report an antecedent infection, such as an upper respiratory infection or Campylobacter jejuni gastroenteritis. It is typically characterized by progressive, symmetric muscle weakness with absent/decreased deep tendon reflexes. Most cases in the literature report that the paralysis begins in the legs distally and ascends to the extremities. Patients may have sensory symptoms or dysautonomia as well. Notable variant forms include acute motor axonal neuropathy, acute motor/sensory neuropathy, Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Diagnosis is confirmed if a lumbar puncture shows albuminocytologic dissociation (typically 45 to 200 mg/dL). Nerve conduction studies may also be considered but are not necessary. Management is largely supportive, but intravenous immunoglobulin and/or plasmapheresis for more severe cases may be considered.
摘要：
当触发因素引起外周神经表位的免疫反应时，通过分子模仿发生格林-巴利综合征。患者通常会报告先前的感染，如上呼吸道感染或空肠弯曲杆菌肠胃炎。它的典型特征是渐进的，对称肌肉无力，深腱反射缺失/减少。文献中的大多数病例报道，瘫痪始于远端腿部，并上升到四肢。患者可能有感觉症状或自主神经障碍。值得注意的变体形式包括急性运动性轴索神经病，急性运动/感觉神经病变，MillerFisher综合征,还有Bickerstaff脑干脑炎.如果腰椎穿刺显示白蛋白细胞解离（通常为45至200mg/dL），则可确诊。神经传导研究也可以考虑，但不是必要的。管理层在很大程度上是支持的，但对于更严重的病例,可以考虑静脉注射免疫球蛋白和/或血浆置换.
