格林-巴利综合征:回顾和总结

Mary Shannon Byers
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摘要

乌兰-巴罗综合征是一种危及生命的脱髓鞘性自身免疫性疾病,机体免疫系统会攻击周围神经系统的髓磷脂。格林-巴罗综合征的特征是上升性运动无力和急性弛缓性麻痹。脱髓鞘导致神经炎症、麻木、刺痛、肌肉无力、髓鞘结构损伤以及可能的呼吸系统并发症。全世界的年发病率为每10万人1.1至1.8人。吉兰-巴罗综合征被认为是由先前的感染引发的,如病毒、胃肠道或细菌感染、食物中毒或对疫苗的反应。大约9-11%的病例导致严重残疾或死亡。急性期的长度从几天到几个月不等,尽管90%以上的患者在四周内开始康复。病人护理包括一个由神经科医生、物理医生、内科医生、护士、物理、职业和语言治疗师、社会工作者、心理学家和家庭医生组成的团队。脑脊液蛋白升高、对称性肌肉无力、症状出现的速度和顺序以及反射的缺失或延迟时间延长是诊断格林-巴-巴综合征的标志。腰椎穿刺检测脑和脊髓中的蛋白质水平,以及神经传导速度测试可能有助于正确诊断,这对于优化治疗方案和减少进一步进展至关重要。虽然无法治愈,但治疗可能包括血浆置换,通常在住院期间进行四次,或静脉注射免疫球蛋白。应避免静脉注射免疫球蛋白联合血浆置换。虽然糖皮质激素可以修复血神经屏障的损伤,但口服糖皮质激素可能会延迟恢复。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Guillain-Barre Syndrome: Review and Summary
uillain-Barré Syndrome is a life-threatening, demyelinating, autoimmune condition in which the body’s immune system attacks the myelin of the peripheral nervous system. Guillain-Barré Syndrome is characterized by ascending motor weakness and acute flaccid paralysis. Demyelination results in nerve inflammation, numbness, tingling, muscle weakness, structural damage to the myelin sheath, and possible respiratory system complications. The annual incidence rate is 1.1 to 1.8 per 100,000 persons worldwide. Guillain-Barré Syndrome is thought to be triggered by an antecedent infection such as a viral, gastrointestinal, or bacterial infection, food poisoning, or reaction to a vaccine. Approximately 9-11% of cases result in severe disability or death. The acute phase can vary in length from a few days to several months, although over 90% of patients begin rehabilitation within four weeks. Patient care involves a team of neurologists, physiatrist, internist, nurses, physical, occupational, and speech therapists, social worker, psychologist and family physician. Elevated cerebrospinal fluid protein, symmetrical muscle weakness, the rate and order at which symptoms appear, and the absence or prolonged latency of reflexes are hallmarks for diagnosing Guillain-Barré Syndrome. A lumbar puncture to test for protein levels in the brain and spinal cord, and nerve conduction velocity test may aid in proper diagnosis, critical for optimizing treatment options and minimizing further progression. Although there is no cure, treatment may consist of plasmapheresis, typically performed four times during hospitalization, or intravenous immunoglobulin. Intravenous immunoglobulin combined with plasmapheresis should be avoided. Although glucocorticoids could repair damage to the blood-nerve barrier, oral corticosteroids could delay recovery.
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