中国现代神经疾病杂志 ›› 2019, Vol. 19 ›› Issue (2): 120-124. doi: 10.3969/j.issn.1672-6731.2019.02.009

• 临床研究 • 上一篇    下一篇

2 创伤相关性吉兰-巴雷综合征六例临床分析

李平, 李峰, 李双英, 张巧莲, 张赛   

  1. 300162 天津,武警特色医学中心神经内科(李平、李双英、张巧莲),神经外科(张赛);272049 山东省济宁市第二人民医院神经外科(李峰)
  • 出版日期:2019-02-25 发布日期:2019-02-03
  • 通讯作者: 张赛,Email:zhangsai11@163.com

Clinical analysis on six cases of post-traumatic Guillain-Barré syndrome

LI Ping1, LI Feng2, LI Shuang-ying1, ZHANG Qiao-lian1, ZHANG Sai3   

  1. 1Department of Neurology, 3Department of Neurosurgery, Characteristic Medical Center of Chinese PAP, Tianjin 300162, China
    2Department of Neurosurgery, Jining No. 2 People's Hospital, Jining 272049, Shandong, China
  • Online:2019-02-25 Published:2019-02-03
  • Contact: ZHANG Sai (Email: zhangsai11@163.com)

摘要:

目的 总结创伤相关性吉兰-巴雷综合征的临床特征。方法 回顾分析 2013 年 8 月至2017 年 6 月共 6 例创伤相关性吉兰-巴雷综合征患者的临床资料,包括临床症状与体征、神经电生理学、血清抗神经节苷脂抗体谱、脑脊液、临床诊断、治疗与转归。结果 本组 6 例患者发病前均有外伤或手术史,创伤至吉兰-巴雷综合征发病时间平均 8 d,临床主要表现为四肢进行性对称性肌无力(6 例)、呼吸肌麻痹(4 例)和脑神经损害(4 例);1 例血清抗神经节苷脂抗体 GM1 IgG 阳性,1 例 GM1 和 GD1b IgG 阳性;2 例脑脊液白细胞计数增加、6 例蛋白定量升高、4 例出现蛋白-细胞分离现象;神经电生理学以运动神经轴索损害为主。3 例临床诊断为急性运动轴索性神经病,1 例为急性运动感觉轴索性神经病,2 例为急性炎性脱髓鞘性多发性神经根神经病。发病至呼吸肌麻痹时间平均 3.25 d,1 例呼吸机辅助通气 27 d后放弃治疗,死亡;1 例拒绝呼吸机辅助通气,死亡。5 例静脉注射免疫球蛋白 0.40 g/ (kg·d),1 例仅静脉滴注糖皮质激素 500 mg/d。平均随访 9.50 个月,4 例生存患者均有不同程度肌萎缩,3 例肌力恢复良好,1例肌力3 ~ 4级。结论 创伤相关性吉兰-巴雷综合征可以发生于不同的创伤应激后,临床表现较严重,病死率较高,预后较差,及时的神经电生理学检查有助于早期诊断。 

关键词: 格林-巴利综合征, 创伤和损伤, 外科手术

Abstract:

Objective To explore the clinical features of post?traumatic Guillain-Barré syndrome (GBS). Methods A retrospective analysis on clinical data of 6 cases was performed from August 2013 to June 2017 in our hospital, including clinical symptoms and signs, electrophysiological examinations, serum anti-ganglioside antibodies (AGA), cerebrospinal fluid (CSF), clinical diagnosis, treatment and prognosis. Results All cases had different histories of trauma or surgery, and the average duration from trauma to onset of GBS was 8 d. Clinical symptoms included progressive symmetrical weakness of limbs in 6 cases, respiratory muscle paralysis in 4 cases and cranial nerve damage in 4 cases. Serum anti-GM1 IgG antibodies were detected in one case, and anti-GM1 and GD1b IgG antibodies were detected in one case. CSF examination showed increased white blood cell (WBC) count in 2 cases, increased protein quantification in 6 cases, protein-cell separation in 4 cases, and the main electrophysiological findings were axonal injuries of motor fibers. Three cases were diagnosed as acute motor axonal neuropathy (AMAN), one case was acute motor-sensory axonal neuropathy (AMSAN), and 2 cases were acute inflammatory demyelinating polyradiculoneuropathy (AIDP). The average duration from onset to respiratory muscle paralysis was 3.25 d. One case abandoned treatment 27 d after mechanical ventilation and died. One case refused mechanical ventilation and died. Five cases were injected intravenous immunoglobulin (IVIg) for 0.40 g/(kg·d), and one case were only given glucocorticoid by intervenous drip for 500 mg/d. The average follow-up was 9.50 months. Four survival cases suffered from different degrees of muscle atrophy, 3 cases had good recovery and one had muscle grade 3-4. Conclusions Post-traumatic GBS can occur after different traumatic stress, with severe clinical manifestations, high mortality and poor prognosis. Timely electrophysiological examination helps to make an early diagnosis.

Key words: Guillain-Barre syndrome, Wounds and injuries, Surgical procedures, operative