创伤相关性吉兰-巴雷综合征六例临床分析
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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。
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 aRnetsi u-lgtasn glioside antibodies(AGA), cerebrospinal fluid(CSF), clinical diagnosis, treatment and prognosis.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.
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 aRnetsi u-lgtasn glioside antibodies(AGA), cerebrospinal fluid(CSF), clinical diagnosis, treatment and prognosis.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.
引文
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[6]Duncan R, Kennedy PG. Guillain-Barrésyndrome followingacute head trauma[J]. Postgrad Med J, 1987, 63:479-480.
[7]Kaida K, Kamakura K, Ogawa G, Ueda M, Motoyoshi K, AritaM, Kusunoki S. GD1b-specific antibody induces ataxia inGuillain-Barrésyndrome[J]. Neurology, 2008, 71:196-201.
[8]Battaglia F, Sevy A, Moyse E, Roche PH. Guillain-Barrésyndrome following severe head trauma and spine surgery[J].Rev Neurol(Paris), 2013, 169:166-168.
[9]Boghani Z, Livingston AD, Simpson EP, Holman PJ, GrossmanRG. Acute onset of Guillain-Barrésyndrome after electivespinal surgery[J]. World Neurosurg, 2015, 84:376-379.
[10]Carr KR, Shah M, Garvin R, Shakir A, Jackson C. Post-traumatic brain injury(TBI)presenting with Guillain-Barrésyndrome and elevated anti-ganglioside antibodies:a casereport and review of the literature[J]. Int J Neurosci, 2015, 125:486-492.
[11]Liu CF, Han T, Bai YH, Fei CD. Guillain-Barrésyndrome aftertraumatic brain injury:a case report[J]. Xi'nan Guo Fang YiYao, 2012, 22:1131-1132.[刘春凤,韩涛,白月辉,费长东.脑外伤合并吉兰-巴雷综合征1例[J].西南国防医药, 2012, 22:1131-1132.]
[12]Tan IL, Ng T, Vucic S. Severe Guillain-Barrésyndromefollowing head trauma[J]. Clin Neurosci, 2010, 17:1452-1454.
[13]Rashid A, Kurra S, Lavelle W. Guillain-Barrésyndrome afterrevision lumbar surgery:a case report[J]. Cureus, 2017, 9:E1393.
[14]Al-Hashel JY, John JK, Vembu P. Unusual presentation ofGuillain-Barrésyndrome following traumatic bone injuries:report of two cases[J]. Med Princ Pract, 2013, 22:597-599.
[15]Kusunoki S, Kaida K. Antibodies against ganglioside complexesin Guillain-Barrésyndrome and related disorders[J]. JNeurochem, 2011, 116:828-832.
[16]Lopez PH, Zhang G, Zhang J, Lehmann HC, Griffin JW,Schnaar RL, Sheikh KA. Passive transfer of IgG anti-GM1antibodies impairs peripheral nerve repair[J]. J Neurosci,2010, 30:9533-9541.
[2]Wang L, Xia C, Zhang Y, Wang TT, Sun XH. Clinicalobservation in rare causes of Guillain-Barrésyndrome[J]. LinChuang Hui Cui, 2016, 31:1332-1335.[王丽,夏程,张颖,王婷婷,孙显辉.少见诱因引起的吉兰-巴雷综合征临床研究[J].临床荟萃, 2016, 31:1332-1335.]
[3]Li X, Xiao J, Ding Y, Xu J, Li C, He Y, Zhai H, Xie B, Hao J.Clinical and electrophysiological features of post-traumaticGuillain-Barrésyndrome[J]. BMC Neurol, 2017, 17:142-152.
[4]Yang B, Lian Y, Liu Y, Wu BY, Duan RS. A retrospectiveanalysis of possible triggers of Guillain-Barrésyndrome[J]. JNeuroimmunol, 2016, 293:17-21.
[5]Neuromuscular Disease Study Group; EMG and ClinicalNeuroelectrophysiology Study Group; Neuroimmunology StudyGroup, Chinese Society of Neurology, Chinese MedicalAssociation. Guidelines for the diagnosis and treatment ofGuillain-Barrésyndrome[J]. Zhonghua Shen Jing Ke Za Zhi,2010, 43:583-586.[中华医学会神经病学分会神经肌肉病学组,中华医学会神经病学分会肌电图及临床神经电生理学组,中华医学会神经病学分会神经免疫学组.中国吉兰-巴雷综合征诊治指南[J].中华神经科杂志, 2010, 43:583-586.]
[6]Duncan R, Kennedy PG. Guillain-Barrésyndrome followingacute head trauma[J]. Postgrad Med J, 1987, 63:479-480.
[7]Kaida K, Kamakura K, Ogawa G, Ueda M, Motoyoshi K, AritaM, Kusunoki S. GD1b-specific antibody induces ataxia inGuillain-Barrésyndrome[J]. Neurology, 2008, 71:196-201.
[8]Battaglia F, Sevy A, Moyse E, Roche PH. Guillain-Barrésyndrome following severe head trauma and spine surgery[J].Rev Neurol(Paris), 2013, 169:166-168.
[9]Boghani Z, Livingston AD, Simpson EP, Holman PJ, GrossmanRG. Acute onset of Guillain-Barrésyndrome after electivespinal surgery[J]. World Neurosurg, 2015, 84:376-379.
[10]Carr KR, Shah M, Garvin R, Shakir A, Jackson C. Post-traumatic brain injury(TBI)presenting with Guillain-Barrésyndrome and elevated anti-ganglioside antibodies:a casereport and review of the literature[J]. Int J Neurosci, 2015, 125:486-492.
[11]Liu CF, Han T, Bai YH, Fei CD. Guillain-Barrésyndrome aftertraumatic brain injury:a case report[J]. Xi'nan Guo Fang YiYao, 2012, 22:1131-1132.[刘春凤,韩涛,白月辉,费长东.脑外伤合并吉兰-巴雷综合征1例[J].西南国防医药, 2012, 22:1131-1132.]
[12]Tan IL, Ng T, Vucic S. Severe Guillain-Barrésyndromefollowing head trauma[J]. Clin Neurosci, 2010, 17:1452-1454.
[13]Rashid A, Kurra S, Lavelle W. Guillain-Barrésyndrome afterrevision lumbar surgery:a case report[J]. Cureus, 2017, 9:E1393.
[14]Al-Hashel JY, John JK, Vembu P. Unusual presentation ofGuillain-Barrésyndrome following traumatic bone injuries:report of two cases[J]. Med Princ Pract, 2013, 22:597-599.
[15]Kusunoki S, Kaida K. Antibodies against ganglioside complexesin Guillain-Barrésyndrome and related disorders[J]. JNeurochem, 2011, 116:828-832.
[16]Lopez PH, Zhang G, Zhang J, Lehmann HC, Griffin JW,Schnaar RL, Sheikh KA. Passive transfer of IgG anti-GM1antibodies impairs peripheral nerve repair[J]. J Neurosci,2010, 30:9533-9541.