• 急性中枢神经系统损伤与吉兰-巴雷综合征
  • Acute central nervous system injury and Guillain-Barré syndrome
  • 吴茜,唐洲平,刘娜,潘超,胡洋,张萍.急性中枢神经系统损伤与吉兰-巴雷综合征[J].内科急危重症杂志,2017,23(2):
    DOI:
    中文关键词:  中枢神经系统损伤  吉兰-巴雷综合征  肌电图  可逆性血管收缩综合征
    英文关键词:CNS injury  GBS  electrophysiological examination  Reversible cerebral vasoconstriction syndrome
    基金项目:国家自然科学基金资助项目:微创血肿清除术治疗脑出血在细胞分子水平多靶点的机制研究(81171089)及脂肪干细胞来源的神经前体细胞移植治疗脑出血及其机制研究(81471201)
    作者单位E-mail
    吴茜 华中科技大学同济医学院附属同济医院神经科 wuqian890110@163.com 
    唐洲平 华中科技大学同济医学院附属同济医院神经科 ddjtzp@163.com 
    刘娜 华中科技大学同济医学院附属同济医院神经科  
    潘超 华中科技大学同济医学院附属同济医院神经科  
    胡洋 华中科技大学同济医学院附属同济医院神经科  
    张萍 华中科技大学同济医学院附属同济医院神经科  
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    中文摘要:
          目的 探讨急性中枢神经系统损伤(Central nervous system injury,CNS injury)与吉兰-巴雷综合征(Guillain-Barré syndrome ,GBS)并发的临床特征及机制。方法 搜集同济医院2011年1月-2016年1月之间住院诊断为GBS患者的资料,筛选并总结继发于急性中枢神经系统损伤的GBS患者资料,复习文献,分析两种疾病之间的关系。结果 我院5年收治GBS共239例,其中继发于急性神经系统损伤后的GBS患者12例(5%),包括男性8例,女性4例,发病年龄在42~61岁。患者周围神经损伤的症状继发于原发性或者外伤性中枢神经系统损伤,表现为原发病的基础上出现进行性加重的四肢迟缓性瘫痪、脑干功能异常、反射消失等症状和体征。脑脊液提示蛋白-细胞分离,电生理检查提示周围神经损伤,F波出现率降低,结合病史确诊为不同亚型的GBS。通过复习文献发现中枢神经系统损伤与GBS有密切的关系,两种疾病可以相继发生,或GBS继发于中枢神经系统损伤或中枢神经系统损伤继发于GBS。目前认为,GBS可以继发于多种中枢神经系统损伤,如脑外伤、出血性脑卒中、脊髓外伤、脊髓相关手术相关操作,主要与患者应激状态下体液-细胞免疫失衡以及炎性血液成分渗漏到蛛网膜下腔引起的神经根损伤有关。而中枢神经系统损伤继发于GBS则以脑梗死多见,也有一些出血性卒中的报道,可能与静脉使用免疫球蛋白导致的血液粘滞度改变、GBS自主神经功能失调导致的血管痉挛、难以控制的高血压有关。结论 两种疾病都是高致残率的神经重症,因此在临床工作需要严谨仔细的体格检查以便尽早发现病情变化,做到早诊断、早治疗。
    英文摘要:
          Objectives To investigate the clinical characteristics and pathogenesis of acute central nervous system injury (CNS injury) complicated with Guillain-Barré syndrome syndrome (GBS). Methods Collecting clinical data of GBS patients in Tongji hospital from January 2011 to 2016 January, we screened those patients who suffered GBS secondary to acute CNS injury and reviewed literatures to analysis their relationships. Results The total number of GBS patients admitted was 239 for 5 years while the number of GBS secondary to CNS injury was 12 cases(accounted for 5%), including eight male and four female patients. Onset age concentrated at 42~61 years old and all patients had GBS secondary to primary or traumatic CNS injury. Clinical manifestations were progressive flaccid paralysis, brainstem dysfunction, weakened or diminished tendon reflexes based on primary CNS diseases. Cerebrospinal fluid results showed protein-cell isolation and electrophysiological examinations showed peripheral nerve injury and decreased F-waves ratio. Combined with the history, 12 patients were diagnosed as different subtypes of GBS. Literature review showed CNS injury and GBS had close relationship and these two diseases may occur successively. One is GBS secondary to CNS injury, the other is CNS injury secondary to GBS. It is thought GBS secondary to a variety of CNS injury, such as traumatic brain injury, hemorrhage stroke, spinal cord injury or surgery are related to humoral-cell immune imbalances under stress state and inflammatory nerve root injury induced by blood components penetration. Cerebral infarction was common to see in CNS injury patients secondary to GBS. Intravenously immunoglobulin injection induced blood viscosity changes, GBS caused autonomic dysfunction such as reversible vasospasm and unstable blood pressures might be responsible for those patients. Conclusions Both CNS injury and GBS are severe neurological diseases therefore physicians require carefully physical examinations to arrive at early diagnosis and treatment.