吉兰巴雷综合征神经电生理研究
|
摘要
第一部分
吉兰巴雷综合征系列神经电生理研究
目的：
对吉兰巴雷综合征(GBS)患者进行系列的神经电生理随诊,明确急性炎性脱髓鞘性多发神经根神经病(AIDP)和急性运动轴索性神经病(AMAN)在病程的不同阶段其系列的神经电生理改变。依据目前的GBS分型诊断标准对GBS进行分型,研究系列神经电生理随诊后GBS分型的变化,并探讨分型发生改变的原因。研究传导阻滞在GBS中的转归,探讨传导阻滞潜在的病理生理机制。
方法：
连续收集北京协和医院2010年9月至2013年3月GBS患者21例,在发病2周和4周左右至少完成2次神经电生理检查,同时回顾性收集北京协和医院1997年至2010年至少完成2次神经电生理检查的GBS住院患者21例,共42例。收集患者临床资料和神经电生理测定参数,包括运动神经传导、感觉神经传导、F波和针极肌电图。利用Hadden等的GBS分型诊断标准对患者进行神经电生理分型：首先依据初次神经电生理检查将患者分为AIDP组、AMAN组、AMSAN组和未分型组；然后依据系列随诊的神经电生理检查再次分组。统计系列随诊后GBS分型发生改变的患者,并分析分型发生改变的原因。统计分析AIDP和AMAN患者的临床和神经电生理特点。分析传导阻滞在GBS中的转归及其原因。
结果：
42例患者中,初次神经电生理检查符合AIDP者26例(62%),AMAN者10例(24%),未分型者6例(14%)。系列随诊后符合AIDP者17例(40%),AMAN者16例(38%),未分型者3例(7%),分型待定者(神经传导异常快速恢复正常)6例(14%)。
AIDP和AMAN两组患者差异具有统计学意义的临床症状是腹泻史(p=0.032)和麻木症状(p=0.015)。两组患者在面瘫、吞咽困难或构音障碍等临床症状上差异无统计学意义。两组患者Hughes评分最低分和发病第4周时Hughes评分差异无统计学意义(t=0.437, p=0.665; t=1.005, p=0.323)。两组患者呼吸机辅助呼吸比例和临床症状快速恢复比例差异无统计学意义(p=0.335；p=0.335)。6例神经传导快速恢复者与AIDP和AMAN患者相比,Hughes评分最低分差异均无统计学意义(t=0.455, p=0.653; t=0.149, p=0.883),但6例患者发病1月内Hughes评分改善均大于2分,发病第4周时Hughes评分与AIDP和AMAN患者相比,差异均有统计学意义(t=2.125, p=0.046; t=3.032, p=0.007)
AIDP患者末端潜伏期(DML)延长在发病第1-2周开始出现,第3-5周达高峰,此后逐渐恢复；远端复合肌肉动作电位(dCMAP)波幅在发病第1周出现下降,在第2-3周最低,此后缓慢恢复。AIDP患者发病第1周F波出现率出现异常,F波平均潜伏期正常,此后F波出现率逐渐恢复,但F波潜伏期逐渐延长,发病第4周左右达高峰。AMAN患者CMAP波幅恢复速度有两种模式：一种是CMAP波幅持续维持在较低的水平,一种是CMAP波幅较快升高,这两种快慢不同的恢复模式可以存在于同—患者不同神经上。
系列随诊GBS分型发生改变者多是初次神经电生理检查为AIDP者分型发生改变,或者是初次神经电生理检查未分型者系列随诊分型明确。11例AIDP患者分型发生改变,其原因包括传导阻滞演变为轴索变性(4例),传导阻滞快速恢复(5例),短暂性DML延长(2例)。
结论：
AIDP和AMAN患者病情严重程度和临床预后是相似的,电生理上AMAN患者CMAP波幅可以持续维持在很低的水平,也可以相对快速的恢复,AMAN潜在的病理生理机制不仅包括轴索变性,也包括可逆性传导障碍。
系列神经电生理随诊GBS分型改变主要由AIDP组转变为AMAN组或者AIDP组神经电生理快速恢复,发生转变的原因包括传导阻滞演变为轴索变性、传导阻滞快速恢复和短暂的末端潜伏期的延长。
第二部分
Miller Fisher综合征和Bickerstaff脑干脑炎临床及电生理特点分析
目的：
总结Miller Fisher综合征(MFS)和Bickerstaff脑干脑炎(BBE)患者临床及电生理特点,并探索其发病机制。
方法：
回顾性分析北京协和医院2000年至2011年符合MFS诊断标准的患者(13例)和BBE诊断标准的患者(7例)的病历资料,收集患者临床资料和电生理测定参数,包括感觉和运动神经传导、针极肌电图、F波、皮肤交感反应(SSR)、脑干听觉诱发电位(BAEP)、瞬目反射等,统计MFS和BBE临床特点和各项电生理检查异常的患者比例。
结果：
MFS和BBE患者前驱感染以呼吸道症状为主,眼球活动障碍、面瘫、延髓部症状较常见,均有脑脊液蛋白细胞分离,都存在抗GQlb抗体。但临床上,BBE还有意识障碍等中枢神经系统受累表现。电生理上,MFS和BBE患者感觉神经受累比例分别为6/13、2/7,主要表现为感觉神经动作电位波幅明显下降,感觉神经传导速度轻度减慢或正常；运动神经受累比例分别为2/13、1/7,多表现为运动末端潜伏期轻度延长,复合肌肉动作电位波幅正常；肢体针极肌电图异常比例分别为1/7、0/4；F波出现率异常比例分别为3/13、5/7,部分患者可出现F波出现率明显下降,但可以恢复；SSR异常比例分别为1/2、1/3;瞬目反射异常比例分别为1/2、1/1,BBE患者表现为中枢性损害；脑干听觉诱发电位异常比例分别为3/5、1/4,均表现为I波潜伏期延长或波幅低。
结论：
MFS和BBE中枢神经系统和周围神经系统均可受累,但BBE以中枢神经系统受累更常见。MFS和BBE可能是中枢神经系统和周围神经系统受累程度不同的同一种疾病的连续疾病谱。
Part1
Serial electrophysiological study of Guillain-Barre syndrome
Objective:
To investigate the serial electrophysiological changes of acute inflammatory demyelinating polyneuropathies(AIDP) and acute motor axonal neuropathy(AMAN) through serial electrophysiological study of Guillain-Barre syndrome(GBS). To electrophysiologically classify GBS patients into AIDP and AMAN subtypes, investigate how serial recordings change the classification, and analyze the causes of classification changes. To investigate the serial electrophysiological changes of conduction block, and analyze the possible underlying mechanisms of conduction block.
Methods:
Prospectively collected21GBS patients in Peking Union Medical College Hospital between September2010and March2013, and performed at least two serial electrophysiological tests around the second and fourth week after disease onset. Retrospectively collected21GBS patients between1997and2010who had at least two serial electrophysiological recordings. The electrophysiological parameters included motor sensory nerve conduction, F waves and electromyography. Based on the first electrophysiological recordings, electrophysiologically classified GBS patients into AIDP and AMAN subtypes according to Hadden's classification criteria. Analyzed how GBS patients changed the initial electrodiagnosis after serial electrophysiological recordings, and analyzed the causes of the changes. Compared and analyzed the clinical and electrophysiological characteristics of AIDP and AMAN patients. Analyzed the serial electrophysiological changes of conduction block.
Results.
At the first test,26of42patients(62%) fulfilled Hadden's criteria for AIDP,10patients(24%) for AMAN and6patients(14%) were classified as equivocal. After follow-up,17patients(40%) were classified as AIDP,16patients(38%) as AMAN,3patients(7%) equivocal and6patients with rapid electrophysiological recovery(classification unclear). Clinically, preceding gastroenteritis were more common in AMAN group (p=0.032), and sensory symptoms were more common in AIDP group(p=0.015). Between the AIDP and AMAN groups, cranial nerve involvement did not differ significantly, and neither the nadir Hughes grade nor Hughes grade at the forth week differed significantly(t=0.437, p=0.665; t=1.005, p=0.323). Compared with AIDP and AMAN group, nadir Hughes grade of the6patients with rapid electrophysiological recovery did not differ significantly. However, all the6patients showed a markedly rapid clinical recovery(improved by two or more Hughes grades within one month), and compared with AIDP and AMAN group the Hughes grades at the forth week differed significantly(t=2.125, p=0.046; t=3.032, p=0.007).
In AIDP group, distal motor latency(DML) prolongation appeared at week1-2, and became prominent at week3-5; The nadir of distal compound muscle action potential(dCMAP) amplitude decrease occurred at week1-2. In AIDP group, the early electrophysiological changes of F waves were decreased frequency with normal F wave latency, and F wave latency prolongation showed up later with nadir abnormality occurring at week4. There were two patterns of CMAP amplitude recovery in AMAN group:rapid increase and persistent at low level, and the two different recovery patterns were found in different nerves of the same patient.
The majority of classification changes were from AIDP and equivocal groups by initial electrophysiological tests. The main reason was the recognition by serial recordings of reversible conduction failure(5patients), axonal degeneration(4patients) and transient prolongation of DML(2patients).
Conclusion:
The clinical severity and prognosis of the AIDP and AMAN groups are similar. In some AMAN patients, the CMAP amplitude can rapidly increase, which could not be explained by axonal degeneration. Besides axonal degeneration, reversible conduction failure might be another underlying mechanisms of AMAN.
The causes of classification changes after serial electrophysiological study include:the length-dependent CMAP amplitude reduction, rapid resolve of conduction block, and transient prolongation of DML.
Part2
Clinical and electrophysiological study of Miller Fisher syndrome and Bickerstaff's brainstem encephalitis
Objective:
To investigate the underlying mechanisms of Miller Fisher syndrome(MFS) and Bickerstaff's brainstem encephalitis(BBE) through study of their clinical and electrophysiological characteristics.
Methods:
Retrospectively analyzed clinical and electrophysiological characteristics of13MFS and7BBE cases in Peking Union Medical College Hospital between2000and2011. The electrophysiological parameters included sensory and motor nerve conduction, electromyography, F wave, sympathetic skin response, brainstem auditory evoked potential and blink reflex.
Results:
MFS and BBE had similar clinical characteristics:respiratory symptoms were the most common infectious symptoms before disease onset; Ophthalmoplegia, facial palsy and bulbar symptoms were common; They both have cerebrospinal fluid albuminocytological dissociation and positive serum anti-GQlb antibody. However, BBE had more central nervous system lesion signs clinically such as conscious disturbance, positive Babinski's sign and central facial palsy. Electrophysiologically, MFS and BBE also had similar electrophysiological features:sensory nerve abnormality ratios were6/13,2/7respectively, with prominently reduced sensory nerve active potential amplitude, normal or slightly slowed sensory conduction velocity; Motor nerves abnormality ratios were2/13,1/7respectively, with slightly prolonged distal motor latency and normal compound muscle action potential; Electromyography abnormality ratios were1/7,0/4respectively; F wave frequency abnormality ratios were3/13,5/7respectively, and in some cases, F wave frequency would restore; Blink reflex abnormality ratios were1/2,1/1respectively, with central involvement in BBE; BAEP abnormality ratios were3/5,1/4respectively, with wave I latency or amplitude abnormality.
Conclusion:
The similarities of clinical and electrophysiological features suggest that MFS and BBE have the same mechanism and they form a continuous spectrum with variable central nervous system and peripheral nervous system involvement.
吉兰巴雷综合征系列神经电生理研究
目的：
对吉兰巴雷综合征(GBS)患者进行系列的神经电生理随诊,明确急性炎性脱髓鞘性多发神经根神经病(AIDP)和急性运动轴索性神经病(AMAN)在病程的不同阶段其系列的神经电生理改变。依据目前的GBS分型诊断标准对GBS进行分型,研究系列神经电生理随诊后GBS分型的变化,并探讨分型发生改变的原因。研究传导阻滞在GBS中的转归,探讨传导阻滞潜在的病理生理机制。
方法：
连续收集北京协和医院2010年9月至2013年3月GBS患者21例,在发病2周和4周左右至少完成2次神经电生理检查,同时回顾性收集北京协和医院1997年至2010年至少完成2次神经电生理检查的GBS住院患者21例,共42例。收集患者临床资料和神经电生理测定参数,包括运动神经传导、感觉神经传导、F波和针极肌电图。利用Hadden等的GBS分型诊断标准对患者进行神经电生理分型：首先依据初次神经电生理检查将患者分为AIDP组、AMAN组、AMSAN组和未分型组；然后依据系列随诊的神经电生理检查再次分组。统计系列随诊后GBS分型发生改变的患者,并分析分型发生改变的原因。统计分析AIDP和AMAN患者的临床和神经电生理特点。分析传导阻滞在GBS中的转归及其原因。
结果：
42例患者中,初次神经电生理检查符合AIDP者26例(62%),AMAN者10例(24%),未分型者6例(14%)。系列随诊后符合AIDP者17例(40%),AMAN者16例(38%),未分型者3例(7%),分型待定者(神经传导异常快速恢复正常)6例(14%)。
AIDP和AMAN两组患者差异具有统计学意义的临床症状是腹泻史(p=0.032)和麻木症状(p=0.015)。两组患者在面瘫、吞咽困难或构音障碍等临床症状上差异无统计学意义。两组患者Hughes评分最低分和发病第4周时Hughes评分差异无统计学意义(t=0.437, p=0.665; t=1.005, p=0.323)。两组患者呼吸机辅助呼吸比例和临床症状快速恢复比例差异无统计学意义(p=0.335；p=0.335)。6例神经传导快速恢复者与AIDP和AMAN患者相比,Hughes评分最低分差异均无统计学意义(t=0.455, p=0.653; t=0.149, p=0.883),但6例患者发病1月内Hughes评分改善均大于2分,发病第4周时Hughes评分与AIDP和AMAN患者相比,差异均有统计学意义(t=2.125, p=0.046; t=3.032, p=0.007)
AIDP患者末端潜伏期(DML)延长在发病第1-2周开始出现,第3-5周达高峰,此后逐渐恢复；远端复合肌肉动作电位(dCMAP)波幅在发病第1周出现下降,在第2-3周最低,此后缓慢恢复。AIDP患者发病第1周F波出现率出现异常,F波平均潜伏期正常,此后F波出现率逐渐恢复,但F波潜伏期逐渐延长,发病第4周左右达高峰。AMAN患者CMAP波幅恢复速度有两种模式：一种是CMAP波幅持续维持在较低的水平,一种是CMAP波幅较快升高,这两种快慢不同的恢复模式可以存在于同—患者不同神经上。
系列随诊GBS分型发生改变者多是初次神经电生理检查为AIDP者分型发生改变,或者是初次神经电生理检查未分型者系列随诊分型明确。11例AIDP患者分型发生改变,其原因包括传导阻滞演变为轴索变性(4例),传导阻滞快速恢复(5例),短暂性DML延长(2例)。
结论：
AIDP和AMAN患者病情严重程度和临床预后是相似的,电生理上AMAN患者CMAP波幅可以持续维持在很低的水平,也可以相对快速的恢复,AMAN潜在的病理生理机制不仅包括轴索变性,也包括可逆性传导障碍。
系列神经电生理随诊GBS分型改变主要由AIDP组转变为AMAN组或者AIDP组神经电生理快速恢复,发生转变的原因包括传导阻滞演变为轴索变性、传导阻滞快速恢复和短暂的末端潜伏期的延长。
第二部分
Miller Fisher综合征和Bickerstaff脑干脑炎临床及电生理特点分析
目的：
总结Miller Fisher综合征(MFS)和Bickerstaff脑干脑炎(BBE)患者临床及电生理特点,并探索其发病机制。
方法：
回顾性分析北京协和医院2000年至2011年符合MFS诊断标准的患者(13例)和BBE诊断标准的患者(7例)的病历资料,收集患者临床资料和电生理测定参数,包括感觉和运动神经传导、针极肌电图、F波、皮肤交感反应(SSR)、脑干听觉诱发电位(BAEP)、瞬目反射等,统计MFS和BBE临床特点和各项电生理检查异常的患者比例。
结果：
MFS和BBE患者前驱感染以呼吸道症状为主,眼球活动障碍、面瘫、延髓部症状较常见,均有脑脊液蛋白细胞分离,都存在抗GQlb抗体。但临床上,BBE还有意识障碍等中枢神经系统受累表现。电生理上,MFS和BBE患者感觉神经受累比例分别为6/13、2/7,主要表现为感觉神经动作电位波幅明显下降,感觉神经传导速度轻度减慢或正常；运动神经受累比例分别为2/13、1/7,多表现为运动末端潜伏期轻度延长,复合肌肉动作电位波幅正常；肢体针极肌电图异常比例分别为1/7、0/4；F波出现率异常比例分别为3/13、5/7,部分患者可出现F波出现率明显下降,但可以恢复；SSR异常比例分别为1/2、1/3;瞬目反射异常比例分别为1/2、1/1,BBE患者表现为中枢性损害；脑干听觉诱发电位异常比例分别为3/5、1/4,均表现为I波潜伏期延长或波幅低。
结论：
MFS和BBE中枢神经系统和周围神经系统均可受累,但BBE以中枢神经系统受累更常见。MFS和BBE可能是中枢神经系统和周围神经系统受累程度不同的同一种疾病的连续疾病谱。
Part1
Serial electrophysiological study of Guillain-Barre syndrome
Objective:
To investigate the serial electrophysiological changes of acute inflammatory demyelinating polyneuropathies(AIDP) and acute motor axonal neuropathy(AMAN) through serial electrophysiological study of Guillain-Barre syndrome(GBS). To electrophysiologically classify GBS patients into AIDP and AMAN subtypes, investigate how serial recordings change the classification, and analyze the causes of classification changes. To investigate the serial electrophysiological changes of conduction block, and analyze the possible underlying mechanisms of conduction block.
Methods:
Prospectively collected21GBS patients in Peking Union Medical College Hospital between September2010and March2013, and performed at least two serial electrophysiological tests around the second and fourth week after disease onset. Retrospectively collected21GBS patients between1997and2010who had at least two serial electrophysiological recordings. The electrophysiological parameters included motor sensory nerve conduction, F waves and electromyography. Based on the first electrophysiological recordings, electrophysiologically classified GBS patients into AIDP and AMAN subtypes according to Hadden's classification criteria. Analyzed how GBS patients changed the initial electrodiagnosis after serial electrophysiological recordings, and analyzed the causes of the changes. Compared and analyzed the clinical and electrophysiological characteristics of AIDP and AMAN patients. Analyzed the serial electrophysiological changes of conduction block.
Results.
At the first test,26of42patients(62%) fulfilled Hadden's criteria for AIDP,10patients(24%) for AMAN and6patients(14%) were classified as equivocal. After follow-up,17patients(40%) were classified as AIDP,16patients(38%) as AMAN,3patients(7%) equivocal and6patients with rapid electrophysiological recovery(classification unclear). Clinically, preceding gastroenteritis were more common in AMAN group (p=0.032), and sensory symptoms were more common in AIDP group(p=0.015). Between the AIDP and AMAN groups, cranial nerve involvement did not differ significantly, and neither the nadir Hughes grade nor Hughes grade at the forth week differed significantly(t=0.437, p=0.665; t=1.005, p=0.323). Compared with AIDP and AMAN group, nadir Hughes grade of the6patients with rapid electrophysiological recovery did not differ significantly. However, all the6patients showed a markedly rapid clinical recovery(improved by two or more Hughes grades within one month), and compared with AIDP and AMAN group the Hughes grades at the forth week differed significantly(t=2.125, p=0.046; t=3.032, p=0.007).
In AIDP group, distal motor latency(DML) prolongation appeared at week1-2, and became prominent at week3-5; The nadir of distal compound muscle action potential(dCMAP) amplitude decrease occurred at week1-2. In AIDP group, the early electrophysiological changes of F waves were decreased frequency with normal F wave latency, and F wave latency prolongation showed up later with nadir abnormality occurring at week4. There were two patterns of CMAP amplitude recovery in AMAN group:rapid increase and persistent at low level, and the two different recovery patterns were found in different nerves of the same patient.
The majority of classification changes were from AIDP and equivocal groups by initial electrophysiological tests. The main reason was the recognition by serial recordings of reversible conduction failure(5patients), axonal degeneration(4patients) and transient prolongation of DML(2patients).
Conclusion:
The clinical severity and prognosis of the AIDP and AMAN groups are similar. In some AMAN patients, the CMAP amplitude can rapidly increase, which could not be explained by axonal degeneration. Besides axonal degeneration, reversible conduction failure might be another underlying mechanisms of AMAN.
The causes of classification changes after serial electrophysiological study include:the length-dependent CMAP amplitude reduction, rapid resolve of conduction block, and transient prolongation of DML.
Part2
Clinical and electrophysiological study of Miller Fisher syndrome and Bickerstaff's brainstem encephalitis
Objective:
To investigate the underlying mechanisms of Miller Fisher syndrome(MFS) and Bickerstaff's brainstem encephalitis(BBE) through study of their clinical and electrophysiological characteristics.
Methods:
Retrospectively analyzed clinical and electrophysiological characteristics of13MFS and7BBE cases in Peking Union Medical College Hospital between2000and2011. The electrophysiological parameters included sensory and motor nerve conduction, electromyography, F wave, sympathetic skin response, brainstem auditory evoked potential and blink reflex.
Results:
MFS and BBE had similar clinical characteristics:respiratory symptoms were the most common infectious symptoms before disease onset; Ophthalmoplegia, facial palsy and bulbar symptoms were common; They both have cerebrospinal fluid albuminocytological dissociation and positive serum anti-GQlb antibody. However, BBE had more central nervous system lesion signs clinically such as conscious disturbance, positive Babinski's sign and central facial palsy. Electrophysiologically, MFS and BBE also had similar electrophysiological features:sensory nerve abnormality ratios were6/13,2/7respectively, with prominently reduced sensory nerve active potential amplitude, normal or slightly slowed sensory conduction velocity; Motor nerves abnormality ratios were2/13,1/7respectively, with slightly prolonged distal motor latency and normal compound muscle action potential; Electromyography abnormality ratios were1/7,0/4respectively; F wave frequency abnormality ratios were3/13,5/7respectively, and in some cases, F wave frequency would restore; Blink reflex abnormality ratios were1/2,1/1respectively, with central involvement in BBE; BAEP abnormality ratios were3/5,1/4respectively, with wave I latency or amplitude abnormality.
Conclusion:
The similarities of clinical and electrophysiological features suggest that MFS and BBE have the same mechanism and they form a continuous spectrum with variable central nervous system and peripheral nervous system involvement.
引文
[1]中华医学会神经病学分会神经肌肉病学组.中国吉兰-巴雷综合征诊治指南[J].中华神经科杂志,2010,43(8)：583-6.
[2]Hadden R D, Cornblath D R, Hughes R A, et al. Electrophysiological classification of Guillain-Barre syndrome:clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group [J]. Ann Neurol,1998,44(5): 780-8.
[3]Ho T W, Li C Y, Cornblath D R, et al. Patterns of recovery in the Guillain-Barre syndromes [J]. Neurology,1997,48(3):695-700.
[4]Kuwabara S, Asahina M, Koga M, et al. Two patterns of clinical recovery in Guillain-Barre syndrome with IgG anti-GM1 antibody [J]. Neurology,1998,51(6):1656-60.
[5]邓晖,吴江,杨薇,等.长春市双阳区群发吉兰-巴雷综合征临床资料分析[J].中华神经科杂志,2009,42(1)：30-3.
[6]Hiraga A, Mori M, Ogawara K, et al. Recovery patterns and long term prognosis for axonal Guillain-Barre syndrome [J]. J Neurol Neurosurg Psychiatry,2005,76(5):719-22.
[7]孙青,邹漳钰,崔丽英.急性运动轴索性神经病与传导阻滞[J].中华神经科杂志,2011,44(11)：774-6.
[8]Kokubun N, Nishibayashi M, Uncini A, et al. Conduction block in acute motor axonal neuropathy [J]. Brain,2010,133(10):2897-908.
[9]Uncini A, Manzoli C, Notturno F, et al. Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1157-63.
[10]Kuwabara S, Yuki N, Koga M, et al. IgG anti-GMl antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barre syndrome [J]. Ann Neurol,1998,44(2):202-8.
[11]Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barre syndrome [J]. Neurology,2005, 64(5):856-60.
[12]Asbury A K, Cornblath D R. Assessment of current diagnostic criteria for Guillain-Barre syndrome [J]. Ann Neurol,1990,27 Suppl(S21-4.
[13]刘银红,崔丽英.传导阻滞[J].国外医学神经病学神经外科学分册2004,31(5)：484-7.
[14]Olney R K. Guidelines in electrodiagnostic medicine. Consensus criteria for the diagnosis of partial conduction block [J]. Muscle Nerve Suppl,1999,8(S225-9.
[15]Nagasawa K, Kuwabara S, Misawa S, et al. Electrophysiological subtypes and prognosis of childhood Guillain-Barre syndrome in Japan [J]. Muscle Nerve,2006,33(6): 766-70.
[16]Ye Y, Wang K, Deng F, et al. Electrophysiological subtypes and prognosis of Guillain-Barre syndrome in northeastern China [J]. Muscle Nerve,2013,47(1):68-71.
[17]Feasby T E, Gilbert J J, Brown W F, et al. An acute axonal form of Guillain-Barre polyneuropathy [J]. Brain,1986,109 (Pt 6)(1115-26.
[18]Albers J W, Donofrio P D, Mcgonagle T K. Sequential electrodiagnostic abnormalities in acute inflammatory demyelinating polyradiculoneuropathy [J]. Muscle Nerve,1985,8(6):528-39.
[19]潘涛,贾志荣,王亭亭,等.早期吉兰-巴雷综合征的神经电生理特点分析[J].中华神经科杂志,2011,44(11)：735-8.
[20]Tamura N, Kuwabara S, Misawa S, et al. Time course of axonal regeneration in acute motor axonal neuropathy [J]. Muscle Nerve,2007,35(6):793-5.
[21]Ho T W, Hsieh S T, Nachamkin I, et al. Motor nerve terminal degeneration provides a potential mechanism for rapid recovery in acute motor axonal neuropathy after Campylobacter infection [J]. Neurology,1997,48(3):717-24.
[22]Poliak S, Peles E. The local differentiation of myelinated axons at nodes of Ranvier [J]. Nat Rev Neurosci,2003,4(12):968-80.
[23]Kaji R. Physiology of conduction block in multifocal motor neuropathy and other demyelinating neuropathies [J]. Muscle Nerve,2003,27(3):285-96.
[24]Uncini A, Yuki N. Electrophysiologic and immunopathologic correlates in Guillain-Barre syndrome subtypes [J]. Expert Rev Neurother,2009,9(6):869-84.
[25]汤晓芙.对传导阻滞的新认识[J].中华神经科杂志,2003,36(6)：404-5.
[26]Capasso M, Caporale C M, Pomilio F, et al. Acute motor conduction block neuropathy Another Guillain-Barre syndrome variant [J]. Neurology,2003,61(5):617-22.
[27]Rajabally Y A, Strens L H, Abbott R J. Acute motor conduction block neuropathy followed by axonal degeneration and poor recovery [J]. Neurology,2006,66(2):287-8.
[28]Susuki K, Rasband M N, Tohyama K, et al. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers [J]. J Neurosci,2007,27(15):3956-67.
[29]Griffin J W, Li C Y, Ho T W, et al. Guillain-Barre syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases [J]. Brain,1995,118 (Pt 3)(577-95.
[30]Griffin J W, Li C Y, Ho T W, et al. Pathology of the motor-sensory axonal Guillain-Barre syndrome [J]. Ann Neurol,1996,39(1):17-28.
[31]Uncini A, England J D, Rhee E K, et al. Tellurium-induced demyelination:an electrophysiological and morphological study [J]. Muscle Nerve,1988,11(8):871-9.
[32]Katirji B. Electromyography in Clinical Practice [M]. the United States of America: Elsevier Inc,2007.
[33]Oda K, Araki K, Totoki T, et al. Nerve conduction study of human tetrodotoxication [J]. Neurology,1989,39(5):743-5.
[34]Kuwabara S, Ogawara K, Mizobuchi K, et al. Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barre syndrome with antiganglioside antibodies [J]. J Neurol Neurosurg Psychiatry,2000,68(2):191-5.
[35]Katirji B. Electromyography in Clinical Practice [M]. the United States of America: Elsevier Inc,2007:335.
[1]Ito M, Kuwabara S, Odaka M, et al. Bickerstaffs brainstem encephalitis and Fisher syndrome form a continuous spectrum:clinical analysis of 581 cases [J]. J Neurol,2008, 255(5):674-82.
[2]Fross R D, Daube J R. Neuropathy in the Miller Fisher syndrome:clinical and electrophysiologic findings [J]. Neurology,1987,37(9):1493-8.
[3]Scelsa S N, Herskovitz S. Miller Fisher syndrome:axonal, demyelinating or both? [J]. Electromyogr Clin Neurophysiol,2000,40(8):497-502.
[4]Aranyi Z, Kovacs T, Sipos I, et al. Miller Fisher syndrome:brief overview and update with a focus on electrophysiological findings [J]. Eur J Neurol,2011,
[5]Van Der Meche F G, Van Doom P A, Meulstee J, et al. Diagnostic and classification criteria for the Guillain-Barre syndrome [J]. Eur Neurol,2001,45(3):133-9.
[6]Odaka M, Yuki N, Yamada M, et al. Bickerstaff s brainstem encephalitis:clinical features of 62 cases and a subgroup associated with Guillain-Barre syndrome [J]. Brain, 2003,126(Pt 10):2279-90.
[7]Kuwabara S, Ogawara K, Mizobuchi K, et al. Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barre syndrome with antiganglioside antibodies [J]. J Neurol Neurosurg Psychiatry,2000,68(2):191-5.
[8]潘涛,贾志荣,王亭亭,等.早期吉兰-巴雷综合征的神经电生理特点分析[J].中华神经科杂志,2011,44(11)：735-8.
[9]Shahrizaila N, Goh K J, Kokubun N, et al. Serial nerve conduction studies provide insight into the pathophysiology of Guillain-Barre and Fisher syndromes [J]. J Neurol Sci, 2011,309(1-2):26-30.
[10]Mori M, Kuwabara S, Fukutake T, et al. Clinical features and prognosis of Miller Fisher syndrome [J]. Neurology,2001,56(8):1104-6.
[11]孙瑶,谢炳均.Miller-Fisher综合征五例的自主神经电生理测定结果[J].中华神经科杂志,2011,44(9)：641-.
[12]Minoda R, Uno K, Toriya T, et al. Neurologic and otologic findings in Fisher's syndrome [J].Auris Nasus Larynx,1999,26(2):153-8.
[13]Hatanaka T, Higashino H, Yasuhara A, et al. Miller Fisher syndrome:etiological significance of serial blink reflexes and MRI study [J]. Electromyogr Clin Neurophysiol, 1992,32(6):317-9.
[14]Odaka M, Yuki N, Hirata K. Anti-GQlb IgG antibody syndrome:clinical and immunological range [J]. J Neurol Neurosurg Psychiatry,2001,70(1):50-5.
[1]中华医学会神经病学分会神经肌肉病学组.中国吉兰-巴雷综合征诊治指南[J].中华神经科杂志,2010,43(8)：583-6.
2] Hadden R D, Cornblath D R, Hughes R A, et al. Electrophysiological classification )f Guillain-Barre syndrome:clinical associations and outcome. Plasma 2xchange/Sandoglobulin Guillain-Barre Syndrome Trial Group [J]. Ann Neurol,1998,44(5): 780-8.
3] Kokubun N, Nishibayashi M, Uncini A, et al. Conduction block in acute motor ixonal neuropathy [J]. Brain,2010,133(10):2897-908.
4] Uncini A, Manzoli C, Notturno F, et al. Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1157-63.
5] Kuwabara S, Yuki N, Koga M, et al. IgG anti-GM1 antibody is associated with eversible conduction failure and axonal degeneration in Guillain-Barre syndrome [J]. Ann Neurol,1998,44(2):202-8.
[6]刘银红,崔丽英.传导阻滞[J].国外医学神经病学神经外科学分册2004,31(5)：484-7.
[7]刘明生,崔丽英.炎性脱髓鞘性周围神经病的电生理诊断[J].中华神经科杂志,2010,43(11)：812-4.
8] Olney R K. Guidelines in electrodiagnostic medicine. Consensus criteria for the liagnosis of partial conduction block [J]. Muscle Nerve Suppl,1999,8(S225-9.
9] Kaji R. Physiology of conduction block in multifocal motor neuropathy and other lemyelinating neuropathies [J]. Muscle Nerve,2003,27(3):285-96.
10] Manganelli F, Pisciotta C, Iodice R, et al. Case of acute motor conduction block leuropathy (AMCBN) [J]. Muscle Nerve,2009,39(2):224-6.
[11]汤晓芙.对传导阻滞的新认识[J].中华神经科杂志,2003,36(6)：404-5.
12] Ho T W, Li C Y, Cornblath D R, et al. Patterns of recovery in the Guillain-Barre syndromes [J]. Neurology,1997,48(3):695-700.
13] Kuwabara S, Asahina M, Koga M, et al. Two patterns of clinical recovery in Guillain-Barre syndrome with IgG anti-GM1 antibody [J]. Neurology,1998,51(6):1656-60.
[14]邓晖,吴江,杨薇,等.长春市双阳区群发吉兰-巴雷综合征临床资料分析[J].中华神经科杂志,2009,42(1)：30-3.
15] Hiraga A, Mori M, Ogawara K, et al. Recovery patterns and long term prognosis for ixonal Guillain-Barre syndrome [J]. J Neurol Neurosurg Psychiatry,2005,76(5):719-22.
[16]Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barre syndrome [J]. Neurology,2005, 64(5):856-60.
[17]Capasso M, Caporale C M, Pomilio F, et al. Acute motor conduction block neuropathy Another Guillain-Barre syndrome variant [J]. Neurology,2003,61(5):617-22.
[18]Uncini A, Manzoli C, Capasso M. Acute motor conduction block neuropathy or acute multifocal motor neuropathy:an attempt at a nosological systematization [J]. Muscle Nerve, 2010,41(2):283-5; author reply 5.
[19]Lefaucheur J P. Acute neuropathy with multiple motor conduction blocks:a variant of Guillain-Barre syndrome or multifocal motor neuropathy with conduction blocks with acute onset? [J]. Neurophysiol Clin,2008,38(4):209-10.
[20]Yuki N, Saperstein D S. Axonal Guillain-Barre syndrome subtypes:do we need more splitting? [J]. Neurology,2003,61(5):598-9.
[21]Uncini A, Capasso M. Acute motor conduction block neuropathy followed by axonal degeneration and poor recovery [J]. Neurology,2006,67(3):543; author reply
[22]Susuki K, Rasband M N, Tohyama K, et al. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers [J]. J Neurosci,2007,27(15):3956-67.
[23]Tamura N, Kuwabara S, Misawa S, et al. Time course of axonal regeneration in acute motor axonal neuropathy [J]. Muscle Nerve,2007,35(6):793-5.
[24]Ho T W, Hsieh S T, Nachamkin I, et al. Motor nerve terminal degeneration provides a potential mechanism for rapid recovery in acute motor axonal neuropathy after Campylobacter infection [J]. Neurology,1997,48(3):717-24.
[25]Kuwabara S. Axonal Guillain-Barre syndrome is underestimated in Europe? [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1063.
[26]Uncini A, Yuki N. Electrophysiologic and immunopathologic correlates in Guillain-Barre syndrome subtypes [J]. Expert Rev Neurother,2009,9(6):869-84.
[1]Yuki N. Infectious origins of, and molecular mimicry in, Guillain-Barre and Fisher syndromes [J]. Lancet Infect Dis,2001,1(1):29-37.
[2]Uncini A, Kuwabara S. Electrodiagnostic criteria for Guillain-Barre syndrome:A critical revision and the need for an update [J]. Clin Neurophysiol,2012,
[3]Hughes R A, Cornblath D R. Guillain-Barre syndrome [J]. Lancet,2005,366(9497): 1653-66.
[4]Chowdhury D, Arora A. Axonal Guillain-Barre syndrome:a critical review [J]. Acta Neurol Scand,2001,103(5):267-77.
[5]Feasby T E, Gilbert J J, Brown W F, et al. An acute axonal form of Guillain-Barre polyneuropathy [J]. Brain,1986,109 (Pt 6)(1115-26.
[6]Triggs W J, Cros D, Gominak S C, et al. Motor nerve inexcitability in Guillain-Barre syndrome. The spectrum of distal conduction block and axonal degeneration [J]. Brain,1992, 115(Pt5)(1291-302.
[7]Mckhann G M, Cornblath D R, Ho T, et al. Clinical and electrophysiological aspects of acute paralytic disease of children and young adults in northern China [J]. Lancet,1991, 338(8767):593-7.
[8]Mckhann G M, Cornblath D R, Griffin J W, et al. Acute motor axonal neuropathy:a frequent cause of acute flaccid paralysis in China [J]. Ann Neurol,1993,33(4):333-42.
[9]Uncini A, Yuki N. Electrophysiologic and immunopathologic correlates in Guillain-Barre syndrome subtypes [J]. Expert Rev Neurother,2009,9(6):869-84.
[10]Griffin J W, Li C Y, Ho T W, et al. Pathology of the motor-sensory axonal Guillain-Barre syndrome [J]. Ann Neurol,1996,39(1):17-28.
[11]Hafer-Macko C, Hsieh S T, Li C Y, et al. Acute motor axonal neuropathy:an antibody-mediated attack on axolemma [J]. Ann Neurol,1996,40(4):635-44.
[12]Hafer-Macko C E, Sheikh K A, Li C Y, et al. Immune attack on the Schwann cell surface in acute inflammatory demyelinating polyneuropathy [J]. Ann Neurol,1996,39(5): 625-35.
[13]Ho T W, Mishu B, Li C Y, et al. Guillain-Barre syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies [J]. Brain, 1995,118 (Pt 3)(597-605.
[14]Hadden R D, Karch H, Hartung H P, et al. Preceding infections, immune factors, and outcome in Guillain-Barre syndrome [J]. Neurology,2001,56(6):758-65.
[15]Ogawara K, Kuwabara S, Mori M, et al. Axonal Guillain-Barre syndrome:relation to anti-ganglioside antibodies and Campylobacter jejuni infection in Japan [J]. Ann Neurol, 2000,48(4):624-31.
[16]Kuwabara S, Ogawara K, Misawa S, et al. Does Campylobacter jejuni infection elicit "demyelinating" Guillain-Barre syndrome? [J]. Neurology,2004,63(3):529-33.
[17]Yuki N, Hartung H P. Guillain-Barre syndrome [J]. N Engl J Med,2012,366(24): 2294-304.
[18]Yuki N, Yoshino H, Sato S, et al. Acute axonal polyneuropathy associated with anti-GM1 antibodies following Campylobacter enteritis [J]. Neurology,1990,40(12):1900-2.
[19]Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barre syndrome [J]. Neurology,2005, 64(5):856-60.
[20]Sekiguchi Y, Uncini A, Yuki N, et al. Antiganglioside antibodies are associated with axonal Guillain-Barre syndrome:a Japanese-Italian collaborative study [J]. J Neurol Neurosurg Psychiatry,2012,83(1):23-8.
[21]Susuki K, Rasband M N, Tohyama K, et al. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers [J]. J Neurosci,2007,27(15):3956-67.
[22]A.K. A, B.G. A, H.R. K, et al. Criteria for diagnosis of Guillain-Barre syndrome [J]. Ann Neurol,1978,3(6):565-6.
[23]Capasso M, Caporale C M, Pomilio F, et al. Acute motor conduction block neuropathy Another Guillain-Barre syndrome variant [J]. Neurology,2003,61(5):617-22.
[24]Kuwabara S, Yuki N, Koga M, et al. IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barre syndrome [J]. Ann Neurol,1998,44(2):202-8.
[25]Rajabally Y A, Strens L H, Abbott R J. Acute motor conduction block neuropathy followed by axonal degeneration and poor recovery [J]. Neurology,2006,66(2):287-8.
[26]Kokubun N, Nishibayashi M, Uncini A, et al. Conduction block in acute motor axonal neuropathy [J]. Brain,2010,133(10):2897-908.
[27]Uncini A, Manzoli C, Notturno F, et al. Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1157-63.
[28]孙青,邹漳钰,崔丽英.急性运动轴索性神经病与传导阻滞[J].中华神经科杂 志,2011,44(11)：774-6.
[29]Kuwabara S, Ogawara K, Mizobuchi K, et al. Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barre syndrome with antiganglioside antibodies [J]. J Neurol Neurosurg Psychiatry,2000,68(2):191-5.
[30]Griffin J W, Li C Y, Ho T W, et al. Guillain-Barre syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases [J]. Brain,1995,118 (Pt 3)(577-95.
[31]Griffin J W, Li C Y, Macko C, et al. Early nodal changes in the acute motor axonal neuropathy pattern of the Guillain-Barre syndrome [J]. J Neurocytol,1996,25(1):33-51.
[32]Ho T W, Li C Y, Cornblath D R, et al. Patterns of recovery in the Guillain-Barre syndromes [J]. Neurology,1997,48(3):695-700.
[33]Hadden R D, Cornblath D R, Hughes R A, et al. Electrophysiological classification of Guillain-Barre syndrome:clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group [J]. Ann Neurol,1998,44(5): 780-8.
[34]Kuwabara S, Asahina M, Koga M, et al. Two patterns of clinical recovery in Guillain-Barre syndrome with IgG anti-GM1 antibody [J]. Neurology,1998,51(6):1656-60.
[35]邓晖,吴江,杨薇,等.长春市双阳区群发吉兰-巴雷综合征临床资料分析[J].中华神经科杂志,2009,42(1)：30-3.
[36]Hiraga A, Mori M, Ogawara K, et al. Recovery patterns and long term prognosis for axonal Guillain-Barre syndrome [J]. J Neurol Neurosurg Psychiatry,2005,76(5):719-22.
[37]侯世芳,许贤豪,刘银红,等.急性运动轴索型神经病的预后分析[J].中华神经医学杂志,2009,8(5)：4.
[2]Hadden R D, Cornblath D R, Hughes R A, et al. Electrophysiological classification of Guillain-Barre syndrome:clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group [J]. Ann Neurol,1998,44(5): 780-8.
[3]Ho T W, Li C Y, Cornblath D R, et al. Patterns of recovery in the Guillain-Barre syndromes [J]. Neurology,1997,48(3):695-700.
[4]Kuwabara S, Asahina M, Koga M, et al. Two patterns of clinical recovery in Guillain-Barre syndrome with IgG anti-GM1 antibody [J]. Neurology,1998,51(6):1656-60.
[5]邓晖,吴江,杨薇,等.长春市双阳区群发吉兰-巴雷综合征临床资料分析[J].中华神经科杂志,2009,42(1)：30-3.
[6]Hiraga A, Mori M, Ogawara K, et al. Recovery patterns and long term prognosis for axonal Guillain-Barre syndrome [J]. J Neurol Neurosurg Psychiatry,2005,76(5):719-22.
[7]孙青,邹漳钰,崔丽英.急性运动轴索性神经病与传导阻滞[J].中华神经科杂志,2011,44(11)：774-6.
[8]Kokubun N, Nishibayashi M, Uncini A, et al. Conduction block in acute motor axonal neuropathy [J]. Brain,2010,133(10):2897-908.
[9]Uncini A, Manzoli C, Notturno F, et al. Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1157-63.
[10]Kuwabara S, Yuki N, Koga M, et al. IgG anti-GMl antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barre syndrome [J]. Ann Neurol,1998,44(2):202-8.
[11]Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barre syndrome [J]. Neurology,2005, 64(5):856-60.
[12]Asbury A K, Cornblath D R. Assessment of current diagnostic criteria for Guillain-Barre syndrome [J]. Ann Neurol,1990,27 Suppl(S21-4.
[13]刘银红,崔丽英.传导阻滞[J].国外医学神经病学神经外科学分册2004,31(5)：484-7.
[14]Olney R K. Guidelines in electrodiagnostic medicine. Consensus criteria for the diagnosis of partial conduction block [J]. Muscle Nerve Suppl,1999,8(S225-9.
[15]Nagasawa K, Kuwabara S, Misawa S, et al. Electrophysiological subtypes and prognosis of childhood Guillain-Barre syndrome in Japan [J]. Muscle Nerve,2006,33(6): 766-70.
[16]Ye Y, Wang K, Deng F, et al. Electrophysiological subtypes and prognosis of Guillain-Barre syndrome in northeastern China [J]. Muscle Nerve,2013,47(1):68-71.
[17]Feasby T E, Gilbert J J, Brown W F, et al. An acute axonal form of Guillain-Barre polyneuropathy [J]. Brain,1986,109 (Pt 6)(1115-26.
[18]Albers J W, Donofrio P D, Mcgonagle T K. Sequential electrodiagnostic abnormalities in acute inflammatory demyelinating polyradiculoneuropathy [J]. Muscle Nerve,1985,8(6):528-39.
[19]潘涛,贾志荣,王亭亭,等.早期吉兰-巴雷综合征的神经电生理特点分析[J].中华神经科杂志,2011,44(11)：735-8.
[20]Tamura N, Kuwabara S, Misawa S, et al. Time course of axonal regeneration in acute motor axonal neuropathy [J]. Muscle Nerve,2007,35(6):793-5.
[21]Ho T W, Hsieh S T, Nachamkin I, et al. Motor nerve terminal degeneration provides a potential mechanism for rapid recovery in acute motor axonal neuropathy after Campylobacter infection [J]. Neurology,1997,48(3):717-24.
[22]Poliak S, Peles E. The local differentiation of myelinated axons at nodes of Ranvier [J]. Nat Rev Neurosci,2003,4(12):968-80.
[23]Kaji R. Physiology of conduction block in multifocal motor neuropathy and other demyelinating neuropathies [J]. Muscle Nerve,2003,27(3):285-96.
[24]Uncini A, Yuki N. Electrophysiologic and immunopathologic correlates in Guillain-Barre syndrome subtypes [J]. Expert Rev Neurother,2009,9(6):869-84.
[25]汤晓芙.对传导阻滞的新认识[J].中华神经科杂志,2003,36(6)：404-5.
[26]Capasso M, Caporale C M, Pomilio F, et al. Acute motor conduction block neuropathy Another Guillain-Barre syndrome variant [J]. Neurology,2003,61(5):617-22.
[27]Rajabally Y A, Strens L H, Abbott R J. Acute motor conduction block neuropathy followed by axonal degeneration and poor recovery [J]. Neurology,2006,66(2):287-8.
[28]Susuki K, Rasband M N, Tohyama K, et al. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers [J]. J Neurosci,2007,27(15):3956-67.
[29]Griffin J W, Li C Y, Ho T W, et al. Guillain-Barre syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases [J]. Brain,1995,118 (Pt 3)(577-95.
[30]Griffin J W, Li C Y, Ho T W, et al. Pathology of the motor-sensory axonal Guillain-Barre syndrome [J]. Ann Neurol,1996,39(1):17-28.
[31]Uncini A, England J D, Rhee E K, et al. Tellurium-induced demyelination:an electrophysiological and morphological study [J]. Muscle Nerve,1988,11(8):871-9.
[32]Katirji B. Electromyography in Clinical Practice [M]. the United States of America: Elsevier Inc,2007.
[33]Oda K, Araki K, Totoki T, et al. Nerve conduction study of human tetrodotoxication [J]. Neurology,1989,39(5):743-5.
[34]Kuwabara S, Ogawara K, Mizobuchi K, et al. Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barre syndrome with antiganglioside antibodies [J]. J Neurol Neurosurg Psychiatry,2000,68(2):191-5.
[35]Katirji B. Electromyography in Clinical Practice [M]. the United States of America: Elsevier Inc,2007:335.
[1]Ito M, Kuwabara S, Odaka M, et al. Bickerstaffs brainstem encephalitis and Fisher syndrome form a continuous spectrum:clinical analysis of 581 cases [J]. J Neurol,2008, 255(5):674-82.
[2]Fross R D, Daube J R. Neuropathy in the Miller Fisher syndrome:clinical and electrophysiologic findings [J]. Neurology,1987,37(9):1493-8.
[3]Scelsa S N, Herskovitz S. Miller Fisher syndrome:axonal, demyelinating or both? [J]. Electromyogr Clin Neurophysiol,2000,40(8):497-502.
[4]Aranyi Z, Kovacs T, Sipos I, et al. Miller Fisher syndrome:brief overview and update with a focus on electrophysiological findings [J]. Eur J Neurol,2011,
[5]Van Der Meche F G, Van Doom P A, Meulstee J, et al. Diagnostic and classification criteria for the Guillain-Barre syndrome [J]. Eur Neurol,2001,45(3):133-9.
[6]Odaka M, Yuki N, Yamada M, et al. Bickerstaff s brainstem encephalitis:clinical features of 62 cases and a subgroup associated with Guillain-Barre syndrome [J]. Brain, 2003,126(Pt 10):2279-90.
[7]Kuwabara S, Ogawara K, Mizobuchi K, et al. Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barre syndrome with antiganglioside antibodies [J]. J Neurol Neurosurg Psychiatry,2000,68(2):191-5.
[8]潘涛,贾志荣,王亭亭,等.早期吉兰-巴雷综合征的神经电生理特点分析[J].中华神经科杂志,2011,44(11)：735-8.
[9]Shahrizaila N, Goh K J, Kokubun N, et al. Serial nerve conduction studies provide insight into the pathophysiology of Guillain-Barre and Fisher syndromes [J]. J Neurol Sci, 2011,309(1-2):26-30.
[10]Mori M, Kuwabara S, Fukutake T, et al. Clinical features and prognosis of Miller Fisher syndrome [J]. Neurology,2001,56(8):1104-6.
[11]孙瑶,谢炳均.Miller-Fisher综合征五例的自主神经电生理测定结果[J].中华神经科杂志,2011,44(9)：641-.
[12]Minoda R, Uno K, Toriya T, et al. Neurologic and otologic findings in Fisher's syndrome [J].Auris Nasus Larynx,1999,26(2):153-8.
[13]Hatanaka T, Higashino H, Yasuhara A, et al. Miller Fisher syndrome:etiological significance of serial blink reflexes and MRI study [J]. Electromyogr Clin Neurophysiol, 1992,32(6):317-9.
[14]Odaka M, Yuki N, Hirata K. Anti-GQlb IgG antibody syndrome:clinical and immunological range [J]. J Neurol Neurosurg Psychiatry,2001,70(1):50-5.
[1]中华医学会神经病学分会神经肌肉病学组.中国吉兰-巴雷综合征诊治指南[J].中华神经科杂志,2010,43(8)：583-6.
2] Hadden R D, Cornblath D R, Hughes R A, et al. Electrophysiological classification )f Guillain-Barre syndrome:clinical associations and outcome. Plasma 2xchange/Sandoglobulin Guillain-Barre Syndrome Trial Group [J]. Ann Neurol,1998,44(5): 780-8.
3] Kokubun N, Nishibayashi M, Uncini A, et al. Conduction block in acute motor ixonal neuropathy [J]. Brain,2010,133(10):2897-908.
4] Uncini A, Manzoli C, Notturno F, et al. Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1157-63.
5] Kuwabara S, Yuki N, Koga M, et al. IgG anti-GM1 antibody is associated with eversible conduction failure and axonal degeneration in Guillain-Barre syndrome [J]. Ann Neurol,1998,44(2):202-8.
[6]刘银红,崔丽英.传导阻滞[J].国外医学神经病学神经外科学分册2004,31(5)：484-7.
[7]刘明生,崔丽英.炎性脱髓鞘性周围神经病的电生理诊断[J].中华神经科杂志,2010,43(11)：812-4.
8] Olney R K. Guidelines in electrodiagnostic medicine. Consensus criteria for the liagnosis of partial conduction block [J]. Muscle Nerve Suppl,1999,8(S225-9.
9] Kaji R. Physiology of conduction block in multifocal motor neuropathy and other lemyelinating neuropathies [J]. Muscle Nerve,2003,27(3):285-96.
10] Manganelli F, Pisciotta C, Iodice R, et al. Case of acute motor conduction block leuropathy (AMCBN) [J]. Muscle Nerve,2009,39(2):224-6.
[11]汤晓芙.对传导阻滞的新认识[J].中华神经科杂志,2003,36(6)：404-5.
12] Ho T W, Li C Y, Cornblath D R, et al. Patterns of recovery in the Guillain-Barre syndromes [J]. Neurology,1997,48(3):695-700.
13] Kuwabara S, Asahina M, Koga M, et al. Two patterns of clinical recovery in Guillain-Barre syndrome with IgG anti-GM1 antibody [J]. Neurology,1998,51(6):1656-60.
[14]邓晖,吴江,杨薇,等.长春市双阳区群发吉兰-巴雷综合征临床资料分析[J].中华神经科杂志,2009,42(1)：30-3.
15] Hiraga A, Mori M, Ogawara K, et al. Recovery patterns and long term prognosis for ixonal Guillain-Barre syndrome [J]. J Neurol Neurosurg Psychiatry,2005,76(5):719-22.
[16]Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barre syndrome [J]. Neurology,2005, 64(5):856-60.
[17]Capasso M, Caporale C M, Pomilio F, et al. Acute motor conduction block neuropathy Another Guillain-Barre syndrome variant [J]. Neurology,2003,61(5):617-22.
[18]Uncini A, Manzoli C, Capasso M. Acute motor conduction block neuropathy or acute multifocal motor neuropathy:an attempt at a nosological systematization [J]. Muscle Nerve, 2010,41(2):283-5; author reply 5.
[19]Lefaucheur J P. Acute neuropathy with multiple motor conduction blocks:a variant of Guillain-Barre syndrome or multifocal motor neuropathy with conduction blocks with acute onset? [J]. Neurophysiol Clin,2008,38(4):209-10.
[20]Yuki N, Saperstein D S. Axonal Guillain-Barre syndrome subtypes:do we need more splitting? [J]. Neurology,2003,61(5):598-9.
[21]Uncini A, Capasso M. Acute motor conduction block neuropathy followed by axonal degeneration and poor recovery [J]. Neurology,2006,67(3):543; author reply
[22]Susuki K, Rasband M N, Tohyama K, et al. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers [J]. J Neurosci,2007,27(15):3956-67.
[23]Tamura N, Kuwabara S, Misawa S, et al. Time course of axonal regeneration in acute motor axonal neuropathy [J]. Muscle Nerve,2007,35(6):793-5.
[24]Ho T W, Hsieh S T, Nachamkin I, et al. Motor nerve terminal degeneration provides a potential mechanism for rapid recovery in acute motor axonal neuropathy after Campylobacter infection [J]. Neurology,1997,48(3):717-24.
[25]Kuwabara S. Axonal Guillain-Barre syndrome is underestimated in Europe? [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1063.
[26]Uncini A, Yuki N. Electrophysiologic and immunopathologic correlates in Guillain-Barre syndrome subtypes [J]. Expert Rev Neurother,2009,9(6):869-84.
[1]Yuki N. Infectious origins of, and molecular mimicry in, Guillain-Barre and Fisher syndromes [J]. Lancet Infect Dis,2001,1(1):29-37.
[2]Uncini A, Kuwabara S. Electrodiagnostic criteria for Guillain-Barre syndrome:A critical revision and the need for an update [J]. Clin Neurophysiol,2012,
[3]Hughes R A, Cornblath D R. Guillain-Barre syndrome [J]. Lancet,2005,366(9497): 1653-66.
[4]Chowdhury D, Arora A. Axonal Guillain-Barre syndrome:a critical review [J]. Acta Neurol Scand,2001,103(5):267-77.
[5]Feasby T E, Gilbert J J, Brown W F, et al. An acute axonal form of Guillain-Barre polyneuropathy [J]. Brain,1986,109 (Pt 6)(1115-26.
[6]Triggs W J, Cros D, Gominak S C, et al. Motor nerve inexcitability in Guillain-Barre syndrome. The spectrum of distal conduction block and axonal degeneration [J]. Brain,1992, 115(Pt5)(1291-302.
[7]Mckhann G M, Cornblath D R, Ho T, et al. Clinical and electrophysiological aspects of acute paralytic disease of children and young adults in northern China [J]. Lancet,1991, 338(8767):593-7.
[8]Mckhann G M, Cornblath D R, Griffin J W, et al. Acute motor axonal neuropathy:a frequent cause of acute flaccid paralysis in China [J]. Ann Neurol,1993,33(4):333-42.
[9]Uncini A, Yuki N. Electrophysiologic and immunopathologic correlates in Guillain-Barre syndrome subtypes [J]. Expert Rev Neurother,2009,9(6):869-84.
[10]Griffin J W, Li C Y, Ho T W, et al. Pathology of the motor-sensory axonal Guillain-Barre syndrome [J]. Ann Neurol,1996,39(1):17-28.
[11]Hafer-Macko C, Hsieh S T, Li C Y, et al. Acute motor axonal neuropathy:an antibody-mediated attack on axolemma [J]. Ann Neurol,1996,40(4):635-44.
[12]Hafer-Macko C E, Sheikh K A, Li C Y, et al. Immune attack on the Schwann cell surface in acute inflammatory demyelinating polyneuropathy [J]. Ann Neurol,1996,39(5): 625-35.
[13]Ho T W, Mishu B, Li C Y, et al. Guillain-Barre syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies [J]. Brain, 1995,118 (Pt 3)(597-605.
[14]Hadden R D, Karch H, Hartung H P, et al. Preceding infections, immune factors, and outcome in Guillain-Barre syndrome [J]. Neurology,2001,56(6):758-65.
[15]Ogawara K, Kuwabara S, Mori M, et al. Axonal Guillain-Barre syndrome:relation to anti-ganglioside antibodies and Campylobacter jejuni infection in Japan [J]. Ann Neurol, 2000,48(4):624-31.
[16]Kuwabara S, Ogawara K, Misawa S, et al. Does Campylobacter jejuni infection elicit "demyelinating" Guillain-Barre syndrome? [J]. Neurology,2004,63(3):529-33.
[17]Yuki N, Hartung H P. Guillain-Barre syndrome [J]. N Engl J Med,2012,366(24): 2294-304.
[18]Yuki N, Yoshino H, Sato S, et al. Acute axonal polyneuropathy associated with anti-GM1 antibodies following Campylobacter enteritis [J]. Neurology,1990,40(12):1900-2.
[19]Hiraga A, Kuwabara S, Ogawara K, et al. Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barre syndrome [J]. Neurology,2005, 64(5):856-60.
[20]Sekiguchi Y, Uncini A, Yuki N, et al. Antiganglioside antibodies are associated with axonal Guillain-Barre syndrome:a Japanese-Italian collaborative study [J]. J Neurol Neurosurg Psychiatry,2012,83(1):23-8.
[21]Susuki K, Rasband M N, Tohyama K, et al. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers [J]. J Neurosci,2007,27(15):3956-67.
[22]A.K. A, B.G. A, H.R. K, et al. Criteria for diagnosis of Guillain-Barre syndrome [J]. Ann Neurol,1978,3(6):565-6.
[23]Capasso M, Caporale C M, Pomilio F, et al. Acute motor conduction block neuropathy Another Guillain-Barre syndrome variant [J]. Neurology,2003,61(5):617-22.
[24]Kuwabara S, Yuki N, Koga M, et al. IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barre syndrome [J]. Ann Neurol,1998,44(2):202-8.
[25]Rajabally Y A, Strens L H, Abbott R J. Acute motor conduction block neuropathy followed by axonal degeneration and poor recovery [J]. Neurology,2006,66(2):287-8.
[26]Kokubun N, Nishibayashi M, Uncini A, et al. Conduction block in acute motor axonal neuropathy [J]. Brain,2010,133(10):2897-908.
[27]Uncini A, Manzoli C, Notturno F, et al. Pitfalls in electrodiagnosis of Guillain-Barre syndrome subtypes [J]. J Neurol Neurosurg Psychiatry,2010,81(10):1157-63.
[28]孙青,邹漳钰,崔丽英.急性运动轴索性神经病与传导阻滞[J].中华神经科杂 志,2011,44(11)：774-6.
[29]Kuwabara S, Ogawara K, Mizobuchi K, et al. Isolated absence of F waves and proximal axonal dysfunction in Guillain-Barre syndrome with antiganglioside antibodies [J]. J Neurol Neurosurg Psychiatry,2000,68(2):191-5.
[30]Griffin J W, Li C Y, Ho T W, et al. Guillain-Barre syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases [J]. Brain,1995,118 (Pt 3)(577-95.
[31]Griffin J W, Li C Y, Macko C, et al. Early nodal changes in the acute motor axonal neuropathy pattern of the Guillain-Barre syndrome [J]. J Neurocytol,1996,25(1):33-51.
[32]Ho T W, Li C Y, Cornblath D R, et al. Patterns of recovery in the Guillain-Barre syndromes [J]. Neurology,1997,48(3):695-700.
[33]Hadden R D, Cornblath D R, Hughes R A, et al. Electrophysiological classification of Guillain-Barre syndrome:clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group [J]. Ann Neurol,1998,44(5): 780-8.
[34]Kuwabara S, Asahina M, Koga M, et al. Two patterns of clinical recovery in Guillain-Barre syndrome with IgG anti-GM1 antibody [J]. Neurology,1998,51(6):1656-60.
[35]邓晖,吴江,杨薇,等.长春市双阳区群发吉兰-巴雷综合征临床资料分析[J].中华神经科杂志,2009,42(1)：30-3.
[36]Hiraga A, Mori M, Ogawara K, et al. Recovery patterns and long term prognosis for axonal Guillain-Barre syndrome [J]. J Neurol Neurosurg Psychiatry,2005,76(5):719-22.
[37]侯世芳,许贤豪,刘银红,等.急性运动轴索型神经病的预后分析[J].中华神经医学杂志,2009,8(5)：4.
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |