接触性热痛诱发电位在吉兰—巴雷综合征中的应用价值
|
摘要
目的:建立接触性热痛诱发电位检测方法,研究正常受试者接触性热痛诱发电位表现,探讨其在吉兰-巴雷综合征中的应用价值。
资料和方法:收集自2007年1月-2008年9月收住于我院的吉兰-巴雷综合征患者60名,年龄平均38.10±15.81岁,男33例,女27例。正常对照组50名,年龄平均36.20±13.29岁,男30例,女20例。所检吉兰-巴雷综合征患者均无客观感觉障碍,部分有主观感觉障碍,按有无主观感觉障碍,分为两组:无主观感觉障碍组(39例,男23,女16)和有主观感觉障碍组(21例,男10,女11)。应用接触性热痛诱发电位刺激器,加热速度70℃/s,可调节脉冲于47℃强度水平,刺激小腿内踝上方和腰背部髂前上嵴水平。刺激方式为单个脉冲刺激,刺激间隔10 s,连续刺激10次。记录电极按国际脑电图10-20系统置于Cz和Pz,参考电极置于前额。以Keypoint.net仪器记录60名吉兰-巴雷综合征患者和50名健康对照者的接触性热痛诱发电位。受试者在每个部位第一次刺激3～5s后,对刺激强度分级。测定刺激强度和疼痛分级的关系、诱发电位的主要成分及外周神经传导速度。
结果:GBS患者出现肢体弛缓性瘫痪呈对称性,且下肢受累出现较早,症状较重。为获得更加准确的试验结果,我们选取右侧小腿内踝上方和右侧腰背部髂前上嵴水平皮肤进行测试,而未选择上肢。所选受试部位为有毛的皮肤,其内主要为低阈值的Aδ伤害性痛觉感受器(AMH2型)。试验选取47℃强度刺激是由于此刺激强度高于低阈值的Aδ伤害性痛觉感受器(AMH2型)的域刺激水平,又不至于温度过高引起受试者不能耐受。所有受试者均可于头顶记录到接触性热痛诱发电位,该电位主要包含负相N1波及正相P1波,极少数患者(3例)可出现正相P2波。得出正常对照组右侧小腿内踝上方N1潜伏期为402.50±23.14 ms,N1-P1峰间波幅为44.68±17.68μV,疼痛等级评分为6.25±0.92;腰背部髂前上嵴水平N1潜伏期为352.03±20.38 ms,N1-P1峰间波幅为49.92±19.69μV,疼痛等级评分为6.82±0.97;所测痛觉周围神经传导速度为13.28±2.31 m/s。所得GBS患者刺激强度和疼痛分级的关系为:刺激右侧下肢及右侧腰部时,有主观感觉障碍组较正常对照组疼痛等级评分显著降低(P＜0.01),无主观感觉障碍组与正常对照组比较及有主观感觉障碍组与无主观感觉障碍组比较疼痛等级评分无统计学意义(P＞0.05)。47℃刺激小腿内侧皮肤时,有主观感觉障碍组N1潜伏期较正常组延长(P＜0.05),有主观感觉障碍组N1-P1峰间波幅较正常对照组降低(P＜0.05)。有主观感觉障碍组痛觉神经纤维传导速度与正常对照组比较明显减慢(P＜0.01)。无主观感觉障碍组与正常对照组比较及有主观感觉障碍组与无主观感觉障碍组比较N1潜伏期、N1-P1峰间波幅、痛觉神经纤维传导速度均无统计学意义(P＞0.05)。47℃腰部髂前上嵴水平刺激时,三组N1潜伏期、N1-P1峰间波幅比较均无统计学意义(P＞0.05)。
结论:接触性热痛诱发电位是一种简便的检测方法,所得试验结果稳定,因而可用于临床实践研究。经本试验验证接触性热痛诱发电位可以选择性的兴奋伤害性痛觉感受器,从而为评价由Aδ和C纤维介导的伤害性痛觉传导通路的功能状态提供了一种有效地检测方法,并拟定了正常人群的下肢和腰部的接触性热痛诱发电位各成分的参考值。将接触性热痛诱发电位应用于吉兰-巴雷综合征患者中,试验发现有肢体末梢主观感觉障碍的患者对疼痛等级的主观评价明显降低,Aδ纤维的外周传导速度明显减慢及接触性热痛诱发电位N1-P1峰间波幅降低。这些改变表明有主观感觉障碍的吉兰-巴雷综合征患者Aδ纤维存在脱髓鞘改变,以及部分轴索变性,这与吉兰-巴雷综合征的病理改变相一致。从而证实接触性热痛诱发电位可以有效地检测吉兰-巴雷综合征患者Aδ纤维的功能状态。并且其操作简便、波形稳定、耐受性好,因此CHEP可以为临床评价细纤维神经病和神经性疼痛提供一种实用的、快速的和非侵入性的检测手段。
Objective:to establish a new method of contact heat evoked potential by stimulating nociceptive fibers,,and study the representation of contact heat evoked potential when we applicated it on normal subjects,and assesse the application of contact heat evoked potential in Guillain-Barr(?) syndrome.
Data and method:we collected 60 patients of Guillain-Barr(?) syndrome participating in the study,whom accepted the cure in hospital from January in 2007 to September in 2008,average age 38.10±15.81years old,male 33,female 27.we also maked a normal control group,which contain 50 healthy volunteers participated in the study,,average age 36.20±13.29 years old,male 30,female 20.None of the patients had objective sensory disability,parts of the Guillain-Barr(?) syndrome had subjective sensory disability,so we divided the patients into two groups according to sensory disability, as existing sensory abnormal group and normal subjective sensory group.The former contained 21 patients,man 10,women 11.And the latter included 39 patients,man 23,women 16.All of people underwent stimulation of contact heat evoked potential stimulator,delivered via a circular thermode to excite selectively nocieeptors with a rapid rising time at 70℃/s to elicit pain and contact heat evoked potential(CHEP).The intensity level of temperature we choosed for stimulating was 47℃,then we sent it to two sites of body of entire subjects:skin of leg above internal malleolus and skin of waist at the anterior superior iliac spine level.The way we selected for stimulating was single pulse stimulation,the interval time between two consecutive stimulation was 10s,and we would consecutive stimulate 10 times on every sites at 47℃.Recording electrodes were put in Cz and Pz and reference electrode was put in forehead according to the international eletroencephalogram 10-20 systerm.,at where we could obtain the wave form of contact heat evoked potential.We used Keypoint.net equipment for recording the representation of contact heat evoked potential when we stimulated on 60 Guillain-Barr(?) syndrome and 50 healthy volunteers.After the first stimulation 3～5s on evey body sites we selected,all of subjects would assessed the stimulus intensity on oral according to visual analog scale(VAS).In this study,we need record the relationship between stimulus intensity and pain ranking,the main components of contact heat evoked potential and nerve conduction velocity of peripheral nerve.The nerve conduction velocity was calculated from the latency difference of the CHEP and center to center distance from leg above internal malleolus to waist at the anterior superior iliac spine level. Result:When we stimulated skin of leg above internal malleolus and skin of waist at the anterior superior iliac spine level at 47℃,we could record the wave form of contact heat evoked potential at corona from all of person whom participated in this study.The evoked potential mainly contained two parts,they were normal phase wave N1 and negative phase wave P1,very few people we could record negative phase wave P2.The average latency of N1 wave was 402.50±23.14 ms,the average amplitude of N1-P1 inter-peak was 44.68±17.68μV,and the average pain raking was 6.25±0.92,when we stimulated the skin of leg above internal malleolus on normal control group.Then we stimulated the skin of waist at the anterior superior iliac spine level,recorded the average latency of N1 wave was 352.03±20.38 ms,the average amplitude of N1-P1 inter-peak was 49.92±19.69μV,and the average pain raking was 6.82±0.97.the average peripheral nerve conduction velocity of normal subjects was 13.28±2.31m/s.The relation ship between stimulus intensity and pain raking when we stimulated skin at 47℃was:the pain raking of existing sensory abnormal group was significantly reduced(P＜0.01),comparing to normal control group when we stimulated the skin of leg above internal malleolus and of waist at the anterior superior iliac spine level at 47℃,but the difference of pain raking between normal subjective sensory group and normal control group,and between existing sensory abnormal grouP and normal subjective sensory group were not statistically significant(P＞0.05).When we stimulated the leg skin,the N1 latency we obtained of existing sensory abnormal group was highly prolonged comparing to that of normal control group(P＜0.05),the N1-P1 inter-peak amplitude of existing sensory abnormal groupalso highly reduced comparing to that of normal control group(P＜0.05),the peripheral nerve conduction velocity of existing sensory abnormal group was significantly slowed down comparing to that of normal control group(P＜0.01).But the difference of N1 latency and N1-P1 inter-peak amplitude and the peripheral nerve conduction velocity between normal subjective sensory group and normal control group,and between existing sensory abnormal group and normal subjective sensory group were not statistically significant(P＞0.05).when choosed the skin of waist at the anterior superior iliac spine level as stimulus,the difference of N1 latency and N1-P1 inter-peak amplitude between this three groups was not statistically significant(P＞0.05).
Conclusion:Our study show that contact heat evoked potential could electively excite the pain nociceptor,which maked it has the capability to assess the functional ststus of conduction tract of pain perception mediated by AS-fiber and C-fiber.So,when contact heat evoked potential was applicated on Guillain-Barr(?) syndrome,we could find the functional disturbance of Aδ-fiber according the N1 latency and N1 -P1 inter-peak and nerve conduction velocity.Furthermore,it was operated convenient,stable wave form,easy tolerance.Therefore contact heat evoked potential can provide a practical,rapid and non-invasive additional clinical tool of potential utility in the evaluation of small fibre neuropathy and neuropathic pain states.
资料和方法:收集自2007年1月-2008年9月收住于我院的吉兰-巴雷综合征患者60名,年龄平均38.10±15.81岁,男33例,女27例。正常对照组50名,年龄平均36.20±13.29岁,男30例,女20例。所检吉兰-巴雷综合征患者均无客观感觉障碍,部分有主观感觉障碍,按有无主观感觉障碍,分为两组:无主观感觉障碍组(39例,男23,女16)和有主观感觉障碍组(21例,男10,女11)。应用接触性热痛诱发电位刺激器,加热速度70℃/s,可调节脉冲于47℃强度水平,刺激小腿内踝上方和腰背部髂前上嵴水平。刺激方式为单个脉冲刺激,刺激间隔10 s,连续刺激10次。记录电极按国际脑电图10-20系统置于Cz和Pz,参考电极置于前额。以Keypoint.net仪器记录60名吉兰-巴雷综合征患者和50名健康对照者的接触性热痛诱发电位。受试者在每个部位第一次刺激3～5s后,对刺激强度分级。测定刺激强度和疼痛分级的关系、诱发电位的主要成分及外周神经传导速度。
结果:GBS患者出现肢体弛缓性瘫痪呈对称性,且下肢受累出现较早,症状较重。为获得更加准确的试验结果,我们选取右侧小腿内踝上方和右侧腰背部髂前上嵴水平皮肤进行测试,而未选择上肢。所选受试部位为有毛的皮肤,其内主要为低阈值的Aδ伤害性痛觉感受器(AMH2型)。试验选取47℃强度刺激是由于此刺激强度高于低阈值的Aδ伤害性痛觉感受器(AMH2型)的域刺激水平,又不至于温度过高引起受试者不能耐受。所有受试者均可于头顶记录到接触性热痛诱发电位,该电位主要包含负相N1波及正相P1波,极少数患者(3例)可出现正相P2波。得出正常对照组右侧小腿内踝上方N1潜伏期为402.50±23.14 ms,N1-P1峰间波幅为44.68±17.68μV,疼痛等级评分为6.25±0.92;腰背部髂前上嵴水平N1潜伏期为352.03±20.38 ms,N1-P1峰间波幅为49.92±19.69μV,疼痛等级评分为6.82±0.97;所测痛觉周围神经传导速度为13.28±2.31 m/s。所得GBS患者刺激强度和疼痛分级的关系为:刺激右侧下肢及右侧腰部时,有主观感觉障碍组较正常对照组疼痛等级评分显著降低(P＜0.01),无主观感觉障碍组与正常对照组比较及有主观感觉障碍组与无主观感觉障碍组比较疼痛等级评分无统计学意义(P＞0.05)。47℃刺激小腿内侧皮肤时,有主观感觉障碍组N1潜伏期较正常组延长(P＜0.05),有主观感觉障碍组N1-P1峰间波幅较正常对照组降低(P＜0.05)。有主观感觉障碍组痛觉神经纤维传导速度与正常对照组比较明显减慢(P＜0.01)。无主观感觉障碍组与正常对照组比较及有主观感觉障碍组与无主观感觉障碍组比较N1潜伏期、N1-P1峰间波幅、痛觉神经纤维传导速度均无统计学意义(P＞0.05)。47℃腰部髂前上嵴水平刺激时,三组N1潜伏期、N1-P1峰间波幅比较均无统计学意义(P＞0.05)。
结论:接触性热痛诱发电位是一种简便的检测方法,所得试验结果稳定,因而可用于临床实践研究。经本试验验证接触性热痛诱发电位可以选择性的兴奋伤害性痛觉感受器,从而为评价由Aδ和C纤维介导的伤害性痛觉传导通路的功能状态提供了一种有效地检测方法,并拟定了正常人群的下肢和腰部的接触性热痛诱发电位各成分的参考值。将接触性热痛诱发电位应用于吉兰-巴雷综合征患者中,试验发现有肢体末梢主观感觉障碍的患者对疼痛等级的主观评价明显降低,Aδ纤维的外周传导速度明显减慢及接触性热痛诱发电位N1-P1峰间波幅降低。这些改变表明有主观感觉障碍的吉兰-巴雷综合征患者Aδ纤维存在脱髓鞘改变,以及部分轴索变性,这与吉兰-巴雷综合征的病理改变相一致。从而证实接触性热痛诱发电位可以有效地检测吉兰-巴雷综合征患者Aδ纤维的功能状态。并且其操作简便、波形稳定、耐受性好,因此CHEP可以为临床评价细纤维神经病和神经性疼痛提供一种实用的、快速的和非侵入性的检测手段。
Objective:to establish a new method of contact heat evoked potential by stimulating nociceptive fibers,,and study the representation of contact heat evoked potential when we applicated it on normal subjects,and assesse the application of contact heat evoked potential in Guillain-Barr(?) syndrome.
Data and method:we collected 60 patients of Guillain-Barr(?) syndrome participating in the study,whom accepted the cure in hospital from January in 2007 to September in 2008,average age 38.10±15.81years old,male 33,female 27.we also maked a normal control group,which contain 50 healthy volunteers participated in the study,,average age 36.20±13.29 years old,male 30,female 20.None of the patients had objective sensory disability,parts of the Guillain-Barr(?) syndrome had subjective sensory disability,so we divided the patients into two groups according to sensory disability, as existing sensory abnormal group and normal subjective sensory group.The former contained 21 patients,man 10,women 11.And the latter included 39 patients,man 23,women 16.All of people underwent stimulation of contact heat evoked potential stimulator,delivered via a circular thermode to excite selectively nocieeptors with a rapid rising time at 70℃/s to elicit pain and contact heat evoked potential(CHEP).The intensity level of temperature we choosed for stimulating was 47℃,then we sent it to two sites of body of entire subjects:skin of leg above internal malleolus and skin of waist at the anterior superior iliac spine level.The way we selected for stimulating was single pulse stimulation,the interval time between two consecutive stimulation was 10s,and we would consecutive stimulate 10 times on every sites at 47℃.Recording electrodes were put in Cz and Pz and reference electrode was put in forehead according to the international eletroencephalogram 10-20 systerm.,at where we could obtain the wave form of contact heat evoked potential.We used Keypoint.net equipment for recording the representation of contact heat evoked potential when we stimulated on 60 Guillain-Barr(?) syndrome and 50 healthy volunteers.After the first stimulation 3～5s on evey body sites we selected,all of subjects would assessed the stimulus intensity on oral according to visual analog scale(VAS).In this study,we need record the relationship between stimulus intensity and pain ranking,the main components of contact heat evoked potential and nerve conduction velocity of peripheral nerve.The nerve conduction velocity was calculated from the latency difference of the CHEP and center to center distance from leg above internal malleolus to waist at the anterior superior iliac spine level. Result:When we stimulated skin of leg above internal malleolus and skin of waist at the anterior superior iliac spine level at 47℃,we could record the wave form of contact heat evoked potential at corona from all of person whom participated in this study.The evoked potential mainly contained two parts,they were normal phase wave N1 and negative phase wave P1,very few people we could record negative phase wave P2.The average latency of N1 wave was 402.50±23.14 ms,the average amplitude of N1-P1 inter-peak was 44.68±17.68μV,and the average pain raking was 6.25±0.92,when we stimulated the skin of leg above internal malleolus on normal control group.Then we stimulated the skin of waist at the anterior superior iliac spine level,recorded the average latency of N1 wave was 352.03±20.38 ms,the average amplitude of N1-P1 inter-peak was 49.92±19.69μV,and the average pain raking was 6.82±0.97.the average peripheral nerve conduction velocity of normal subjects was 13.28±2.31m/s.The relation ship between stimulus intensity and pain raking when we stimulated skin at 47℃was:the pain raking of existing sensory abnormal group was significantly reduced(P＜0.01),comparing to normal control group when we stimulated the skin of leg above internal malleolus and of waist at the anterior superior iliac spine level at 47℃,but the difference of pain raking between normal subjective sensory group and normal control group,and between existing sensory abnormal grouP and normal subjective sensory group were not statistically significant(P＞0.05).When we stimulated the leg skin,the N1 latency we obtained of existing sensory abnormal group was highly prolonged comparing to that of normal control group(P＜0.05),the N1-P1 inter-peak amplitude of existing sensory abnormal groupalso highly reduced comparing to that of normal control group(P＜0.05),the peripheral nerve conduction velocity of existing sensory abnormal group was significantly slowed down comparing to that of normal control group(P＜0.01).But the difference of N1 latency and N1-P1 inter-peak amplitude and the peripheral nerve conduction velocity between normal subjective sensory group and normal control group,and between existing sensory abnormal group and normal subjective sensory group were not statistically significant(P＞0.05).when choosed the skin of waist at the anterior superior iliac spine level as stimulus,the difference of N1 latency and N1-P1 inter-peak amplitude between this three groups was not statistically significant(P＞0.05).
Conclusion:Our study show that contact heat evoked potential could electively excite the pain nociceptor,which maked it has the capability to assess the functional ststus of conduction tract of pain perception mediated by AS-fiber and C-fiber.So,when contact heat evoked potential was applicated on Guillain-Barr(?) syndrome,we could find the functional disturbance of Aδ-fiber according the N1 latency and N1 -P1 inter-peak and nerve conduction velocity.Furthermore,it was operated convenient,stable wave form,easy tolerance.Therefore contact heat evoked potential can provide a practical,rapid and non-invasive additional clinical tool of potential utility in the evaluation of small fibre neuropathy and neuropathic pain states.
引文
[1]L.Arendt-Nielsen,A.C.N,Chen.Lasers and other thermal stimulators for activation of skin nociceptors in humans.Neurophysiologie clinique,2003,33(6):259-268.
[2]Iannetti GD,Zambreanu L,Cruccu G,et al.Operculoinsular cortex encodes pain intensity at the earliest stages of cortical processing as indicated by amplitude of laser-evoked potentials in humans[J].Neuroscience,2005,1 31(1):199-208.
[3]郑菊阳,徐迎胜等.接触性热痛诱发电位检测方法的建立.中华神经科杂志,2007,4(2):129-132.
[4]Chi-Chao Chao,Song-Chou Hsieh,Ming-Tsung Tseng,et al.Patterns of contact heat evoked potentials(CHEP) in neuropathy with skin denervation:Correlation of CHEP amplitude with intraepidermal nerve fiber density.Clinical Neurophysiology,2008,119(3):653-661.
[5]Asbury AK,Comblath DR.Assessment of current diagnostic criteria for Guillain-Barre syndrome.Ann Neurol.1990,27(supp):S21-4.
[6]Bromm B,Lorenz J.Neurophysiological evaluation of pain.Electroencephalogr Clin Neurophysiol,1998,107:227-253.
[7]Tran TD,Inui K,Hoshiyama M,et al.Conduction velocity of the spinothalamic tract following CO_2 laser stimulation of C-fibers in human.Pain,2002,95:125-131.
[8]Kakigi R,Watanabe S,Yamasaki H.Pain-related somatosensery evoked potentials.J Clin Neurophysiol,2000,17:295-308.
[9]Valeriani M,Restuccia D,Le pera D,et al.Unmask-ing of an early laser evoked potential by apoint localization task.Clin Neurophysiol,2000,111:1927-1933.
[10]Valeriani M,Rambaud L,Maugn iere F.Scalp topography and dipolar source modeling of potentials evoked by C02 laser stimulation of the hand.Electroenceph clin Neurophysiol,1996,100:343-353.
[11]Iannetti GD,Zambreanu L,Cruccu G,et al.Operculoinsular cortex encodes pain intensity at the earliest stages of cortical processing as indicated by amplitude of laser.evoked potentials in humans.Neuroscience,2005,131(1):199-208.
[12]Bragard D,Chen AC,plaghki L.Direck isolation of ultralate(C-fibre) evoked brain potentials by CO2 laser stimulation of tiny cutaneous surface areas in man.Neurosci Lett,1996,209:81-84.
[13]Chen AC,Niddam DM,Arendt-Nielsen L.Contact heat evoked Potentials as a valid means to study nocicePtive Pathways in human subjects.Neurosci Lett 2001;316:79-82.
[14]Granovsky Y,Matre D,Sokolik A,Lorenz J,Casey KL.ThermorecePtive innervation of human glabrous and hairy skin:a contact heat evoked Potential analysis.Pain 2005;115:238-247.
[15]Walter M,Zahid A,Jens E,et al.C- and A δ fiber components of heat-evoked cerebral potentials in healthy human subjects.Pain.1999,82(2):127-137.
[16]Towell AD,Purves AM,Boyd SG CO2 laser activation of nociceptive and non-nociceptive thermal afferents from hairy and glabrous skin.Pain 1996;66:79-86.
[17]Valeriani M,Le pera D,Niddam D,Chen AC,Arendt-Nielsen L.Dipolar modelling of the scalp evoked potentials to painful contact heat stimulation of the human skin.Neurosci Lett 2002;318:44-48.
[18]Walter M,Zahid A,Jens E,et al.C- and Aδfiber components of heat-evoked cerebral potentials in healthy human subjects.Pain.1999,82:127-137.
[19]Duncan D Atherton,Paul Facer,Katherine M Roberts,et al.Use of the novel contact heat evoked potential stimulator(CHEPS)for the assessment of small fibre neuropathy:correlations with skin flare responses and intra-epidermal nerve fibre counts[J].BMC Neurology 2007,7:21
[20]彭茂,贾建平.吉兰-巴雷综合征严重程度早期预测因素[J].中华神经科杂志.2004,37(2):154-157.
[21]张晓君,汤晓芙.格林-巴利综合征的电诊断新发展[J].临床脑电学杂志,1997,6(3):188-91.
[22]PTopcu M,Ergin M,Nurlu G,et al.Evoked potentials in Guillain-Barr(?) syndrome[J].Turk J Pediatr,1993,35(2):79-85.
[23]Angie L.F.Soetanto,Joanne W.Y.Chung,Thomas K.S.Wong.Are There Gender Differences in pain perception?.Journal of Neuroscience Nursing.2006,38(3):172-176.
[24]Chi-Chao Chao,Sung-TSANG Hsieh,Ming-Jang Chiu.Effect of aging on contact heat-evoked potentials :the physiological assessment of thermal perception .Muscle Nerve,2007,36(1):30-38.
[25]Jacobs JM,Love S.Qualitative and quantitative morPhology of human sural nerve at different ages.Brain 1985;108:897-924.
[1]李彩霞.格林-巴利综合征12例的肌电图观察[J].中国临床康复,2002,6(19):2875
[2]Zhang X,Tang X,Zhang Z,et al.Electrophysiological forms of Guillain-Barre syndrome in Beijing suburb[J].Chin Med J,1997,110(11):856-8.
[3]孙海锋,刘南平.肌电图、神经电图在Guillain-Barre综合征中的应用[J].临床神经病学杂志.2001,14(1):35-36.
[4]Zifko U,Chen R,Remtulla H,et al.Respiratory electrophysiological studies in Guillain-Barre syndrome[J].Neurol Neurosurg Psychiatry,1996,60(2):191-4.
[5]Sakakibara R,Hattori T,Kuwabara S,et al.Micturitional disturbance in patients with Guillain-Barre syndrome[J].Neurol Neurosurg Psychiatry,1997,63(5):649-53.
[6]Spaans F,Vredeveld JW,Morr(?) HH,et al.Dysfunction at the motor end-plate and axon membrane in Guillain-Barre syndrome:a single-fiber EMG study[J].Muscle Nerve,2003,27(4):426-34.
[7]Sartucci F,Cafforio G,Borghetti D,et al.Electrophysiological evidence by single fibre electromyography of neuromuscular transmission impairment in a case of Miller Fisher syndrome[J].Neurol Sci,2005,;26(2):125-8.
[8]张晓君,汤晓芙.格林-巴利综合征的电诊断新发展[J].临床脑电学杂志,1997,6(3):188-91.
[9]Capasso M,Caporale CM,Pomilio F,et al.Acute motor conduction block neuropathy Another Guillain-Barr(?) syndrome variant[J].Neurology,2004,62(6):1026-7.
[10]李春岩,王桂荣.感觉性共济失调型格林-巴利综合征3例临床与电生理[J].脑与神经疾病杂志,2001,9(1):11-13.
[11]Miralles F,Montro J.Sensory Guillain-Barresyndrome[J].Neuroi Neuurosurgpsychiat,1992,(55):411.
[12]Carvalho M,Cordeiro E,Alves M,et al.The Miller Fisher syndrome.Review of the cases of the Santa Maria Hospital[J].Acta Med Port,1996,9(4-6):167-70.
[13]Kuwabara S,Asahina M,Nakajima M,et al.Special romendsensory ataxia in Miller Fisher syndrome detected by postural body sway analysis[J].Ann Neurol,1999,45(4):533-6.
[14]马亚玲,朱永庆.格林-巴利综合征电生理改变与预后的关系[J].延安大学学报,2005,3(3):19-21.
[15]Vucic S,Cairns KD,Black KR,et al.Neurophysiologic findings in early acute inflammatory demyelinating polyradiculoneuropathy[J].Clin Neurophysiol,2004,115(10):2329-35.
[16]康维礼,洪军.瞬目反射对颅神经型格林-巴利综合征的诊断价值[J].中华物理医学与康复杂志,2001,23(3):96-98.
[17]罗伟,李靖.瞬目反射检测在GBS中的应用价值[J].山东医药,2005,45(1):19-20.
[18]Ogawara K,Kuwabara S.Fisher syndrome or Bickerstaff brainstem encephalitis?Anti-GQ1b IgG antibody syndrome involving both the peripheral and central nervous systems[J].Muscle Nerve.,2002,26(6):845-9.
[19]齐进兴,赵燕民.急性格林-巴利综合征患者CSFIg与神经电生理检测[J].郑州大学学报,2002,37(2):229-230.
[20]Wong V.A neurophysiological study in children with Miller Fisher syndrome and Guillain-Barre syndrome[j].Brain Dev,1997,19(3):197-204.
[21]Zgorzalewicz M,Zieli(?)ska M,Kilarski D.Brain stem auditory and visual evoked potentials in children and adolescents with Guillain-Barr(?) syndrome[J].Neurol Neurochir Pol,2004,38(1 Suppl 1):S31-7.
[22]Durand MC,Goulon-Go(?)au C,Schweitzer A,et al.Electrophysiologic study of 10 cases of Miller Fisher syndrome[J].Rev Neurol,2001,157(1):72-9.
[23]PTopcu M,Ergin M,Nurlu G,et al.Evoked potentials in Guillain-Barr(?)syndrome[J].Turk J Pediatr,1993,35(2):79-85.
[24]Takada H,Ravnborg M.Magnetically evoked motorpotentials in demyelinating and axonal polyneuropathy:a comparative study[J].Eur J Neurol,2000,7(1):63-69.
[25]刘英,邹艺,胥勋成,等.MEP在吉兰一巴雷综合征患者中的应用价值[J].临床神经电生理学杂志,2005,14(1):22-33.
[26]杨林萍.磁运动诱发电位对小儿格林A巴利综合征的评估[J].中国临床康复,2002,6(9):1283-1284.
[27]Kakigi R,Endo C,Neshige R,et al.Estimation of conduction velocity of A delta fibers in humans[J].Muscle Nerve,1991,14(12):1193-6.
[28]Bromm B,Treede RD.Human cerebral potentials evoked by C02 laser stimuli causing pain[J].Exp Brain Res,1987;67(1):153-62.
[29]Chi-Chao Chao ,Song-Chou Hsieh,Ming-Tsung Tseng ,et al.Pattems of contact heat evoked potentials (CHEP) in neuropathy with skin denervation:Correlation of CHEP amplitude with intraepidermal nerve fiber density.Clinical Neurophysiology ,2008,119(3):653-661.
[2]Iannetti GD,Zambreanu L,Cruccu G,et al.Operculoinsular cortex encodes pain intensity at the earliest stages of cortical processing as indicated by amplitude of laser-evoked potentials in humans[J].Neuroscience,2005,1 31(1):199-208.
[3]郑菊阳,徐迎胜等.接触性热痛诱发电位检测方法的建立.中华神经科杂志,2007,4(2):129-132.
[4]Chi-Chao Chao,Song-Chou Hsieh,Ming-Tsung Tseng,et al.Patterns of contact heat evoked potentials(CHEP) in neuropathy with skin denervation:Correlation of CHEP amplitude with intraepidermal nerve fiber density.Clinical Neurophysiology,2008,119(3):653-661.
[5]Asbury AK,Comblath DR.Assessment of current diagnostic criteria for Guillain-Barre syndrome.Ann Neurol.1990,27(supp):S21-4.
[6]Bromm B,Lorenz J.Neurophysiological evaluation of pain.Electroencephalogr Clin Neurophysiol,1998,107:227-253.
[7]Tran TD,Inui K,Hoshiyama M,et al.Conduction velocity of the spinothalamic tract following CO_2 laser stimulation of C-fibers in human.Pain,2002,95:125-131.
[8]Kakigi R,Watanabe S,Yamasaki H.Pain-related somatosensery evoked potentials.J Clin Neurophysiol,2000,17:295-308.
[9]Valeriani M,Restuccia D,Le pera D,et al.Unmask-ing of an early laser evoked potential by apoint localization task.Clin Neurophysiol,2000,111:1927-1933.
[10]Valeriani M,Rambaud L,Maugn iere F.Scalp topography and dipolar source modeling of potentials evoked by C02 laser stimulation of the hand.Electroenceph clin Neurophysiol,1996,100:343-353.
[11]Iannetti GD,Zambreanu L,Cruccu G,et al.Operculoinsular cortex encodes pain intensity at the earliest stages of cortical processing as indicated by amplitude of laser.evoked potentials in humans.Neuroscience,2005,131(1):199-208.
[12]Bragard D,Chen AC,plaghki L.Direck isolation of ultralate(C-fibre) evoked brain potentials by CO2 laser stimulation of tiny cutaneous surface areas in man.Neurosci Lett,1996,209:81-84.
[13]Chen AC,Niddam DM,Arendt-Nielsen L.Contact heat evoked Potentials as a valid means to study nocicePtive Pathways in human subjects.Neurosci Lett 2001;316:79-82.
[14]Granovsky Y,Matre D,Sokolik A,Lorenz J,Casey KL.ThermorecePtive innervation of human glabrous and hairy skin:a contact heat evoked Potential analysis.Pain 2005;115:238-247.
[15]Walter M,Zahid A,Jens E,et al.C- and A δ fiber components of heat-evoked cerebral potentials in healthy human subjects.Pain.1999,82(2):127-137.
[16]Towell AD,Purves AM,Boyd SG CO2 laser activation of nociceptive and non-nociceptive thermal afferents from hairy and glabrous skin.Pain 1996;66:79-86.
[17]Valeriani M,Le pera D,Niddam D,Chen AC,Arendt-Nielsen L.Dipolar modelling of the scalp evoked potentials to painful contact heat stimulation of the human skin.Neurosci Lett 2002;318:44-48.
[18]Walter M,Zahid A,Jens E,et al.C- and Aδfiber components of heat-evoked cerebral potentials in healthy human subjects.Pain.1999,82:127-137.
[19]Duncan D Atherton,Paul Facer,Katherine M Roberts,et al.Use of the novel contact heat evoked potential stimulator(CHEPS)for the assessment of small fibre neuropathy:correlations with skin flare responses and intra-epidermal nerve fibre counts[J].BMC Neurology 2007,7:21
[20]彭茂,贾建平.吉兰-巴雷综合征严重程度早期预测因素[J].中华神经科杂志.2004,37(2):154-157.
[21]张晓君,汤晓芙.格林-巴利综合征的电诊断新发展[J].临床脑电学杂志,1997,6(3):188-91.
[22]PTopcu M,Ergin M,Nurlu G,et al.Evoked potentials in Guillain-Barr(?) syndrome[J].Turk J Pediatr,1993,35(2):79-85.
[23]Angie L.F.Soetanto,Joanne W.Y.Chung,Thomas K.S.Wong.Are There Gender Differences in pain perception?.Journal of Neuroscience Nursing.2006,38(3):172-176.
[24]Chi-Chao Chao,Sung-TSANG Hsieh,Ming-Jang Chiu.Effect of aging on contact heat-evoked potentials :the physiological assessment of thermal perception .Muscle Nerve,2007,36(1):30-38.
[25]Jacobs JM,Love S.Qualitative and quantitative morPhology of human sural nerve at different ages.Brain 1985;108:897-924.
[1]李彩霞.格林-巴利综合征12例的肌电图观察[J].中国临床康复,2002,6(19):2875
[2]Zhang X,Tang X,Zhang Z,et al.Electrophysiological forms of Guillain-Barre syndrome in Beijing suburb[J].Chin Med J,1997,110(11):856-8.
[3]孙海锋,刘南平.肌电图、神经电图在Guillain-Barre综合征中的应用[J].临床神经病学杂志.2001,14(1):35-36.
[4]Zifko U,Chen R,Remtulla H,et al.Respiratory electrophysiological studies in Guillain-Barre syndrome[J].Neurol Neurosurg Psychiatry,1996,60(2):191-4.
[5]Sakakibara R,Hattori T,Kuwabara S,et al.Micturitional disturbance in patients with Guillain-Barre syndrome[J].Neurol Neurosurg Psychiatry,1997,63(5):649-53.
[6]Spaans F,Vredeveld JW,Morr(?) HH,et al.Dysfunction at the motor end-plate and axon membrane in Guillain-Barre syndrome:a single-fiber EMG study[J].Muscle Nerve,2003,27(4):426-34.
[7]Sartucci F,Cafforio G,Borghetti D,et al.Electrophysiological evidence by single fibre electromyography of neuromuscular transmission impairment in a case of Miller Fisher syndrome[J].Neurol Sci,2005,;26(2):125-8.
[8]张晓君,汤晓芙.格林-巴利综合征的电诊断新发展[J].临床脑电学杂志,1997,6(3):188-91.
[9]Capasso M,Caporale CM,Pomilio F,et al.Acute motor conduction block neuropathy Another Guillain-Barr(?) syndrome variant[J].Neurology,2004,62(6):1026-7.
[10]李春岩,王桂荣.感觉性共济失调型格林-巴利综合征3例临床与电生理[J].脑与神经疾病杂志,2001,9(1):11-13.
[11]Miralles F,Montro J.Sensory Guillain-Barresyndrome[J].Neuroi Neuurosurgpsychiat,1992,(55):411.
[12]Carvalho M,Cordeiro E,Alves M,et al.The Miller Fisher syndrome.Review of the cases of the Santa Maria Hospital[J].Acta Med Port,1996,9(4-6):167-70.
[13]Kuwabara S,Asahina M,Nakajima M,et al.Special romendsensory ataxia in Miller Fisher syndrome detected by postural body sway analysis[J].Ann Neurol,1999,45(4):533-6.
[14]马亚玲,朱永庆.格林-巴利综合征电生理改变与预后的关系[J].延安大学学报,2005,3(3):19-21.
[15]Vucic S,Cairns KD,Black KR,et al.Neurophysiologic findings in early acute inflammatory demyelinating polyradiculoneuropathy[J].Clin Neurophysiol,2004,115(10):2329-35.
[16]康维礼,洪军.瞬目反射对颅神经型格林-巴利综合征的诊断价值[J].中华物理医学与康复杂志,2001,23(3):96-98.
[17]罗伟,李靖.瞬目反射检测在GBS中的应用价值[J].山东医药,2005,45(1):19-20.
[18]Ogawara K,Kuwabara S.Fisher syndrome or Bickerstaff brainstem encephalitis?Anti-GQ1b IgG antibody syndrome involving both the peripheral and central nervous systems[J].Muscle Nerve.,2002,26(6):845-9.
[19]齐进兴,赵燕民.急性格林-巴利综合征患者CSFIg与神经电生理检测[J].郑州大学学报,2002,37(2):229-230.
[20]Wong V.A neurophysiological study in children with Miller Fisher syndrome and Guillain-Barre syndrome[j].Brain Dev,1997,19(3):197-204.
[21]Zgorzalewicz M,Zieli(?)ska M,Kilarski D.Brain stem auditory and visual evoked potentials in children and adolescents with Guillain-Barr(?) syndrome[J].Neurol Neurochir Pol,2004,38(1 Suppl 1):S31-7.
[22]Durand MC,Goulon-Go(?)au C,Schweitzer A,et al.Electrophysiologic study of 10 cases of Miller Fisher syndrome[J].Rev Neurol,2001,157(1):72-9.
[23]PTopcu M,Ergin M,Nurlu G,et al.Evoked potentials in Guillain-Barr(?)syndrome[J].Turk J Pediatr,1993,35(2):79-85.
[24]Takada H,Ravnborg M.Magnetically evoked motorpotentials in demyelinating and axonal polyneuropathy:a comparative study[J].Eur J Neurol,2000,7(1):63-69.
[25]刘英,邹艺,胥勋成,等.MEP在吉兰一巴雷综合征患者中的应用价值[J].临床神经电生理学杂志,2005,14(1):22-33.
[26]杨林萍.磁运动诱发电位对小儿格林A巴利综合征的评估[J].中国临床康复,2002,6(9):1283-1284.
[27]Kakigi R,Endo C,Neshige R,et al.Estimation of conduction velocity of A delta fibers in humans[J].Muscle Nerve,1991,14(12):1193-6.
[28]Bromm B,Treede RD.Human cerebral potentials evoked by C02 laser stimuli causing pain[J].Exp Brain Res,1987;67(1):153-62.
[29]Chi-Chao Chao ,Song-Chou Hsieh,Ming-Tsung Tseng ,et al.Pattems of contact heat evoked potentials (CHEP) in neuropathy with skin denervation:Correlation of CHEP amplitude with intraepidermal nerve fiber density.Clinical Neurophysiology ,2008,119(3):653-661.