慢性肌筋膜触发点大鼠模型的电生理和病理组织学研究
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摘要
研究目的：
日常生命活动或体育运动损伤后常常出现一些慢性疼痛后遗症状,这些疼痛往往会引起关节和脊柱周围疼痛,导致关节障碍。这些慢性疼痛大部分为骨骼肌疼痛,而肌筋膜疼痛触发点是导致骨骼肌疼痛的常见原因之一。临床上慢性肌筋膜疼痛综合症是以疼痛为主一组症候群,这种症候群表现为疼痛、牵涉痛、自主神经的和骨骼肌功能的障碍等症状。肌筋膜疼痛严重影响了人们的生活和工作,并成为消耗卫生资源的重要原因。目前认为受累肌内存在有骨骼肌或肌筋膜内的疼痛触发点。为了研究其发病机制,目前有关触发点的模型多为模拟模型或隐性触发点模型,无法代表活化触发点的全貌；因此无法说明触发点的自发肌电位和动作电位的真实变化,而且也无法说明到真实活化触发点的病理组织学的真实改变。本研究通过经济实惠的大鼠作为实验动物,采用股内侧肌打击结合离心运动的方法建立创伤性肌筋膜疼痛触发点的动物模型,在经历不同恢复时间后,检测触发点肌电图表现和观察触发点的病理组织学的改变,了解肌筋膜疼痛触发点的本质和发病特点,以推论触发点的可能发病机制。
研究方法：
32只七周龄雄性SD大鼠,平均体重220g-260g,随机分为ABCD四组,每组8只,A组为正常对照组,BCD三组为实验干预组。A组正常对照组在造模期与恢复期均正常喂养,不进行任何干预。实验干预组造模期每周第一天打击左下肢股内侧肌,打击后第二天配合离心运动,造模期为8周。实验干预组恢复期同对照组,不进行任何实验干预,正常喂养,其中B组恢复4周,C组恢复8周,D.组恢复12周。分别在不同时期分批对大鼠进行造模效果检查和取材,手术暴露大鼠股内侧肌,触摸打击处及周围肌肉的紧张带和收缩结节、针刺紧张带引起局部抽搐反应、记录紧张带处的自发性电位和记录结节数目。最后,对紧张带或结节处的局部组织进行组织活检取材：1.组织进行HE染色后,光镜下观察病理切片的结节数目、形态及大小等变化；2.使用透射电子显微镜超薄切片技术制作电镜标本,电镜观察触发点组织的肌丝排列、肌小节、线粒体等超微结构特点。将实验干预组和对照组所得结果进行比较分析,所用数据统计分析均采用SPSS17.0软件包进行分析。
研究结果：
A组对照组股内侧肌附近发现紧张带或触发点个数平均0.13个(1/8)；B、C、D组平均发现触发点个数分别为3.00个(24/8)、2.63个(21/8)、2.25个(18/8),紧张带或触发点在针刺时均出现局部抽搐反应。静息状态下,大鼠股内侧肌附测量肌肉的自发电位,A、B、C、D各组一分钟内出现自发电位的频数分别为2.75±2.87,172.57±102.88,151.63±65.37,168.14±64.53。对照组与实验组两两比较,P<0.01具有高度显著性差异,实验组之间两两比较P>0.05没有统计意义。A、B、C、D各组自发电位的波幅分别为26.06±16.67μV,33.08±18.40μV,93.26±163.18μV,78.27±161.68μV,其中A、B两组与C、D两组比较有显著性差异P＜0.05,而A、B组之间与C、D组之间不具有显著性差异。
病理切片横切面显示,对照组肌细胞形态规则、大小均匀,未发现有大小不一、圆形、增大、深染的肌细胞,实验组横切面均发现增大、圆形深染的挛缩结节,实验组各组均出现炎细胞浸润和核内移(>10%)现象。纵切面,对照组表现为排列紧密而规律的纵向肌纤维。实验组B、C、D组均出现排列紊乱、中央膨大两端变细或相间出现粗细不等的梭形肌纤维。ABCD各组肌细胞直径分别为22.84±0.48μm,44.73±9.50μm,45.77±8.70μm,47.81±5.84μm,实验组与A组对照组比较具有高度显著差异性,P<0.01,而实验组之间无显著差异性。
电子显微镜观察：对照组横切显示,粗细肌丝排列规则,大量线粒体存在,线粒体形态呈卵圆形并存在折叠嵴结构；纵切显示,肌原纤维排列整齐,明暗带交替出现。实验组横切均显示,线粒体数量明显减少,呈圆形且嵴结构减少或消失；纵切显示,肌原纤维排列紊乱、模糊不清,Z线呈水纹样改变。ABCD各组肌小节长度分别为1.95±0.02μm,1.92±0.08μm,1.53±0.06μm,1.48±0.07μm,实验组C、D组与A组对照组和B组实验组比较具有高度显著差异性,P<0.01,另外,C、D组之间比较无显著性差异,B组与A组比较无显著差异性,P>0.05。
研究结论：
1.紧张带或触发点,局部抽搐反应、自发电位等电生理特征和病理组织学改变证明打击结合离心运动方式建立的肌筋膜疼痛触发点大鼠模型成功。延长恢复期,肌筋膜疼痛触发点仍然存在,说明大鼠模型复制的MTrPs可长期存在,符合临床肌筋膜疼痛触发点的特征。
2.恢复4周组肌筋膜疼痛触发点为早期触发点,存在明显炎症变化和肌肉损伤现象,恢复8周和恢复12周,肌筋膜疼痛触发点表现相似,为慢性触发点,说明触发点在恢复8周时已稳定存在,建立肌筋膜疼痛触发点模型时无需恢复12周即可复制稳定肌筋膜疼痛触发点。
3.肌筋膜疼痛触发点产生的自发性电位是一种高频率的异常终板电位,说明肌筋膜触发点位于运动终板附近。
4.病理组织学光镜观察受累骨骼肌触发点处聚集的圆形结节及膨大并相间出现的变细肌纤维结构,说明骨骼肌触发点存在异常收缩的收缩结节和因收缩而导致结节两端的变细,肌筋膜疼痛触发点是一种异常肌纤维改变。炎性浸润提示肌筋膜触发点存在慢性的炎症过程,核内移则提示可能存在神经肌肉接头功能异常现象。
5.电镜观察肌小节排列紊乱,Z线水纹样改变,线粒体数量减少,结构异常,提示为受累肌肌筋膜疼痛触发点处存在能量危机现象,并且超微结构显示肌筋膜疼痛触发点肌纤维维存在损伤现象；肌小节显著性缩短进一步验证肌纤维存在异常收缩现象。
Objective:
Daily life activities or sports injury usually cause some chronic pain, which could lead to the pain at joint and spine or the disorders of skeletomuscular system. Most of this chronic pain is muscle pain, and myofascial pain is a common cause of muscle pain. Clinically, chronic myofascial pain syndrome has been characterized by pain, referred pain, autonomic nerve dysfunction and muscle disorders. Myofascial pain could seriously affect people's living and work lead to an increase of the financial burden of society. Now it is believed that myofascial trigger points locate in skeletal muscle or fascia muscularis. In order to study the pathogenesis of the myofascial trigger points, most of current models are simulation models of latent trigger points models which can not represent the whole characters of myofascial trigger points. Therefore, all of these models couldn't explain real changes of trigger points' spontaneous electrical activity (SEA) and histopathological changes. In this study, we will use rats as experimental animals. During experiment, rats were dealt with striking and eccentric exercise to produce the myofascial trigger points in rats. After different longed recovery time, the EMG and histopathological changes at trigger points will be inspected on the nature and pathological character of myofascial trigger points which could infer the possible pathogenesis of myofascial trigger points.
Methods:
32 male SD rats seven week-old, average weight of 220g-260g, were randomly divided into 4 groups which were A group, B group, C group and D group. There were 8 rats in every group. A group was control group and B group, C group and D groups were experimental groups. A group:During periods of modeling and recovery, all rats in A group weren't given any intervention. Experimental groups:in the first day of every week during modeling period, all rats in experimental groups were stroked at the left vastus medialis, and the next day, all rats were taken to eccentric exercise for 90 min. The modeling period lasted 8 weeks. During recovery periods, without any experimental intervention and normal feeding, all experimental rats were dealt as the control group. The recovery periods of BCD group separately lasted 4,8 and 12 weeks. After recovery period, all groups were detected taut band, contraction knots, local twitch response (LTR) and SEA. Finally, diagnose myofascial trigger points and make muscle biopsy:1.After HE staining, use microscope to record the modules number and observe the shape and size of modules; 2.Using transmission electron microscope (TEM), observe arrangement of myoneme, sarcomere, mitochondria, etc. All the results of experimental groups and control group were compared and analyzed by SPSS17.0 software package.
Results:
The average number of myofascial trigger points or taut band of A group was 0.13(1/8) and that of B, C, D group was respectively 3.00 (24/8),2.63 (21/8),2.25 (18/8). When acupunctured, all taut band or nodules could be induced LTR. During resting state, the frequency of SEA in a minute of A, B, C, D group was respectively 2.75±2.87,172.57±102.88,151.63±65.37,168.14±64.53. When the control group was compared with every experimental group, P<0.01 which has highly significant difference; while each experimental group was compared, P> 0.05 which didn't have statistical significance. The amplitude of each group's SEA was 26.06±16.67μV,33.08±18.40μV,93.26±163.18μV,78.27±161.68μV. When A, B group and C, D group were compared, there was significant difference, P<0.05, while there was no significant difference between A group and B group and between C group and D group.
The cross-section of pathological section showed:A group had regular muscle cell and uniform size, and was not found different sized, round, augmented and deeply stained muscle cell; All experimental groups were found augmented, round and deeply stained contracture nodules, and also found inflammatory cell infiltration and nuclear transfer phenomena (>10%). The Longitudinal section of pathological section showed:the control group showed a tightly and regular arrangement of longitudinal muscle fibers; all experimental groups were appeared disorganized shuttle-shaped muscle fibers which were swollen in central and thin at both ends. The average muscle cell diameter in each group were 22.84±0.48μm,44.73±9.50μm,45.77±8.70μm,47.81±5.84μm. There was a highly significant difference between experimental groups and the control group, P<0.01, while there was no significant difference between experimental groups.
The observation of TEM showed:cross-section of the control group showed regularly arranged thin filament and thick filament, a large number of mitochondria which were ovoid and had whole ridge structures; the longitudinal section shows regularly arranged myofibrils with alternating light band and dark band. The cross-section of experimental groups all showed significantly decreased mitochondria which were round and had less ridge structures or abnormal ones; the longitudinal section showed disordered myofibrils which were blurred and whose Z lines had a water-patterns-like changing. The main sarcomere length in each groups were 1.95±0.02μm,1.92±0.08μm,1.53±0.06μm,1.48±0.071μm, there was a highly significant difference between C, D group and A group,p<0.01, while there was no significant difference between A group and B group and between C group and D group,p>0.05.
Conclusions:
1. All founds of the experiment which conclude taut band or myofascial trigger points, LTR, SEA and pathological changes demonstrate that myofascial trigger points rat model though striking and eccentric exercise is successful. When the recovery period was extended, myofascial trigger points did not disappeared and could prove that myofacial trigger points can exist in the long time, which is in accordance with the characteristics of clinical MTrPs.
2.The SEA generated in MTrPs is a kind of abnormal end plate potential with high frequency and low amplitude, which could prove that MTrPs locate near motor end plate.
3.The pathological observation of microscopy illustrate that there are abnormally contracted nodules in myofascial trigger points and MTrPs is a kind of abnormal muscle fiber. Inflammatory infiltration suggests that there may be a inflammatory process during the pathogenesis of MTrPs, and the nuclear transfer may point out a muscle repairing process or muscle that is lost of neural control.
4.The observation of TEM suggests that muscle with MTrPs has a energy crisis and injury phenomenon; significantly shorten sarcomere can further prove that the muscle fibers near MTrPs are abnormally contracted fiber.
日常生命活动或体育运动损伤后常常出现一些慢性疼痛后遗症状,这些疼痛往往会引起关节和脊柱周围疼痛,导致关节障碍。这些慢性疼痛大部分为骨骼肌疼痛,而肌筋膜疼痛触发点是导致骨骼肌疼痛的常见原因之一。临床上慢性肌筋膜疼痛综合症是以疼痛为主一组症候群,这种症候群表现为疼痛、牵涉痛、自主神经的和骨骼肌功能的障碍等症状。肌筋膜疼痛严重影响了人们的生活和工作,并成为消耗卫生资源的重要原因。目前认为受累肌内存在有骨骼肌或肌筋膜内的疼痛触发点。为了研究其发病机制,目前有关触发点的模型多为模拟模型或隐性触发点模型,无法代表活化触发点的全貌；因此无法说明触发点的自发肌电位和动作电位的真实变化,而且也无法说明到真实活化触发点的病理组织学的真实改变。本研究通过经济实惠的大鼠作为实验动物,采用股内侧肌打击结合离心运动的方法建立创伤性肌筋膜疼痛触发点的动物模型,在经历不同恢复时间后,检测触发点肌电图表现和观察触发点的病理组织学的改变,了解肌筋膜疼痛触发点的本质和发病特点,以推论触发点的可能发病机制。
研究方法：
32只七周龄雄性SD大鼠,平均体重220g-260g,随机分为ABCD四组,每组8只,A组为正常对照组,BCD三组为实验干预组。A组正常对照组在造模期与恢复期均正常喂养,不进行任何干预。实验干预组造模期每周第一天打击左下肢股内侧肌,打击后第二天配合离心运动,造模期为8周。实验干预组恢复期同对照组,不进行任何实验干预,正常喂养,其中B组恢复4周,C组恢复8周,D.组恢复12周。分别在不同时期分批对大鼠进行造模效果检查和取材,手术暴露大鼠股内侧肌,触摸打击处及周围肌肉的紧张带和收缩结节、针刺紧张带引起局部抽搐反应、记录紧张带处的自发性电位和记录结节数目。最后,对紧张带或结节处的局部组织进行组织活检取材：1.组织进行HE染色后,光镜下观察病理切片的结节数目、形态及大小等变化；2.使用透射电子显微镜超薄切片技术制作电镜标本,电镜观察触发点组织的肌丝排列、肌小节、线粒体等超微结构特点。将实验干预组和对照组所得结果进行比较分析,所用数据统计分析均采用SPSS17.0软件包进行分析。
研究结果：
A组对照组股内侧肌附近发现紧张带或触发点个数平均0.13个(1/8)；B、C、D组平均发现触发点个数分别为3.00个(24/8)、2.63个(21/8)、2.25个(18/8),紧张带或触发点在针刺时均出现局部抽搐反应。静息状态下,大鼠股内侧肌附测量肌肉的自发电位,A、B、C、D各组一分钟内出现自发电位的频数分别为2.75±2.87,172.57±102.88,151.63±65.37,168.14±64.53。对照组与实验组两两比较,P<0.01具有高度显著性差异,实验组之间两两比较P>0.05没有统计意义。A、B、C、D各组自发电位的波幅分别为26.06±16.67μV,33.08±18.40μV,93.26±163.18μV,78.27±161.68μV,其中A、B两组与C、D两组比较有显著性差异P＜0.05,而A、B组之间与C、D组之间不具有显著性差异。
病理切片横切面显示,对照组肌细胞形态规则、大小均匀,未发现有大小不一、圆形、增大、深染的肌细胞,实验组横切面均发现增大、圆形深染的挛缩结节,实验组各组均出现炎细胞浸润和核内移(>10%)现象。纵切面,对照组表现为排列紧密而规律的纵向肌纤维。实验组B、C、D组均出现排列紊乱、中央膨大两端变细或相间出现粗细不等的梭形肌纤维。ABCD各组肌细胞直径分别为22.84±0.48μm,44.73±9.50μm,45.77±8.70μm,47.81±5.84μm,实验组与A组对照组比较具有高度显著差异性,P<0.01,而实验组之间无显著差异性。
电子显微镜观察：对照组横切显示,粗细肌丝排列规则,大量线粒体存在,线粒体形态呈卵圆形并存在折叠嵴结构；纵切显示,肌原纤维排列整齐,明暗带交替出现。实验组横切均显示,线粒体数量明显减少,呈圆形且嵴结构减少或消失；纵切显示,肌原纤维排列紊乱、模糊不清,Z线呈水纹样改变。ABCD各组肌小节长度分别为1.95±0.02μm,1.92±0.08μm,1.53±0.06μm,1.48±0.07μm,实验组C、D组与A组对照组和B组实验组比较具有高度显著差异性,P<0.01,另外,C、D组之间比较无显著性差异,B组与A组比较无显著差异性,P>0.05。
研究结论：
1.紧张带或触发点,局部抽搐反应、自发电位等电生理特征和病理组织学改变证明打击结合离心运动方式建立的肌筋膜疼痛触发点大鼠模型成功。延长恢复期,肌筋膜疼痛触发点仍然存在,说明大鼠模型复制的MTrPs可长期存在,符合临床肌筋膜疼痛触发点的特征。
2.恢复4周组肌筋膜疼痛触发点为早期触发点,存在明显炎症变化和肌肉损伤现象,恢复8周和恢复12周,肌筋膜疼痛触发点表现相似,为慢性触发点,说明触发点在恢复8周时已稳定存在,建立肌筋膜疼痛触发点模型时无需恢复12周即可复制稳定肌筋膜疼痛触发点。
3.肌筋膜疼痛触发点产生的自发性电位是一种高频率的异常终板电位,说明肌筋膜触发点位于运动终板附近。
4.病理组织学光镜观察受累骨骼肌触发点处聚集的圆形结节及膨大并相间出现的变细肌纤维结构,说明骨骼肌触发点存在异常收缩的收缩结节和因收缩而导致结节两端的变细,肌筋膜疼痛触发点是一种异常肌纤维改变。炎性浸润提示肌筋膜触发点存在慢性的炎症过程,核内移则提示可能存在神经肌肉接头功能异常现象。
5.电镜观察肌小节排列紊乱,Z线水纹样改变,线粒体数量减少,结构异常,提示为受累肌肌筋膜疼痛触发点处存在能量危机现象,并且超微结构显示肌筋膜疼痛触发点肌纤维维存在损伤现象；肌小节显著性缩短进一步验证肌纤维存在异常收缩现象。
Objective:
Daily life activities or sports injury usually cause some chronic pain, which could lead to the pain at joint and spine or the disorders of skeletomuscular system. Most of this chronic pain is muscle pain, and myofascial pain is a common cause of muscle pain. Clinically, chronic myofascial pain syndrome has been characterized by pain, referred pain, autonomic nerve dysfunction and muscle disorders. Myofascial pain could seriously affect people's living and work lead to an increase of the financial burden of society. Now it is believed that myofascial trigger points locate in skeletal muscle or fascia muscularis. In order to study the pathogenesis of the myofascial trigger points, most of current models are simulation models of latent trigger points models which can not represent the whole characters of myofascial trigger points. Therefore, all of these models couldn't explain real changes of trigger points' spontaneous electrical activity (SEA) and histopathological changes. In this study, we will use rats as experimental animals. During experiment, rats were dealt with striking and eccentric exercise to produce the myofascial trigger points in rats. After different longed recovery time, the EMG and histopathological changes at trigger points will be inspected on the nature and pathological character of myofascial trigger points which could infer the possible pathogenesis of myofascial trigger points.
Methods:
32 male SD rats seven week-old, average weight of 220g-260g, were randomly divided into 4 groups which were A group, B group, C group and D group. There were 8 rats in every group. A group was control group and B group, C group and D groups were experimental groups. A group:During periods of modeling and recovery, all rats in A group weren't given any intervention. Experimental groups:in the first day of every week during modeling period, all rats in experimental groups were stroked at the left vastus medialis, and the next day, all rats were taken to eccentric exercise for 90 min. The modeling period lasted 8 weeks. During recovery periods, without any experimental intervention and normal feeding, all experimental rats were dealt as the control group. The recovery periods of BCD group separately lasted 4,8 and 12 weeks. After recovery period, all groups were detected taut band, contraction knots, local twitch response (LTR) and SEA. Finally, diagnose myofascial trigger points and make muscle biopsy:1.After HE staining, use microscope to record the modules number and observe the shape and size of modules; 2.Using transmission electron microscope (TEM), observe arrangement of myoneme, sarcomere, mitochondria, etc. All the results of experimental groups and control group were compared and analyzed by SPSS17.0 software package.
Results:
The average number of myofascial trigger points or taut band of A group was 0.13(1/8) and that of B, C, D group was respectively 3.00 (24/8),2.63 (21/8),2.25 (18/8). When acupunctured, all taut band or nodules could be induced LTR. During resting state, the frequency of SEA in a minute of A, B, C, D group was respectively 2.75±2.87,172.57±102.88,151.63±65.37,168.14±64.53. When the control group was compared with every experimental group, P<0.01 which has highly significant difference; while each experimental group was compared, P> 0.05 which didn't have statistical significance. The amplitude of each group's SEA was 26.06±16.67μV,33.08±18.40μV,93.26±163.18μV,78.27±161.68μV. When A, B group and C, D group were compared, there was significant difference, P<0.05, while there was no significant difference between A group and B group and between C group and D group.
The cross-section of pathological section showed:A group had regular muscle cell and uniform size, and was not found different sized, round, augmented and deeply stained muscle cell; All experimental groups were found augmented, round and deeply stained contracture nodules, and also found inflammatory cell infiltration and nuclear transfer phenomena (>10%). The Longitudinal section of pathological section showed:the control group showed a tightly and regular arrangement of longitudinal muscle fibers; all experimental groups were appeared disorganized shuttle-shaped muscle fibers which were swollen in central and thin at both ends. The average muscle cell diameter in each group were 22.84±0.48μm,44.73±9.50μm,45.77±8.70μm,47.81±5.84μm. There was a highly significant difference between experimental groups and the control group, P<0.01, while there was no significant difference between experimental groups.
The observation of TEM showed:cross-section of the control group showed regularly arranged thin filament and thick filament, a large number of mitochondria which were ovoid and had whole ridge structures; the longitudinal section shows regularly arranged myofibrils with alternating light band and dark band. The cross-section of experimental groups all showed significantly decreased mitochondria which were round and had less ridge structures or abnormal ones; the longitudinal section showed disordered myofibrils which were blurred and whose Z lines had a water-patterns-like changing. The main sarcomere length in each groups were 1.95±0.02μm,1.92±0.08μm,1.53±0.06μm,1.48±0.071μm, there was a highly significant difference between C, D group and A group,p<0.01, while there was no significant difference between A group and B group and between C group and D group,p>0.05.
Conclusions:
1. All founds of the experiment which conclude taut band or myofascial trigger points, LTR, SEA and pathological changes demonstrate that myofascial trigger points rat model though striking and eccentric exercise is successful. When the recovery period was extended, myofascial trigger points did not disappeared and could prove that myofacial trigger points can exist in the long time, which is in accordance with the characteristics of clinical MTrPs.
2.The SEA generated in MTrPs is a kind of abnormal end plate potential with high frequency and low amplitude, which could prove that MTrPs locate near motor end plate.
3.The pathological observation of microscopy illustrate that there are abnormally contracted nodules in myofascial trigger points and MTrPs is a kind of abnormal muscle fiber. Inflammatory infiltration suggests that there may be a inflammatory process during the pathogenesis of MTrPs, and the nuclear transfer may point out a muscle repairing process or muscle that is lost of neural control.
4.The observation of TEM suggests that muscle with MTrPs has a energy crisis and injury phenomenon; significantly shorten sarcomere can further prove that the muscle fibers near MTrPs are abnormally contracted fiber.
引文
[1]Yap E C. Myofascial pain—an overview. Ann Acad Med [J],2007,36(1):43-8.
[2]Partanen J V, Ojala T A, Arokoski J P. Myofascial syndrome and pain:A neurophysiological approach [J]. Pathophysiology,2010,17(1):19-28.
[3]Hong CZ. Myofascial Pain Therapy[J]. J Musculoskel Pain,2004,12(3):37-43.
[4]Hong CZ. Pathophysiology of myofascial trigger point[J]. J Formos Med Assoc, 1996,95(2):93-104.
[5]Simons DG, Travell JG, Simons LS. Travell and Simons' myofascial pain and dysfunction:the trigger point manual[M]. Volume 1:upper half of body.2nd ed. Baltimore:Williams & Wilkins,1999.71-72.
[6]Lucas KR, Polus BI, Rich PS. Latent myofascial trigger points:Their effect on muscle activation and movement efficient [J]. J Bodywork Mov Ther,2004,8(3): 160-166.
[7]Weissmann RD. Uberlegungen zur Biomechanik in der Myofaszialen Triggerpunkttherapie [German; Considerations with regard to the biomechanics related to myofascial trigger point therapy [J]. Physiotherapie 2000; 35(10):13-21.
[8]黄强民.肌筋膜触发点及肌筋膜疼痛综合征[J].颈腰痛杂志,2004,25(5)：360-362.
[9]姚明华,黄强民.肌筋膜触发点疼痛的实验动物模型研究[J].中国运动医学,2009,28(4)：415-418.
[10]Dommerholt J, Bron C, Franssen J. Myofascial trigger points:an evidence-informed review [J]. The Journal of Manual & Manipulative Therapy,2006, 14(4):203-221.
[11]Hagg G M. The Cinderella Hypothesis. In:Johansson H, et al, eds. Chronic Work-Related Myalgia [M]. Gavle, Sweden:Gavle University Press,2003:127-132.
[12]Larsson B, Bjork J, Kadi F, et al. Blood supply and oxidative metabolism in muscle biopsies of female cleaners with and without myalgia [J]. Clin J Pain 2004, 20(6):440-446.
[13]Gissel H. Ca2+ accumulation and cell damage in skeletal muscle during low frequency stimulation [J]. Eur J Appl Physiol 2000,83(2-3):175-180.
[14]Febbraio M A, Pedersen B K. Contraction-induced myokine production and release:Is skeletal muscle an endocrine organ? [J]. Exerc Sport Sci Rev 2005.33(3): 114-119.
[15]Pedersen B K, Febbraio M. Muscle-derived interleukin-6:A possible link between skeletal muscle, adipose tissue, liver, and brain [J]. Brain Behav Immun. 2005,19(5):371-376.
[16]Treaster D, Marras W S, Burr D, Sheedy J E, Hart D. Myofascial trigger point development from visual and postural stressors during computer work [J]. J Electromyogr Kinesiol,2006,16(2):115-124.
[17]Otten E. Concepts and models of functional architecture in skeletal muscle [J]. Exerc Sport Sci Rev,1988,16:89-137.
[18]Simons D G. Understanding effective treatments of myofascial trigger points [J]. J Bodywork Mov Ther.2002,6:81-88.
[19]Dommerholt J, Royson M W, Whyte-Ferguson L. Neck pain and dysfunction following whiplash [M]. In:Whyte-Ferguson L, Gerwin RD, eds. Clinical Mastery of Myofascial Pain Syndrome. Baltimore, MD:Lippincott, Williams&Wilkins,2005: 57-89.
[20]Schuller E, Eisenmenger W, Beier G. Whiplash injury in low speed car accidents [J]. J Musculoskeletal Pain.2000,8(1/2):55-67.
[21]Gerwin R D, Dommerholt J. Myofascial trigger points in chronic cervical whiplash syndrome [J]. J Musculoskeletal Pain.1998,6(Suppl.2):28.
[22]Fernandez-de-las-Penas C, Fernandez-Carnero J, Palomeque-del-Cerro L, et al. Manipulative treatment vs. conventional physiotherapy treatment in whiplash injury: A randomized controlled trial [J]. J Whiplash Rel Disord.2004,3(2):73-90.
[23]Scott D, Jull G, Sterling M. Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain [J]. Clin J Pain.2005,21(2):175-181.
[24]Simons D G. Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal pain and dysfunction [J]. J Electromyogr Kinesiol.2004,14(1): 95-107.
[25]Gerwin R D, Dommerholt J, Shah J. An expansion of Simons' integrated hypothesis of trigger point formation [J]. Curr Pain Headache Rep.2004,8(6): 468-475.
[26]Kawakita K, Itoh K, Okada K. Experimental model of trigger points using eccentric exercise [J]. J Musculoskeletal Pain,2008,16(1-2):29-35.
[27]Mense S. The pathogenesis of muscle pain [J]. Curr Pain Headache Rep,2003, 7(6):419-425.
[28]Shah J P, Phillips T M, Danoff J V, et al. An in-vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle [J]. J Appl Physiol.2005,99(5):1980-1987.
[29]Fernandez-de-las-Penas C, Alonso-Blanco C, Cuadrado ML, et al. Trigger points in the suboccipital muscles and forward head posture in tension-type headache[J]. Headche,2006,46:454-460.
[30]Gerwin R D. A review of myofascial pain and fibromyalgia:Factors that promote their persistence [J]. Acupunct Med.2005,23(3):121-134.
[31]Gerwin RD. Factores que promueven la persistencia de mialgia en el sindrome de dolor miofascial y en la fibromyalgia [Spanish; Factors that promote the continued existence of myalgia in myofascial pain syndrome and fibromyalgia[J]. Fisioterapia 2005; 27(2):76-86.
[32]Andres E, Loukili N H, Noel E, et al. Vitamin B12 (cobalamin) deficiency in elderly patients [J]. CMAJ,2004,171(3):251-259.
[33]Gerwin R. A study of 96 subjects examined both for fibromyalgia and myofascial pain (abstract)[J]. J Musculoskeletal Pain 1995; 3 (Suppl 1):121.
[34]Pruthi RK, Tefferi A. Pernicious anemia revisited[J]. Mayo Clin Proc 1994; 69: 144-150.
[35]Kadi F, Waling K, Ahlgren C, et al. Pathological mechanisms implicated in localized female trapezius myalgia[J]. Pain 1998;78:191-196.
[36]Plotnikoff G A, Quigley J M. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain [J]. Mayo Clin Proc,2003,78(12): 1463-1470
[37]Dommerholt J, Issa T. Differential diagnosis:Myofascial pain [M]. In:Chaitow L, ed. Fibromyalgia Syndrome:A Practitioner's Guide to Treatment. Edinburgh, UK: Churchill Livingstone,2003:149-177
[38]Lewis C, Gevirtz R, Hubbard D, et al. Needle trigger point and surface frontal EMG measurements of psychophysiological responses in tension-type headache patients[J]. Biofeedback & Self-Regulation 1994; 3:274-275.
[39]McNulty WH, Gevirtz RN, Hubbard DR, et al. Needle electromyographic evaluation of trigger point response to a psychological stressor[J]. Psychophysiology 1994; 31:313-316.
[40]Banks SL, Jacobs DW, Gevirtz R, et al. Effects of autogenic relaxation training on electromyographic activity in active myofascial trigger points[J]. J Musculoskeletal Pain 1998; 6(4):23-32.
[41]Linton SJ. A review of psychological risk factors in back and neck pain[J]. Spine 2000; 25:1148-1156.
[42]Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain:A state of the art[J]. Pain 2000; 85:317-332.
[43]Menefee LA, Cohen MJ, Anderson WR, et al. Sleep disturbance and nonmalignant chronic pain:A comprehensive review of the literature [J]. Pain Med 2000; 1:156-172.
[44]Hubbard DR, Berkoff GM. Myofascial trigger points show spontaneous needle EMG activity[J]. Spine,1993,18(13):1803-1807.
[45]Kuan TS, Hsieh YL, Chen SM, et al. The myofascial trigger point region: correlation between the degree of irritability and the prevalence of endplate noise[J]. Am J Phys Med Rehabil,2007,86(3):183-189.
[46]McPartland JM, Simons DG.Myofascial trigger points:translating molecular theory into manual therapy[J]. J Man Manipulative,2006,14(4):232-239.
[47]Kuan TS, Chen SM, Chien CH, et al. Effect of botulinum toxin on endplate noise in myofascial trigger spots of rabbit skeletal muscle[J]. Am J Phys Med Rehabil.2002, 81(7):512-520.
[48]Mense S, Simons DG, Hoheisel U, et al. Lesion of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation[J]. J ApplPhysiol,2003, 94(4):2494-2501.
[49]Gerwin RD, Dommerholt J, shal JP. An expansion of Simons' intergrated hypothesis of trigger point formation[J]. Curr Pain Headache Rep,2004,8(6): 468-475.
[50]Sluka KA, Kalra A, Moore SA. Unilateral intramuscular injections of acidic saline produce a bilateral, long-lasting hyperalgesia[J]. Muscle Nerve,2001,24(1): 37-46.
[51]Wang X, Li Y, Engisch KL, et al. Activity-dependent presynaptic regulation of quantal size at the mammalian neuromuscular junction in vivo[J]. J Neurosci,2005, 25(2):343-351.
[52]Nakanishi ST, Cope TC, Rich MM, et al. Regulation of motoneuron excitability via motor endplate acetylcholine receptor activation[J]. J Neurosci,2005,25(9): 2226-2232.
[53]Butler DS. The sensitive Nervous System[M]. Adelaide, Austrlia:Noigroup Publications,2000.
[54]Chaitow L, Morrison S, Baldary P, et al. Fibromyalgia syndrome:a practitioner's guide to treatment[M].2nd ed. North Thames(West), UK:Churchill Livingstone,2003. 16-16.
[55]Chaitow L, Morrison S, Baldary P, et al. Fibromyalgia syndrome:a practitioner's guide to treatment[M].2nd ed. North Thames(West), UK:Churchill Livingstone,2003. 15-15.
[56]Bruckle W, Suckfull M, Fleckenstein W, et al. Gewebe-pO2-Messung in der verspanntenRuckenmuskulatur(m.erectorspinae)[J]. Z Rheumatol,1990,49(4): 208-216.
[57]Giniatullin RA, Sokolova EM. ATP and adenosine inhibit transmitter release at the frog neuromuscular junction through distinct presynaptic receptors[J]. Br J Pharmacol,1998; 124(4):839-844.
[58]Hong CZ. New trends in myofascial pain syndrome[J]. Chin Med J (Taipei),2002, 65(11),501-512.
[59]Bukharaeva EA, GainulovRKh, Nikol'skii EE. The effects of noradrenaline on the amplitude-time characteristics of multiquantum endplate currents and the kinetics of induced secretion of transmitter quanta[J]. NeurosciBehav Physiol.2002,32(5): 549-554.
[60]Chen JT, Chen SM, Kuan TS, et al. Phentolamine effect on the spontaneous electrical activity of active loci in a myofascial trigger spot of rabbit skeletal muscle[J]. Arch Phys Med Rehabil,1998,79(7):790-794.
61 Delaney JP, Leong KS, Watkins A. et al. The short-term effects of myofascial trigger point massage therapy on cardiac autonomic tone in healthy subjects. J AdvNurs,2002,37(4):364-371.
[62]黄强民,敖丽娟,刘燕.肌筋膜触发点疼痛特征的要点分析[J].中国临床康复杂,2004,8(23)：4822-4824.
[63]Butler DS. The Sensitive Nervous System[M]. Adelaide, Australia:Noigroup Publications,2000.
[64]Mense S. Biochemical pathogenesis of myofascial pain [J]. J Musculoskeletal Pain,1996,4(1-2):145-162.
[65]Shah JP, Gilliams EA. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis:An application of muscle pain concepts to myofascial pain syndrome [J]. J Bodywork Movement Ther,2008,12(4):371-384.
[66]Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points [J]. Arch Phys Med Rehabil,2008,89(1):16-23.
[67]Simons DG. Review of microanalytical in vivo study of biochemical milieu of myofascial trigger points [J]. J Bodywork Mov Ther,2006,10(1):10-11.
[68]Shah JP. Uncovering the biechemical milieu of myofascial trigger points using in vivo microdialysis [J]. J Musculoskeletal Pain,2008,16(1-2):17-20.
[69]Itoh K, Kawakita K:Effect of indomethacin on the development of eccentric exercise-induced localized sensitive region in the fascia of rabbit [J]. Jpn J Physiol, 2002,52(2):173-180.
[70]韩济生.神经科学[M].第3版.北京：北京大学医学出版社,2008.
[71]鞠躬,吕国蔚,王百忍.神经生物学(供研究生用).北京：人民卫生出版社,2004.
[72]Butler DS. The sensitive Nervous System [M]. Adelaide, Austrlia:Noigroup Publications,2000.
[73]Chaitow L, Morrison S, Baldary P, et al. Fibromyalgia syndrome:a practitioner's guide to treatment [M].2nd ed. North Thames(West), UK:Churchill Livingstone, 2003.
[74]Hoheisel U, Koch K, Mense S. Functional reorganization in the rat dorsal horn during an experimental myositis [J]. Pain,1994,59(1):111-118.
[75]Young BO, Dubo HY, Fisher AA, et al.肌筋膜痛综合征基于脊髓节段性敏感的诊断和治疗(一)[J].中国康复理论与实践,2009,15(6)：589-590.
[76]Young BO, Dubo HY, Fisher AA, et al.肌筋膜痛综合征基于脊髓节段性敏感的诊断和治疗(二)[J].中国康复理论与实践,2009,15(7)：691-693.
[77]Issberner U, Reeh PW. Steen KH. Pain due to tissue acidosis:a mechanism for inflammatory and ischemic myalgia? [J]. Neuroscience Letters,1996,208(3): 191-194.
[78]Ambalavanar R. Dessem D, Moutanni A, et al. Muscle inflamma- tion induces a rapid increase in calcitonin gene-related peptide(CGRP)mRNA that temporally relates to CGRP immunoreactivity and nociceptive behavior [J]. Neuroscience,2006,143(3): 875-884.
[79]Luo G, Hershko DD, Robb BW, et al. IL-lbeta stimulates IL-6 production in cultured skeletal muscle cells through activation of MAP kinase signaling pathway and NF-kappa B [J]. Am J Physiol Regul Integr Comp Physiol.2003,284(5): 1249-1254.
[80]Tough E A, White A R, Cummings T M, et al. Acupuncture and dry needling in the management of myofascial trigger point pain:A systematic review and meta-analysis of randomized controlled trials [J]. Eur J Pain.2009,13(1):3-10.
[81]Tough E A, White A R, Richards S, et al. Variability of criteria used to diagnose myofascial trigger point pain syndrome-evidence from a review of the literature [J]. Clin J Pain,2007,23(3):278-86.
[82]Lavelle E D, Lavelle W, Smith H S. Myofascial trigger points [J]. Anesthesiology, 2007,25(4):841-851.
[83]黄强民,庄小强,谭树生.肌筋膜疼痛触发点的诊断与治疗[M].广西：广西科学技术出版社,2010：202-203.
[84]Kiralp M Z, Uzun G, Dincer U, et al. A Novel Treatment Modality for Myofascial Pain Syndrome:Hyperbaric Oxygen Therapy [J]. J Nati Assoc,2009,101(1):77-80.
[85]Baldry P. Management of myofascial trigger point pain [J]. Acupunct Med,2002, 20(1):2-10.
[86]Harden R N, Cottrill J, Gagnon C M, et al. Botulinum toxin A in the treatment of chronic tension-type headache with cervical myofascial trigger points:A randomized, double-blind, placebo-controlled pilot study [J]. Headache,2009,49(5):732-743.
[87]McPartland J M, Brodeur R, Hallgren R C. Chronic neck pain, standing balance, and suboccipital muscle atrophy [J]. J Manipulative Physiol Ther 1997,20(1):24-29.
[88]Katsura M, Mohri Y, Shuto K, et al. Up-regulation of L-type uoltage-dependent calcium channels after long-term exposure to nicotine in cerebral cortical neurons [J]. J Biol Chem 2002,277(10):7979-7988.
[89]Berger J. Vermont DO urges peers to learn about herbal medicine [J]. The DO, 1999,40(3):58-60.
[90]Re L, Barocci S, Sonnino S, et al. Linalool modifies the nicotinic receptor-ion channel kinetics at the mouse neuromuscular junction [J]. Pharmacol Res,2000,42(2): 177-182.
[91]陈疾忤,陈世益,李云霞.骨骼肌钝挫伤后肌电检测的应用研究[J].中华物理医学有康复杂志,2005,27(1)：23-25.
[92]徐建鸣.疼痛管理概述[J].上海护理,2002,2(4)：56-57.
[93]Itoh K, Okada K, Kawakita K. A proposed experimental model of myofascial trigger points in human muscle after slow eccentric exercise[J]. Acupunct Med,2004, 22(1):2-13.
[94]Kawakita K, Itoh K, Okada. Experimental model of trigger points using eccentric exercise[J]. J Musculoskeletal Pain,2008,16(1-2):29-35.
[95]Mense S. Pathophysiologic basis of muscle pain syndromes[M]. In:Fischer AA, ed. Myofascial Pain:Update in Diagnosis and Treatment. Philadelphia, PA:W.B. Saunders Company,1997:23-53.
[96]Itoh K, Okada K, Kawakita K. A proposed experimental model of myofascial trigger points in human muscle after slow eccentric exercise[J]. Acupunct Med,2004, 22(1):2-13.
[97]Ficton JR, Auvinen MD, Dykstra D et al. Myofascial pain syndrome: Electromyographic changes associated with local twitch response[J]. Arch Phys Med Rehabil,1985,66:314-317.
[98]Kawakita K, Gotoh K. Role of polymodal receptors in the acupuncture-mediated endogenous pain inhibitory systems[M]. In:Kumazawa I, Kruger L, Mizumura K, editors, Prog Brain Res 113. Amsterdam:Elsevier,1996:507-523.
[99]Gerwin RD, Shannon S, Simons DG, et al. Identification of myofascial trigger points:interrater agreement and effect of training[J]. Pain,1997:69:65-73.
[100]Simons DG, Travell JG. Myofascial trigger points, a possible explanation[J]. Pain,1981,10:106-109.
[101]Mense S. Considerations concerning the neurobilogical basis of muscle pain[J]. Pain,1991,69:610-616.
[102]Gerwin RD, Duranleau D. Ultrasound identification of the myofascial trigger point[J]. Muscle Nerve,1997,20:767-768.
[103]Hong CZ. Persistence of local twitch response with loss of conduction to and from the spinal cord[J]. Arch Phys Med Rehabil,1994,75:12-16.
[104]Hong C-Z, Yu J. Spontaneous electrical activity of rabbit trigger spot after transection of spinal cord and peripheral nerve[J]. J Musculoskeletal Pain,1998,6(4): 45-58.
[105]Wang F, Audette J. Electrophysiological characteristics of the local twitch response with active myofascial pain of neck compared with a control group with latent trigger points [J]. Am J Phys Med Rehabil,2000,79:203.
[106]Hong CZ. Myofascial trigger points:Pathophysiology and correlation with acupuncture[J]. Acup Med 2000,18:41-47.
[107]姚泰,曹济民,樊小力等.生理学[M].北京：人民卫生出版社.第2版,2010.
[108]Jun Kimura著,郭铁城,朱愈译.神经肌肉疾病电诊断(原理与实践)[M].第3版.天津：天津科技翻译出版公司,2008.
[109]李作汉,张平.神经肌肉疾病的临床与病理[M].北京：人民卫生出版社,2007.
[110]Mense S, Simons DG, Russell IJ原著,郭传友主译.肌痛[M].北京： 人民卫生出版社,2005.
[111]Dubowitz V, Sewry CA原著,袁云主译.肌肉活检[M].第3版.北京：北京大学医学出版社,2009.
[112]沈燕国,徐建光,顾玉东等.成肌调节因子Myogenin和MRF4在人体失神经骨骼肌中的表达及其临床意义[J].中华手外科杂志,200218(3)：177-180.
[113]Rodrigues S, Schmalbruch L. Satellite cells and myonuclei in long-term denervated rat muscle[J]. Anat Rec,1995,243:430-437.
[114]Koishi CA, Lu DX, Faulkner JA. MyoD protein accumulates in satellite cells and its neurally regulated in regenerating myotubes and skeletal muscle fibers[J]. Dev Dyn,1995,202:244-254.
[115]Friden J, Lieber RL. Segmental muscle fiber lesions after repetitive eccentric contractions[J]. Cell Tissue Res,1998,293:165-171.
[116]Lieber RL, Shah S, Friden J. Cytoskeletal disruption after eccentric contraction-induced muscle injury[J]. Clin Orthop,2002,403:90-99.
[117]Barash IA, Peters D, Friden J, et al. Desmin cytoskeletal modifications after a bout of eccentric exercise in the rat[J]. Am J Physiol Regul Integr Comp Physiol, 2002,283:958-963.
[118]Lieber RL, Friden J. Mechanisms of muscle injury gleaned from animal models[J]. Am J Phys Med Rehabil,2002,81(11 Suppl):70-79.
[119]Peters D, Barash IA, Burdi M, et al. Asynchronous functional, cellular and transcriptional changes after a bout of eccentric exercise in the rat[J]. J Physiol,2003, 553(3):947-957.
[120]Partanen JV, Ojala TA, Arokoski JP. Myofascial syndrome and pain:A neurophysiological approach. Pathophysiology,2010,7(1):19-28.
[121]Ge HY, Fernandez-de-Las-Penas C, etal. Myofascial trigger points:spontaneous electrical activity and its consequences for pain induction and propagation. Chin Med, 2011,25,6:13.
[122]Gissel H. The role of Ca2 in muscle cell damage. Ann N Y Acad Sci 2006,1066: 166-180.
[123]McBride TA, Stockert BW, Gorin FA, etal. Stretch-activated ion channels contribute to membrane depolarization after eccentric contractions. J Appl Physiol 2000,88:91-101.
[124]Chung Jw, Ohrbach R, McCall WD. Effect of increased sympathetic activity on electrical activity from myofascial painful areas. Am J Phys Med Rehabil,2004, 83(11):842-850.
[125]Chen WK, Liu IY, Chang YT, etal. Cav3.2 T-Type Ca2+ Channel-Dependent Activation of ERK in Paraventricular Thalamus Modulates Acid-Induced Chronic Muscle Pain. J Neurosci,2010,30(31):10360-8.
[126]Cordero MD, De Miguel M, Moreno Fernandez AM, etal. Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients:implications in the pathogenesis of the disease. Arthritis Res Ther.2010, 12(1):R17. Epub 2010 Jan 28.
[127]Lieber RL, Friden J. Mechanisms of Muscle Injury Gleaned from Animal Models. Am J Phys Med Rehabil.2002,81(11 Suppl):70-79.
[2]Partanen J V, Ojala T A, Arokoski J P. Myofascial syndrome and pain:A neurophysiological approach [J]. Pathophysiology,2010,17(1):19-28.
[3]Hong CZ. Myofascial Pain Therapy[J]. J Musculoskel Pain,2004,12(3):37-43.
[4]Hong CZ. Pathophysiology of myofascial trigger point[J]. J Formos Med Assoc, 1996,95(2):93-104.
[5]Simons DG, Travell JG, Simons LS. Travell and Simons' myofascial pain and dysfunction:the trigger point manual[M]. Volume 1:upper half of body.2nd ed. Baltimore:Williams & Wilkins,1999.71-72.
[6]Lucas KR, Polus BI, Rich PS. Latent myofascial trigger points:Their effect on muscle activation and movement efficient [J]. J Bodywork Mov Ther,2004,8(3): 160-166.
[7]Weissmann RD. Uberlegungen zur Biomechanik in der Myofaszialen Triggerpunkttherapie [German; Considerations with regard to the biomechanics related to myofascial trigger point therapy [J]. Physiotherapie 2000; 35(10):13-21.
[8]黄强民.肌筋膜触发点及肌筋膜疼痛综合征[J].颈腰痛杂志,2004,25(5)：360-362.
[9]姚明华,黄强民.肌筋膜触发点疼痛的实验动物模型研究[J].中国运动医学,2009,28(4)：415-418.
[10]Dommerholt J, Bron C, Franssen J. Myofascial trigger points:an evidence-informed review [J]. The Journal of Manual & Manipulative Therapy,2006, 14(4):203-221.
[11]Hagg G M. The Cinderella Hypothesis. In:Johansson H, et al, eds. Chronic Work-Related Myalgia [M]. Gavle, Sweden:Gavle University Press,2003:127-132.
[12]Larsson B, Bjork J, Kadi F, et al. Blood supply and oxidative metabolism in muscle biopsies of female cleaners with and without myalgia [J]. Clin J Pain 2004, 20(6):440-446.
[13]Gissel H. Ca2+ accumulation and cell damage in skeletal muscle during low frequency stimulation [J]. Eur J Appl Physiol 2000,83(2-3):175-180.
[14]Febbraio M A, Pedersen B K. Contraction-induced myokine production and release:Is skeletal muscle an endocrine organ? [J]. Exerc Sport Sci Rev 2005.33(3): 114-119.
[15]Pedersen B K, Febbraio M. Muscle-derived interleukin-6:A possible link between skeletal muscle, adipose tissue, liver, and brain [J]. Brain Behav Immun. 2005,19(5):371-376.
[16]Treaster D, Marras W S, Burr D, Sheedy J E, Hart D. Myofascial trigger point development from visual and postural stressors during computer work [J]. J Electromyogr Kinesiol,2006,16(2):115-124.
[17]Otten E. Concepts and models of functional architecture in skeletal muscle [J]. Exerc Sport Sci Rev,1988,16:89-137.
[18]Simons D G. Understanding effective treatments of myofascial trigger points [J]. J Bodywork Mov Ther.2002,6:81-88.
[19]Dommerholt J, Royson M W, Whyte-Ferguson L. Neck pain and dysfunction following whiplash [M]. In:Whyte-Ferguson L, Gerwin RD, eds. Clinical Mastery of Myofascial Pain Syndrome. Baltimore, MD:Lippincott, Williams&Wilkins,2005: 57-89.
[20]Schuller E, Eisenmenger W, Beier G. Whiplash injury in low speed car accidents [J]. J Musculoskeletal Pain.2000,8(1/2):55-67.
[21]Gerwin R D, Dommerholt J. Myofascial trigger points in chronic cervical whiplash syndrome [J]. J Musculoskeletal Pain.1998,6(Suppl.2):28.
[22]Fernandez-de-las-Penas C, Fernandez-Carnero J, Palomeque-del-Cerro L, et al. Manipulative treatment vs. conventional physiotherapy treatment in whiplash injury: A randomized controlled trial [J]. J Whiplash Rel Disord.2004,3(2):73-90.
[23]Scott D, Jull G, Sterling M. Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain [J]. Clin J Pain.2005,21(2):175-181.
[24]Simons D G. Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal pain and dysfunction [J]. J Electromyogr Kinesiol.2004,14(1): 95-107.
[25]Gerwin R D, Dommerholt J, Shah J. An expansion of Simons' integrated hypothesis of trigger point formation [J]. Curr Pain Headache Rep.2004,8(6): 468-475.
[26]Kawakita K, Itoh K, Okada K. Experimental model of trigger points using eccentric exercise [J]. J Musculoskeletal Pain,2008,16(1-2):29-35.
[27]Mense S. The pathogenesis of muscle pain [J]. Curr Pain Headache Rep,2003, 7(6):419-425.
[28]Shah J P, Phillips T M, Danoff J V, et al. An in-vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle [J]. J Appl Physiol.2005,99(5):1980-1987.
[29]Fernandez-de-las-Penas C, Alonso-Blanco C, Cuadrado ML, et al. Trigger points in the suboccipital muscles and forward head posture in tension-type headache[J]. Headche,2006,46:454-460.
[30]Gerwin R D. A review of myofascial pain and fibromyalgia:Factors that promote their persistence [J]. Acupunct Med.2005,23(3):121-134.
[31]Gerwin RD. Factores que promueven la persistencia de mialgia en el sindrome de dolor miofascial y en la fibromyalgia [Spanish; Factors that promote the continued existence of myalgia in myofascial pain syndrome and fibromyalgia[J]. Fisioterapia 2005; 27(2):76-86.
[32]Andres E, Loukili N H, Noel E, et al. Vitamin B12 (cobalamin) deficiency in elderly patients [J]. CMAJ,2004,171(3):251-259.
[33]Gerwin R. A study of 96 subjects examined both for fibromyalgia and myofascial pain (abstract)[J]. J Musculoskeletal Pain 1995; 3 (Suppl 1):121.
[34]Pruthi RK, Tefferi A. Pernicious anemia revisited[J]. Mayo Clin Proc 1994; 69: 144-150.
[35]Kadi F, Waling K, Ahlgren C, et al. Pathological mechanisms implicated in localized female trapezius myalgia[J]. Pain 1998;78:191-196.
[36]Plotnikoff G A, Quigley J M. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain [J]. Mayo Clin Proc,2003,78(12): 1463-1470
[37]Dommerholt J, Issa T. Differential diagnosis:Myofascial pain [M]. In:Chaitow L, ed. Fibromyalgia Syndrome:A Practitioner's Guide to Treatment. Edinburgh, UK: Churchill Livingstone,2003:149-177
[38]Lewis C, Gevirtz R, Hubbard D, et al. Needle trigger point and surface frontal EMG measurements of psychophysiological responses in tension-type headache patients[J]. Biofeedback & Self-Regulation 1994; 3:274-275.
[39]McNulty WH, Gevirtz RN, Hubbard DR, et al. Needle electromyographic evaluation of trigger point response to a psychological stressor[J]. Psychophysiology 1994; 31:313-316.
[40]Banks SL, Jacobs DW, Gevirtz R, et al. Effects of autogenic relaxation training on electromyographic activity in active myofascial trigger points[J]. J Musculoskeletal Pain 1998; 6(4):23-32.
[41]Linton SJ. A review of psychological risk factors in back and neck pain[J]. Spine 2000; 25:1148-1156.
[42]Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain:A state of the art[J]. Pain 2000; 85:317-332.
[43]Menefee LA, Cohen MJ, Anderson WR, et al. Sleep disturbance and nonmalignant chronic pain:A comprehensive review of the literature [J]. Pain Med 2000; 1:156-172.
[44]Hubbard DR, Berkoff GM. Myofascial trigger points show spontaneous needle EMG activity[J]. Spine,1993,18(13):1803-1807.
[45]Kuan TS, Hsieh YL, Chen SM, et al. The myofascial trigger point region: correlation between the degree of irritability and the prevalence of endplate noise[J]. Am J Phys Med Rehabil,2007,86(3):183-189.
[46]McPartland JM, Simons DG.Myofascial trigger points:translating molecular theory into manual therapy[J]. J Man Manipulative,2006,14(4):232-239.
[47]Kuan TS, Chen SM, Chien CH, et al. Effect of botulinum toxin on endplate noise in myofascial trigger spots of rabbit skeletal muscle[J]. Am J Phys Med Rehabil.2002, 81(7):512-520.
[48]Mense S, Simons DG, Hoheisel U, et al. Lesion of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation[J]. J ApplPhysiol,2003, 94(4):2494-2501.
[49]Gerwin RD, Dommerholt J, shal JP. An expansion of Simons' intergrated hypothesis of trigger point formation[J]. Curr Pain Headache Rep,2004,8(6): 468-475.
[50]Sluka KA, Kalra A, Moore SA. Unilateral intramuscular injections of acidic saline produce a bilateral, long-lasting hyperalgesia[J]. Muscle Nerve,2001,24(1): 37-46.
[51]Wang X, Li Y, Engisch KL, et al. Activity-dependent presynaptic regulation of quantal size at the mammalian neuromuscular junction in vivo[J]. J Neurosci,2005, 25(2):343-351.
[52]Nakanishi ST, Cope TC, Rich MM, et al. Regulation of motoneuron excitability via motor endplate acetylcholine receptor activation[J]. J Neurosci,2005,25(9): 2226-2232.
[53]Butler DS. The sensitive Nervous System[M]. Adelaide, Austrlia:Noigroup Publications,2000.
[54]Chaitow L, Morrison S, Baldary P, et al. Fibromyalgia syndrome:a practitioner's guide to treatment[M].2nd ed. North Thames(West), UK:Churchill Livingstone,2003. 16-16.
[55]Chaitow L, Morrison S, Baldary P, et al. Fibromyalgia syndrome:a practitioner's guide to treatment[M].2nd ed. North Thames(West), UK:Churchill Livingstone,2003. 15-15.
[56]Bruckle W, Suckfull M, Fleckenstein W, et al. Gewebe-pO2-Messung in der verspanntenRuckenmuskulatur(m.erectorspinae)[J]. Z Rheumatol,1990,49(4): 208-216.
[57]Giniatullin RA, Sokolova EM. ATP and adenosine inhibit transmitter release at the frog neuromuscular junction through distinct presynaptic receptors[J]. Br J Pharmacol,1998; 124(4):839-844.
[58]Hong CZ. New trends in myofascial pain syndrome[J]. Chin Med J (Taipei),2002, 65(11),501-512.
[59]Bukharaeva EA, GainulovRKh, Nikol'skii EE. The effects of noradrenaline on the amplitude-time characteristics of multiquantum endplate currents and the kinetics of induced secretion of transmitter quanta[J]. NeurosciBehav Physiol.2002,32(5): 549-554.
[60]Chen JT, Chen SM, Kuan TS, et al. Phentolamine effect on the spontaneous electrical activity of active loci in a myofascial trigger spot of rabbit skeletal muscle[J]. Arch Phys Med Rehabil,1998,79(7):790-794.
61 Delaney JP, Leong KS, Watkins A. et al. The short-term effects of myofascial trigger point massage therapy on cardiac autonomic tone in healthy subjects. J AdvNurs,2002,37(4):364-371.
[62]黄强民,敖丽娟,刘燕.肌筋膜触发点疼痛特征的要点分析[J].中国临床康复杂,2004,8(23)：4822-4824.
[63]Butler DS. The Sensitive Nervous System[M]. Adelaide, Australia:Noigroup Publications,2000.
[64]Mense S. Biochemical pathogenesis of myofascial pain [J]. J Musculoskeletal Pain,1996,4(1-2):145-162.
[65]Shah JP, Gilliams EA. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis:An application of muscle pain concepts to myofascial pain syndrome [J]. J Bodywork Movement Ther,2008,12(4):371-384.
[66]Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points [J]. Arch Phys Med Rehabil,2008,89(1):16-23.
[67]Simons DG. Review of microanalytical in vivo study of biochemical milieu of myofascial trigger points [J]. J Bodywork Mov Ther,2006,10(1):10-11.
[68]Shah JP. Uncovering the biechemical milieu of myofascial trigger points using in vivo microdialysis [J]. J Musculoskeletal Pain,2008,16(1-2):17-20.
[69]Itoh K, Kawakita K:Effect of indomethacin on the development of eccentric exercise-induced localized sensitive region in the fascia of rabbit [J]. Jpn J Physiol, 2002,52(2):173-180.
[70]韩济生.神经科学[M].第3版.北京：北京大学医学出版社,2008.
[71]鞠躬,吕国蔚,王百忍.神经生物学(供研究生用).北京：人民卫生出版社,2004.
[72]Butler DS. The sensitive Nervous System [M]. Adelaide, Austrlia:Noigroup Publications,2000.
[73]Chaitow L, Morrison S, Baldary P, et al. Fibromyalgia syndrome:a practitioner's guide to treatment [M].2nd ed. North Thames(West), UK:Churchill Livingstone, 2003.
[74]Hoheisel U, Koch K, Mense S. Functional reorganization in the rat dorsal horn during an experimental myositis [J]. Pain,1994,59(1):111-118.
[75]Young BO, Dubo HY, Fisher AA, et al.肌筋膜痛综合征基于脊髓节段性敏感的诊断和治疗(一)[J].中国康复理论与实践,2009,15(6)：589-590.
[76]Young BO, Dubo HY, Fisher AA, et al.肌筋膜痛综合征基于脊髓节段性敏感的诊断和治疗(二)[J].中国康复理论与实践,2009,15(7)：691-693.
[77]Issberner U, Reeh PW. Steen KH. Pain due to tissue acidosis:a mechanism for inflammatory and ischemic myalgia? [J]. Neuroscience Letters,1996,208(3): 191-194.
[78]Ambalavanar R. Dessem D, Moutanni A, et al. Muscle inflamma- tion induces a rapid increase in calcitonin gene-related peptide(CGRP)mRNA that temporally relates to CGRP immunoreactivity and nociceptive behavior [J]. Neuroscience,2006,143(3): 875-884.
[79]Luo G, Hershko DD, Robb BW, et al. IL-lbeta stimulates IL-6 production in cultured skeletal muscle cells through activation of MAP kinase signaling pathway and NF-kappa B [J]. Am J Physiol Regul Integr Comp Physiol.2003,284(5): 1249-1254.
[80]Tough E A, White A R, Cummings T M, et al. Acupuncture and dry needling in the management of myofascial trigger point pain:A systematic review and meta-analysis of randomized controlled trials [J]. Eur J Pain.2009,13(1):3-10.
[81]Tough E A, White A R, Richards S, et al. Variability of criteria used to diagnose myofascial trigger point pain syndrome-evidence from a review of the literature [J]. Clin J Pain,2007,23(3):278-86.
[82]Lavelle E D, Lavelle W, Smith H S. Myofascial trigger points [J]. Anesthesiology, 2007,25(4):841-851.
[83]黄强民,庄小强,谭树生.肌筋膜疼痛触发点的诊断与治疗[M].广西：广西科学技术出版社,2010：202-203.
[84]Kiralp M Z, Uzun G, Dincer U, et al. A Novel Treatment Modality for Myofascial Pain Syndrome:Hyperbaric Oxygen Therapy [J]. J Nati Assoc,2009,101(1):77-80.
[85]Baldry P. Management of myofascial trigger point pain [J]. Acupunct Med,2002, 20(1):2-10.
[86]Harden R N, Cottrill J, Gagnon C M, et al. Botulinum toxin A in the treatment of chronic tension-type headache with cervical myofascial trigger points:A randomized, double-blind, placebo-controlled pilot study [J]. Headache,2009,49(5):732-743.
[87]McPartland J M, Brodeur R, Hallgren R C. Chronic neck pain, standing balance, and suboccipital muscle atrophy [J]. J Manipulative Physiol Ther 1997,20(1):24-29.
[88]Katsura M, Mohri Y, Shuto K, et al. Up-regulation of L-type uoltage-dependent calcium channels after long-term exposure to nicotine in cerebral cortical neurons [J]. J Biol Chem 2002,277(10):7979-7988.
[89]Berger J. Vermont DO urges peers to learn about herbal medicine [J]. The DO, 1999,40(3):58-60.
[90]Re L, Barocci S, Sonnino S, et al. Linalool modifies the nicotinic receptor-ion channel kinetics at the mouse neuromuscular junction [J]. Pharmacol Res,2000,42(2): 177-182.
[91]陈疾忤,陈世益,李云霞.骨骼肌钝挫伤后肌电检测的应用研究[J].中华物理医学有康复杂志,2005,27(1)：23-25.
[92]徐建鸣.疼痛管理概述[J].上海护理,2002,2(4)：56-57.
[93]Itoh K, Okada K, Kawakita K. A proposed experimental model of myofascial trigger points in human muscle after slow eccentric exercise[J]. Acupunct Med,2004, 22(1):2-13.
[94]Kawakita K, Itoh K, Okada. Experimental model of trigger points using eccentric exercise[J]. J Musculoskeletal Pain,2008,16(1-2):29-35.
[95]Mense S. Pathophysiologic basis of muscle pain syndromes[M]. In:Fischer AA, ed. Myofascial Pain:Update in Diagnosis and Treatment. Philadelphia, PA:W.B. Saunders Company,1997:23-53.
[96]Itoh K, Okada K, Kawakita K. A proposed experimental model of myofascial trigger points in human muscle after slow eccentric exercise[J]. Acupunct Med,2004, 22(1):2-13.
[97]Ficton JR, Auvinen MD, Dykstra D et al. Myofascial pain syndrome: Electromyographic changes associated with local twitch response[J]. Arch Phys Med Rehabil,1985,66:314-317.
[98]Kawakita K, Gotoh K. Role of polymodal receptors in the acupuncture-mediated endogenous pain inhibitory systems[M]. In:Kumazawa I, Kruger L, Mizumura K, editors, Prog Brain Res 113. Amsterdam:Elsevier,1996:507-523.
[99]Gerwin RD, Shannon S, Simons DG, et al. Identification of myofascial trigger points:interrater agreement and effect of training[J]. Pain,1997:69:65-73.
[100]Simons DG, Travell JG. Myofascial trigger points, a possible explanation[J]. Pain,1981,10:106-109.
[101]Mense S. Considerations concerning the neurobilogical basis of muscle pain[J]. Pain,1991,69:610-616.
[102]Gerwin RD, Duranleau D. Ultrasound identification of the myofascial trigger point[J]. Muscle Nerve,1997,20:767-768.
[103]Hong CZ. Persistence of local twitch response with loss of conduction to and from the spinal cord[J]. Arch Phys Med Rehabil,1994,75:12-16.
[104]Hong C-Z, Yu J. Spontaneous electrical activity of rabbit trigger spot after transection of spinal cord and peripheral nerve[J]. J Musculoskeletal Pain,1998,6(4): 45-58.
[105]Wang F, Audette J. Electrophysiological characteristics of the local twitch response with active myofascial pain of neck compared with a control group with latent trigger points [J]. Am J Phys Med Rehabil,2000,79:203.
[106]Hong CZ. Myofascial trigger points:Pathophysiology and correlation with acupuncture[J]. Acup Med 2000,18:41-47.
[107]姚泰,曹济民,樊小力等.生理学[M].北京：人民卫生出版社.第2版,2010.
[108]Jun Kimura著,郭铁城,朱愈译.神经肌肉疾病电诊断(原理与实践)[M].第3版.天津：天津科技翻译出版公司,2008.
[109]李作汉,张平.神经肌肉疾病的临床与病理[M].北京：人民卫生出版社,2007.
[110]Mense S, Simons DG, Russell IJ原著,郭传友主译.肌痛[M].北京： 人民卫生出版社,2005.
[111]Dubowitz V, Sewry CA原著,袁云主译.肌肉活检[M].第3版.北京：北京大学医学出版社,2009.
[112]沈燕国,徐建光,顾玉东等.成肌调节因子Myogenin和MRF4在人体失神经骨骼肌中的表达及其临床意义[J].中华手外科杂志,200218(3)：177-180.
[113]Rodrigues S, Schmalbruch L. Satellite cells and myonuclei in long-term denervated rat muscle[J]. Anat Rec,1995,243:430-437.
[114]Koishi CA, Lu DX, Faulkner JA. MyoD protein accumulates in satellite cells and its neurally regulated in regenerating myotubes and skeletal muscle fibers[J]. Dev Dyn,1995,202:244-254.
[115]Friden J, Lieber RL. Segmental muscle fiber lesions after repetitive eccentric contractions[J]. Cell Tissue Res,1998,293:165-171.
[116]Lieber RL, Shah S, Friden J. Cytoskeletal disruption after eccentric contraction-induced muscle injury[J]. Clin Orthop,2002,403:90-99.
[117]Barash IA, Peters D, Friden J, et al. Desmin cytoskeletal modifications after a bout of eccentric exercise in the rat[J]. Am J Physiol Regul Integr Comp Physiol, 2002,283:958-963.
[118]Lieber RL, Friden J. Mechanisms of muscle injury gleaned from animal models[J]. Am J Phys Med Rehabil,2002,81(11 Suppl):70-79.
[119]Peters D, Barash IA, Burdi M, et al. Asynchronous functional, cellular and transcriptional changes after a bout of eccentric exercise in the rat[J]. J Physiol,2003, 553(3):947-957.
[120]Partanen JV, Ojala TA, Arokoski JP. Myofascial syndrome and pain:A neurophysiological approach. Pathophysiology,2010,7(1):19-28.
[121]Ge HY, Fernandez-de-Las-Penas C, etal. Myofascial trigger points:spontaneous electrical activity and its consequences for pain induction and propagation. Chin Med, 2011,25,6:13.
[122]Gissel H. The role of Ca2 in muscle cell damage. Ann N Y Acad Sci 2006,1066: 166-180.
[123]McBride TA, Stockert BW, Gorin FA, etal. Stretch-activated ion channels contribute to membrane depolarization after eccentric contractions. J Appl Physiol 2000,88:91-101.
[124]Chung Jw, Ohrbach R, McCall WD. Effect of increased sympathetic activity on electrical activity from myofascial painful areas. Am J Phys Med Rehabil,2004, 83(11):842-850.
[125]Chen WK, Liu IY, Chang YT, etal. Cav3.2 T-Type Ca2+ Channel-Dependent Activation of ERK in Paraventricular Thalamus Modulates Acid-Induced Chronic Muscle Pain. J Neurosci,2010,30(31):10360-8.
[126]Cordero MD, De Miguel M, Moreno Fernandez AM, etal. Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients:implications in the pathogenesis of the disease. Arthritis Res Ther.2010, 12(1):R17. Epub 2010 Jan 28.
[127]Lieber RL, Friden J. Mechanisms of Muscle Injury Gleaned from Animal Models. Am J Phys Med Rehabil.2002,81(11 Suppl):70-79.