-腰痛和腰椎间盘突出症(英文)-（PPT课件）.ppt

1、腰痛和腰椎腰痛和腰椎间盘突出症间盘突出症lStructural support and balance for upright posturelProtection Spinal cord and nerve rootsInternal organslFlexibility of motion in six degrees of freedomLeft and RightSide BendingFlexion and ExtensionLeft and Right RotationlCranial - the head or towards the headlCaudal - the tail

2、 or towards the taillAnterior - the front section or towards the frontlPosterior - the back section or towards the backlVentral - the front or anterior surfacelDorsal - the back or posterior surfaceCranialCaudalAnteriorPosteriorDorsal VentrallPedicle notchesSlight NotchDeep NotchIntervertebral Foram

3、enlIntervertebral foramenlNerve roots exitBodyPedicleLaminaSuperior Articular ProcessSpinousProcessTransverse ProcessVertebral ForamenlBody - L1 to L5 progressive increase in masslPedicles - longer and wider than thoracic; oval shapedlSpinous processes - horizontal, square shapedlTransverse processe

4、s - smaller than in thoracic regionlSpinal foramen- large to allow for cauda equina and nerve rootslIntervertebral foramen - large, but with increased incidence of nerve root compressionlIntervertebral DisclEnd PlatelApophyseal RingCartilaginousBonylThe FUNCTIONAL UNITFUNCTIONAL UNIT of the spinelCo

5、mprised of:Two adjacent vertebraeIntervertebral discConnecting ligamentsTwo facet joints and capsuleslFibrocartilaginous joint of the motion segmentlMakes up the length of the spinal columnlPresent at levels C2-C3 to L5-S1lAllows compressive, tensile, and rotational motionlLargest avascular structur

6、es in the bodylAnnulus FibrosusOuter portion of the discLamellaelGreat tensile strengthMade up of lamellaeAnnulus FibrosusLayers of collagen fiberslArranged obliquely 30 lReversed contiguous layerslNucleus PulposusNucleus PulposusInner structureGelatinousHigh water contentResists axial forceslLarges

7、t avascular structurelBlood supply by diffusion through end plateslDamage to the blood supply leads to degradation of the discThe Vertebral Body (VB)lKey RolesCarry 80% of the axial loads through VB and discEndplates enable nutrition to diffuse to discHas two rolesShock absorber of axial forcesPivot

8、 point in motion segmentLigamentum flavumPosterior longitudinal ligamentAnterior longitudinal ligamentlBands or sheets of tough, fibrous tissue that connect bones, cartilage, or other structureslBecome active when stressed to maximum range of motionlProtect the joints from being hyperflexedTwo major

9、 components of IVDAnnulus fibrosis: thick, fibrous “radial tire”LamellaeNucleus pulposus: ball-like gelBy age 50, 95% of people show lumbar disc degenerationlNot all have symptomslSignificant changes to IVD are:Water and proteoglycan content decreasesCollagen fibers of AF become distortedTears may o

10、ccur in the lamellaelResults in:Disc loses height and volumeLoses resistance to loading forceslNo longer acts as a shock absorberlThe motion segment is the functional unit of the spine and consists ofMuscle (activators)Ligaments (passive restraints)Adjacent vertebral bodies A 3-joint complex of two

11、facet joints and a disc (pivots)lDegeneration can begin in one or more of these joints, but ultimately all three will be affectedProvide an overview of degenerative conditionsDegenerative DiseaseSpinal StenosisHerniated DisclLoss of normal tissue structure and function due to aging processlChanges a

12、re usually gradual, trauma sometimes accelerateslDegenerative changes do not always lead to clinical symptomslWhen changes cause symptoms (often pain), the process is referred to as osteoarthritislSpondylosis is degenerative changes in the spineThe Vertebral Body (VB)lDegenerative ChangesSclerosis:

13、Increased bone formation adjacent to endplateslReduces nutrition diffusing to disclStiffens endplate, and reduces ability to absorb loadsOsteophytes: Formation of small bony spurslCan project into neuro structuresKey RolesCarry 20% of compressive loadsHelp stabilize spinelDegenerative ChangesCartila

14、ge lining loses water contentCartilage wears awayFacets override each otherLeads to abnormal function of motion segmentLigaments and MuscleslLigaments attach bone to boneProvide stability, enable normal motionlDegenerative ChangesPartial ruptures, necrosis and calcificationsNegatively impact functio

15、n of motion segmentlChanges include:Disc loses height and volumeCompressive loads transfer away from nucleus to margins Sclerosis of endplate reduces disc nutritionFacet joints wear away cartilage, begin to overrideMotion segment becomes hypermobileOsteophytes develop to attempt to stabilize motion

16、segmentOsteophytes may encroach on neuro structureslNarrowing of the spinal canal and/or lateral foramen through which the nerves travellThree types:Central stenosis: in central spinal canal where cord or cauda equina are locatedLateral recess stenosis: in the tract where nerve roots exit canalAcqui

17、red: in lateral foramen where nerve roots exit to bodylMost frequent in lower cervical and lower lumbar spinelOften called “ruptured disc”lVery common pathologylL3-4, L4-5, L5-S1 common locationslThought to be a culmination of acute traumatic events to the disc Nuclear herniation: nucleus ruptures.

18、No disruption of outer annular fiberslDisc protrusion: ruptured nucleus causes outer fibers to bulgelNuclear extrusion: Complete split in annulus. Material leaks but remains attached to nucleuslSequestered nucleus: Leaked substance no longer attached to nucleuslThe back and leg pain since - Greeks r

19、ecognized it.lIn the fifth century AD Aurelianus clearly described the symptoms of sciatica. lThe sciatica arose from either hidden causes or observable causes- a fall, a violent blow, pulling, or straining. lThe most notable of these is the Lasgue sign, or straight-leg raising test, described by Fo

20、rst in 1881 but attributed to Lasgue, his teacher. This test was devised to distinguish hip disease from sciatica.lMixter and Barr in their classic paper published in 1934 again attributed sciatica to lumbar disc herniation.lRuptured discs are among the most common and painful of all back ailments.

21、lThe condition occurs when the outer cover of a disc is torn and the soft inner tissue extrudes. The extrusion often puts pressure on the spinal nerves, causing back and leg pain which can be severe.l腰椎间盘突出症是因椎间盘变性，纤维环破裂，髓核腰椎间盘突出症是因椎间盘变性，纤维环破裂，髓核突出刺激或压迫神经根、马尾神经所表现的一种综合突出刺激或压迫神经根、马尾神经所表现的一种综合征。征。lIt

22、usually occurs in the L4/5 or L5/S1 intervertebral disc regions and is most often seen on only one side but may be bilateral. lIt may occur in other regions, especially at the L3/4 level, and occasionally disc protrusion may occur at more than one level simultaneously.lIt is often due to degeneratio

23、n of the disc and therefore occurs most commonly in middle or old age.lDegeneration of the annulus fibrosus allows the nucleus pulposus to herniate throughl压迫改变神经根的传导、营养状态，通过压迫改变神经根的传导、营养状态，通过影响局部血运和脑脊液的营养，影响局部血运和脑脊液的营养，l机械直接损伤神经内部，神经根受压变形，机械直接损伤神经内部，神经根受压变形，有张力，压迫神经根可引传导性损伤，功有张力，压迫神经根可引传导性损伤，功能改变。能

24、改变。l同周围神经一样，单纯压迫不引起根痛，同周围神经一样，单纯压迫不引起根痛，没有炎症和刺激因素压迫只产生感觉缺失，没有炎症和刺激因素压迫只产生感觉缺失，运动无力，反射异常，但无痛。如有化学运动无力，反射异常，但无痛。如有化学炎症和代谢因素产生炎性反应存在炎症和代谢因素产生炎性反应存在l压力从压力从1013.33kPa引起了神经传导功能的逐引起了神经传导功能的逐渐减弱。其中，传入神经传导功能的减弱更加渐减弱。其中，传入神经传导功能的减弱更加明显，而去压迫后，运动神经能更加容易和迅明显，而去压迫后，运动神经能更加容易和迅速地恢复到几乎正常的速地恢复到几乎正常的CMAP水平。水平。l压迫在压迫在

25、26.67kPa时，引起了神经传导功能的迅时，引起了神经传导功能的迅速减弱，而且去压迫后传入神经几乎没有恢复，速减弱，而且去压迫后传入神经几乎没有恢复，传出神经仍有传出神经仍有30%40%的恢复。将压迫时间的恢复。将压迫时间从从2h延长到延长到4h，对神经恢复能力的影响更加对神经恢复能力的影响更加明显明显3。lHowe发现背根节对中度压迫极发现背根节对中度压迫极度敏感，当压力解除后感觉神度敏感，当压力解除后感觉神经释放的信号可持续经释放的信号可持续25分钟。分钟。l从神经生理学角度背根节是特从神经生理学角度背根节是特有的、有的、“捣鬼捣鬼”的疼痛源，突的疼痛源，突出椎间盘能挤压它出椎间盘能挤压

26、它l对于周围神经来说，当刺激解对于周围神经来说，当刺激解除后，神经冲动马上停止除后，神经冲动马上停止.实验结果背根节在尼龙线牵拉产生实验结果背根节在尼龙线牵拉产生60秒的发电，秒的发电，而玻璃棒压迫会产生而玻璃棒压迫会产生4分钟的冲动分钟的冲动l背根节的神经细胞与突触相交背根节的神经细胞与突触相交处的细胞膜上有高密度的钠通处的细胞膜上有高密度的钠通道，使其对机械压力特别敏感。道，使其对机械压力特别敏感。l这种高密度的钠通道可能是导这种高密度的钠通道可能是导致神经冲动持续，在背根节受致神经冲动持续，在背根节受压时产生生骨神经痛压时产生生骨神经痛.lOlmarker等应用不同的化学标记物来等应用不

27、同的化学标记物来研究压力的大小和压迫发生的速度与研究压力的大小和压迫发生的速度与水肿形成和营养障碍的关系。水肿形成和营养障碍的关系。l结果提示，压迫产生越迅速，神经根结果提示，压迫产生越迅速，神经根水肿的形成和营养供给障碍越明显。水肿的形成和营养供给障碍越明显。l与与DRG不同，背根对机械压力不是始终有不同，背根对机械压力不是始终有反应，除非神经根有炎性或处可易惹状态。反应，除非神经根有炎性或处可易惹状态。lHowe在被铬肠线结扎神经根后可以引出多在被铬肠线结扎神经根后可以引出多次发电的情况，单一压迫刺激即可引次发电的情况，单一压迫刺激即可引A、d神经纤维放电神经纤维放电5-30秒。秒。l被刺

28、激的神经根是有鞘神位由可能含有神被刺激的神经根是有鞘神位由可能含有神经末梢。经末梢。Jang发现了猫的发现了猫的S1背根中有点状背根中有点状直接受刺激区直接受刺激区l最有效的机械刺激是轻度牵拉，最有效的机械刺激是轻度牵拉，与临床情况相吻合。与临床情况相吻合。l有病间盘水平的神经根比邻近有病间盘水平的神经根比邻近正常的神经根更敏感正常的神经根更敏感lKuslich在局麻下椎间盘手术中，在局麻下椎间盘手术中，对有炎症或压迫的神经根压迫对有炎症或压迫的神经根压迫特别敏感，压迫它再现坐骨神特别敏感，压迫它再现坐骨神经痛经痛lSmyth用尼龙线绕过受累神经用尼龙线绕过受累神经根，轻拉即再现坐骨神经痛的根

29、，轻拉即再现坐骨神经痛的 损伤和炎症的组织释放的化学介质损伤和炎症的组织释放的化学介质使神经末梢致敏。使神经末梢致敏。l这些神经致敏物质包括由这些神经致敏物质包括由C纤维释纤维释放出的放出的P物质、物质、11氨基酸神经肽。氨基酸神经肽。lP物质导致血管扩张，血浆外渗，物质导致血管扩张，血浆外渗，肥大细胞释放组胺。肥大细胞释放组胺。l这些炎性介质的持续释放引起了疼这些炎性介质的持续释放引起了疼痛。痛。l虽然原因还不清楚，虽然原因还不清楚，P物质可能直物质可能直接作用神经末梢或间接通过血管扩接作用神经末梢或间接通过血管扩张，释放组胺、血浆外渗起作用。张，释放组胺、血浆外渗起作用。lP物质在神经致敏

30、中起重要作用，物质在神经致敏中起重要作用，这有重临床意义，这有重临床意义，l脊柱的运动正常是无痛的，但在炎脊柱的运动正常是无痛的，但在炎症条件下引起疼痛症条件下引起疼痛l在组织损伤中产生的可以激活和致敏神经末在组织损伤中产生的可以激活和致敏神经末梢的化学介质包括：缓激肽、血清素梢的化学介质包括：缓激肽、血清素(5-HT)、组织胺、钾离子、前列腺素。组织胺、钾离子、前列腺素。l已在椎小关节及邻近组织中发现了已在椎小关节及邻近组织中发现了P物质，物质，l使用使用10-g即能同时兴奋低痛阈和高痛阈神经即能同时兴奋低痛阈和高痛阈神经纤维，纤维，l30分钟后这些神经对机械刺激的痛阈明显降分钟后这些神经对

31、机械刺激的痛阈明显降低低l当将角叉菱胶或陶土注入关节后，当将角叉菱胶或陶土注入关节后，神经纤维致敏兴奋性增加，神经纤维致敏兴奋性增加，1-2mm的各方关节活动即可导致关的各方关节活动即可导致关节支配神经的持续释放冲动电位。节支配神经的持续释放冲动电位。l最近的研究表现在神经感受器对最近的研究表现在神经感受器对机械压力敏感的部位，注入角叉机械压力敏感的部位，注入角叉菱胶，会导致神经元放电达菱胶，会导致神经元放电达3小时小时l这些研究的临床意义：如这些研究的临床意义：如果关节囊、韧带、肌肉受果关节囊、韧带、肌肉受牵拉，例如脊柱滑脱和椎牵拉，例如脊柱滑脱和椎间盘突出症，引起组织损间盘突出症，引起组织

32、损伤会导致持久的伤害性刺伤会导致持久的伤害性刺激，激，l并可以导致一种循环状态，并可以导致一种循环状态，肌肉痉挛，痛觉过敏，以肌肉痉挛，痛觉过敏，以致持续性疼痛致持续性疼痛l有关椎间盘的神经生理学有关椎间盘的神经生理学研究是有限的。研究是有限的。lCavanaugh报告了椎间盘报告了椎间盘受机械刺激时只偶有少量受机械刺激时只偶有少量冲动，只有腹侧硬膜受牵冲动，只有腹侧硬膜受牵拉才有持续冲动。拉才有持续冲动。l只有电刺激椎间盘和后纵只有电刺激椎间盘和后纵韧带引起韧带引起A-d纤维冲动，纤维冲动，同椎管内注入致痛物质，同椎管内注入致痛物质，像组胺作用一样像组胺作用一样lYamashita报告了椎间

33、盘对机械压力大部分情况是报告了椎间盘对机械压力大部分情况是没有反应。椎间盘内只有静止伤害感受器，它只没有反应。椎间盘内只有静止伤害感受器，它只对损伤或炎症产生的致痛电学物质有反应。对损伤或炎症产生的致痛电学物质有反应。lMcCarron向狗硬膜外腔注入自体的髓核，表现出向狗硬膜外腔注入自体的髓核，表现出它的致炎作用。它的致炎作用。lOlmarker 发现身体髓核在神经发现身体髓核在神经l组织中产生炎性和退行性改变组织中产生炎性和退行性改变l腰腿痛当中，原因很复杂，椎间盘突出腰腿痛当中，原因很复杂，椎间盘突出l的大小与疼痛程度不一，的大小与疼痛程度不一，l生化和机械因素交互作用。生化和机械因素交

34、互作用。l有很多证据表明髓核有致免疫原性，有很多证据表明髓核有致免疫原性，l自体髓核与血液接触，对髓核自身抗体已发现，虽然很多证自体髓核与血液接触，对髓核自身抗体已发现，虽然很多证据表明介导免疫炎性，绝大多数以前的研究都注意到椎间盘据表明介导免疫炎性，绝大多数以前的研究都注意到椎间盘退变和疼痛的产生中的免疫现象标志物。退变和疼痛的产生中的免疫现象标志物。lSaal证明突出间盘边缘有免疫细胞，发现了证明突出间盘边缘有免疫细胞，发现了T淋巴细胞淋巴细胞IL-1、2，据细胞。浸润的不同程度分级与症状相关。反应程度与术据细胞。浸润的不同程度分级与症状相关。反应程度与术前症状时间相关前症状时间相关l但病

35、人没有全身的自身免疫性疾病表现但病人没有全身的自身免疫性疾病表现, 疼痛直接原因不清。疼痛直接原因不清。l在风湿性关节炎、急性胰腺炎、血清单阴性关节炎、脓毒症表现出明显的炎症作用。它在体内的源性：l表1 PLA2 activiyu l PMN3,2l Platelet1.4l Plasma0.006l Sperm28.0l inflammatory synovial fluid 12.1l herniated lumbar disc1212.0l正常椎间盘内PLA2就有致水肿作用lSteroid局部应用非常有效，在没有免疫反应的生化炎症，局部应用非常有效，在没有免疫反应的生化炎症，作为疼痛发生

36、机制的另一个原因作为疼痛发生机制的另一个原因l髓核有介导炎性的能力，含有高浓度的髓核有介导炎性的能力，含有高浓度的PLA2。 lSaal在有腰痛病人病变节段的椎间盘组织内会有不正常高在有腰痛病人病变节段的椎间盘组织内会有不正常高浓度的磷酸激酶浓度的磷酸激酶A2-PLA2。髓核、髓核、PLA2及别的致炎物质及别的致炎物质作用到椎间盘的伤害感觉受器，它激活痛感纤维的作用比作用到椎间盘的伤害感觉受器，它激活痛感纤维的作用比单纯压力更大单纯压力更大lPLA2进入神经根后进入神经根后神经水肿，髓鞘轴突损伤，同注射神经水肿，髓鞘轴突损伤，同注射蛇毒蛇毒 PLA2，但作用程度轻，支持了但作用程度轻，支持了P

37、LA2的神经毒性的神经毒性l硬腰外使用自体髓核，发生传导阻滞，神经周围组织炎硬腰外使用自体髓核，发生传导阻滞，神经周围组织炎症症 。 lIncision of the anulus fibrosus induces nerve root morphologic, vascular, and functional changes. An experimental study.lKayama -Japan: Spine 1996 lThe nerve conduction velocity was significantly lower in the incision group (13 14 m

38、/sec) compared with the nonincision group (73 5 m/sec). lThe obvious signs of capillary stasis with an increased number and diameter of the intraneural capillaries in the incision group. lKayama -Sweden : Spine 1998 lNucleus pulposus cells and fibroblasts were cultured for 3 weeks, and various prepa

39、rations were applied to the cauda equina in 29 pigs. After 1 week, nerve conduction velocity was determined by local electrical stimulation. lApplication of nucleus pulposus cells reproduced the previously seen reduction in nerve conduction velocity induced.lKuslich在在144例椎间盘手术中，在病变椎间盘外侧检查刺激例椎间盘手术中，在

40、病变椎间盘外侧检查刺激或电刺激产生中度疼痛占或电刺激产生中度疼痛占70%，重度占，重度占30%。l突出椎间盘或狭窄的椎间只对突出椎间盘或狭窄的椎间只对DRG或突炎神经根的机械压迫或突炎神经根的机械压迫是持续的，就能导致持续性疼痛，或是持续的，就能导致持续性疼痛，或DRG或炎性神经根内压或炎性神经根内压增加这种持续性疼痛就会变为进行性加重。增加这种持续性疼痛就会变为进行性加重。lCavanaugh将自体髓核注入将自体髓核注入DRG引起引起1-3分钟的神经释放分钟的神经释放l致炎因素；直接作用伤害感受器；磷脂酶本致炎因素；直接作用伤害感受器；磷脂酶本身的直接造成神经损伤。炎症介定导致源发性神经身的

41、直接造成神经损伤。炎症介定导致源发性神经根坏死，根坏死，l体外证实体外证实PLA2直接刺激纤维环伤害感受器。直接刺激纤维环伤害感受器。l这些化学物质可直接刺激纤维环和周围神细胞中的这些化学物质可直接刺激纤维环和周围神细胞中的细小的无髓纤维细小的无髓纤维C或或Adeltal。致病物质作用后，伤害致病物质作用后，伤害感受器的痛域下降。感受器的痛域下降。l（对机械刺激）正常的生理活动就可以导致腰痛、（对机械刺激）正常的生理活动就可以导致腰痛、障碍痛、根性痛（在纤维环外障碍痛、根性痛（在纤维环外1/3后纵韧带）后纵韧带）.l临床、组织化学、生理化学、神经组织学研究，髓核含有化临床、组织化学、生理化学、

42、神经组织学研究，髓核含有化学性致炎、神经退变，急性期有神经兴奋的作用。学性致炎、神经退变，急性期有神经兴奋的作用。l同样化学物质有氢离子、同样化学物质有氢离子、PLA2免疫球蛋白免疫球蛋白G等，在椎间盘性等，在椎间盘性疼痛中，增加炎性神经根的敏感性起重要作用疼痛中，增加炎性神经根的敏感性起重要作用lOzaktay USA ：Spine 1998 JunlPhospholipase A2 appeared to be neurotoxic when doses ranging from 100 to 400 U were applied on the mechanically sensitive

43、 segments of the dorsal root ganglia. lPLA2 doses comparable to serum concentrations in human rheumatoid arthritis when applied to dorsal root ganglia. lThese results suggest that dorsal roots and dorsal root ganglion may be impaired by phospholipase A2, leading to sciatica and low back pain. l中枢致敏中

44、枢致敏l组织损伤可能导致连续的神经冲动至脊髓，这使后组织损伤可能导致连续的神经冲动至脊髓，这使后角神经元致敏角神经元致敏l致敏的神经元痛阈下降，致敏的神经元痛阈下降，l对传入冲动的反应增强，对传入冲动的反应增强，l对重复刺激的反应也增强，对重复刺激的反应也增强，l接受刺激的阈值变宽。接受刺激的阈值变宽。l恶性刺激导致中枢致敏时，有明确证据后角释放了恶性刺激导致中枢致敏时，有明确证据后角释放了兴奋性胺基酸和神经肽兴奋性胺基酸和神经肽l在中枢致敏状态下，在中枢致敏状态下，l机械刺激的致痛阈值已下降，使很低机械刺激的致痛阈值已下降，使很低的机械刺激就可以让后角发出疼痛信的机械刺激就可以让后角发出疼痛

45、信号。号。l变宽的接受阈能把损伤处及附近正常变宽的接受阈能把损伤处及附近正常组织的传入信号变为疼痛信号向上传组织的传入信号变为疼痛信号向上传递，递，l这就解释了腰疼痛位不清和持久、及这就解释了腰疼痛位不清和持久、及牵涉痛的原因牵涉痛的原因lGilleffe发现了后角单个神经发现了后角单个神经元可接受从各种脊柱组织传入元可接受从各种脊柱组织传入的信号，呈一种高度会聚接收的信号，呈一种高度会聚接收状态。状态。l脊髓后角的神经元可以由压迫脊髓后角的神经元可以由压迫皮肤、椎小关节、韧带、及肌皮肤、椎小关节、韧带、及肌肉而兴奋，这种高度会聚功能肉而兴奋，这种高度会聚功能也是腰痛不易定位的原因也是腰痛不易

46、定位的原因lHu SJ- Xian, PR China Pain 1998 JullAn experimental model in the rat.lA small stainless steel rod (0.5-0.8 mm in diameter) was inserted into the L5 intervertebral foramenlThese neurons had a greatly enhanced sensitivity to mechanical stimulation of the injured DRG and a prolonged after dischar

47、ge. la persistent heat hyperalgesia 5-35 days lThe excitatory responses were evoked in the injured, but not the uninjured, DRG neurons. lMultiple factors affect the development of back pain. lsmoking, pro-longed daily driving of motor vehicles, jobs requiring frequent repetitive lifting of heavy obj

48、ects and twisting, the use of jackhammers and machine tools, and the operation of motor vehicles episodes of anxiety and depression.lIt is more common in males than females and has a maximal incidence in the third and fourth decades of life.lBack pain may be caused by stimulation of the pain fibers

49、in the outer layers of the annulus fibrosus. lAlternatively, distortion of the posterior longitudinal ligament, which is richly innervated by pain fibers, may result in back pain. lLeg pain can result from compression of a nerve root by an HNPl腰痛可以起自于椎间盘、椎小关节、肌肉的腰痛可以起自于椎间盘、椎小关节、肌肉的神经末梢。神经末梢。l化学炎性介质释

50、放，使正常无痛的运动变为化学炎性介质释放，使正常无痛的运动变为疼痛性的。疼痛性的。l髓核是强列的神经根和神经末梢致炎和刺激髓核是强列的神经根和神经末梢致炎和刺激物质物质l椎间盘与神经根的位置、椎间盘与神经根的位置、 DRG的特殊神经生的特殊神经生理特点、神经根和理特点、神经根和DRG易被压迫而出现坐骨易被压迫而出现坐骨种经痛。种经痛。l系列恶性冲动使后角感觉神经元致敏，导致系列恶性冲动使后角感觉神经元致敏，导致的慢性疼痛状态的慢性疼痛状态lThe following are risk factors for herniated disc disease in the lumbar spine: