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1、LOWER BACK PAIN AND HERNIA OF INTERVERTEBRAL DISC,腰痛和腰椎间盘突出症,Structural support and balance for upright posture,Functions of the Spine,Protection Spinal cord and nerve roots,Functions of the Spine,Internal organs,Flexibility of motion in six degrees of freedom,Functions of the Spine,Left and RightSi
2、de Bending,Flexion and Extension,Left and Right Rotation,Cranial - the head or towards the headCaudal - the tail or towards the tailAnterior - the front section or towards the frontPosterior - the back section or towards the backVentral - the front or anterior surfaceDorsal - the back or posterior s
3、urface,Basic Terminology,Cranial,Caudal,Anterior,Posterior,Dorsal,Ventral,Vertebral Structures,Pedicle notches,Slight Notch,Deep Notch,Intervertebral Foramen,Intervertebral foramen,Nerve roots exit,Vertebral Structures,Body,Pedicle,Lamina,Superior Articular Process,SpinousProcess,Transverse Process,
4、Vertebral Foramen,Lumbar Vertebrae,Body - L1 to L5 progressive increase in mass,Pedicles - longer and wider than thoracic; oval shaped,Spinous processes - horizontal, square shaped,Transverse processes - smaller than in thoracic region,Spinal foramen- large to allow for cauda equina and nerve roots,
5、Intervertebral foramen - large, but with increased incidence of nerve root compression,Intervertebral Disc,Vertebral Structures,End Plate,Apophyseal Ring,Cartilaginous,Bony,The FUNCTIONAL UNIT of the spineComprised of:Two adjacent vertebraeIntervertebral discConnecting ligamentsTwo facet joints and
6、capsules,The Motion Segment,Fibrocartilaginous joint of the motion segmentMakes up the length of the spinal columnPresent at levels C2-C3 to L5-S1Allows compressive, tensile, and rotational motionLargest avascular structures in the body,Intervertebral Disc,Intervertebral Disc,Annulus FibrosusOuter p
7、ortion of the disc,Lamellae,Great tensile strength,Made up of lamellae,Annulus Fibrosus,Layers of collagen fibersArranged obliquely 30 Reversed contiguous layers,Intervertebral Disc,Nucleus Pulposus,Nucleus Pulposus,Inner structureGelatinousHigh water contentResists axial forces,Intervertebral Disc,
8、Largest avascular structureBlood supply by diffusion through end platesDamage to the blood supply leads to degradation of the disc,Anatomy and Degenerative Change,The Vertebral Body (VB)Key RolesCarry 80% of the axial loads through VB and discEndplates enable nutrition to diffuse to disc,Interverteb
9、ral Disc,The Intervertebral Disc,Has two rolesShock absorber of axial forcesPivot point in motion segment,Intervertebral Disc,Ligaments,Ligamentum flavum,Posterior longitudinal ligament,Anterior longitudinal ligament,Spinal Ligaments,Bands or sheets of tough, fibrous tissue that connect bones, carti
10、lage, or other structuresBecome active when stressed to maximum range of motionProtect the joints from being hyperflexed,The Intervertebral Disc and Degenerative Change,Two major components of IVDAnnulus fibrosis: thick, fibrous “radial tire”LamellaeNucleus pulposus: ball-like gel,The Intervertebral
11、 Disc (IVD) and Degenerative Change,By age 50, 95% of people show lumbar disc degenerationNot all have symptomsSignificant changes to IVD are:Water and proteoglycan content decreasesCollagen fibers of AF become distortedTears may occur in the lamellaeResults in:Disc loses height and volumeLoses resi
12、stance to loading forcesNo longer acts as a shock absorber,Overview - cont.,The 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 facet joints and a disc (pivots)Degeneration can begin
13、 in one or more of these joints, but ultimately all three will be affected,Degenerative Conditions,Provide an overview of degenerative conditionsDegenerative DiseaseSpinal StenosisHerniated Disc,Degenerative Disease - Overview,Loss of normal tissue structure and function due to aging processChanges
14、are usually gradual, trauma sometimes acceleratesDegenerative changes do not always lead to clinical symptomsWhen changes cause symptoms (often pain), the process is referred to as osteoarthritisSpondylosis is degenerative changes in the spine,Anatomy and Degenerative Change,The Vertebral Body (VB)D
15、egenerative ChangesSclerosis: Increased bone formation adjacent to endplatesReduces nutrition diffusing to discStiffens endplate, and reduces ability to absorb loadsOsteophytes: Formation of small bony spursCan project into neuro structures,Facet Joints and Degenerative Change,Key RolesCarry 20% of
16、compressive loadsHelp stabilize spineDegenerative ChangesCartilage lining loses water contentCartilage wears awayFacets override each otherLeads to abnormal function of motion segment,Anatomy and Degenerative Change,Ligaments and MusclesLigaments attach bone to boneProvide stability, enable normal m
17、otionDegenerative ChangesPartial ruptures, necrosis and calcificationsNegatively impact function of motion segment,Degenerative Disc Disease,Changes include:Disc loses height and volumeCompressive loads transfer away from nucleus to margins Sclerosis of endplate reduces disc nutritionFacet joints we
18、ar away cartilage, begin to overrideMotion segment becomes hypermobileOsteophytes develop to attempt to stabilize motion segmentOsteophytes may encroach on neuro structures,Spinal Stenosis,Narrowing of the spinal canal and/or lateral foramen through which the nerves travelThree types:Central stenosi
19、s: in central spinal canal where cord or cauda equina are locatedLateral recess stenosis: in the tract where nerve roots exit canalAcquired: in lateral foramen where nerve roots exit to bodyMost frequent in lower cervical and lower lumbar spine,Herniated Disc,Often called “ruptured disc”Very common
20、pathologyL3-4, L4-5, L5-S1 common locationsThought to be a culmination of acute traumatic events to the disc,Herniated Disc: 4 degrees,Nuclear herniation: nucleus ruptures. No disruption of outer annular fibersDisc protrusion: ruptured nucleus causes outer fibers to bulgeNuclear extrusion: Complete
21、split in annulus. Material leaks but remains attached to nucleusSequestered nucleus: Leaked substance no longer attached to nucleus,INTRODUCTION,The back and leg pain since - Greeks recognized it.In the fifth century AD Aurelianus clearly described the symptoms of sciatica. The sciatica arose from e
22、ither hidden causes or observable causes- a fall, a violent blow, pulling, or straining.,The most notable of these is the Lasgue sign, or straight-leg raising test, described by Forst in 1881 but attributed to Lasgue, his teacher.,This test was devised to distinguish hip disease from sciatica.,Biome
23、chanics of the lumbar spine,Biomechanics of the lumbar spine,Biomechanics of the lumbar spine,Biomechanics of the lumbar spine,Biomechanics of the lumbar spine,Biomechanics of the lumbar spine,INTRODUCTION,Mixter and Barr in their classic paper published in 1934 again attributed sciatica to lumbar d
24、isc herniation.,Definition,Ruptured discs are among the most common and painful of all back ailments. The 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.
25、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征。,Prolapsed intervertebral disc,It 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. It may occur in other regions, especially at the L3/4 level, and occasionally disc protrusio
26、n may occur at more than one level simultaneously.It is often due to degeneration of the disc and therefore occurs most commonly in middle or old age.Degeneration of the annulus fibrosus allows the nucleus pulposus to herniate through,压迫对神经根的作用,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，机械直接损伤神经内部，神经根受压变形，有张力，
27、压迫神经根可引传导性损伤，功能改变。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，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,压迫对神经根的作用,压力从1013.33kPa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CMAP水平。压迫在26.67kPa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，传出神经仍有30%40%的恢复。将压迫时间从2h延长到4h，对神经恢复能力的影响更加明显3。,产生腰痛的组织 -背根节,Howe发现背根节对中度压迫极
28、度敏感，当压力解除后感觉神经释放的信号可持续25分钟。从神经生理学角度背根节是特有的、“捣鬼”的疼痛源，突出椎间盘能挤压它对于周围神经来说，当刺激解除后，神经冲动马上停止.,产生腰痛的组织-背根节,实验结果背根节在尼龙线牵拉产生60秒的发电，而玻璃棒压迫会产生4分钟的冲动,产生腰痛的组织-背根节,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道，使其对机械压力特别敏感。这种高密度的钠通道可能是导致神经冲动持续，在背根节受压时产生生骨神经痛.,产生腰痛的组织-神经根,Olmarker等应用不同的化学标记物来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。结果提示，压迫产生越迅速，
29、神经根水肿的形成和营养供给障碍越明显。,产生腰痛的组织-脊神经背根,与DRG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。Howe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A、d神经纤维放电5-30秒。被刺激的神经根是有鞘神位由可能含有神经末梢。Jang发现了猫的S1背根中有点状直接受刺激区,产生腰痛的组织-脊神经背根,最有效的机械刺激是轻度牵拉，与临床情况相吻合。有病间盘水平的神经根比邻近正常的神经根更敏感Kuslich在局麻下椎间盘手术中，对有炎症或压迫的神经根压迫特别敏感，压迫它再现坐骨神经痛Smyth用尼龙线绕过受累神经根，轻拉即再现坐骨神经
30、痛的,神经源的化学介质,损伤和炎症的组织释放的化学介质使神经末梢致敏。这些神经致敏物质包括由C纤维释放出的P物质、11氨基酸神经肽。P物质导致血管扩张，血浆外渗，肥大细胞释放组胺。这些炎性介质的持续释放引起了疼痛。,神经源的化学介质,虽然原因还不清楚，P物质可能直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。P物质在神经致敏中起重要作用，这有重临床意义，脊柱的运动正常是无痛的，但在炎症条件下引起疼痛,腰痛症状持续的原因非神经源的化学介质,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(5-HT)、组织胺、钾离子、前列腺素。已在椎小关节及邻近组织中发现了P物
31、质，使用10-g即能同时兴奋低痛阈和高痛阈神经纤维，30分钟后这些神经对机械刺激的痛阈明显降低,非神经源的化学介质,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，1-2mm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。最近的研究表现在神经感受器对机械压力敏感的部位，注入角叉菱胶，会导致神经元放电达3小时,非神经源的化学介质,这些研究的临床意义：如果关节囊、韧带、肌肉受牵拉，例如脊柱滑脱和椎间盘突出症，引起组织损伤会导致持久的伤害性刺激，并可以导致一种循环状态，肌肉痉挛，痛觉过敏，以致持续性疼痛,椎间盘及神经根周围的炎症,有关椎间盘的神经生理学研究是有限的。Cavanaugh报告
32、了椎间盘受机械刺激时只偶有少量冲动，只有腹侧硬膜受牵拉才有持续冲动。只有电刺激椎间盘和后纵韧带引起A-d纤维冲动，同椎管内注入致痛物质，像组胺作用一样,椎间盘及神经根周围的炎症,Yamashita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，它只对损伤或炎症产生的致痛电学物质有反应。McCarron向狗硬膜外腔注入自体的髓核，表现出它的致炎作用。Olmarker 发现身体髓核在神经组织中产生炎性和退行性改变,免疫和炎症反应,腰腿痛当中，原因很复杂，椎间盘突出的大小与疼痛程度不一，生化和机械因素交互作用。有很多证据表明髓核有致免疫原性，自体髓核与血液接触，对髓核自身抗体
33、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退变和疼痛的产生中的免疫现象标志物。Saal证明突出间盘边缘有免疫细胞，发现了T淋巴细胞IL-1、2，据细胞。浸润的不同程度分级与症状相关。反应程度与术前症状时间相关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。,磷脂酶A2 -PLA2,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：表1 PLA2 activiyu PMN3,2 Platelet1.4 Plasma0.006 Sperm28.0 inflammatory synovial fluid 12.1 herni
34、ated lumbar disc1212.0正常椎间盘内PLA2就有致水肿作用,PLA2的神经毒性,Steroid局部应用非常有效，在没有免疫反应的生化炎症，作为疼痛发生机制的另一个原因髓核有介导炎性的能力，含有高浓度的PLA2。 Saal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A2-PLA2。髓核、PLA2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单纯压力更大PLA2进入神经根后神经水肿，髓鞘轴突损伤，同注射蛇毒 PLA2，但作用程度轻，支持了PLA2的神经毒性硬腰外使用自体髓核，发生传导阻滞，神经周围组织炎症 。,Leakage of nucleu
35、s pulposus material to nerve roots, is a pathophysiologic mechanism in LBP and sciatica,Incision of the anulus fibrosus induces nerve root morphologic, vascular, and functional changes. An experimental study.Kayama -Japan: Spine 1996 The nerve conduction velocity was significantly lower in the incis
36、ion group (13 14 m/sec) compared with the nonincision group (73 5 m/sec). The obvious signs of capillary stasis with an increased number and diameter of the intraneural capillaries in the incision group.,Cultured, autologous nucleus pulposus cells induce functional changes in spinal nerve roots,Kaya
37、ma -Sweden : Spine 1998 Nucleus pulposus cells and fibroblasts were cultured for 3 weeks, and various preparations were applied to the cauda equina in 29 pigs. After 1 week, nerve conduction velocity was determined by local electrical stimulation. Application of nucleus pulposus cells reproduced the
38、 previously seen reduction in nerve conduction velocity induced.,腰痛症状持续的原因椎间盘及神经根周围的炎症,Kuslich在144例椎间盘手术中，在病变椎间盘外侧检查刺激或电刺激产生中度疼痛占70%，重度占30%。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是持续的，就能导致持续性疼痛，或DRG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。Cavanaugh将自体髓核注入DRG引起1-3分钟的神经释放,PLA2致痛原因,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根坏死，体
39、外证实PLA2直接刺激纤维环伤害感受器。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C或Adeltal。致病物质作用后，伤害感受器的痛域下降。（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1/3后纵韧带）.,第二部分：腰痛症状持续的原因椎间盘及神经根周围的炎症,临床、组织化学、生理化学、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。同样化学物质有氢离子、PLA2免疫球蛋白G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,Phospholipase A2 sensitivity of the dorsal root and d
40、orsal root ganglion,Ozaktay USA ：Spine 1998 JunPhospholipase A2 appeared to be neurotoxic when doses ranging from 100 to 400 U were applied on the mechanically sensitive segments of the dorsal root ganglia. PLA2 doses comparable to serum concentrations in human rheumatoid arthritis when applied to d
41、orsal root ganglia. These results suggest that dorsal roots and dorsal root ganglion may be impaired by phospholipase A2, leading to sciatica and low back pain.,脊髓水平,中枢致敏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致敏的神经元痛阈下降，对传入冲动的反应增强，对重复刺激的反应也增强，接受刺激的阈值变宽。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,脊髓水平-中枢致敏,在中枢致敏状态下，机械刺激的致
42、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号。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递，这就解释了腰疼痛位不清和持久、及牵涉痛的原因,脊髓水平-中枢致敏,Gilleffe发现了后角单个神经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状态。脊髓后角的神经元可以由压迫皮肤、椎小关节、韧带、及肌肉而兴奋，这种高度会聚功能也是腰痛不易定位的原因,Chronic Compression of Dorsal Root Ganglion Produced by Intervertebral Foramen Stenosis,Hu SJ- Xian, PR Chin
43、a Pain 1998 JulAn experimental model in the rat.A small stainless steel rod (0.5-0.8 mm in diameter) was inserted into the L5 intervertebral foramenThese neurons had a greatly enhanced sensitivity to mechanical stimulation of the injured DRG and a prolonged after discharge. a persistent heat hyperal
44、gesia 5-35 days The excitatory responses were evoked in the injured, but not the uninjured, DRG neurons.,EPIDEMIOLOGY-risk factors,Multiple factors affect the development of back pain. smoking, pro-longed daily driving of motor vehicles, jobs requiring frequent repetitive lifting of heavy objects an
45、d twisting, the use of jackhammers and machine tools, and the operation of motor vehicles episodes of anxiety and depression.It is more common in males than females and has a maximal incidence in the third and fourth decades of life.,LUMBAR DlSC HERNlATION,Back pain may be caused by stimulation of t
46、he pain fibers in the outer layers of the annulus fibrosus. Alternatively, distortion of the posterior longitudinal ligament, which is richly innervated by pain fibers, may result in back pain. Leg pain can result from compression of a nerve root by an HNP,腰痛可以起自于椎间盘、椎小关节、肌肉的神经末梢。化学炎性介质释放，使正常无痛的运动变为
47、疼痛性的。髓核是强列的神经根和神经末梢致炎和刺激物质椎间盘与神经根的位置、 DRG的特殊神经生理特点、神经根和DRG易被压迫而出现坐骨种经痛。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,CIinicaI Presentation,The following are risk factors for herniated disc disease in the lumbar spine:smoking, pro-longed daily driving of motor vehicles, and frequent repetitive lifting of heavy objects
48、and twisting. It is more common in males than females and has a maximal incidence in the third and fourth decades of life.,The clinician must rule out a compressive lesion of the sciatic nerve peripherally before ascribing the pain to a herniated disc.There may be a history of a previous injury.,CIi
49、nicaI Presentation,A symptom- HNP. Sciatica is pain along the course of the sciatic nerve. The classic symptom is low back pain with radiation of severe pain down the back of the leg to the ankle and foot.It may be associated with neurological signs such as motor and sensory loss and occasionally bl
50、adder involvement.,The levels of lumbar HNP,The most common levels - L4-L5 and L5-Sl. For this reason, radicular symptoms almost always refer to symptoms below the level of the knee, in the L5 or S1 dermatome. Leg symptoms can vary from numbness to dysesthesia to true pain.The herniation of the L4-L
