【专题文献】之下腰痛---腰椎关节突关节（小关节）源性腰痛的发病机制，诊断和治疗『0206』
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Pathogenesis, Diagnosis, and Treatment of Lumbar Zygapophysial (Facet) Joint Pain
Steven P. Cohen, M.D.,* Srinivasa N. Raja, M.D.?
腰椎关节突关节（小关节）源性腰痛的发病机制，诊断和治疗
This article has been selected for the Anesthesiology CME Program. After reading the article, go to http://www.asahq.org/journal-cme to take the test and apply for Category 1 credit. Complete instructions may be found in the CME section at the back of this issue.
Lumbar zygapophysial joint arthropathy is a challenging condition affecting up to 15% of patients with chronic low backpain. The onset of lumbar facet joint pain is usually insidious,with predisposing factors including spondylolisthesis, degenerativedisc pathology, and old age. Despite previous reports of a“facet syndrome,” the existing literature does not support the use of historic or physical examination findings to diagnose lumbar zygapophysial joint pain. The most accepted method for diagnosing pain arising from the lumbar facet joints is with low-volume intraarticular or medial branch blocks, both of which are associated with high false-positive rates. Standard treatment modalities for lumbar zygapophysial joint pain include intraarticular steroid injections and radiofrequency denervation of the medial branches innervating the joints, but the evidence supporting both of these is conflicting. In this article,the authors provide a comprehensive review of the anatomy,biomechanics, and function of the lumbar zygapophysial joints,along with a systematic analysis of the diagnosis and treatmentof facet joint pain.
腰椎小关节病占慢性腰痛的15%，已成为极具挑战性的课题。腰椎小关节源性疼痛常常隐匿起病，伴有既往椎体滑脱、椎间盘退变、和老龄等问题。尽管以前曾报道多“小关节综合征”，然而目前的文献多不支持采用组织学或体格检查的方式诊断小关节源性疼痛。最令人接受的诊断方式是采用微量关节内注射或内侧支阻滞的方法，然而两者的假阳性率都较高。标准的质量方式包括关节内注射类固醇和射频消融支配关节的内侧支。但是这两种治疗方法也存在争议。在本文中，作者综合阐述了腰椎小关节源性疼痛相关的解剖，生物力学，和功能特点，并对诊断和治疗做了系统分析。
SINCE its original description almost 100 yr ago, thousands of scientific articles have been published on lumbarzygapophysial (l-z) joint pain, and facet interventions represent the second most common type of procedure performed in pain management centers throughout the United States.1 But despite the plethora of research and clinical emphasis on this disorder, almost every aspect of l-z joint pain, from diagnosis to treatment, remains mired in controversy. Even among pain specialists, lumbarfacet joint pain remains a misunderstood, misdiagnosed,and improperly treated medical condition. In this article,l-z joint pain is defined in a functional capacity as pain originating from any structure integral to both the function and configuration of the lumbar facet joints, including the fibrous capsule, synovial membrane, hyaline cartilagesurfaces, and bony articulations.
自从100多年前该概念提出以来，发表了大量关于腰椎小关节（L-Z）痛的文章。小关节干预曾经成为美国疼痛治疗中心的第二常见的处理方式。但是虽然有越来越多的研究证实这种疾病，对此的临床关注也越来越重视。然而腰椎小关节疼痛的各个方面，从诊断到治疗，却皆存在争论。即使在疼痛科医生眼中，腰椎小关节疼痛也仍是一种难以理解，难于诊断的临床情况。本文中，L-Z疼痛定义为一种功能性的疼痛，包括来源于腰椎小关节的各种功能及结构成分，如关节囊，滑膜，透明软骨以及骨性关节。A critical issue that must be addressed before embarking on any review of l-z joint pain is whether pain can be definitively attributed to these joints. In the 1960s and1970s, this question posed a legitimate controversy that was vigorously debated in the medical literature.2,3 However,in the past 20 yr, the scales of this controversy have resolutely tipped toward the conviction that l-z joints can be and often are a primary source of low back pain(LBP).4
在着手讨论L-z疼痛之前，明确小关节究竟是否可以产生疼痛这个概念非常重要。从1960s 到1970s，这个问题曾通过文献产生过激烈的争论。然而在过去的20年间，对于l-z可以产生疼痛的观点已经被十分坚定的接受，且l-z源性疼痛常常是下腰痛发生的最主要的原因。
Compelling evidence underlies this paradigmatic shift in thinking. The facet joint capsule and surrounding structures are richly imbued with nociceptors that fire when the capsule is stretched or subjected to local compressive forces.5,6 In both pain patients and volunteers,chemical or mechanical stimulation of the facet joints and their nerve supply has been shown to elicit back and/or leg pain.7–10 During spine surgery performed under local anesthetic (LA), lumbar facet capsule stimulation elicits significant pain in approximately 20% of patients.11 Last and most significantly, LA blocks of either the facet joints themselves or the medial branches innervating them have been shown to relieve pain in a substantial percentage of patients with chronic LBP.12Therefore, like other synovial joints in the human body,the l-z joints represent a potential pain generator inpatients with chronic LBP.
一些证据已为这种想法的基础。小关节囊及其周围结构富含疼痛感受器，当收到拉伸或局部压缩力时，可以被刺激。腰痛患者和志愿者的研究均表明，针对小关节和其支配神经的化学性或机械性刺激均可引发腰痛或腿痛。在局麻（LA）下的腰椎手术中，刺激腰椎小关节囊可以引发近20%患者产生腰痛。最后且最重要的是，局麻不仅阻滞了小关节本身，而且阻滞了内侧支，而阻滞内侧支本可以在部分病人中减轻疼痛。因此，像身体其他的滑膜关节一样，腰椎小关节也是慢性腰痛的发生器。In light of the prevalence of lumbar facet joint pain and the frequency with which facet blocks are performed,several reviews have been undertaken on this phenomenonin the past 15 yr. Although some of these articles provided keen insight on various aspects of the condition,most were limited by their confined scope and specialized target audiences. The purpose of this reviewis therefore to provide a comprehensive, evidence-basedframework on the anatomy, pathophysiology, prevalence,diagnosis, and treatment of lumbar facet pain.Articles reviewed were obtained via MEDLINE and Ovidsearch engines, books and book chapters, and bibliographic references dating to the early 1900s.
鉴于腰椎小关节疼痛的发病率较高及小关节阻滞的频繁开展，过去15年间已经对此种现象进行了一些回顾。虽然一些文章在不同的方面提出了敏锐的观点，但是大部分还是具有领域局限性及病患针对性。本文的目的是针对此现象做一综合的，基于证据的回顾，内容涉及解剖，病理，流行病，诊断及治疗等多方面。回顾所用的稳扎个来自MEDLINE 和 Ovidsearch搜索引擎，相关书及章节，参考文献最早到1900sHistoric Review
The l-z joints, often referred to as facet joints, have long been recognized as a potential source of LBP. In1911, Goldthwaite13 first noted that the peculiarities of the facet joints could be a significant source of back pain and instability. Sixteen years later, after anatomical dissectionsof 75 cadavers, Putti14 suggested that local inflammation and degenerative changes in lumbar facet joints could result in sciatica from irritation of nerveroots. In 1933, Ghormley15 coined the term “facet syndrome,”which he defined as lumbosacral pain, with or without sciatica, that was likely to occur after a sudden rotatory strain. Shortly thereafter, interest in the l-z joints as potential sources of back pain waned after the landmarkarticle by Mixter and Barr16 implicating lumbar discrupture as the major cause of low back and leg pain. The1940s saw a resurgence in the interest of l-z joints as pain generators when Badgley17 suggested that up to 80% of cases of LBP and sciatica are due to referred pain from l-z joint pathology, rather than direct nerve root compression.In 1963, Hirsch et al.7 published the first account whereby the injection of l-z joints reproduced patients’ back pain. Rees,18 who reported a success rate of 99.8%,is generally credited with promoting percutaneous“facet rhizolysis” with his ground-breaking report in the early 1970s. Later, it was shown that the technique advocated by Rees may not have been sufficient to achieve rhizotomy in most patients.3 Buoyed by a high incidence of hemorrhagic complications, Shealy19,20 pioneered the use of fluoroscopically guided radiofrequency facet denervation to treat l-z joint pain in the mid-1970s.
历史回顾：
L-z关节常常被称为小关节，长期以来被视为腰痛发生的潜在诱因。1911年，Goldthwaite首次说明小关节的结构特性可以引发腰痛和不稳。16年后在解剖了75例标本以后，Putti认为小关节的局部炎症和退化能刺激神经从而引起坐骨神经痛。1933年，Ghormley创造了“小关节综合征”一词，指腰骶部疼痛伴有或不伴有坐骨神经痛，可能来源于突然的腰部扭转。此后，Mixter and Barr暗示椎间盘破裂时导致腰腿痛的主要原因后，以此为标志，l-z关节作为腰痛的潜在来源的说法开始减弱。1940s，Badgley指出高达80%的腰痛和坐骨神经痛的病人疼痛来源于小关节产生的牵涉痛，而非由直接药品神经根而引起，由此l-z关节源性疼痛的关注有开始得到复苏。1963年，Hirsch用小关节注射的方法复制了患者的腰痛。由于Ree报道小关节射频神经切断术的成功率高达99.8%，1970s这一手术得到广泛开展。此后，Rees的方法被证实在大部分患者中不能有效切断神经。Buoyed报道这种方法并发血肿的概率很高。1970s中期，Shealy又首创了透视引导下射频消融达到小关节去神经化的方法。
Anatomy and Innervation
The lumbar facet joints form the posterolateral articulations connecting the vertebral arch of one vertebra to the arch of the adjacent vertebra. As true synovial joints,each facet joint contains a distinct joint space capable of accommodating between 1 and 1.5 ml of fluid, a synovial membrane, hyaline cartilage surfaces, and a fibrous capsule.21 The fibrous capsule of the lumbar facet joint is approximately 1 mm thick and composed mostly of collagenous tissue arranged in a more or less transversefashion to provide maximum resistance to flexion.22,23The joint capsule is thick posteriorly, supported by fibers arising from the multifidus muscle. Superiorly and inferiorly, the capsule attaches further away from the osteochondral margins, forming subcapsular recessesthat in the normal joint are filled with fibroadipose menisci.Anteriorly, the fibrous capsule is replaced by the ligamentum flavum.24
腰椎小关节组成后外侧关节，链接椎体的椎弓和其临近的椎弓。作为真正的滑膜关节，每个小关节包含明显的关节间隙，容纳1到1.5ml关节液。小关节由滑膜，透明软骨表面，和纤维囊组成。纤维囊厚约1mm，大部分有白色纤维组成，横向排列，以在屈曲时提供最大的张力。囊的后部很厚，纤维来源与多裂肌。囊的上部和下部较薄，附着于远离骨软骨边缘的地方，形成了囊下隐窝，正常情况下填充有纤维脂肪性软骨版。囊前部被黄韧带所取代。
Each facet joint receives dual innervation from medial branches arising from posterior primary rami at the same level and one level above the z-joint.25,26 For example,the inferior pole of the L4–L5 facet joint receives innervation from the L4 medial branch and its superior pole is innervated by the L3 medial branch, L1–L4 dorsal rami course across the top of their respective transverse processes one level below the named spinal nerve (e.g., L4 crosses the transverse process of L5), traversing the dorsal leaf of the intertransverse ligament at the base of the transverse process. Each nerve then runs downward along the junction of the transverse and superior articular processes, passing beneath the mamilloaccessory ligamentand dividing into multiple branches as it crosses the vertebral lamina (fig. 1). In some cases, the mamilloaccessory ligament becomes calcified, which may lead to nerve entrapment.27 This is most common at L5 (approximately 20%) but also occurs at L4 (10%) and L3(4%). In addition to two l-z joints, the medial branches also innervate the multifidus muscle, the interspinous muscle and ligament, and the periosteum of the neural arch.7,28–30 The L5 nerve differs in that it is the dorsal ramus itself that runs along the junction of the sacral ala and superior articular process of the sacrum.29,31 Its medial branch arises opposite the inferolateral corner of the base of the lowest facet joint. At this level, it is the dorsal ramus rather than its medial branch that is am enable to blockade.
每个小关节都受双重神经支配，分别来自同节段及上一临近节段背侧主支的内侧支。例如，L4-L5关节囊的下极接受L4内侧支支配，而其上极接受L3内侧支的支配，分别可在L5和L4的横突处阻滞。L1-L4 脊神经背侧支的内侧支行经各自横突的上端，为同名的下一个阶段脊神经（例如L4穿过L5的横突）。在横突基底部穿越横突间韧带的背侧叶。沿着横突和上关节突下行的神经支穿过乳突副突韧带的基底部，在椎板处分为多支小枝（图1）。在一部分病例中，乳突副突韧带骨化，使神经被包埋于其中。这种情况在L5中最常见（将近20%），单也常发生于L4 (10%) 和 L3(4%)。除了l-z关节以外，内侧支还支配多裂肌，棘间肌和韧带以及椎弓处的骨膜。L5神经有所不同，其背侧支本身走行于髂骨翼和髂骨的上关节突。其内侧支在最低关节囊的基底部下外侧角的对面发出。因此阻滞时只能针对背侧支而非内侧支。
Some people may have aberrant or additional innervation of the facet joints. In a study conducted in asymptomatic volunteers, Kaplan et al.32 found that 1 in 9 subjects who underwent L4–L5 (n = 5) and L5–S1 (n =4) facet joint medial branch blocks (MBB) felt pain during repeated capsular distension concordant with pain experienced during previous l-z joint provocation without MBB. Assuming the blocks were technically successful,one explanation for this finding is that in a small subset of individuals, aberrant innervation may account for false-negative diagnostic MBB. Some authors have suggested that l-z joints may also receive innervation from the medial branch below the joint (i.e., S1 for theL5–S1 joint),33,34 the dorsal root ganglion,35 and the paravertebral sympathetic ganglia,36,37 but these assertions remain unproven (fig. 2).
一部分患者的小关节可能存在异常的或其他的神经支配。在一项针对无症状志愿者的研究中Kaplan等发现，在接受L4–L5 (n = 5) 或 L5–S1 (n =4)小关节内侧支阻滞（MBB）的患者，每9例中有1人在阻滞后牵拉小关节仍会产生疼痛，性质与未阻滞前牵拉小关节所产生的疼痛一致。假设阻滞在技术上已经成功，那么这种现象的解释就是存在一部分患者，其小关节支配神经发生了变异，从而产生了小关节阻滞性诊断假阴性的结果。一些作者认为l-z关节也接受来自关节下部的内侧支及背侧根神经节，椎旁交感神经节的支配，但这些假设尚未得到证实（图2）。
Histologic studies have demonstrated that the lumbar facet joints are richly innervated with encapsulated (Ruffini-type endings, pacinian corpuscles), unencapsulated, and free nerve endings.5 The presence of low-threshold, rapidly adapting mechanosensitive neurons suggests that in addition to transmitting nociceptive information, the l-z facet capsule also serves a proprioceptive function. Besides substance P and calcitonin gene–related peptide, a substantial percentage of nerve endings in facet capsules have also been found containing neuropeptide Y, indicating the presence of sympathetic efferent fibers.38,39 Nervefibers have also been found in subchondral bone and intraarticular inclusions of l-z joints, that facet-mediated pain may originate in structures besides the joint capsule.40–42 In degenerative lumbar spinal disorders, inflammatory mediators such as prostaglandins43 and the inflammatory cytokines interleukin 1B， interleukin 6, and tumor necrosis factor _44 have been found in facet joint cartilage and synovial tissue.
组织学研究证实，腰椎小关节含有丰富的神经支配。包括有包膜（Ruffini型末梢，尼氏小体）、无包膜及游离神经末梢。低阈值，快适应型动力敏感神经元表明，l-z关节囊不仅传导伤害性信号，还起到本体感受器的作用。除了P物质，降钙素基因相关肽，还在一定数量的小关节神经末梢发现了神经肽Y，表明了存在一定比例的交感传出纤维。在软骨下骨及关节囊内也发现了神经纤维。因此小关节介导性疼痛可能是一种结构依赖性而非关节囊依赖性。在腰椎退变的病例中，在小关节软骨及滑膜组织中也发现了炎症介质如PG，炎性细胞因子，白介素1B，白介素6以及肿瘤坏死因子等。Function and Biomechanics
功能及生物力学
The basic anatomical unit of the spine, often referred to as the three-joint complex, consists of the paired zygapophysial joints and the intervertebral disc. Together,these joints function to support and stabilize the spine, and prevent injury by limiting motion in all planes of movement. Macroscopically, each facet joint is composed of a posteromedially facing concave superior articularprocess from the inferior vertebral body, and as maller anterolaterally facing inferior articular processfrom the superior spinal level. The shape and orientationof the l-z joints determine the role each plays in protectingthe spine against excessive motion. Facet joints oriented parallel to the sagittal plane provide substantial resistance to axial rotation but minimal resistance to shearing forces (backward and forward sliding), whereas joints oriented more in a coronal plane tend to protect against flexion and shearing forces but provide minimal protection against rotation (fig. 3).24 In an anatomical study published in 1940 by Horwitz and Smith,45 the authors found that the L4–L5 z-joints tended to be more coronally positioned (almost 70° with respect to the sagittal plane), whereas the L2–L3 and L3–L4 joints were likely to be oriented more parallel (<40°) to the sagittal plane. In more recent studies by Masharawi et al.46 andPunjabi et al.,47 the investigators found that the upper lumbar facet joints (T12–L2) were oriented closer to the midsagittal plane of the vertebral body (mean range,26°–34°), whereas the lower facet joints tended to be oriented away from that plane (40°–56°). In the upper lumbar spine, approximately 80% of the facet joints are curved, and 20% are flat. In the lower lumbar spine,these numbers are reversed.45 Studies by Grobler et al.48and Boden et al.49 found a positive association between degenerative spondylolisthesis and more sagittally oriented lower lumbar facet joints. In young people, the l-z joints are quite strong, capable of supporting almost twice body weight.23 As aging occurs, the joints become weaker and more biplanar,transitioning from a largely coronal orientation to a more prominent sagittal positioning. The orientation of each joint to the sagittal plane can also differ between the paired facet joints at the same spinal level. This phenomenonis known as tropism and has a 20–40% incidence among the general population.24,50 Most50–55 but not all49,56 studies have demonstrated a positive relation between facet joint tropism and intervertebral disc degeneration and herniation.
脊柱的基本解剖单元，常被称为三关节复合体，有成对的关节突关节和椎间盘组成。这些关节共同支持并稳定脊柱，限制其在各个方向上的运动以防止损伤发生。大体观，每个小关节由下位椎体朝向后内侧凹陷的上关节突以及上位椎体朝向前外侧的的下关节突组成。L-z关节的形状及朝向决定了其作用为阻止脊柱过度运动。小关节朝向趋于矢状位可以限制脊柱的轴向旋转但是减少了对剪应力的限制（前后运动时）。而趋于水平的小关节可以更好的保护屈曲和剪切下的应力，但对旋转的抵抗力降低（图3）。在1940年的一项解剖学研究中，Horwitz 和 Smith发现L4-L5小关节更趋向冠状位（相对于矢状面近70°），而L2–L3 和 L3–L4关节趋向与矢状面平行(<40°)。近期，Masharawi 和Punjabi等人的研究发现，上位小关节（T12–L2）的趋向更接近椎体的正中矢状面（平均角度26°–34°），而低位腰椎小关节的趋向远离正中矢状面(40°–56°)。在上位腰椎，近80%的小关节为屈曲面，而20%小关节为平面，而下位腰椎则刚好相反。Grobler和 Boden等人的研究发现，下位腰椎小关节的矢状走向的程度与退变性腰椎滑脱之间存在相关性。年轻人的l-z关节足够强大，可以支持2倍体重的重量。随着年龄增长，关节强度减弱，且多变为双平面，从大部分冠状位过度矢状位。同一脊柱节段的两个小关节的趋向也可以不同。这种现象称为趋向性，在人群中的发生率约为20–40%。大部分但并非所有的文献都报道了趋向性与椎间盘退变及突出之间存在的联系。
Although most of the axial load is borne by the intervertebral discs, the two other components of the three-joint complex, the l-z joints, also play a role in weight bearing, with the proportion dependent on several factors. In a study by Yang and King,57 the authors determined that normal facet joints typically carry 3–25% of the axial burden, which can increase even higher in patients with degenerative disc disease facet arthritis. During this seminal experiment, it was observed that with significant facet loading the inferior tip of the facets bottomed against the laminae below, functioning as pivots for the entire vertebral body to rotate backward. This resulted in considerable stretching of the superior facet capsules, manifesting as blood extravasating onto the outer surface of the capsule. In another cadaveric study, Adams and Hutton58found that the lumbar facet joints resist approximately16% of the intervertebral compressive force when standing erect versus near 0% when sitting, which helps explain the high intra discal pressures during unsupported sitting.59 Finally, after conducting in vitro experiments measuring induced loads on cadaveric lumbar facets, Lorenz et al.60 concluded that with increasing compressive loads, the absolute facet loads increases only slightly, so that the proportion of the axial burden borne by the l-z joints actually decreases with increasing stress. During extension, the normal load on the facet joints is always higher when compared with the neutral mode. After facetectomy, while the remaining load on the vestigial facet is substantially reduced, the peak pressure increases.60In summary, the l-z joints serve primarily a protective role, functioning to limit movement in all planes of motion. Whereas they do play a part in weight bearing, the proportion of the axial load they bear is inversely proportional to the amount of stress.
虽然大部分轴向负荷由椎间盘负担，但是作为三关节复合体的小关节仍在承担负荷中发挥了一定作用，其作用的大小取决于许多因素。Yang 和 King的一项研究表明，正常情况下，小关节承担3–25%的轴向负荷，在椎间盘退变小关节炎的患者，其承担的负荷增大。初步研究发现，小关节负荷明显增加后，，其关节底部尖端顶向椎板的下面，称为整个椎体向后旋转的功能结构。这导致了小关节囊上部明显拉伸，表现为血液渗出到关节囊的外表面。另一项尸体标本的研究中，Adam和Hutton发现，当直立站立时，小关节承担了逐渐压力的近16%，而坐位时进0%，这解释了为什么在无支持的坐位时椎间的压力非常高。最后，Lorenz在尸体标本加载负荷后测量小关节的应力后，认为增加压力负荷时，小关节间的应力仅轻微增加，因此在轴向负荷中，小关节承担的比例实际随着应力的增加而减少。当拉伸时，小关节承受的应力相对于中立位来说有所增加。小关节切除后，残存小关节的应力也减少，但应力的峰值增大。总之，l-z关节的主要作用是保护，功能是限制脊柱在各个方向上的运动。它也起一部分的体重承载作用，其承载的轴向负荷的部分与整体负荷程反向相关。
Mechanisms of Injury Cadaveric and Animal Studies
损伤机制 尸体标本及动物研究
Although in rare instances the development of facet joint arthropathy can be traced to a specific inciting event,61 the overwhelming majority of cases of l-z joint pain are the result of repetitive strain and/or low-grade trauma accumulated over the course of a lifetime. Khalsa et al. conducted a series of cadaveric experiments designed to determine which physiologic movements are associated with the greatest degree of facet joint capsule strains. They found that the joint moments measured at any given motion increased with greater magnitudes of joint displacement, and were significantly larger in the two most caudad facet joints (L4–L5 and L5–S1).62 With lateral bending, strains of the joint capsule tended to be larger in magnitude in the three most caudad joints(L3–S1) during contralateral flexion (i.e., the left facet joints are most strained during right lateral flexion),whereas the two most cephalad joints (L1–L2 and L2–L3)bore the greatest strain during bending to the ipsilateral side. For the upper three facet joints, the maximum joint displacement and greatest strain was associated with lateral bending, usually to the right. For the two lowest joints, the greatest degree of strain occurred during forward flexion (table 1).
虽然在少数病例中，小关节病变的发展史由于特殊的刺激造成的，但是绝大部分的病例中，l-z关节性疼痛是源于反复的牵拉以及/或低强度的损伤积累的结果。Khalsa等进行了一系列尸体标本的实验研究，以确定何种生理运动下关节囊收到的拉伸力量最大。他们发现任何运动使关节发生位移时，都会增加关节的力矩，并且在尾部两个关节中增加更显著(L4–L5 和 L5–S1)。当向对侧弯曲时侧弯时最尾端(L3–S1)的三个椎体的小关节囊的拉伸强度增大（例如右侧屈曲时左侧小关节达到最大的应力）。而头端的两个关节(L1–L2 和L2–L3)在向同侧屈曲运动时拉伸力量最大。对于上位的三个小关节，最大的应力与最大的形变与侧曲相关，右侧屈曲时尤甚。对于尾端的两个小关节，最大应力在前屈时发生（表1）
In a follow-up study, the authors fixated human lumbar spine specimens with a single anterior thoracolumbar plate on L4–L5, and then measured capsular displacement and strains for a wide range of physiologic motions.63 For all motions, increased joint moments occurred at the level of fixation and both adjacent levels.There was also an increase in intervertebral angulation at L3–L4 and L5–S1, and decreased motion at L4–L5. Increased strain was noted bilaterally at L3–L4 and L5–S1,and contralaterally at L4–L5. On the side ipsilateral to the fixation, decreased strain was found at L4–L5. These findings support the work of other investigators demonstrating that fusing two vertebrae results in a transfer of motion previously occurring at the operated level to adjacent segments, particularly L5–S1, which in turn can lead to accelerated degeneration.64–68
随后的研究中，作者用前路胸腰椎钢板固定了人脊柱标本的L4–L5节段的一侧，测量大范围生理运动时关节囊的位移和应力。所有运动都导致固定节段及其临近节段的力矩增大。L3–L4 和 L5–S1的椎间成角也增大, L4–L5的活动度减小。L3–L4 和 L5–S1双侧关节应力均增加，L4–L5固定对侧的应力增大，其固定同侧的应力减小。这些结果支持了其他学者的研究结果，表明两个节段固定以后可以导致运动转移，主要发生在手术节段和临近节段，尤其是L5–S1，可导致其退变加速。
In a subsequent study, Little and Khalsa69 found that both sustained and repetitive lumbar flexion increased capsular motion and joint strain from L3–L4 to L5–S1,with creep developing more rapidly during sustained flexion than with repetitive movements. Interestingly,these parameters remained elevated even after a 20-min recovery period. Although these studies provide a theoretical framework for the development of micro injury associated with repetitive spine movements, cadavers can not experience pain, and the viscoelastic material properties factored into computational cadaveric spine models may differ from those found in live patients.70
后来的研究中，Little 和Khalsa发现反复和持续性的腰椎屈曲运动增加从L3–L4到L5–S1关节囊的运动及小关节的应力，持续屈曲比反复运动时增加更快。有趣的是，在恢复了20分钟以后，这些参数仍然持续增加。虽然这些研究为反复运动导致微小创伤的观点提供了理论框架，但是尸体不能感受疼痛，而且尸体和活体的粘弹性材料属性也不同。
In response to repetitive strain and inflammation, the synovial l-z joints can fill with fluid and distend, resulting in pain from stretching the joint capsule.71 Distension of the articular recesses can also compress the exiting nerve root in the neural foramen or spinal canal, especially when the foramen is already narrowed by joint hypertrophy and/or osteophytes. 72–75 This can lead to concomitant sciatica and mask the facet pathology underlying the radiculopathy. Capsular irritation may also result in reflex spasm of the erector spinae, multifidus,and other paraspinal muscles.72,76,77
反复的应力与炎症反应，可使滑膜l-z关节充满滑液并扩张，导致关节囊收到牵拉产生疼痛。关节囊隐窝的扩张可以压迫神经孔出的神经根出口或压迫椎管内脊髓，尤其当由于关节肥大和/或骨赘形成已经存在椎间孔狭窄时发生率更高。这可以导致伴随性坐骨神经痛的发生，且在此神经根病的影响下可能忽略小关节病的存在。关节囊收到刺激也可以导致反应性竖脊肌，多裂肌和其他椎旁肌的痉挛。
In in vivo and in vitro experiments designed to reproduce facet capsular stretch, nerves typically cease firing shortly after the stimulus is removed.78–80 Although these findings indicate that capsular strain could cause acute facetogenic pain, they do not explain its persistence.The pathophysiologic basis for persistent lumbarfacet pain was established in a series of elegant experiment sconducted by Cavanaugh, Yama***a, Ozaktay, etal. in New Zealand white rabbits. In these studies, the application of inflammatory chemicals or algesic mediators such as substance P and phospholipase A2, were found to result in inflammatory changes consisting of vasodilation, venous congestion, and the accumulation of polymorphonuclear leukocytes. Neuronal sensitization occurred in both nociceptive and proprioceptive nerve endings, being manifested by reduced mechanical thresholds, increases in multiunit discharge rate and recruitment of previously silent units.81–84 Persistent nociceptive input invariably leads to peripheral sensitization,and if the underlying stimulus is not removed,central sensitization and neuroplasticity can develop.85Whereas the spinal structures in humans are subject to greater stress than other mammals, because of the array of anatomical and functional differences that exist between the l-z joints in various mammalian species,86caution should be exercised when extrapolating the results of animal studies to humans.
体内和体外实验再现了关节囊的拉伸，当去掉刺激后神经也停止了放电。虽然这些研究表明关节囊的应力可以导致急性关节源性疼痛，但并不能解释其疼痛的持续性。Cavanaugh, Yama***a, Ozaktay等人在新西兰大白兔上已经建立了一系列相关实验以解释持续性疼痛发生的病理生理学。P物质，磷脂酶A2等炎性化学物质或疼痛介质的作用下，导致一系列炎性反应，包括血管舒张，静脉充血以及多形核白细胞聚集。在疼痛感受神经和本体感受神经末梢，都发生神经致敏作用，这可以通过机械刺激阈值降低得以证实，从而导致了多单位放电率的升高以及原来静默单位的恢复放电。持续不断的刺激输入疼痛感受神经，导致其神经末梢致敏，如果潜在的刺激因素继续存在，可导致中枢致敏。然而由于人类脊柱小关节的解剖及功能结构较其他哺乳动物不同，使其较能承受更大的压力，所以将动物实验的结果推到人类身上时要尤其谨慎。
One inferential interpretation of these preclinical findingsis that chronic l-z joint pain is likely to occur with repetitive, chronic strains as might be seen in the elderly or, less frequently, after an acute event such as tearing the joint capsule by stretching it beyond its physiologic limits. This hypothesis is supported by clinical studies indicating a higher prevalence of facet arthropathy in elderly patients87–89 and numerous cases of lumbar facet arthropathy after high-energy trauma.61
对于慢性l-z关节疼痛的一项推论性的解释是疼痛发生于慢性反复的牵拉，这种情况多见于老年人。另一种非常见的解释是其发生于突破关节囊生理极限的急性撕裂。一些临床证据支持上述解释，如临床常见老年患者及高能量损伤后经常发生小关节病变
Human Studies
患者研究
Clinically, several conditions may predispose individuals to chronic facet joint strain. Radiologic studies conducted in LBP patients and asymptomatic controls have shown a positive correlation between sagittally oriented facet joints and degenerative spondylolisthesis.48,49 In these patients, recurrent rotational strains result in myriad changes to the discs and paired l-z joints, including loss of disc height, osteophyte formation, and degenerative hypertrophy of the facets.90,91
在临床上，多种情况可以造成慢性小关节劳损。放射学研究表明，下腰痛患者及无症状的对照组中，小关节矢状面方向及退行性滑脱之间存在正相关。在这些患者中，反复的旋转性应力导致椎间盘和小关节的多种改变，包括椎间盘高度丢失，骨赘形成和退变性关节面增生等。
Changes in any component of the three-joint spinal unit lead to predictable changes in the other components.Degeneration and loss of structural integrity of the intervertebral discs have been shown to result in concomitant degenerative changes in the l-z joints.92–94 The reverse is also true. Degeneration and motion abnormalities at the l-z joints can induce and accelerate degeneration of the intervertebral discs.58,95,96 In a magnetic resonance imaging (MRI)study evaluating the relation between facet joint osteoarthritis and degenerative disc disease (DDD), Fujiwara et al. 97 found that facet joint osteoarthritis was rarely found in the absence of disc degeneration but tended to be most pronounced at spinal levels associated with advanced DDD. The authors concluded that disc degeneration is a more reliable indicator of aging than facet joint osteoarthritis, and in most people,DDD precedes facet osteoarthritis.
脊柱三关节复合体单位中的任何一个组分的改变均会导致其他组分相应的变化。椎间盘的退变和结构组分的丢失均可导致l-z关节的退变。反之亦然。L-z关节退变及异常运动可以导致椎间盘退变加速。一项MRI的研究评估了小关节骨性关节炎与椎间盘退变性疾病（DDD）之间的关系。Fujiwara等人发现小关节骨性关节炎在无椎间盘退变中发生率不高，但是在退变相关节段较显著。作者总结认为，椎间盘退变是老化更可靠的依据，且在大多数人中，椎间盘退变疾病发生于小关节之前。
Paradoxically, in the only clinical study evaluating the relative contributions of DDD and facet arthropathy to chronic LBP, Schwarzer et al.98 found the combination of discogenic and l-z joint pain to be a relatively rare occurrence. In 92 patients who underwent both discography and confirmatory l-z joint blocks with lidocaine and bupivacaine, 39% had at least one positive discogram with a negative control disc, and 9% obtained concordant pain relief after the series of analgesic facet joint blocks. But only 3% of patients had both positive discography and a symptomatic l-z joint. The discrepancy between the handful of basic science studies demonstrating a correlation between DDD and facet joint degeneration and the lone clinical study finding minima loverlap between the two pain generators indicates that more research is needed on this topic.
相反的是，在单纯的临床研究中，评价DDD及小关节病在下腰痛中的地位时，Schwarzer等发现，椎间盘源性和小关节源性的腰痛发生率皆不高。在一项研究中，92例患者同时接受了椎间盘造影和确切的利多卡因布比卡因联合阻滞，39%在阴性对照下至少存在一个阳性的椎间盘X线照片结果。在接受了阻滞后，9%的患者疼痛缓解。但是仅有3%的患者同时存在椎间盘造影阳性和l-z关节疼痛缓解。基础研究结果的不一致性表明DDD与小关节退化间存在一定联系。唯一的临床研究发现两种疼痛源之间存在交叉也说明了此问题需要更进一步的研究。
Aside from osteoarthritis, several other conditions may affect the facet joints. These include inflammatory arthritides such as rheumatoid arthritis, ankylosing spondylitis and reactive arthritis,99–101 synovial impingement,meniscoid entrapment, chondromalacia facetae, pseudogout,synovial inflammation, villonodular synovitis, and acute and chronic infection.102–106 Intrafacetal synovial cysts can be a source of pain because of distension and pressure on adjacent pain-generating structures, calcification,and asymmetrical facet hypertrophy.107–110 In a retrospective review of MRI scans in 303 consecutive patients with LBP, Doyle and Merrilees111 found that9.5% had facet joint synovial cysts, the large majority of which were located posteriorly. Trauma may also cause lumbar facetogenic pain. There are more than two dozen reported cases of lumbar facet dislocation after rapid deceleration injuries (e.g., traffic accidents), most involving L5–S1.61,112–115 The mechanism of injury in these cases is purported to be a combination of hyperflexion, distraction, and rotation.61,112,116 In a posthumous study conducted in 31 lumbar spines of subjects who died of traumatic injuries (mostly motor vehicle accidents),Twomey et al.117 found occult bony fractures in the superior articular process or subchondral bone plate in 35% of victims, and z-joint capsular and/or articular cartilage damage in 77% of cases. The authors concluded that occult bony and soft tissue injuries to the l-z joints may be a common cause of LBP after trauma.
除了骨性关节炎，许多其他的疾病亦可影响小关节。包括炎症性关节炎如类风湿性关节炎，强直性脊柱炎及反应性关节炎等，还有滑液撞击，关节软骨版卡压，关节面软骨软化，假性痛风，滑液炎症，绒毛结节性滑膜炎和急慢性感染。小关节内滑囊囊肿可由于拉伸和压缩临近的疼痛发生结构，骨化及不对称关节增生等原因引起疼痛。在一项303例连续患者的MRI研究中，Doyle 和 Merrilees发现其中9.5%存在小关节囊肿，大部分发生于关节囊后部。创伤也可导致腰椎小关节源性疼痛。多项研究报道了急性减速伤（如交通事故）后发生腰椎小关节分离，多数发生于L5-S1，其机制可能为过度屈曲，分离和旋转。在一项对死亡病例的研究中，Twomey 等发现，31例因交通事故死亡的人中有35%的腰椎上关节突或软骨下骨性终板存在隐匿骨折，77%存在小关节囊和/或关节软骨损伤。作者总结创伤后隐匿性股和软组织损伤也许是腰痛的来源。
Steven P. Cohen, M.D.,* Srinivasa N. Raja, M.D.?
腰椎关节突关节（小关节）源性腰痛的发病机制，诊断和治疗
This article has been selected for the Anesthesiology CME Program. After reading the article, go to http://www.asahq.org/journal-cme to take the test and apply for Category 1 credit. Complete instructions may be found in the CME section at the back of this issue.
Lumbar zygapophysial joint arthropathy is a challenging condition affecting up to 15% of patients with chronic low backpain. The onset of lumbar facet joint pain is usually insidious,with predisposing factors including spondylolisthesis, degenerativedisc pathology, and old age. Despite previous reports of a“facet syndrome,” the existing literature does not support the use of historic or physical examination findings to diagnose lumbar zygapophysial joint pain. The most accepted method for diagnosing pain arising from the lumbar facet joints is with low-volume intraarticular or medial branch blocks, both of which are associated with high false-positive rates. Standard treatment modalities for lumbar zygapophysial joint pain include intraarticular steroid injections and radiofrequency denervation of the medial branches innervating the joints, but the evidence supporting both of these is conflicting. In this article,the authors provide a comprehensive review of the anatomy,biomechanics, and function of the lumbar zygapophysial joints,along with a systematic analysis of the diagnosis and treatmentof facet joint pain.
腰椎小关节病占慢性腰痛的15%，已成为极具挑战性的课题。腰椎小关节源性疼痛常常隐匿起病，伴有既往椎体滑脱、椎间盘退变、和老龄等问题。尽管以前曾报道多“小关节综合征”，然而目前的文献多不支持采用组织学或体格检查的方式诊断小关节源性疼痛。最令人接受的诊断方式是采用微量关节内注射或内侧支阻滞的方法，然而两者的假阳性率都较高。标准的质量方式包括关节内注射类固醇和射频消融支配关节的内侧支。但是这两种治疗方法也存在争议。在本文中，作者综合阐述了腰椎小关节源性疼痛相关的解剖，生物力学，和功能特点，并对诊断和治疗做了系统分析。
SINCE its original description almost 100 yr ago, thousands of scientific articles have been published on lumbarzygapophysial (l-z) joint pain, and facet interventions represent the second most common type of procedure performed in pain management centers throughout the United States.1 But despite the plethora of research and clinical emphasis on this disorder, almost every aspect of l-z joint pain, from diagnosis to treatment, remains mired in controversy. Even among pain specialists, lumbarfacet joint pain remains a misunderstood, misdiagnosed,and improperly treated medical condition. In this article,l-z joint pain is defined in a functional capacity as pain originating from any structure integral to both the function and configuration of the lumbar facet joints, including the fibrous capsule, synovial membrane, hyaline cartilagesurfaces, and bony articulations.
自从100多年前该概念提出以来，发表了大量关于腰椎小关节（L-Z）痛的文章。小关节干预曾经成为美国疼痛治疗中心的第二常见的处理方式。但是虽然有越来越多的研究证实这种疾病，对此的临床关注也越来越重视。然而腰椎小关节疼痛的各个方面，从诊断到治疗，却皆存在争论。即使在疼痛科医生眼中，腰椎小关节疼痛也仍是一种难以理解，难于诊断的临床情况。本文中，L-Z疼痛定义为一种功能性的疼痛，包括来源于腰椎小关节的各种功能及结构成分，如关节囊，滑膜，透明软骨以及骨性关节。A critical issue that must be addressed before embarking on any review of l-z joint pain is whether pain can be definitively attributed to these joints. In the 1960s and1970s, this question posed a legitimate controversy that was vigorously debated in the medical literature.2,3 However,in the past 20 yr, the scales of this controversy have resolutely tipped toward the conviction that l-z joints can be and often are a primary source of low back pain(LBP).4
在着手讨论L-z疼痛之前，明确小关节究竟是否可以产生疼痛这个概念非常重要。从1960s 到1970s，这个问题曾通过文献产生过激烈的争论。然而在过去的20年间，对于l-z可以产生疼痛的观点已经被十分坚定的接受，且l-z源性疼痛常常是下腰痛发生的最主要的原因。
Compelling evidence underlies this paradigmatic shift in thinking. The facet joint capsule and surrounding structures are richly imbued with nociceptors that fire when the capsule is stretched or subjected to local compressive forces.5,6 In both pain patients and volunteers,chemical or mechanical stimulation of the facet joints and their nerve supply has been shown to elicit back and/or leg pain.7–10 During spine surgery performed under local anesthetic (LA), lumbar facet capsule stimulation elicits significant pain in approximately 20% of patients.11 Last and most significantly, LA blocks of either the facet joints themselves or the medial branches innervating them have been shown to relieve pain in a substantial percentage of patients with chronic LBP.12Therefore, like other synovial joints in the human body,the l-z joints represent a potential pain generator inpatients with chronic LBP.
一些证据已为这种想法的基础。小关节囊及其周围结构富含疼痛感受器，当收到拉伸或局部压缩力时，可以被刺激。腰痛患者和志愿者的研究均表明，针对小关节和其支配神经的化学性或机械性刺激均可引发腰痛或腿痛。在局麻（LA）下的腰椎手术中，刺激腰椎小关节囊可以引发近20%患者产生腰痛。最后且最重要的是，局麻不仅阻滞了小关节本身，而且阻滞了内侧支，而阻滞内侧支本可以在部分病人中减轻疼痛。因此，像身体其他的滑膜关节一样，腰椎小关节也是慢性腰痛的发生器。In light of the prevalence of lumbar facet joint pain and the frequency with which facet blocks are performed,several reviews have been undertaken on this phenomenonin the past 15 yr. Although some of these articles provided keen insight on various aspects of the condition,most were limited by their confined scope and specialized target audiences. The purpose of this reviewis therefore to provide a comprehensive, evidence-basedframework on the anatomy, pathophysiology, prevalence,diagnosis, and treatment of lumbar facet pain.Articles reviewed were obtained via MEDLINE and Ovidsearch engines, books and book chapters, and bibliographic references dating to the early 1900s.
鉴于腰椎小关节疼痛的发病率较高及小关节阻滞的频繁开展，过去15年间已经对此种现象进行了一些回顾。虽然一些文章在不同的方面提出了敏锐的观点，但是大部分还是具有领域局限性及病患针对性。本文的目的是针对此现象做一综合的，基于证据的回顾，内容涉及解剖，病理，流行病，诊断及治疗等多方面。回顾所用的稳扎个来自MEDLINE 和 Ovidsearch搜索引擎，相关书及章节，参考文献最早到1900sHistoric Review
The l-z joints, often referred to as facet joints, have long been recognized as a potential source of LBP. In1911, Goldthwaite13 first noted that the peculiarities of the facet joints could be a significant source of back pain and instability. Sixteen years later, after anatomical dissectionsof 75 cadavers, Putti14 suggested that local inflammation and degenerative changes in lumbar facet joints could result in sciatica from irritation of nerveroots. In 1933, Ghormley15 coined the term “facet syndrome,”which he defined as lumbosacral pain, with or without sciatica, that was likely to occur after a sudden rotatory strain. Shortly thereafter, interest in the l-z joints as potential sources of back pain waned after the landmarkarticle by Mixter and Barr16 implicating lumbar discrupture as the major cause of low back and leg pain. The1940s saw a resurgence in the interest of l-z joints as pain generators when Badgley17 suggested that up to 80% of cases of LBP and sciatica are due to referred pain from l-z joint pathology, rather than direct nerve root compression.In 1963, Hirsch et al.7 published the first account whereby the injection of l-z joints reproduced patients’ back pain. Rees,18 who reported a success rate of 99.8%,is generally credited with promoting percutaneous“facet rhizolysis” with his ground-breaking report in the early 1970s. Later, it was shown that the technique advocated by Rees may not have been sufficient to achieve rhizotomy in most patients.3 Buoyed by a high incidence of hemorrhagic complications, Shealy19,20 pioneered the use of fluoroscopically guided radiofrequency facet denervation to treat l-z joint pain in the mid-1970s.
历史回顾：
L-z关节常常被称为小关节，长期以来被视为腰痛发生的潜在诱因。1911年，Goldthwaite首次说明小关节的结构特性可以引发腰痛和不稳。16年后在解剖了75例标本以后，Putti认为小关节的局部炎症和退化能刺激神经从而引起坐骨神经痛。1933年，Ghormley创造了“小关节综合征”一词，指腰骶部疼痛伴有或不伴有坐骨神经痛，可能来源于突然的腰部扭转。此后，Mixter and Barr暗示椎间盘破裂时导致腰腿痛的主要原因后，以此为标志，l-z关节作为腰痛的潜在来源的说法开始减弱。1940s，Badgley指出高达80%的腰痛和坐骨神经痛的病人疼痛来源于小关节产生的牵涉痛，而非由直接药品神经根而引起，由此l-z关节源性疼痛的关注有开始得到复苏。1963年，Hirsch用小关节注射的方法复制了患者的腰痛。由于Ree报道小关节射频神经切断术的成功率高达99.8%，1970s这一手术得到广泛开展。此后，Rees的方法被证实在大部分患者中不能有效切断神经。Buoyed报道这种方法并发血肿的概率很高。1970s中期，Shealy又首创了透视引导下射频消融达到小关节去神经化的方法。
Anatomy and Innervation
The lumbar facet joints form the posterolateral articulations connecting the vertebral arch of one vertebra to the arch of the adjacent vertebra. As true synovial joints,each facet joint contains a distinct joint space capable of accommodating between 1 and 1.5 ml of fluid, a synovial membrane, hyaline cartilage surfaces, and a fibrous capsule.21 The fibrous capsule of the lumbar facet joint is approximately 1 mm thick and composed mostly of collagenous tissue arranged in a more or less transversefashion to provide maximum resistance to flexion.22,23The joint capsule is thick posteriorly, supported by fibers arising from the multifidus muscle. Superiorly and inferiorly, the capsule attaches further away from the osteochondral margins, forming subcapsular recessesthat in the normal joint are filled with fibroadipose menisci.Anteriorly, the fibrous capsule is replaced by the ligamentum flavum.24
腰椎小关节组成后外侧关节，链接椎体的椎弓和其临近的椎弓。作为真正的滑膜关节，每个小关节包含明显的关节间隙，容纳1到1.5ml关节液。小关节由滑膜，透明软骨表面，和纤维囊组成。纤维囊厚约1mm，大部分有白色纤维组成，横向排列，以在屈曲时提供最大的张力。囊的后部很厚，纤维来源与多裂肌。囊的上部和下部较薄，附着于远离骨软骨边缘的地方，形成了囊下隐窝，正常情况下填充有纤维脂肪性软骨版。囊前部被黄韧带所取代。
Each facet joint receives dual innervation from medial branches arising from posterior primary rami at the same level and one level above the z-joint.25,26 For example,the inferior pole of the L4–L5 facet joint receives innervation from the L4 medial branch and its superior pole is innervated by the L3 medial branch, L1–L4 dorsal rami course across the top of their respective transverse processes one level below the named spinal nerve (e.g., L4 crosses the transverse process of L5), traversing the dorsal leaf of the intertransverse ligament at the base of the transverse process. Each nerve then runs downward along the junction of the transverse and superior articular processes, passing beneath the mamilloaccessory ligamentand dividing into multiple branches as it crosses the vertebral lamina (fig. 1). In some cases, the mamilloaccessory ligament becomes calcified, which may lead to nerve entrapment.27 This is most common at L5 (approximately 20%) but also occurs at L4 (10%) and L3(4%). In addition to two l-z joints, the medial branches also innervate the multifidus muscle, the interspinous muscle and ligament, and the periosteum of the neural arch.7,28–30 The L5 nerve differs in that it is the dorsal ramus itself that runs along the junction of the sacral ala and superior articular process of the sacrum.29,31 Its medial branch arises opposite the inferolateral corner of the base of the lowest facet joint. At this level, it is the dorsal ramus rather than its medial branch that is am enable to blockade.
每个小关节都受双重神经支配，分别来自同节段及上一临近节段背侧主支的内侧支。例如，L4-L5关节囊的下极接受L4内侧支支配，而其上极接受L3内侧支的支配，分别可在L5和L4的横突处阻滞。L1-L4 脊神经背侧支的内侧支行经各自横突的上端，为同名的下一个阶段脊神经（例如L4穿过L5的横突）。在横突基底部穿越横突间韧带的背侧叶。沿着横突和上关节突下行的神经支穿过乳突副突韧带的基底部，在椎板处分为多支小枝（图1）。在一部分病例中，乳突副突韧带骨化，使神经被包埋于其中。这种情况在L5中最常见（将近20%），单也常发生于L4 (10%) 和 L3(4%)。除了l-z关节以外，内侧支还支配多裂肌，棘间肌和韧带以及椎弓处的骨膜。L5神经有所不同，其背侧支本身走行于髂骨翼和髂骨的上关节突。其内侧支在最低关节囊的基底部下外侧角的对面发出。因此阻滞时只能针对背侧支而非内侧支。
Some people may have aberrant or additional innervation of the facet joints. In a study conducted in asymptomatic volunteers, Kaplan et al.32 found that 1 in 9 subjects who underwent L4–L5 (n = 5) and L5–S1 (n =4) facet joint medial branch blocks (MBB) felt pain during repeated capsular distension concordant with pain experienced during previous l-z joint provocation without MBB. Assuming the blocks were technically successful,one explanation for this finding is that in a small subset of individuals, aberrant innervation may account for false-negative diagnostic MBB. Some authors have suggested that l-z joints may also receive innervation from the medial branch below the joint (i.e., S1 for theL5–S1 joint),33,34 the dorsal root ganglion,35 and the paravertebral sympathetic ganglia,36,37 but these assertions remain unproven (fig. 2).
一部分患者的小关节可能存在异常的或其他的神经支配。在一项针对无症状志愿者的研究中Kaplan等发现，在接受L4–L5 (n = 5) 或 L5–S1 (n =4)小关节内侧支阻滞（MBB）的患者，每9例中有1人在阻滞后牵拉小关节仍会产生疼痛，性质与未阻滞前牵拉小关节所产生的疼痛一致。假设阻滞在技术上已经成功，那么这种现象的解释就是存在一部分患者，其小关节支配神经发生了变异，从而产生了小关节阻滞性诊断假阴性的结果。一些作者认为l-z关节也接受来自关节下部的内侧支及背侧根神经节，椎旁交感神经节的支配，但这些假设尚未得到证实（图2）。
Histologic studies have demonstrated that the lumbar facet joints are richly innervated with encapsulated (Ruffini-type endings, pacinian corpuscles), unencapsulated, and free nerve endings.5 The presence of low-threshold, rapidly adapting mechanosensitive neurons suggests that in addition to transmitting nociceptive information, the l-z facet capsule also serves a proprioceptive function. Besides substance P and calcitonin gene–related peptide, a substantial percentage of nerve endings in facet capsules have also been found containing neuropeptide Y, indicating the presence of sympathetic efferent fibers.38,39 Nervefibers have also been found in subchondral bone and intraarticular inclusions of l-z joints, that facet-mediated pain may originate in structures besides the joint capsule.40–42 In degenerative lumbar spinal disorders, inflammatory mediators such as prostaglandins43 and the inflammatory cytokines interleukin 1B， interleukin 6, and tumor necrosis factor _44 have been found in facet joint cartilage and synovial tissue.
组织学研究证实，腰椎小关节含有丰富的神经支配。包括有包膜（Ruffini型末梢，尼氏小体）、无包膜及游离神经末梢。低阈值，快适应型动力敏感神经元表明，l-z关节囊不仅传导伤害性信号，还起到本体感受器的作用。除了P物质，降钙素基因相关肽，还在一定数量的小关节神经末梢发现了神经肽Y，表明了存在一定比例的交感传出纤维。在软骨下骨及关节囊内也发现了神经纤维。因此小关节介导性疼痛可能是一种结构依赖性而非关节囊依赖性。在腰椎退变的病例中，在小关节软骨及滑膜组织中也发现了炎症介质如PG，炎性细胞因子，白介素1B，白介素6以及肿瘤坏死因子等。Function and Biomechanics
功能及生物力学
The basic anatomical unit of the spine, often referred to as the three-joint complex, consists of the paired zygapophysial joints and the intervertebral disc. Together,these joints function to support and stabilize the spine, and prevent injury by limiting motion in all planes of movement. Macroscopically, each facet joint is composed of a posteromedially facing concave superior articularprocess from the inferior vertebral body, and as maller anterolaterally facing inferior articular processfrom the superior spinal level. The shape and orientationof the l-z joints determine the role each plays in protectingthe spine against excessive motion. Facet joints oriented parallel to the sagittal plane provide substantial resistance to axial rotation but minimal resistance to shearing forces (backward and forward sliding), whereas joints oriented more in a coronal plane tend to protect against flexion and shearing forces but provide minimal protection against rotation (fig. 3).24 In an anatomical study published in 1940 by Horwitz and Smith,45 the authors found that the L4–L5 z-joints tended to be more coronally positioned (almost 70° with respect to the sagittal plane), whereas the L2–L3 and L3–L4 joints were likely to be oriented more parallel (<40°) to the sagittal plane. In more recent studies by Masharawi et al.46 andPunjabi et al.,47 the investigators found that the upper lumbar facet joints (T12–L2) were oriented closer to the midsagittal plane of the vertebral body (mean range,26°–34°), whereas the lower facet joints tended to be oriented away from that plane (40°–56°). In the upper lumbar spine, approximately 80% of the facet joints are curved, and 20% are flat. In the lower lumbar spine,these numbers are reversed.45 Studies by Grobler et al.48and Boden et al.49 found a positive association between degenerative spondylolisthesis and more sagittally oriented lower lumbar facet joints. In young people, the l-z joints are quite strong, capable of supporting almost twice body weight.23 As aging occurs, the joints become weaker and more biplanar,transitioning from a largely coronal orientation to a more prominent sagittal positioning. The orientation of each joint to the sagittal plane can also differ between the paired facet joints at the same spinal level. This phenomenonis known as tropism and has a 20–40% incidence among the general population.24,50 Most50–55 but not all49,56 studies have demonstrated a positive relation between facet joint tropism and intervertebral disc degeneration and herniation.
脊柱的基本解剖单元，常被称为三关节复合体，有成对的关节突关节和椎间盘组成。这些关节共同支持并稳定脊柱，限制其在各个方向上的运动以防止损伤发生。大体观，每个小关节由下位椎体朝向后内侧凹陷的上关节突以及上位椎体朝向前外侧的的下关节突组成。L-z关节的形状及朝向决定了其作用为阻止脊柱过度运动。小关节朝向趋于矢状位可以限制脊柱的轴向旋转但是减少了对剪应力的限制（前后运动时）。而趋于水平的小关节可以更好的保护屈曲和剪切下的应力，但对旋转的抵抗力降低（图3）。在1940年的一项解剖学研究中，Horwitz 和 Smith发现L4-L5小关节更趋向冠状位（相对于矢状面近70°），而L2–L3 和 L3–L4关节趋向与矢状面平行(<40°)。近期，Masharawi 和Punjabi等人的研究发现，上位小关节（T12–L2）的趋向更接近椎体的正中矢状面（平均角度26°–34°），而低位腰椎小关节的趋向远离正中矢状面(40°–56°)。在上位腰椎，近80%的小关节为屈曲面，而20%小关节为平面，而下位腰椎则刚好相反。Grobler和 Boden等人的研究发现，下位腰椎小关节的矢状走向的程度与退变性腰椎滑脱之间存在相关性。年轻人的l-z关节足够强大，可以支持2倍体重的重量。随着年龄增长，关节强度减弱，且多变为双平面，从大部分冠状位过度矢状位。同一脊柱节段的两个小关节的趋向也可以不同。这种现象称为趋向性，在人群中的发生率约为20–40%。大部分但并非所有的文献都报道了趋向性与椎间盘退变及突出之间存在的联系。
Although most of the axial load is borne by the intervertebral discs, the two other components of the three-joint complex, the l-z joints, also play a role in weight bearing, with the proportion dependent on several factors. In a study by Yang and King,57 the authors determined that normal facet joints typically carry 3–25% of the axial burden, which can increase even higher in patients with degenerative disc disease facet arthritis. During this seminal experiment, it was observed that with significant facet loading the inferior tip of the facets bottomed against the laminae below, functioning as pivots for the entire vertebral body to rotate backward. This resulted in considerable stretching of the superior facet capsules, manifesting as blood extravasating onto the outer surface of the capsule. In another cadaveric study, Adams and Hutton58found that the lumbar facet joints resist approximately16% of the intervertebral compressive force when standing erect versus near 0% when sitting, which helps explain the high intra discal pressures during unsupported sitting.59 Finally, after conducting in vitro experiments measuring induced loads on cadaveric lumbar facets, Lorenz et al.60 concluded that with increasing compressive loads, the absolute facet loads increases only slightly, so that the proportion of the axial burden borne by the l-z joints actually decreases with increasing stress. During extension, the normal load on the facet joints is always higher when compared with the neutral mode. After facetectomy, while the remaining load on the vestigial facet is substantially reduced, the peak pressure increases.60In summary, the l-z joints serve primarily a protective role, functioning to limit movement in all planes of motion. Whereas they do play a part in weight bearing, the proportion of the axial load they bear is inversely proportional to the amount of stress.
虽然大部分轴向负荷由椎间盘负担，但是作为三关节复合体的小关节仍在承担负荷中发挥了一定作用，其作用的大小取决于许多因素。Yang 和 King的一项研究表明，正常情况下，小关节承担3–25%的轴向负荷，在椎间盘退变小关节炎的患者，其承担的负荷增大。初步研究发现，小关节负荷明显增加后，，其关节底部尖端顶向椎板的下面，称为整个椎体向后旋转的功能结构。这导致了小关节囊上部明显拉伸，表现为血液渗出到关节囊的外表面。另一项尸体标本的研究中，Adam和Hutton发现，当直立站立时，小关节承担了逐渐压力的近16%，而坐位时进0%，这解释了为什么在无支持的坐位时椎间的压力非常高。最后，Lorenz在尸体标本加载负荷后测量小关节的应力后，认为增加压力负荷时，小关节间的应力仅轻微增加，因此在轴向负荷中，小关节承担的比例实际随着应力的增加而减少。当拉伸时，小关节承受的应力相对于中立位来说有所增加。小关节切除后，残存小关节的应力也减少，但应力的峰值增大。总之，l-z关节的主要作用是保护，功能是限制脊柱在各个方向上的运动。它也起一部分的体重承载作用，其承载的轴向负荷的部分与整体负荷程反向相关。
Mechanisms of Injury Cadaveric and Animal Studies
损伤机制 尸体标本及动物研究
Although in rare instances the development of facet joint arthropathy can be traced to a specific inciting event,61 the overwhelming majority of cases of l-z joint pain are the result of repetitive strain and/or low-grade trauma accumulated over the course of a lifetime. Khalsa et al. conducted a series of cadaveric experiments designed to determine which physiologic movements are associated with the greatest degree of facet joint capsule strains. They found that the joint moments measured at any given motion increased with greater magnitudes of joint displacement, and were significantly larger in the two most caudad facet joints (L4–L5 and L5–S1).62 With lateral bending, strains of the joint capsule tended to be larger in magnitude in the three most caudad joints(L3–S1) during contralateral flexion (i.e., the left facet joints are most strained during right lateral flexion),whereas the two most cephalad joints (L1–L2 and L2–L3)bore the greatest strain during bending to the ipsilateral side. For the upper three facet joints, the maximum joint displacement and greatest strain was associated with lateral bending, usually to the right. For the two lowest joints, the greatest degree of strain occurred during forward flexion (table 1).
虽然在少数病例中，小关节病变的发展史由于特殊的刺激造成的，但是绝大部分的病例中，l-z关节性疼痛是源于反复的牵拉以及/或低强度的损伤积累的结果。Khalsa等进行了一系列尸体标本的实验研究，以确定何种生理运动下关节囊收到的拉伸力量最大。他们发现任何运动使关节发生位移时，都会增加关节的力矩，并且在尾部两个关节中增加更显著(L4–L5 和 L5–S1)。当向对侧弯曲时侧弯时最尾端(L3–S1)的三个椎体的小关节囊的拉伸强度增大（例如右侧屈曲时左侧小关节达到最大的应力）。而头端的两个关节(L1–L2 和L2–L3)在向同侧屈曲运动时拉伸力量最大。对于上位的三个小关节，最大的应力与最大的形变与侧曲相关，右侧屈曲时尤甚。对于尾端的两个小关节，最大应力在前屈时发生（表1）
In a follow-up study, the authors fixated human lumbar spine specimens with a single anterior thoracolumbar plate on L4–L5, and then measured capsular displacement and strains for a wide range of physiologic motions.63 For all motions, increased joint moments occurred at the level of fixation and both adjacent levels.There was also an increase in intervertebral angulation at L3–L4 and L5–S1, and decreased motion at L4–L5. Increased strain was noted bilaterally at L3–L4 and L5–S1,and contralaterally at L4–L5. On the side ipsilateral to the fixation, decreased strain was found at L4–L5. These findings support the work of other investigators demonstrating that fusing two vertebrae results in a transfer of motion previously occurring at the operated level to adjacent segments, particularly L5–S1, which in turn can lead to accelerated degeneration.64–68
随后的研究中，作者用前路胸腰椎钢板固定了人脊柱标本的L4–L5节段的一侧，测量大范围生理运动时关节囊的位移和应力。所有运动都导致固定节段及其临近节段的力矩增大。L3–L4 和 L5–S1的椎间成角也增大, L4–L5的活动度减小。L3–L4 和 L5–S1双侧关节应力均增加，L4–L5固定对侧的应力增大，其固定同侧的应力减小。这些结果支持了其他学者的研究结果，表明两个节段固定以后可以导致运动转移，主要发生在手术节段和临近节段，尤其是L5–S1，可导致其退变加速。
In a subsequent study, Little and Khalsa69 found that both sustained and repetitive lumbar flexion increased capsular motion and joint strain from L3–L4 to L5–S1,with creep developing more rapidly during sustained flexion than with repetitive movements. Interestingly,these parameters remained elevated even after a 20-min recovery period. Although these studies provide a theoretical framework for the development of micro injury associated with repetitive spine movements, cadavers can not experience pain, and the viscoelastic material properties factored into computational cadaveric spine models may differ from those found in live patients.70
后来的研究中，Little 和Khalsa发现反复和持续性的腰椎屈曲运动增加从L3–L4到L5–S1关节囊的运动及小关节的应力，持续屈曲比反复运动时增加更快。有趣的是，在恢复了20分钟以后，这些参数仍然持续增加。虽然这些研究为反复运动导致微小创伤的观点提供了理论框架，但是尸体不能感受疼痛，而且尸体和活体的粘弹性材料属性也不同。
In response to repetitive strain and inflammation, the synovial l-z joints can fill with fluid and distend, resulting in pain from stretching the joint capsule.71 Distension of the articular recesses can also compress the exiting nerve root in the neural foramen or spinal canal, especially when the foramen is already narrowed by joint hypertrophy and/or osteophytes. 72–75 This can lead to concomitant sciatica and mask the facet pathology underlying the radiculopathy. Capsular irritation may also result in reflex spasm of the erector spinae, multifidus,and other paraspinal muscles.72,76,77
反复的应力与炎症反应，可使滑膜l-z关节充满滑液并扩张，导致关节囊收到牵拉产生疼痛。关节囊隐窝的扩张可以压迫神经孔出的神经根出口或压迫椎管内脊髓，尤其当由于关节肥大和/或骨赘形成已经存在椎间孔狭窄时发生率更高。这可以导致伴随性坐骨神经痛的发生，且在此神经根病的影响下可能忽略小关节病的存在。关节囊收到刺激也可以导致反应性竖脊肌，多裂肌和其他椎旁肌的痉挛。
In in vivo and in vitro experiments designed to reproduce facet capsular stretch, nerves typically cease firing shortly after the stimulus is removed.78–80 Although these findings indicate that capsular strain could cause acute facetogenic pain, they do not explain its persistence.The pathophysiologic basis for persistent lumbarfacet pain was established in a series of elegant experiment sconducted by Cavanaugh, Yama***a, Ozaktay, etal. in New Zealand white rabbits. In these studies, the application of inflammatory chemicals or algesic mediators such as substance P and phospholipase A2, were found to result in inflammatory changes consisting of vasodilation, venous congestion, and the accumulation of polymorphonuclear leukocytes. Neuronal sensitization occurred in both nociceptive and proprioceptive nerve endings, being manifested by reduced mechanical thresholds, increases in multiunit discharge rate and recruitment of previously silent units.81–84 Persistent nociceptive input invariably leads to peripheral sensitization,and if the underlying stimulus is not removed,central sensitization and neuroplasticity can develop.85Whereas the spinal structures in humans are subject to greater stress than other mammals, because of the array of anatomical and functional differences that exist between the l-z joints in various mammalian species,86caution should be exercised when extrapolating the results of animal studies to humans.
体内和体外实验再现了关节囊的拉伸，当去掉刺激后神经也停止了放电。虽然这些研究表明关节囊的应力可以导致急性关节源性疼痛，但并不能解释其疼痛的持续性。Cavanaugh, Yama***a, Ozaktay等人在新西兰大白兔上已经建立了一系列相关实验以解释持续性疼痛发生的病理生理学。P物质，磷脂酶A2等炎性化学物质或疼痛介质的作用下，导致一系列炎性反应，包括血管舒张，静脉充血以及多形核白细胞聚集。在疼痛感受神经和本体感受神经末梢，都发生神经致敏作用，这可以通过机械刺激阈值降低得以证实，从而导致了多单位放电率的升高以及原来静默单位的恢复放电。持续不断的刺激输入疼痛感受神经，导致其神经末梢致敏，如果潜在的刺激因素继续存在，可导致中枢致敏。然而由于人类脊柱小关节的解剖及功能结构较其他哺乳动物不同，使其较能承受更大的压力，所以将动物实验的结果推到人类身上时要尤其谨慎。
One inferential interpretation of these preclinical findingsis that chronic l-z joint pain is likely to occur with repetitive, chronic strains as might be seen in the elderly or, less frequently, after an acute event such as tearing the joint capsule by stretching it beyond its physiologic limits. This hypothesis is supported by clinical studies indicating a higher prevalence of facet arthropathy in elderly patients87–89 and numerous cases of lumbar facet arthropathy after high-energy trauma.61
对于慢性l-z关节疼痛的一项推论性的解释是疼痛发生于慢性反复的牵拉，这种情况多见于老年人。另一种非常见的解释是其发生于突破关节囊生理极限的急性撕裂。一些临床证据支持上述解释，如临床常见老年患者及高能量损伤后经常发生小关节病变
Human Studies
患者研究
Clinically, several conditions may predispose individuals to chronic facet joint strain. Radiologic studies conducted in LBP patients and asymptomatic controls have shown a positive correlation between sagittally oriented facet joints and degenerative spondylolisthesis.48,49 In these patients, recurrent rotational strains result in myriad changes to the discs and paired l-z joints, including loss of disc height, osteophyte formation, and degenerative hypertrophy of the facets.90,91
在临床上，多种情况可以造成慢性小关节劳损。放射学研究表明，下腰痛患者及无症状的对照组中，小关节矢状面方向及退行性滑脱之间存在正相关。在这些患者中，反复的旋转性应力导致椎间盘和小关节的多种改变，包括椎间盘高度丢失，骨赘形成和退变性关节面增生等。
Changes in any component of the three-joint spinal unit lead to predictable changes in the other components.Degeneration and loss of structural integrity of the intervertebral discs have been shown to result in concomitant degenerative changes in the l-z joints.92–94 The reverse is also true. Degeneration and motion abnormalities at the l-z joints can induce and accelerate degeneration of the intervertebral discs.58,95,96 In a magnetic resonance imaging (MRI)study evaluating the relation between facet joint osteoarthritis and degenerative disc disease (DDD), Fujiwara et al. 97 found that facet joint osteoarthritis was rarely found in the absence of disc degeneration but tended to be most pronounced at spinal levels associated with advanced DDD. The authors concluded that disc degeneration is a more reliable indicator of aging than facet joint osteoarthritis, and in most people,DDD precedes facet osteoarthritis.
脊柱三关节复合体单位中的任何一个组分的改变均会导致其他组分相应的变化。椎间盘的退变和结构组分的丢失均可导致l-z关节的退变。反之亦然。L-z关节退变及异常运动可以导致椎间盘退变加速。一项MRI的研究评估了小关节骨性关节炎与椎间盘退变性疾病（DDD）之间的关系。Fujiwara等人发现小关节骨性关节炎在无椎间盘退变中发生率不高，但是在退变相关节段较显著。作者总结认为，椎间盘退变是老化更可靠的依据，且在大多数人中，椎间盘退变疾病发生于小关节之前。
Paradoxically, in the only clinical study evaluating the relative contributions of DDD and facet arthropathy to chronic LBP, Schwarzer et al.98 found the combination of discogenic and l-z joint pain to be a relatively rare occurrence. In 92 patients who underwent both discography and confirmatory l-z joint blocks with lidocaine and bupivacaine, 39% had at least one positive discogram with a negative control disc, and 9% obtained concordant pain relief after the series of analgesic facet joint blocks. But only 3% of patients had both positive discography and a symptomatic l-z joint. The discrepancy between the handful of basic science studies demonstrating a correlation between DDD and facet joint degeneration and the lone clinical study finding minima loverlap between the two pain generators indicates that more research is needed on this topic.
相反的是，在单纯的临床研究中，评价DDD及小关节病在下腰痛中的地位时，Schwarzer等发现，椎间盘源性和小关节源性的腰痛发生率皆不高。在一项研究中，92例患者同时接受了椎间盘造影和确切的利多卡因布比卡因联合阻滞，39%在阴性对照下至少存在一个阳性的椎间盘X线照片结果。在接受了阻滞后，9%的患者疼痛缓解。但是仅有3%的患者同时存在椎间盘造影阳性和l-z关节疼痛缓解。基础研究结果的不一致性表明DDD与小关节退化间存在一定联系。唯一的临床研究发现两种疼痛源之间存在交叉也说明了此问题需要更进一步的研究。
Aside from osteoarthritis, several other conditions may affect the facet joints. These include inflammatory arthritides such as rheumatoid arthritis, ankylosing spondylitis and reactive arthritis,99–101 synovial impingement,meniscoid entrapment, chondromalacia facetae, pseudogout,synovial inflammation, villonodular synovitis, and acute and chronic infection.102–106 Intrafacetal synovial cysts can be a source of pain because of distension and pressure on adjacent pain-generating structures, calcification,and asymmetrical facet hypertrophy.107–110 In a retrospective review of MRI scans in 303 consecutive patients with LBP, Doyle and Merrilees111 found that9.5% had facet joint synovial cysts, the large majority of which were located posteriorly. Trauma may also cause lumbar facetogenic pain. There are more than two dozen reported cases of lumbar facet dislocation after rapid deceleration injuries (e.g., traffic accidents), most involving L5–S1.61,112–115 The mechanism of injury in these cases is purported to be a combination of hyperflexion, distraction, and rotation.61,112,116 In a posthumous study conducted in 31 lumbar spines of subjects who died of traumatic injuries (mostly motor vehicle accidents),Twomey et al.117 found occult bony fractures in the superior articular process or subchondral bone plate in 35% of victims, and z-joint capsular and/or articular cartilage damage in 77% of cases. The authors concluded that occult bony and soft tissue injuries to the l-z joints may be a common cause of LBP after trauma.
除了骨性关节炎，许多其他的疾病亦可影响小关节。包括炎症性关节炎如类风湿性关节炎，强直性脊柱炎及反应性关节炎等，还有滑液撞击，关节软骨版卡压，关节面软骨软化，假性痛风，滑液炎症，绒毛结节性滑膜炎和急慢性感染。小关节内滑囊囊肿可由于拉伸和压缩临近的疼痛发生结构，骨化及不对称关节增生等原因引起疼痛。在一项303例连续患者的MRI研究中，Doyle 和 Merrilees发现其中9.5%存在小关节囊肿，大部分发生于关节囊后部。创伤也可导致腰椎小关节源性疼痛。多项研究报道了急性减速伤（如交通事故）后发生腰椎小关节分离，多数发生于L5-S1，其机制可能为过度屈曲，分离和旋转。在一项对死亡病例的研究中，Twomey 等发现，31例因交通事故死亡的人中有35%的腰椎上关节突或软骨下骨性终板存在隐匿骨折，77%存在小关节囊和/或关节软骨损伤。作者总结创伤后隐匿性股和软组织损伤也许是腰痛的来源。
