Lumbar Facet Syndrome

Zygapophysial Joints (ZGAs) in Lumbar Spine

International Publicized Data

GMCD Instructional Course Lectures

Author:

Dr. med. Guy MC Declerck MD (GMCD)

Medical FRCS-, FRCS Ed Orth-, M Ch Orth-, PhD-studies

Spinal Surgical and Research Fellow, Perth, Western Australia

Spinal Orthopaedic Surgeon and Surgical Instructor

Consultant R&D Innovative & Restorative Spinal Technologies

President International Association of Andullation Therapy (IAAT)

Copywriter / Translator:   Filip Vanhaecke PhD

Illustrative expertise:   Jasper Baele, HHP and ProVision, Waregem, Flanders, Belgium

Review scientific literature:   Medical Consulting Advice, Ostend, Flanders, Belgium

Support:   International Association of Andullation Therapy

Legal advice:   Anthony De Zutter, kornukopia.be

Dedication to my mysterious girlfriends. March 2014

What happens if you are submerged by (Facebook) friends, suffers digibesitas, and having no free time? Why did you all walked behind me? I don’t lead. Why did you all walked in front of me? I don’t follow. Why did you all not simply walked beside me to become my friend (Albert Camus)?

It is not a lack of love, but a lack of friendship that makes unhappy relationships (Friedrich Nietzsche).

Although free time is a terrible thing to waste, you all kept your free time in the past where nobody could touch it!  And it’s what men/women do in their free time that will see them free or enslave them (Kintz).

There is consistent evidence that human beings underestimate that time is a powerful force altering their personalities, reshaping their values, and transforming their preferences in the future (Sedikides & Alicke).

Denying this tendency leads to suboptimal decision-making which can be regretted in the future. I hear and feel it’s regretted already. Indeed, prospection is a constructive process, retrospection is a reconstructive process, and constructing new things is typically more difficult than reconstructing old ones (Addis & Wong & Schacter).

However, thanks to you all, I found the insight on the twisted logic of love and enmity, attraction and repulsion, affinity and antagonism (Terry Eagleton).

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Introduction

Relying on the work of giants is the lifeblood of scientific research. Indeed, if I have seen further, it is by standing on the shoulders of giants. One might even say that I have always depended on the kindness of strangers in this regard (*).

The continuous support by professor BA Kakulas (Neuropathology), professor JR Taylor (Spinal Anatomy and Human Biology), and Sir George M Bedbrook (Spinal Orthopaedic and Rehabilitation Surgeon) made it possible to analyse 23539 post-mortem human spines, normal and pathological, in the Department of Neuropathology, Royal Perth Hospital/University Western Australia, Perth.

Note: in order not to disturb easy reading of the underneath scientifically based chapters, only a few authors are mentioned in the text where dr. Guy considered it essential. Their names are placed between brackets. Further information on their individual research can be read in the last chapter ‘Literature Encyclopedia’.

(*) Mirsky Steve. Copy That. Technology is making it harder for word thieves to earn outrageous fortunes.

    Scientific American, February 2014, p.64

Table of Contents

1. The Greek term ‘zygapophysial’ joint (ZGA)

2. The ZGA joint is an articulation with hyaline cartilage and synovial lining>

3. The capsule of the ZGA joint

4. Small anatomic openings in the capsule surrounding the ZGA joint

5. Shape and orientation of the articular facets of the ZGA joints

6. The orientation of the lumbar ZGA joints varies

7. Bilateral asymmetry (tropism) and its significance

8. Functional interrelationship between intervertebral disc and ZGA joints.

9. Essentials of the degenerative processes in the intervertebral discs (IVDs)

10. The stabilising role of the ZGA joints

11. ZGA joints are load sharing structures

12. ZGA joints guide but limit segmental motion

13. Traumatic intra-articular lesions of the ZGA joints

14. Degenerative arthritis of the ZGA joints

15. Can the ZGA joint(s) cause low back pain?

16. Can the ‘facet joint syndrome’ - dorsal ramus syndrome - really be defined by clinical

      examination and radiological examination?

17. Innervation of the lumbar ZGA joints contains substance P pain sensitive receptors

18. Intraarticular and/or pericapsular ZGA joint needling procedures

19. A ‘simple’ and ‘diagnostic’ ZGA joint arthrogram?

20. A diagnostic and/or therapeutic intraarticular ZGA joint injection

21. Which - and how many – ZGA joints need to be ‘blocked’ intraarticularly?

22. Nearly all intraarticular ZGA joint injections are epidural blocks

23. What to conclude from intraarticular ZGA joint ‘blocking’ injections?

24. Extraarticular nerve block or thermocoagulation of the pericapsular nerves

25. Andullation: additional conservative pain relieving and healing method

26. Literature Encyclopaedia

1. Greek term ‘zygapophysial’ (ZGA) joint

Zygos’ in Greek means bridge and ‘apophysis’ signifies outgrowth. The spinal ‘bridging outgrowths’ form the posteriorly located articulations between two adjacent vertebrae (Fig. 1a, 1b, 1c) and are called the zygapophysial joints (ZGAs). The shorter term, ‘apophyseal’ joint, is an acceptable term and used regularly.

Because the ZGAs contain various intra-articular facets, each responsible for a particular functional aspect of the ZGA, describing a ZGA joint simply as a ‘facet’ joint is incorrect and too simplistic. Most joints in the human body are multifaceted but all have been well defined with simple names (e.a. knee, ankle, elbow, wrist joint etc…). As there is no rational reason to discard the original Greek term, zygapophysial will be respected in the underneath text.

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Fig. 1a. (Left): radiological images of the L3-L4, L4-L5, and L5-S1 ZGA joints (X90-879)

Fig. 1b. (Middle): anatomical views of the L3-L4, L4-L5, and L5-S1 ZGA joints (X90-879)

Fig. 1c. (Right): sagittal view at L1 and L2 pedicular levels with T12-L1 and L1-L2 ZGA joints (X90-879)

2. ZGA joint: hyaline cartilage and synovial lining

Each ZGA joint is composed by two posterior articular processes (= ‘outgrowths’) of two consecutive vertebrae (Fig. 2a, 2b). The superior articular process (SAP) embraces the inferior articular process (IAP). The diarthrodial joint is coated with hyaline articular cartilage and lined with synovium. Like any other synovial joint, the ZGA will undergo the normal course of aging. When degeneration starts, the initial arthritic changes are mostly seen at the proximal and distal ends of the processes because the tips of the ZGAs have no cartilage.

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Fig. 2a. (Left) and Fig. 2b. (Right): the zygapophysial joint is a diarthrodial and synovial joint. It is well-coated with articular hyaline cartilage (white zone). The tips of the superior articular process (SAP) and inferior articular process (IAP) have no cartilage. The anteromedial part is not covered by fibrous capsular tissue but by the ligamentum flavum (LF). NR = nerve root. VB = vertebral body

3. Capsule of ZGA joint

The ZGA joint is not circumferentially surrounded by a fibrous capsule. The capsule is thick in its posterior and lateral aspects. The anteromedial part of the ZGA near the spinal canal is not closed by fibrous tissue but replaced by the ligamentum flavum which is in direct contact with the synovium in the ZGA joint (Fig. 2b).

4. Normal anatomic openings in the capsule

At the superior and inferior parts of the ZGA joints, the capsule forms small but normal anatomic openings through which extracapsular adipose tissue moves in and out the joints during the lumbar spinal movements. During the performance of an arthrogram, these normal openings provide a direct route for extravasation of dye into the epidural space. When too much contrast is injected in a ZGA (2 ml or more), the dye always will leak through these normal anatomic holes making the physician incorrectly conclude to a ‘rupture’ of the joint capsule (Fig. 4a, 4b, 4c).

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Fig. 4a. (Left): during spinal movements, fat tissue (yellow) moves in an out through normal superior and inferior anatomical openings in the capsule of the ZGA joint

Fig. 4b. (Middle): Author’s conception of an injection of too much blue dye into a ZGA (2 cc or more) resulting in ‘leakages’ through the normal anatomic openings

Fig. 4c. (Right): radiological visualisation of leakages through a normal inferior anatomic opening

5. ZGA joint: shape and orientation of its facets

The shape and orientation of the planes of the articular facets in the ZGA joints determine the relative movements allowed by these joints (Fig. 5a, 5b). The anterior frontally oriented third of the ZGA resists flexion, whereas the posterior sagittally oriented component limits anteroposterior shear movements. As one moves caudally through the lower lumbar levels (L3-L4, L4-L5, L5-S1), a change in the orientation of the articular facets of the ZGAs becomes clear.

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Fig. 5a. (Left): T12-L1 ZGA joint in the axial plane. The surface of the superior articular process (SAP) is concave and projects posteromedially. The surface of the inferior articular process (IAP) is convex and directs anterolaterally. There exists a rounded ‘angle’ (more than 90°) between the horizontal and a sagittal components. At the higher lumbar levels (T12-L1, L1-L2, L2-L3) the sagittal orientation is more prominent

Fig. 5b. (Right): Axial view of a L5-S1 ZGA joint. The ZGA becomes less ‘angled’ as the horizontal component becomes more prominent. Note the asymmetry between both ZGAs at the same level

6. Lumbar ZGA joints: orientation varies

Considering the average angle to the sagittal plane (Fig. 6a, 6b), an increase of that angle is clearly distinguished from the T12-L1 vertebral level down to the L5-S1 lumbosacral level. The angle can vary enormously: between 70° and 80° at L3-4, between 80° and 90° at L4-L5, and even over 100° at L5-S1 levels.

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Fig. 6a. (Left): orientation of a ZGA joints in the lumbar spine, (Middle): in the thoracic spine, and (Right) in the cervical spines

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Fig. 6b. Orientation of the ZGA joints. If oriented 45° to the sagittal axis (red line) there is resistance to forward displacement and rotation. If oriented 0° to the sagittal axis, the ZGA strongly resists rotation. If oriented 90°, there is a strong resistance to forward displacement

7. Bilateral asymmetry (tropism) and its significance

The three-dimensional construction of both ZGA joints at the same lumbar level varies as well. In about 50 % of individuals an average asymmetry varying from 10° to 42° can be measured between left and right ZGAs (Fig. 7a). A difference of 5 degrees or more at one particular lumbar level represents articular tropism.

Tropism strongly suggests the existence of irregular movements. Asymmetry between the ZGAs may lead to increased rotatory hypermobility and torsional strain on the intervertebral disc accelerating the degenerative processes in the nucleus pulposus and creating more annular tears. However, no association has been shown between ZGA joint asymmetry at one particular level and the production of a nuclear herniating pathway at the same level (protrusion, extrusion, or sequestration).

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Fig. 7a. Asymmetry of 5° or more between the two ZGA joints at the same lumbar level is called tropism and may lead to rotatory hypermobility

8. Interrelation: intervertebral disc and ZGA joints

The stability and the flexibility of the lumbar spinal column is provided by interaction between the intervertebral discs (IVDs) in the anterior spinal column and zygapophysial joints in the posterior column (Fig. 8a). But as age advances, degenerative processes usually occur in the IVD and subsequently in the ZGA joints. As can be noted on CAT and MRI and has been confirmed by post-mortem analyses: ‘discs degenerate before ZGA joints’.

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Fig. 8a. Intervertebral discs and ZGA joints interact for spinal stability and flexibility

9. Essentials on the degenerative discogenic processes

The progress of degenerative processes in the lumbar IVDs leads to the decrease of the hydrostatic pressure resulting in disruption of disc tissues. At the upper lumbar L1-L2 and L2-3 levels, the depressurisation rather occurs in the presence of or is associated with endplate erosions. At the lower lumbar levels, the decrease in nuclear pressure rather leads to the transmission of higher compression loads and an increased concentration of compressive stress into the posterior portions of the annulus. Indeed, the prevalence of annular tears is much higher at the L4-L5 and L5-S1 disc levels. However, it is evident that ruptures of the endplates and the annuli can be present at the same time (Fig. 9a). These disruptions in the disc mostly occur in the sitting, standing, or bending posture. Each of these alterations is considered to initiate (chronic) low back pain.

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Fig. 9a. The L4-5 intervertebral disc level (A90/139) presents degenerative internal nuclear disruption, degenerative endplate fissures, anterior and posterior annular bulging, disc height narrowing and osteoporotic vertebral bone

10. ZGA joints: stabilising role

The stabilizing role of the ZGA joints is clearly shown during in vitro experiments and following inadvertent and inappropriate surgery. Partial removal or total resection of the ZGA joints, unilaterally or bilaterally, induce a significant non-physiological segmental range of motion in axial rotation and anteroposterior sagittal translation (Fig. 10a).

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Fig. 10a. Inappropriate (surgical) removal of parts of the ZGA joints induce abnormal intervertebral hypermobilities in different directions (red lines)

11. ZGA joints: load sharing structures

Body weight is carried by the vertebral bodies and the adjacent pedicles. In the non-degenerative and healthy lordotic lumbar spine, the axial compressive loads between two vertebral bodies are transmitted by the endplate, nucleus and annulus of the intervertebral discs. Axial compressive loading between the adjacent pedicles is transferred by the ZGAs. The percentage of transmitted load depends on (1) the spinal posture, (2) the degree of intervertebral disc degeneration, and (3) the orientation of the facets in the ZGA joints. In the upright standing position 10 % to a maximum of 20 % of body weight is carried by the ZGAs (measured by mathematical and in vitro models). During increasing hyperextension, more load is transmitted through bony contact at the tips of the inferior articular processes (IAP) with the laminae of the vertebra below. At that moment, the capsules of the ZGAs may be extensively stretched. In forward flexed positions and sitting postures the posterior spinal joints are relatively unloaded in compression but they carry more than 50 % of the anterior shear load. The ZGAs are loaded most heavily in torsion under compression.

When the intervertebral discs start degenerating and disc space narrowing ensues, the forces (N) and stresses (N/m²) on the ZGA joints may increase up to 70 % depending on the spinal posture. An average of 36 % increase in the ZGA pressure has been measured for a 1-mm loss in disc height and an average of 61 % for a 4-mm disc narrowing.

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Fig. 11a. (Left) and 11b.(Right): Typical and routine radiological views of internal disc degeneration with subsequent structural destruction of the ZGA joints. This patient never experienced low back pain

As there is no cartilage at the tip of the ZGA joints, these structures are not supposed to resist compressive forces. As narrowing of the IVD progressively occurs, the ZGAs undergo subluxation until the tips of the inferior facets impinge on the vertebral laminae. This evolution increases the contact areas as well as the load transmission between the ZGAs (especially during extension movements). Increased compressive forces cause increased peak pressures and initiate thinning of the articular cartilage in the ZGAs. Both processes of subluxation and cartilage thinning cause capsular laxity allowing more abnormal motions and hypermobility in the motion segment which already was initiated by IVD degeneration. In the more advanced stages of IVD degeneration (and more disc space narrowing), the neural arch starts stress shielding the posterior annulus (in extension) allowing even more compressive load to be transmitted through the ZGAs and the neutral arch (and the anterior annulus). In these stages of IVD degeneration, more degeneration of the cartilage at the ZGAs will occur and give rise to bony hypertrophy and osteophytes, stabilising the segmental hypermobility and altering other spinal motion segments. The final immobilisation of the deformed ZGAs and motion segments may be associated with the development of lumbar spinal stenosis compressing the cauda equina, lateral canals and the nerve roots (Fig.11a and 11b).

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Fig. 11b. R. (A90/149): Paramedian sagittal section through two adjacent degenerated intervertebral discs. Both upper L1-L2 and L2-3 IVDS are grossly disrupted. The ZGA joint is grossly degenerated: hypertrophic, reactively remodeled assuming a transverse orientation and no longer the ball-and-socket configuration

12. ZGA joints guide but limit segmental motion

The ZGAs maintain alignment, allow but limit segmental mobility between two adjacent lumbar vertebrae when exposed to flexion-extension, lateral bending and/or rotational forces. However, once the aging and degenerative processes start with ensuing narrowing of the disc space, the intervertebral disc (IVD) always will lead to alterations in the biomechanical loading patterns of the zygapophysial joints.

The amplitude and direction of the movements at each spinal segment (= 2 vertebrae, the IVD and the 2 ZGA joints) are determined by the 3-D orientation of the planes of the ZGAs. These posterior articulations limit lateral bending but are mainly designed for resisting torsion movements and forces. Although the twisting movements in the lumbar spine are coupled with various combinations of lateral bending, flexion, and extension, the normal motion segment is stiff when pure axial rotation is attempted (McFadden; Farfan). The ZGAs block the lumbar axial rotation which has been calculated to be extremely limited to allow only 2° to 3° in each direction (to the left and to the right).The resistance to torsional stress is greater in the more sagittally oriented L1-L2, L2-L3, and L3-4 ZGAs. This explains why the corresponding IVDs are better protected from severe rotational injuries. Indeed, degenerative annular tears are much more frequent in the IVDs at the lower L4-5 and L5-S1 segments where the ZGAs are more frontally oriented.

13. ZGA joints: traumatic intra-articular lesions

When victims of road traffic accidents or falls need surgical procedures to stabilize their spinal fractures,capsular and cartilaginous lesions with exposure of the subchondral bone are frequent findings in the various facets of the ZGA joints. Accidents directly can tear the articular capsule and the ligamentum flavum and even damage the articulation causing cartilaginous fibrillation, synovitis and cysts. None of these intra-articular injuries can be visualized with the existing radiological methods. Then, pre-operative radiological absence of traumatic injuries to the vertebral bodies and/or to the intervertebral discs does not mean that the victims did not sustain lesions in the ZGA joints.

Post-mortem macroscopic and histologic analysis of ZGAs are presently the only available methods to diagnose various subtle lesions. This type of investigations is been performed in the Departments of Anatomy and Embryology (Prof JR Taylor), and Neuropathology (Prof BA Kakulas) at the University of Western Australia in Perth since 1958. Frequently encountered ‘subtle’ aberrations are: synovial plicae, intra-articular haemorrhages, splits in the articular cartilage, separations of the articular cartilage from the subchondral bone, subchondral bone infarctions, tears of the articular capsule, and fractures of the (mostly superior) articular processes (Fig. 13a, 13b, 13c, 13d). Tears of the ligamentum flavum in one or more joints are seen in +/- 77%.

Similar lesions are routine findings in all other synovial joints. All these abnormalities can be arthroscopically diagnosed and handled in the shoulder, elbow, hip, and knee. In the absence of degenerative lesions into the lumbar intervertebral discs, all the mentioned aberrations in the posterior joints may be the primary sources of continuing low back pain (Taylor).

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Fig. 13a. (Left): intra-articular fracture at the tip of the IAP in an ZGA joint

Fig. 13b. (Right): intra-articular ZGA haemorrhages (M-A83-58)

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Fig. 13c. (Left) and 13d. (Right): intra-articular ZGA joint fractures (Courtesy of professor JA Taylor, Perth, Australia)

14. ZGA joints: degenerative arthritis

It is evident that traumatic lesions of the capsules and the articular cartilage of the ZGA joints may consolidate. But when these lesions result in intraarticular irregularities, interfere with the normal gliding mechanism between the joint surfaces, and alter the normal biomechanical loading patterns, the lesioned ZGA is predisposed to early development of degenerative osteoarthritis. This evolution is similar to that in any other synovial joint in such situation.

In the non-traumatic situation, osteoarthritic changes in the ZGAs are secondary to the evolving degenerative processes inside the intervertebral disc. When the intervertebral disc starts losing its height, the cartilaginous surfaces of the inferior articular process (IAP) and the superior articular process (SAP) are subjected to increased pressures and stresses as well as abnormal motions which result in degradative structural and metabolic changes of the cartilage (Fig. 11a).

Unfortunately, not a lot can be done to halt the degenerative osteoarthritic processes. There exists no vaccination to prevent osteoarthritis. What is well known, is that the quantity, the quality and the osmolarity of the remaining synovial tissues and the articular cartilage can be maintained by daily appropriate gentle active and passive mobility exercises.

It needs to be reminded that osteoarthritis does not equal pain. A huge amount of middle-aged adults worldwide have typical radiological signs of OA in their hips, knees, shoulders, elbows, spines and other joints, but only few experience discomfort, disabling pain or functional limits. On the other hand, people with radiological ‘normal ’ joints may have pain.

Likewise, ZGAs with a radiological image of degeneration and/or osteoarthritis can be totally asymptomatic while ZGAs with none or minimal structural derangement may be the source of pain.

15. Can zygapophysial joint(s) cause low back pain?

Yes. The role of the ZGA joints in generating pain was first proposed in 1911 (Goldthwait). But the modern diagnostic methods still do not allow to indicate that the ZGA is the sole responsible factor for developing (chronic) low back pain. Finally ‘diagnosing’ a lumbar zygapophysial joint as the main reason for low back pain is based on ‘trial and error’ thinking and handling. However, it is totally acceptable that a ZGA may account for part of a spinal problem. Indeed, the prevalence of the posterior spinal joint as an additional part of pain symptoms in the lumbar spine has been suggested to vary between 15 % and 40 %.

Some symptoms in some low back pain sufferers can be caused by accidents and/or evolving osteoarthritis of the ZGA joint.

Deformation or stretching or distension of the joint capsule and irritation of synovium in normal, in degenerating and in degenerated ZGAs may be the mechanical sources of pain as they stimulate the available pain receptors. But in the degenerated ZGA, it has been clearly shown that only 30 % of the capsules are sensitive to mechanical stimulation (Kuslich). Because the degenerated ZGAs present irregular or absent cartilaginous lining, pain may be explained as well by irritation of the subchondral bone. Bone tissue contains nerve endings sensitive to substance P, an essential molecule involved in the transmission and sensation of pain.

Although all the above have been scientifically proven, typical and diagnostic clinical and radiological signs and symptoms do not exist to delineate an unique articular disorder of the spine called ‘lumbar facet syndrome’.

16. Can ‘facet joint syndrome’ be defined?

In 1933 the controversial term of ‘facet syndrome’ was brought forward. But as this syndrome was not irrevocably defined, since then a lot has been published regarding this ‘syndrome’. Although there is no doubt at all that low back pain may originate primarily from a ZGA joint complex, it has been estimated that on its own the ZGA is responsible for only 2 % to 7 % of low back pain symptoms.

Even this estimation and based on my own exclusive spinal formation, my spinal surgical experience, and intense review of the spinal literature, I still have no clue what really means a ‘facet syndrome’ and how to diagnose it correctly.

In my opinion, and except for patients who suffer ‘inexplicable’ low back pain problems and presenting totally ‘normal’ discovertebral radiological investigations as a consequence of trauma, it is not at all evident to conclude that a ZGA joint complex may be the solely responsible structure. The patient’s history, physical examination, and imaging studies are unreliable to conclude to the certainty that the ZGA is the sole culprit.

Both the intervertebral discs (IVDs) and the ZGAs share load during all weight bearing situations. However, the ZGAs are loaded most heavily in torsion under compression. Consequently and from clinical perspective, low back pain should be intensified by motions that are known to load the ZGAs primarily. Then, a history of intermittent bouts of low back pain brought on by movements of combined lateral bending, rotating and arching backward with or without causing referred (= non-topographical, non-radicular) leg pain and subsequently lessened by fluently bending forward, is suggestive for a ‘pathological’ ZGA joint. At least when the IVDs are intact and well hydrated. Degenerative disc lesions can excite exactly the same intermittent bouts of low back pain in the chronic intermittent or in the chronic undulating LBP situations.

The presence of a well localized and mostly unilateral tender spot - and in the absence of abnormal neurologic motor findings - further indicates a potential ZGA problem.

Because the ZGA is a synovial joint, rising in the morning may not be easy. Daily appropriate gentle active and passive physical activities ease symptoms in most painful synovial joints as they maintain the quantity, the quality, and the osmolarity of the remaining synovial tissues and the articular cartilage. Then, LBP aggravated by rest in any posture, including recumbency (e.g. pain at night), and subsequently relieved by repeated or continuous gentle movement (Eisenstein) may further suggest the involvement of a ZGA joint.

But the clinical diagnostic problem remains. LBP due to internal degenerative disc disruptions, endplate fissures and annular ruptures are associated with morning stiffness, pain at night, and the urge to move around the settle the pains (even at night).

On top of it - and especially for those who only rely on radiological ‘images’ for their diagnoses - all existing imaging studies have been shown to be invalid and unreliable as diagnosing methods to conclude to a so-called isolated ‘facet’ syndrome. There exists no correlation between the aforementioned symptoms and signs and osteoarthritic features seen on plain XR, CAT, MRI, arthrography etc …. All the aging and degenerative changes are universally present in all synovial joints of the human body in …. asymptomatic individuals!

The ZGA joints are part of low back pain but rarely as primary reason. Evaluations of post-mortem lumbar spines confirm the findings by CAT and MRI findings: ‘facets degenerate after disc degeneration’.

17. Lumbar ZGA joints: substance P pain sensitive receptors

The dorsal rami of the outgoing lumbar nerve roots give rise to medial branch nerves which provide a rich innervation for the lumbar zygapophysial joints. The capsule of each ZGA may receive medial branches from up to three spinal nerve roots. For example, the L3-L4 ZGA may receive rich innervation provided by the medial branches originating from the L2, L3 and L4 spinal nerve roots (Bogduk).

Although less consistent than in the cervical ZGA joints, the fibrous capsules as well as the synovial lining of the lumbar ZGAs are well innervated. They contain a variety of free and encapsulated mechanoreceptive and afferent nociceptive nerve endings which both are substance P immunofluorescent.

As the ZGAs are load bearing structures, excessive physiological loads but especially abnormal loads due to intervertebral disc degeneration, may induce pain by stimulating the pain sensory nerves. Mechanical irritation of intraarticular ZGA synovial inclusions and/or capsular structures during abnormal spinal positions, compression, pinching, tension, stretching, etc … are sensed by the mechanoreceptors. This normally results in a reflex activity of the paraspinal muscles to regulate function, position, and balance of the lumbar spine (Indahl).

18. ZGA joints: intraarticular versus pericapsular needling

All the needling procedures, extraarticular, intraarticular or combined techniques, remain a field of challenge and experimentation. None is superior to the other. None is definitely diagnostic to indicate that the ZGA joint is the only reason inducing low back pain. Some low back pain patients will have ‘spectacular’ pain relieving results. But in one and the same patient, sometimes intraarticular injections will prove to be superior to pericapsular injections, sometimes it will be the opposite. There is simply no rationale for predicting an outcome of an injection in or around a ZGA joint.

19. ZGA joint arthrogram: simple? and diagnostic?

The major reason for performing an arthrography – under guiding radiographic control - is to localize the exact site for precisely inserting a needle and subsequently injecting a ‘therapeutic’ fluid into this small joint.

Only a few drops of dye are necessary (one drop ~ 0,05 cc) to visualise the ‘inside’ of the ZGA which volume is no greater than 1,5 cc. The initial contrast injection may reveal an inflammation of the synovium (synovitis), an occasional synovial cyst, an intraarticular fracture, or even confirm a spondylolysis.

However, the interpretation of a radiographic contrast-filled ZGA has nearly no value compared to similar arthrograms of large joints (hip, knee, shoulder, etc …). The joint is simply too small to visualise the lesions which are frequently encountered during macro- and microscopic investigations of these joints at autopsy.

Inadvertently or unknowingly injecting a larger volume of dye (1,5 to 2 cc) stretches the capsule joint (Fig. 4c) and may irritate the substance P containing mechanoreceptors and nociceptors. The (re)produced low back pain may then be so intense that further ‘therapeutic’ intraarticular or pericapsular injection needs to be abandoned.

20. Intraarticular ZGA injections: diagnostic? therapeutic?

It is well-known that intraarticular ZGA joint injections in asymptomatic volunteers may cause severe but short-term pain in a specific area of the low back. Indeed, the nociceptive nerve endings in the intracapsular synovial structures can react accordingly. In these cases and when referred pain would arise in the buttocks, posterior thigh and below the knee, the temporarily discomfort can even be associated with positive neuromeningeal tension signs which disappear rapidly when the capsule no longer is stretched.

More than 100 years following the suggestion that a lumbar ZGA joint may induce low back pain (1911), it remains frustrating that a diagnostic or therapeutic ‘block’ does not unequivocally indicates that a lumbar zygapophysial joint may be the pain culprit.

Most percutaneous needling procedures of ZGAs were initiated in the late 1970s. Different injections of water (normal, isotonic, or hypertonic saline) and/or an anaesthetic (bupivacaine / lignocaine) and/or corticosteroids (hydrocortisone / methylprednisolone acetate) were and are still tried. Whatever the combination, none has been proven to be better than the other. In other words, corticosteroid injections are no better than saline (water) injections. There exists no rational explanation for it but only indicates that the ZGA joint rarely is the single or primary cause of low back pain and/or referred leg pain.

All types of ZGA joint injections can provoke low back pain and temporary referred leg pain. They can evoke short-term symptomatic relief of low back pain or have no effect at all. Only 68 % of chronic low back pain sufferers report rapid initial but temporary symptomatic relief. Complete long-term relief (more than 6 months) is present in only 6 % to 20 %.

Single ZGA joint ‘blocks’ are reported to have a false-positive rate of 38 % (Schwarzer). ZGA ‘blocks’ have even been associated with a placebo response rate of 32 %. Note that there is nothing wrong with a placebo! Patients who possess the specific genetic variation of the COMT-enzyme (= catecholamine-O-methyltransferase-gene) on their DNA, produce more serotonin and dopamine in their prefrontal cortex, hormones responsible for a satisfying response (Finniss; Hall).

21. How many and which ZGA joints need to be ‘blocked’?

Deciding which ZGA joints should be needled is rather arbitrarily. Because there are no objective grounds to judge which ZGA joint(s) is/are the culprit, the decision can only be made from the patient’s pain distribution and the radiological ‘pictures’.

From an anatomical point of view, at least two (but better three) joints should be injected if only one is ‘found’ to be the culprit, three to four if two ZGAs are considered responsible (Fig. 21), …. Trying to find out which ZGA then finally is the most probable cause of pain remains wishful thinking and handling or as the Germans define:‘fingerspitzengefühl’.

And of course, repetitive anaesthetic blocks at different levels and on separate occasions may eliminate the ‘cheating’ joints. Once the culprit found, the infiltrating technique may be repeated over and over again.

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 Fig. 21. Totally inaccurate investigation as minimum two levels need to be explored The cornerstone for all healing processes is the production of scar tissue. The formation of collagens depends for 80 % on piezoelectric effects (Fukada; Minary-Jolandan). Then, healing effects of andullation are explained by the fact that vibrations penetrate into the body, transform the collagen fibrils, and as such induce the required piezoelectric effects for the fibroblasts to fulfil their synthetic activities.

22. Intraarticular ZGA injections as epidural blocks?

To avoid extravasation, the total injected volume of a diagnostic or therapeutic fluid needs to be as small as possible: maximum 1,5 cc. The volume of the small ZGA joint is estimated at only 1,5 cc.

When excess fluid is injected, greater manual pressure is needed. Then, leakages occur through the normal anatomical openings in the superior and/or the inferior parts of the ZGA joints (Fig. 4b). Leakages may occur as well through unexpected ruptures in the capsule joint caused by trauma and which were never visible during the (repeated) radiographic investigations.

If the volume of the diagnostic or therapeutic fluid to be injected is not respected, surplus of anaesthetic and/or a corticosteroid will leak into the epidural space ending up in a combined ZGA joint and epidural block.

23. Conclusion regarding intraarticular ZGA joint ‘blocks’

It is evident that the diagnosis of a pathologic ZGA joint responsible for low back pain (LBP) is considered when relief of pain is achieved. However, it has long been known that an injection into a ZGA is of little durable value in the treatment of patients with LBP (Carette; Jackson). Any disappearance or decrease of pain is coincidental and eventually transient.

Intraarticular ‘blocking’ of a ZGA remains an aspecific, unreliable and unpredictable modality for potentially diagnosing and/or treating low back pain even if it results in temporarily relieve of pain. The only conclusion that can be made from a ‘successful’ ZGA infiltration is that part of the patient’s low back pain and referred leg pain is attributable to a lumbar ZGA joint. Nothing more. Nothing less.

Pathologic changes in the lumbar spine are rarely isolated to a single ZGA. From biomechanical and functional point of view, this observation is totally normal and logic to explain. In response to the processes of intervertebral disc degeneration, internal nuclear disruption and consequent loss of disc height, the ZGAs will undergo higher mechanical strains during spinal loading. It ultimately affects both the structure and function of the disco-ZGA joint complex bridging two adjacent vertebral bodies. Post-mortem and radiological studies indicate that, except in traumatic cases, the intervertebral disc nearly always degenerates before ZGA joints. The anatomopathological findings during analysis of the different lumbar disco-ZGA joint complexes (including the thoracolumbar and the lumbosacral levels) in over twenty-three thousand post-mortem cases (23,000!) in the Department of Neuropathology in Perth, Western Australia (1958 till 1991), concluded that ZGA joint involvement followed degenerative IVD pathology in 98 % of all examined specimens.

The day innovative scanning devices will be able to monitor the human cellular and molecular damage (Chung) at spinal level, it will become possible to associate directly the post injection period of relief of low back pain with the nature and the ‘degree’ of intervertebral joint and ZGA joint degeneration.

24. Extraarticular nerve block or thermocoagulation

Those who consider an intraarticular ZGA joint procedure a controversial and non-reliable diagnostic and/or therapeutic procedure concentrate on an extraarticular needling procedure of the posterior spinal joints (for anatomic reasons at least two!).

The dorsal rami of identical spinal nerve roots give rise to medial branches whose nerve endings (mechanoreceptors and nociceptors) terminate inside and on the outside capsular structure of the ZGAs.

Extraarticular capsular needle probing techniques are applied frequently. Saline, anaesthetics and/or corticosteroids are injected locally to these medial branches or directly around the capsules of a suspected ZGA joint (Fig. 24).

So-called lumbar ZGA joint denervation by ‘burning’ the nerves with radiofrequency waves through a needle (= percutaneous rhizotomy or rhizolysis) was introduced in the 1970’s (Rees; Shealy). Thermocoagulation of these nerves has no value as the nerves will ‘regenerate’.

However, it remains totally unpredictable if those extraarticular needling procedures will achieve some short-term or no-term pain relief. Conclusions can never been extrapolated.

facet_005.png

Fig. 24. Example of an extraarticular lumbar medial nerve branch block. Because the nerve branch passes at the level between the transverse process and the superior articular process (SAP), the tip of the needle is positioned in this zone to inject local anesthetic, sterile water or a corticosteroid. Skilled and sensitive fingers do inject the ‘therapeutic’ fluids at different points of the capsule without penetrating the ZGA joint

25. Additional conservative pain relieving method

Biophysical methods using energy (e.g. warmth, electric currents, UV light, IR radiation, ultrasonic sound, laser beams, magnetic fields, etc ...) are physiotherapeutic tools to suppress low back pain complaints. Andullation induces energy by applying low frequency vibrations in combination with infrared light. The pain inducing effect of andullation is explained by the theory of Melzack and Wall. The vibrating sensory stimuli applied to the skin are filtered by the T cells in the spinal cord (‘gate control’) before being forwarded to the brain where pain relieving effects result. Because the mechanically generated vibrations are stochastically modulated, andullation can be employed for long times activating the liberation of pain relieving endorphins.

The cornerstone for all healing processes is the production of scar tissue. The formation of collagens depends for 80 % on piezoelectric effects (Fukada; Minary-Jolandan). Then, healing effects of andullation are explained by the fact that vibrations penetrate into the body, transform the collagen fibrils, and as such induce the required piezoelectric effects for the fibroblasts to fulfil their synthetic activities.

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