Lumbar zygapophyseal joint arthropathy

Author(s): Clifford Richard Everett, MD, Mark Bauernfeind, MD, and Maria Vanushkina, MD

Originally published:09/19/2012

Last updated:03/27/2017

1. DISEASE/DISORDER:

Definition

Arthropathy, or joint disease, of the zygapophyseal or “facet” joint (FJA) is a clinical and pathological syndrome that involves the functional failure of facet joints (FJ).1

Etiology

Improper FJ alignment and load distribution are believed to be the major contributors to the development and progression of FJA, with the earliest changes typically occurring in the regions that experience the greatest mechanical forces.1 In patients with healthy spines, the disc is the primary load bearing structure with only 33% of axial load carried through the facets.2 As discs degenerate (DDD) with age, they become functionally incompetent and up to 70% of the load is transferred through the facets.3 As a result, with the shifted transmission of force, pathology beginning in a disc progresses to osteoarthritic changes in the FJ at that vertebral level.1,4 Thus, lumbar FJA frequently occurs at the levels most commonly affected by DDD, L4-S1.5

Epidemiology, risk factors and primary prevention

Asymptomatic facet degeneration can start in teenagers and progresses over a lifetime to affect 90% of the elderly.1 CT imaging studies have shown moderate or severe FJA in 36% of adults age <45 years, 67% of adults age 45-64 years, and 89% of those age 65 years or older; with rates in women nearly twice those in men.6 The risk of FJA increases almost threefold in overweight, and fivefold in obese, individuals.7 Concurrent disc-height narrowing is associated with roughly doubled odds of FJA independent of age, sex, and BMI.6 Primary prevention is directed at modification and reduction of risk factors.

Low back pain (LBP) symptoms can derive from many potential anatomic structures within the back, including FJA, however FJA found on imaging is often asymptomatic.8 Of patients with localized LBP, facetogenic pain accounts for 15-50% depending on the population studied and the means of diagnosis.1,4,8

Patho-anatomy and physiology

Facets consist of the inferior articular process of the superior vertebra and the superior articular process of the inferior vertebra and exhibit features typical of synovial joints including aneural articular cartilage, synovial membrane, capsular pouch, fibroadipose meniscoid, and a fibrous capsule.9 FJs function to stabilize and limit excessive flexion, extension, side-bending, and axial rotation of the spine. Each joint receives dual innervation from the medial branches of the dorsal primary rami of the same level and the level above.1 Studies have demonstrated free and encapsulated nerve endings in lumbar FJs, as well as nerves containing substance P and calcitonin gene-related peptide.1,10 One in nine patients have FJ innervation from other nerves.1,4 Direct pressure on subchondral bone, intramedullary hypertension, trabecular micro-fractures, capsular distension, and synovial inflammation activate nociceptor fibers leading to pain.1

Disease progression including natural history, disease phases or stages, disease trajectory

The earliest changes of FJA involve the articular cartilage, synovium, and capsule. Cartilage breakdown begins focally and superficially, progresses deeper, encompassing the entire joint, and eventually erodes down to the subchondral bone.12 In early arthropathy the joint capsule might show fibrosis and increased vascularization with inflammatory cells. Extensive fibrocartilage proliferation occurs later.13 Osteophyte formation and remodeling of the subchondral bone with formation of sclerosis and subchondral cysts are characteristic of advanced disease.1

Specific secondary or associated conditions and complications

At any stage of the disease, mechanical joint injury can initiate an inflammatory response leading to muscle spasms and radicular symptoms from leakage of cytokines through the ventral capsule.4,10,11 Prolonged peripheral inflammation can lead to central sensitization, neuronal plasticity, and development of chronic spinal pain.4,14 Foraminal stenosis, radicular symptoms, and nerve impingement may occur due to joint hypertrophy and synovial cyst formation.4 Adult degenerative scoliosis and degenerative spondylolisthesis are also related to FJA secondary to failure of motion segments.1

2. ESSENTIALS OF ASSESSMENT

History

There are no symptoms specific/unique to FJA. Common causes of acute and chronic LBP can have similar presentations.10 History is most useful in excluding alternative etiologies, in particular radiculopathies, fractures, infections, neoplasms, or rheumatologic conditions.1,4 “Typical” facetogenic LBP is progressive.4 Referred pain is predominantly in the buttock and thigh, rarely radiating past the knee.15

Physical examination

There are no specific signs or special tests to aid in FJA diagnosis, which is often guided by the absence of signs that suggest alternate etiologies. The only exam finding that correlates with facetogenic LBP is paraspinal tenderness, which has been shown to distinguish facet from discogenic back pain.4,16 “Facet loading”, or pain upon extension and ipsilateral rotation, was popularized in a small, retrospective study; however, larger, higher quality studies have consistently failed to replicate this finding.16, 17,18,19

Functional assessment

Mobility can be impaired due to pain. Studies have repeatedly failed to identify patient reported activities that are associated with the presence of facetogenic LBP.4

Laboratory studies

Laboratory studies are not used to diagnose FJA, but facilitate exclusion of other etiologies of LBP. Renal and hepatic function studies maybe be needed to guide medication management.

Imaging

The current recommendation is to avoid imaging for acute LBP within the first 6 weeks of presentation unless red flag symptoms are present.20,21 The majority of available epidemiologic studies showed no consistent relationship between the presence or severity of FJA on CT, SPECT, fused PET and CT, and/or MRI and the presence of LBP.1,4 Imaging may help to exclude FJA, as multiple radiological studies have demonstrated that DDD almost always precedes JF degeneration, especially in older adults.4

Supplemental assessment tools / Early prediction of outcomes

Lumbar medial branch blocks (MBBs) are recommended (level I) for patients with suspected facetogenic LBP as the gold standard for diagnosis and for definitive therapy patient selection.4,10,22 For MBBs, the false positive rate in the lumbar spine is between 17-44% and the false negative rate is about 8%.4,10,22 Interestingly, false-positive responders have been shown to experience benefits that are indistinguishable from those of treatment responders.23 Dual blocks with at least 80% pain relief following injection are a prognostic indicator for good response to definitive therapy with radiofrequency ablation (RFA). The use of dual blocks has been advocated to reduce the high false positive rate by multiple organizations, however this remains a controversial topic. The consequences of false-negative blocks, commonly caused by aberrant joint innervation by non-medial branch nerves or patient failure to distinguish daily pain from procedure-related pain, are serious because it means a safe, effective treatment will be withheld from a patient.4

Early predictions of outcomes

Environmental

Poor postures and/or heavy lifting have been reported to increase the risk of future sick leave due to back pain.24

Social role and social support system

Chronic LBP can lead to missed work and disability. Biopsychosocial factors such as depression, poor coping skills, lack of home/community support, somatization, secondary gain issues (e.g., ongoing litigation), and greater disease burden (e.g., high dose opioid use, previous spinal surgery) can lead to harder to treat pain and worse interventional outcomes. Poor patient selection, including the aforementioned reasons, for invasive treatments is perhaps the most common reason for treatment failure.1

Professional Issues

From 2000 to 2013, in the Medicare population alone, MBBs and RFAs increased at a rate of 213% and 522% respectively.25 Review of the FJ injections allowed by Medicare Part B in 2006 found that 63% did not meet the program requirements for reimbursement, 38% had a documentation error, 31% had a coding error, 8% did not establish medical need, and 14% had overlapping errors.26

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

Multiple organizations have published guidelines on FJA (ASIPP in 2000 with 5 subsequent updates, American College of Occupational and Environmental Medicine in 2007-2008, American Pain Society in 2009, Official Disability Guidelines in 2010, and SIS) and some have received major scrutiny/criticism by experts for poor methodology.27

At different disease stages

New onset/acute:
No studies have evaluated non-interventional therapy for injection-confirmed FJ pain, so treatment is extrapolated from patients with non-specific LBP.4,28 Initial conservative management, including NSAIDs, home exercise, nutrition/weight reduction, acetaminophen, topical agents, ice/heat, and addressing psychological factors, is recommended for both acute and chronic FJ pain. A multidisciplinary approach should be employed, with minimally invasive interventional techniques offered to patients not responding to conservative treatment. Exercise therapy, especially physical therapy (PT), has the strongest evidence for efficacy compared to all other non-interventional treatments.4 PT, with overall better outcomes than a home program, should address posture, range of motion, muscular strengthening, and activity/risk factor modification.4 Acupuncture and chiropractic or osteopathic manipulation have low quality evidence for short term pain relief; but when compared to sham, other non-interventional treatments, or physical exercise, the results are inconclusive.4 Early interventional modalities are sometimes performed for very painful presentations and may aid in therapy participation.29 Muscle relaxants are effective agents for acute LBP.4 Recent reforms are promoting a decrease in opioid use as new guidelines published by CDC in 2016 noted early opioid exposure increased the risk of long-term use.30 If using opioids, clinicians should prescribe the lowest effective dose of immediate-release formulations for three to seven days maximum.30 A clinically meaningful improvement after initiation of any therapy has been defined as a 30% improvement in scores for both pain and function.31

Subacute:
If symptoms have been present for more than three months and have not responded to conservative treatment, interventional methods are often pursued. These interventions include intra-articular corticosteroid injections, MBB , and RFA, the standard of care, following diagnostic MBB. Therapeutic nerve blocks remain controversial but within a single study using local anesthetics have demonstrated fair to good short and long-term improvement in symptoms but often require multiple injections, with 90% of responsive patients receiving an average of 5 to 6 procedures over a 2 year period.10 At the end of one year, 69% of therapeutic MBB patients showed significant improvement in pain compared to 90% in the RFA group.25 There is good evidence (level I) for RFA efficacy in short term (<6 months) and lesser evidence (level II) for long term pain relief in appropriately selected patients.25 The efficacy of RFA for functional improvement is limited, with only low quality evidence available to suggest that RFA has greater effect than placebo.32 Serious complications from RFA are rare (<1%).4 Comparatively, intra-articular injections (level III evidence), are more difficult to preform, are inferior diagnostic and prognostic indicators of RFA, have limited evidence, and most review studies suggest that they are largely ineffective, save possibly in a certain subset of patients with positive SPECT scans.4,25

Chronic/stable:
If RFA has yielded positive results, it can be repeated every six months with expected relief lasting up to 13 months for repeat treatments.10 Opioid therapy for chronic LBP is a controversial topic and not generally recommended. There is no good evidence that opioids improve pain or function with long-term use, and the complete relief of pain is unlikely.30 Clinicians should use extreme caution when considering increasing opioid dosages for chronic LBP and should follow current guidelines.30 There is a lack of evidence for arthrodesis and surgery for spondylosis or facet-mediated pain. Surgery can however be indicated in patients with symptomatic instability of the spine.

Coordination of care

The physiatrist’s role is to coordinate a multidisciplinary approach to treatment as mentioned above.

Patient & family education

“Back School” can improve the quality of life in patients who suffer from chronic LBP and prevent recurrent injuries.33 Patient education appears to reduce the negative consequences of fear-avoidance behavior that occurs when attempting active exercise-based rehabilitation and thus promotes treatment compliance. Patient and family education should be focused on risk factor reduction and modification and home exercise programs.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

The presence of isolated paramidline LBP increases the probability of symptomatic FJA and mildly reduces the likelihood of lumbar DDD.34 If the patient has failed conservative treatment and injection is the next step, the site of pain can be palpated and confirmed under fluoroscope before diagnostic MBB. By attempting to confirm the level of pain prior to the injection, the accuracy and potential efficacy of the procedure may improve.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

Recent imaging techniques have used fat suppressed, cross-sectional MRI sequences to evaluate changes in the FJs and surrounding structures. Subchondral bone marrow edema-like lesions can be picked up using this sequence and have been associated with clinical manifestations of pain, and are present in the lumbar facets of 14-41% of patients with back pain in at least 8 studies.1 The use of ultrasound instead of fluoroscopy or CT to guide lumbar MBBs has been studied recently with several studies demonstrating feasibility.35–37 Techniques for percutaneous facet fusion are available, but long-term published results are not available.38

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

There is an ongoing need for more and better designed studies examining the efficacy of interventional and conservative management options. For interventional procedures, a true placebo-controlled trial is reportedly difficult to design and has not been performed to date.22

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Original Version of the Topic

Amit Bhargava, MD. Lumbar zygapophyseal joint arthropathy. 05/19/2013.

Author Disclosure

Clifford Richard Everett, MD
Nothing to Disclose

Mark Bauernfeind, MD
Nothing to Disclose

Maria Vanushkina, MD
Nothing to Disclose

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