Lumbar spondylosis without myelopathy

Author(s): D.J. Kennedy, MD, Renata Jarosz, MD, Ryan Demirjian, MD

Originally published:09/20/2013

Last updated:09/20/2013

1. DISEASE/DISORDER:

Definition

Lumbar spondylosis is broadly defined as osteoarthritic changes affecting the triad of joints forming the spinal columns: the paired zygapophysial joints (z-joints) posteriorly and the intervertebral disk anteriorly. These degenerative changes are ubiquitous with increasing age, but in some cases they can be associated with low back pain (LBP). This condition can cause secondary myelopathy if the spondylosis results in cauda equina compression.

Etiology

The exact cause of lumbar spondylosis is unknown. Because it affects synovial joints, lumbar spondylosis can be thought of as being analogous to peripheral osteoarthritis (OA), and likely results from an imbalance in the synthesis and degeneration of the articular cartilage.

Epidemiology including risk factors and primary prevention

The prevalence of radiographic spondylosis increases with age. It is uncommon in the first few decades of life, but ubiquitous by the age of 65. In those with LBP, the prevalence ranges from 7% to 75%, depending on the diagnostic criteria.1 The prevalence in the United States ranges from 15% to 45% among patients with chronic LBP.1,2

Risk Factors

Commonly accepted risk factors are the following: increasing age, genetic predisposition, being a woman, previous injury, and joint overload from malalignment and/or abnormal z-joint orientation.3 After the age of 45 years, advanced cartilage changes, subchondral sclerosis, and osteophyte formation are common.4 Genetic predisposition has also been shown to be a significant contribution to symptomatic and radiographic lumbar spondylosis in several studies. Cadaveric studies demonstrated that when compared with men, women of similar age showed a larger grade of cartilage degeneration and more osteophytes. The presence of estrogen receptors in cartilage was found,2 and higher estrogen expression correlates directly with higher levels of z-joint arthritis.1 Disk desiccation and z-joint malalignment are both associated with spondylosis.5 Greater z-joint sagittal orientation correlated more with degenerative changes in the z-joints and a higher incidence of spondylolisthesis.5,6

Patho-anatomy/physiology

Studies have shown that within the lumbar spine this degradation frequently follows a common degenrative cascade, with the initial step being intervertebral disk desiccation. Collagen cross-linking and inability to hold water stiffens the cartilage and the capsule structures, leading to an altered range of motion. In the lumbar spine, the z-joints have a posterior-lateral orientation to resist axial rotation and translation. Thus, the degenerative changes frequently arise earlier and are more advanced in the regions that resist translation, specifically the anterior-medial portion of the joints and most frequently at the L4/L5 and L5/S1 levels, likely because of their proximity to a fused sacrum.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Although variable, most of the patients experience a benign clinical course. Studies have shown the following:

  1. Radiologic spondylosis directly increases with age, irrespective of pain.7
  2. Spondylosis was shown to be equally present in those with and without LBP.3
  3. No correlation between the magnitude of z-joint arthorpathy and the severity of pain.1

Specific secondary or associated conditions and complications

z-joint hypertrophy, because of osteophyte formation combined with ligament redundancy from the disk desiccation, may collectively lead to spinal canal and/or intervertebral foramen narrowing. The increase in translation forces from disk desiccation, combined with the z-joints decreased ability to resist these factors, may also result in spinal instabilities, specifically spondylolisthesis. Excess synovial fluid production can result in secondary synovial cysts formation. All of these changes can result in central or lateral stenosis, radiculopathy, and/or, in severe cases, cauda equina syndrome.

2. ESSENTIALS OF ASSESSMENT

History

The symptoms are acute or gradual onset of diffuse LBP, possibly with an epicenter. Pain may refer unilaterally or bilaterally to the buttock, hip, groin, and thigh regions; although, typically, it does not extend past the knee.1,8 The pain tends to worsen with extension, rotation, and standing; it is better with lying and L-spine flexion.8 By definition, lumbar spondylosis exhibits no neurologic deficits; however, because of its association with conditions that can affect the neurologic function of the lower limbs, it is imperative to ask about weakness, balance, gait, and bowel/bladder function.

Physical examination

A systematic review revealed that most physical exam maneuvers have limited or no diagnostic validity for spondylosis.1; Paraspinal tenderness is the only physical exam maneuver that seems to correlate with z-joint arthropathy. Although clasically felt to diagnose z-joint pain, joint loading with pain on extension and ipsilateral rotation has been not shown to consistently correlate with spondylosis.9,10 Because the pain distribution may overlap with other clinical entities, a comprehensive exam including hip, sacroiliac joint provocative maneuvers should be performed routinely. Associated neurologic conditions should be ruled out through thorough strength, sensation, reflexes, gait, and balance testing.

Laboratory studies

None are routinely indicated. Laboratory studies, such as C-reactive protein, sedimentation rate, and complete blood count, can be done if there is a clinical suspicion for a more nefarious condition, such as tumor, infection, or rheumatologic disease, such as spondyloarthropathies.

Imaging

z-joint arthropathy is common on all imaging modalities with increasing age, and has a weak to no association with controlled diagnostic blocks. Imaging is therefore typically done to rule out other disorders, and can take the form of plain radiographs, magnetic resonance imaging (MRI), and computed tomorgraphy (CT) studies.9

Plain radiographs are not sensitive for detecting early z-joint OA, but are highly accessible, and often used. Lateral views are important to study sagittal alignment and the presence of spondylolisthesis.

MRI is generally not needed for diagnosis of spondylosis, but it is useful for evaluating the soft tissues and neural elements within the spine. Large amounts of fluid within the z-joints may represent instability, which can be further assessed by flexion/extension films.

CT is typically utilized only when an MRI is unobtainable.

Supplemental assessment tools

Diagnostic Injections

Given the high prevalence of radiographic spondylosis, the only means for an accurate diagnosis of symptomatic lumbar spondylosis are controlled diagnostic blocks11 of the medial branch nerves that innervate the z-joints.

Several key principles exist for diagnostic blocks:

  1. Because of inaccuracy of landmark guidance, all blocks should be preformed utilizing image guidance.
  2. False positive blocks occur at a high rate of 17% to 41% in the lumbar spine, thus necessitating a second control block for confirmation of the diagnosis. The 2 injections are done with anesthetics with differing durations of effect. With dual positive blocks (>1h with lidocaine and >3h with bupivacaine hydrochloride), the sensitivity and specificity are greatly enhanced.10
  3. The greater the percentage of pain relief a patient obtains with a given injection, the more likely that injection correctly targeted the pain generator. Some clinicians accept 50% pain relief as a diagnostic criterion. An 80% pain relief with comparative medial branch blocks results in more successful outcomes with radiofrequency ablation.10,11

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

Although a few guidelines have been created, to date, none are universally accepted for z-joint treatment.

Coordination of care

As with all spine conditions, treatment should ideally be a multidisciplinary team and a coordinated approach with a physical therapist and a phsyician.

Patient & family education

Patients should be educated that the condition typically responds to treatment. Education should be provided regarding warning signs for disease progression into secondary neurologic conditions, such as myleopathy.

Emerging/unique Interventions

There are several validated outcome measures that can be utilized for grading functional limitations including the following: McGill Low Back Pain Scale, Oswestry Disability Index, and the Medical Outcomes Study 36-Item Short-Form Health Survey. These are typically administered at every office visit for following the functional limitations and disease progression.

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

Physicians should have a low threshold for ruling out other serious conditions that also commonly present as LBP in this age group. If injections are required and successful because of a failure of other treatments, patients should be encouragd to engage in daily therapuetic spine exercises to maximize function and hopefully prevent relapse of pain.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

New techniques and methods to enhance RFA lesion size while preserving safety are being developed. Limited literature exists on their efficacy, but 2 such technolgies are water-cooled RFA and Nimbus needles. These will hopefully enhance success rates and minimize technical failures. Studies are also currently underway on biologics to alter disease progression.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Given the limitations of imaging, physical exam, and prognostic blocks, individual characteristics that may help predict a successful response to a particular treatment are crucial. Also, more studies need to be done on those with block proven spondylosis, especially the conservative and interventional therapies.

REFERENCES

1. Kalichman L, Li L, Kim DH, et al. Facet joint osteoarthritis and low back pain in the community-based population. Spine. 2008;33:2560-2565.

2. Rosenberg NJ. Degenerative spondylosithesis. Predisposing factors. J Bone Joint Surg Am. 1975;57:467-474.

3. Bogduk N. Degenerative joint disease of the spine. Radiol Clin North Am. 2012;50:613-628.

4. Lewin T. Osteoarthritis in lumbar synovial joints. A morphologic study. Acta Orthop Scand Suppl. 1964:SUPPL 73:1-112.

5. Fujiwara A, Lim TH, An HS, et al. The effect of disc degeneration and facet joint osteoarthritis on the segmental flexibility of the lumbar spine. Spine. 2000;25:3036-3044.

6. Sharma M, Langrana NA, Rodriguez J. Role of ligaments and facets in lumbar spinal stability. Spine. 1995;20:887-900.

7. Lawrence JS, Bremner JM, Bier F. Osteo-arthrosis. Prevalence in the population and relationship between symptoms and x-ray changes. Ann Rheum Dis. 1966;25:1-24.

8. Eisenstein SM, Parry CR. The lumbar facet arthrosis syndrome. Clinical presentation and articular surface changes. J Bone Joint Surg Br. 1987;69:3-7.

9. Datta S, Lee M, Falco FJ, et al. Systematic assessment of diagnostic accuracy and therapeutic utility of lumbar facet joint interventions. Pain Physician. 2009;12:437-460.

10. Bogduk N, Dreyfuss P, Govind J. A narrative review of lumbar medial branch neurotomy for the treatment of back pain. Pain Med. 2009;10:1035-1045.

11. Macvicar J, Borowczyk JM, Macvicar AM, et al. Lumbar medial branch radiofrequency neurotomy in New Zealand. Pain Med. In press.

12. Lilius G, Laasonen EM, Myllynen P, et al. Lumbar facet joint syndrome. A randomised clinical trial. J Bone Joint Surg Br. 1989;71:681-684.

13. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroids injections into facet joints for chronic low back pain. N Engl J Med. 1991;325:1002-1007.

14. Slipman CW, Bhat AL, Gilchrist RV, et al. A critical review of the evidence for the use of zygapophysial injections and radiofrequency dennervation in the treatment of low back pain. Spine J. 2003;3:310-316.

15. van Kleef M, Barendse GA, Kessels A, et al. Randomized trial of radiofrequencylumbar facet denervation for chronic low back pain. Spine. 1999;24:1937-1942.

16. Nath S, Nath CA, Pettersson K. Percutaneous lumbar zygapophysial (Facet) joint neurotomy using radiofrequency current, in the management of chronic low back pain: a randomized double-blind trial. Spine. 2008;33:1291-1297.

17. Tekin I, Mirzai H, Ok G, et al. A comparison of conventional and pulsed radiofrequency denervation in the treatment of chronic facet joint pain. Clin J Pain. 2007;23:524-529.

18. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine. 2000;25:1270-1277.

19. Schofferman J, Kine G. Effectivness of repeated radiofrequeny neurotomy for lumbar facet pain. Spine. 2004;29:2471-2473.

Bibliography

Kim KY, Wang MY. Magnetic resonance image-based morphological predictors of single photon emission computed tomography-positive facet arthropathy in patients with axial back pain. Neurosurgery. 2006;59:147-156.

Author Disclosure

D.J. Kennedy, MD
Nothing to Disclose

Renata Jarosz, MD
Nothing to Disclose

Ryan Demirjian, MD
Nothing to Disclose

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