Author(s): Jackson Liu, MD, Michael B. Furman, MD
Originally published: September 20, 2013 Last updated: June 22, 2022
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Disease/Disorder

Definition

Lumbar spondylolisthesis (LS) is the subluxation or slipping of one vertebral body relative to another. It is a potential cause of back pain and neurologic deficits.

Etiology

A widely accepted classification scheme divides LS by etiology into the following 5 subtypes. 1-3

  • Dysplastic (or congenital): Results from an abnormality in the upper surface of the sacrum or the dorsal bony arch of the 5th lumbar vertebra. This is most frequently due to underlying spina bifida (SB) or zygapophysial joint (facet or z-joint) malformations2
  • Isthmic: The most common sub-type, caused by a defect in the pars interarticularis (PI), can be further divided into the following 3 subtypes:
    • Subtype A (lytic): Occurring most frequently at L5-S1, this is defined as lysis and bony separation of the PI, related to fatigue or stress fractures
    • Subtype B: Elongation of the PI without separation due to healed chronic microfractures; also related to fatigue or stress fractures  
    • Subtype C: The rarest form caused by acute fracture of the PI
  • Degenerative: Due to age-related chronic z-joint arthropathy which causes remodeling of joint orientation which causes abnormal motion across the joint and thus subluxation with an intact PI
  • Traumatic: Due to acute fracture of the posterior elements, such as pedicle or z-joint, with sparing of the PI; LS occurs over weeks to months. If subluxation occurs immediately after the inciting traumatic event, this is considered a fracture dislocation and is not categorized under this subtype.
  • Pathologic: Results from secondary systemic, localized, or iatrogenic causes. Systemic causes include osteoporosis, osteogenesis imperfecta, Marfan syndrome, and Ehlers-Danlos syndrome. Localized causes include primary or metastatic tumor or infections that weaken posterior element integrity. Iatrogenic causes include excessive PI thinning from surgical decompressive laminectomy and adjacent segment disease following spinal fusion.

Epidemiology including risk factors and primary prevention

Certain genetic factors, such as family history, race, and athletic activities that involve repetitive lumbar hyperextension, have been associated with higher LS risk.1,2 For example, the incidence of LS has been found to be more common in African American women when compared to white women, possibly due in part due to more common sacralization of L5.6 Radiographic LS has been correlated with a history of occupational driving and intense manual activity in the agricultural fishing sector.7

Isthmic spondylolisthesis (IS) is the most clinically encountered subtype and is seen with an incidence of 5-6% in the adult population and about 12% in the adolescent population.1,9 It most commonly involves L5 (90%) and L4 (5%). Although the incidence of IS in women is half that of men, women account for >50% of symptomatic cases, and have higher LS grades. 1 Risk factors include high-impact sports such as football, gymnastics, and patients suffering from Schueuerman’s disease, which are all associated with spondylolysis.2,9

The incidence of degenerative spondylolisthesis (DS) is about 10% and is between 3 to 9 times more common in women than men.4,5,10 This is thought to be due to anatomical differences in increased pelvic incidence, L4 vertebral body inclination, and more sagitally oriented z-joints10. Hysterectomy and multiparity, presumably by causing abdominal muscle deficiency, increase odds of developing DS.5 There is likely increased risk of DS from sedentary work and decreased risk from work that requires walking or climbing slopes or steps.7

There are no specific LS primary prevention methods. However, literature supports exercise for generalized low back pain primary prevention. Back schools and lumbar supports are largely ineffective, and ergonomic interventions have insufficient evidence.8

Patho-anatomy/physiology

Because the lumbar spine has a normative lordotic curve with a relatively anterior center of gravity, the lower lumbar vertebrae shear in the anterior direction relative to their caudal segments. These high segmental loads are shared between the intervertebral disks, which primarily bear the compressive force, and the z-joints, which resist the anterior shearing force.9 These shear forces translate through the z-joints into the PIs and are accentuated with repeated lumbosacral extension in a nutcracker mechanism.1 In IS there is structural discontinuity between the middle and posterior columns of the spine at the level of PI. 9 Certain measurable spinopelvic parameters have been described. In patients with IS for example, there is a higher pelvic incidence, sacral slope, pelvic tilt, and lumbar lordosis.10,11

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

The natural history typically ends in spontaneous stabilization so that significant adult slip progression is rare.12 The following are the 2 major grading systems for LS:

  • Tailard: spondylolisthesis degree as a percentage of the inferior vertebra’s anteroposterior diameter. Spondyloptosis refers to complete dislocation from the inferior vertebral segment.1
  • Meyerding: grades based on dividing the caudal vertebral body into quarters. Grade I is 0% to 25%, grade II is 26% to 50%, grade III is 51% to 75%, grade IV is 76% to 100%, and grade V is more than 100% (spondyloptosis).13

Specific secondary or associated conditions and complications

Cauda equina syndrome (CES) can be a significant complication, particularly of the degenerative subtype, and has been described for all grades.1 Therefore, patients should be monitored for bowel and bladder incontinence, saddle anesthesia, and/or sexual dysfunction. Rarely, traumatic grade V spondylolisthesis or spondyloptosis rostral to L2/L3 results in spinal cord injury.14

Essentials of Assessment

History

Patients typically complain of diffuse and dull axial lower back pain with or without lower limb radiation.1,15 Patients with nerve or cord involvement may have sensory disturbances and/or weakness. Radiculopathy, develops insidiously because of a combination of vertebral subluxation and associated disk degeneration, causing foraminal and/or central stenosis. System review should assess for symptoms indicating neurologic deficits, CES or cord injury such as stool and urinary continence, and other pathologic conditions. Sexual dysfunction may be observed in patients with LS but is frequently under-reported.16 Spondylolysis is the most commonly identified cause of back pain in children. Activity-related pain or specific traumatic event should be queried2 and include a detailed sports-specific history in athletes.

Physical examination

Inspection may reveal paraspinal hypertrophy, increased lumbar lordosis, or postural changes, such as a shortened waistline or flattening of the buttocks.1,15 Evaluate spinal range of motion and alignment. A palpable lumbar step-off is a very specific finding but is more often seen with Grade 3 and Grade 4 LS. Dural tension signs are typically negative although approximately half of adult patients with symptomatic IS will have a positive straight leg test.11 Focal neurologic deficits, such as weakness, sensory loss, or diminished reflexes, may be seen secondary to radiculopathy. Hamstring contractures are common in children.15 If there is clinical concern for CES secondary to LS, perform a rectal exam for sensation and tone and always evaluate for upper motor neuron signs.

Functional assessment

Gait evaluation may reveal a compensated extended lumbar spine position to relieve symptoms, although hyperextension and rotational motions may cause pain, especially during single-limb stance.1,2 Measures for assessing LS include the Oswestry Disability Index, Short Form of Medical Outcomes, and visual analog scale.10 These measures are not specific to LS but may be applied to other musculoskeletal conditions as well.

Imaging

Abnormal imaging findings in asymptomatic patients are common. Weak abdominal musculature, paraspinal muscle hypertrophy, lumbar hyperlordosis, slipping or step-off on palpation and inspection, hamstring muscle spasm, pain with lateral trunk flexion-extension and with double leg raising were found to be correlated with radiological assessment of LS.17 Initial plain radiographs are appropriate for these cases of suspected LS. Oblique views may better visualize a PI fracture2,15, although utility of oblique views in adolescents has been questioned by at least one study.18 Standing radiographs with flexion and extension are ideal to image the weight-bearing spine in dynamic positions, allowing identification of  unstable spondylolisthesis if there is a change in severity grade.19 Normal values have been obtained in asymptomatic volunteers for passively performed flexion-extension and lateral bending in the lumbar spine, providing analysis of segmental rotation and translation.19 Computed tomography (CT) can better visualize spinal bony anatomy and also rule out other pain-contributing factors or tumors. Oblique plain films and CT do result in increased radiation exposure. Consider magnetic resonance imaging (MRI) in patients with signs or symptoms of radiculopathy.1 Instability can be suggested by MRI demonstrating large fluid-filled facet joints with increased signal on T2 axial images. Large facet joint effusions (>1.5mm at L4-5) are highly predictive of DS, even in the absence of findings of measurable listhesis on supine MRI. 20  Facet opening was the strongest predictor for instability, followed by DS, MRI grade, and subchondral sclerosis. LS instability is correlated more with mild Pfirrman grade 3-4 disc degeneration than more severe grade 5 with disc collapse. Such information is clinically relevant because low back pain is significantly more severe in patients with instability.20   

Early predictions of outcomes

Radiographic disease progression develops in 30% to 35% of conservatively treated patients. Progression is least likely if intervertebral height is markedly decreased or there is intervertebral osteophyte formation, subcartilaginous sclerosis, and/or ligamentous ossification. Progression is more likely with higher LS grades, disk degeneration at the slipped level, and a high slip angle. Slip progression occurs in only a small patient percentage and is unlikely after adolescence. Dysplastic slips are more likely to progress.1,15 In 1 prospective study of first-grade children, whereas the prevalence of spondylolysis was 4.4% in 6 year olds and 6% in adulthood, only about 15% of individuals progressed to spondylolisthesis.21

Social role and social support system

As with any chronic low back pain condition, LS treatment requires a thorough understanding of the patient. The clinician must address any biopsychosocial factors that may hinder a positive response. Consider comorbid psychiatric disorders, somatization, and secondary gain.

Professional issues

Missing the diagnosis in an acute spondylolisthesis may lead to chronic pain and spinal instability. Adolescents with acute pars fractures are often noncompliant with bracing; thus, parental education is essential.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Although no specific guidelines have been published, general management starts with rehabilitation and medical management. Surgery may be indicated when conservative measures fail or if there is intractable pain, progressive neurologic deficit, CES, or trauma with spinal instability.

At different disease stages

New onset/acute management:

  • Activity modification: relative rest and avoid active extension.
  • Medications: nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and opioids for breakthrough pain. Consider neuropathic medications in radiculopathy.
  • Orthoses: for acute spondylolysis in children or adolescents, rigid antilordotic thoracolumbosacral orthosis bracing has been suggested for up to 6 months to reduce PI stress.,22,23 Similar approaches have been suggested for LS; however, there is no evidence for bracing in slip progression prevention.

Subacute management:

  • Rehabilitation: spinal stabilization programs are recommended for short- and long-term benefit, with Williams flexion-based exercises suggested over extension exercises. Aggressive physical therapy provides significant short-term benefits and should include lower limb stretching and progressive abdominal, hip, and back muscle strengthening. Lumbar traction is contraindicated.10 
  • Procedures: transforaminal or interlaminar epidural steroid injections (ESIs) may be beneficial for radicular symptoms. Interlaminar ESIs should only be considered after careful image review, ideally MRI. If there is not adequate space at the level of the LS, consider injecting an adjacent segment. Z-joint injections or medial branch blocks may be beneficial for z-joint mediated axial pain.
  • Surgical consultation: consider in cases involving instability, refractory neurologic deficits, with emergent consultation in CES. Surgical options include spinal decompression and/or fusion.

Chronic/stable management:

  • Complementary/alternative treatments: manual therapy, acupuncture, and transcutaneous electric nerve stimulation.
  • Multidiscliplinary approach to chronic pain management: this could include a comprehensive biopsychosocial rehabilitation program.

Coordination of care

The physiatrist plays a crucial role in LS rehabilitation and treatment. The therapy program should be tailored to the individual with close follow-up, communication with therapy staff, and tolerance and compliance monitoring. Worsening or new symptom development requires prompt clinical re-evaluation. Consult a spine surgeon when appropriate.

Patient & family education

Patients should be educated on basic spine biomechanics, posture, and daily ergonomics. The natural history and likelihood of progression should be discussed to manage expectations. The patient should be able to recognize symptoms, such as acute bowel/bladder incontinence, that require emergent care.

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

The patient presenting with low back pain demands a thorough clinical history, physical examination, and diagnostic study review with consideration of a wide differential. More serious issues, such as cord compression, CES, and pathologic diseases, need to be ruled out. Imaging is a useful adjunct but cannot be used alone in establishing a correct diagnosis, because positive findings are common in asymptomatic patients.

Cutting Edge/ Emerging and Unique Concepts and Practice

Some studies show that upright dynamic MRI is superior to recumbent scans by imaging the spine in a physiologic and functional nature, but there is a lack of research and availability.24 There is very limited literature in support of prolotherapy25 and ozone26injections for LS, as well as limited support of PRP as treatment for z-joint pain that can be associated with Degenerative LS.27

Gaps in the Evidence-Based Knowledge

There is no consensus on the most effective conservative treatment, surgical timing, or surgical fusion technique. 22,23 The benefit of fusion in addition to decompression is inconclusive although fusion may be necessary if there is underlying vertebral instability or iatrogenic instability from an extensive surgical decompression.7Bracing has been used in conservative management, mostly in cases of spondylolysis and spondylolisthesis in adolescents and children. No clear guidelines exist for its use.22,23 There is evidence that surgical intervention is superior and more cost-effective to continued failed conservative management.4 However, these studies are often misinterpreted to discount individual nonoperative treatments, such as physical therapy or ESIs. In patients with lumbar stenosis and associated LS, those who underwent surgery had greater improvement in pain and function throughout a 4-year period.28,29 There is no evidence as to the most cost-effective method to treating LS10,withno significant advantage of one fusion technique over another in patients with stenosis and LS.28,29 There is growing interest in minimally invasive surgery with proposed benefits such as shortened length of operation and reduced perioperative complications. 7, 30

References

  1. Ibrahimi DM, Beaty NB, Crandall KM, Hamilton DK, Sansur CA. A review of lumbar spondylolisthesis. Eur Musculoskelet Rev. 2011;6:110-113.
  2. Hu SS, Tribus CB, Diab M, Ghanayem AJ. Spondylolisthesis and spondylolysis. J Bone Joint Surg Am. 2008;90:656-671.
  3. Wiltse LL, Newman PH, Macnab I. Classification of spondylolisis and spondylolisthesis. Clin Orthop Relat Res. 1976;(117):23-29.
  4. Baker JF, Errico TJ, Kim Y, Razi A. Degenerative spondylolisthesis: contemporary review of the role of interbody fusion. Eur J Orthop Surg Traumatol. 2017;27(2):169-180.
  5. Cholewicki J, Lee AS, Popovich JM, et al. Degenerative spondylolisthesis is related to multiparity and hysterectomies in older women. Spine (Phila PA 1976). 2017:Epub
  6. Vogt MT, Rubin DA, Palermo L, et al. Lumbar spine listhesis in older African American women. Spine J. 2003;3:255-261.
  7. Akkawi I, Zmerly H. Degenerative Spondylolisthesis: A Narrative Review. Acta Biomed. 2021; 92: 1-5.
  8. Linton SJ, van Tulder MW. Prevention interventions for back and neck pain problems: what is the evidence? Spine (Phila Pa 1976). 2001;26:778-787.
  9. Schneck CD, et al. Imaging techniques relative to rehabilitation. In: DeLisa JD, ed. Physical Medicine & Rehabilitation: Principles and Practice Volume 1. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010:209-210.
  10. Chaddha R, Keny SM. Current Concepts in the management of spondylolisthesis. Curr Orthop Pract. 2017;28(1):23-30.
  11. Kreiner DS, Baisden J, Mazanec DJ, et al. Guideline summary review: an evidence-based clinical guideline for the diagnosis and treatment of adult isthmic spondylolisthesis. Spine J. 2016;16(12):1478-1485.
  12. Barr KP, Harrast MA. Low back pain. In: Braddom RL, ed. Physical Medicine & Rehabilitation. 4th ed. Philadelphia, PA: Saunders; 2011:897-898.
  13. Spinelli J, Rainville J. Lumbar spondylolysis and spondylolisthesis. In: Frontera WR, ed. Essentials of Physical Medicine and Rehabitation.2nd ed. Philadelphia, PA: Saunders; 2008:253-258.
  14. Yadla S, Lebude B, Tender GC, et al. Traumatic spondyloptosis of the thoracolumbar spine. J Neurosurg Spine. 2008;9:145-151.
  15. Tallarico RA, Madom IA, Palumbo MA. Spondylolysis and spondylolisthesis in the athlete. Sports Med Arthrosc. 2008;16:32-38.
  16. Möller H, Sundin A, Hedlund R. Symptoms, signs, and functional disability in adult spondylolisthesis. Spine. 2000;25(6):683-690
  17. Kalpakcioglu B, Altinbilek T, Senel K. Determination of spondylolisthesis in low back pain by clinical evaluation. J Back Musculoskeletal Rehabil. 2009;22(1):27-32.
  18. Beck NA, Miller R, et al. Do oblique views add value in the diagnosis of spondylolysis in adolescents? J Bone Joint Surg Am. 2013;95(10):e65.
  19. Dvorak  J, Panjabi M, et al. Functional radiographic diagnosis of the lumbar spine flexion-extension and lateral bending. Spine. 1991;16(5):562-571.
  20. Hasegawa K, Shimoda H, et al. What are the reliable radiological indicators of lumbar segmental instability? J Bone Joint Surg. 2011;93-B:650-657.
  21. Beutler WJ, Fredrickson BE, Murtland A, Sweeney CA, Grant WD, Baker D. The natural history of spondylolysis and spondylolithesis. Spine (Phila Pa 1976). 2003;28:1027-1035.
  22. Agabegi SS, Fischgrund JS. Contemporary management of isthmic spondylolisthesis: pediatric and adult. Spine J. 2010;10:530-543.
  23. Bell DF, Ehrlich MG, Zaleske DJ. Brace treatment for symptomatic spondylolisthesis. Clin Orthop Relat Res. 1988;(236):192-198.
  24. Tarantino U, Fanucci E, Iundusi R, et al. Lumbar spine MRI in upright position for diagnosing acute and chronic low back pain: statistical analysis of morphological changes. J Orthop Traumatol. 2013;14:15-22.
  25. Jacks A, Barling T. Lumbosacral prolotherapy: a before-and-after study in an NHS setting. Int Musculoskelet Med. 2012;34:7-12.
  26. Bonetti M, Fontana A, Albertini F. CT-guided oxygen-ozone treatment for first degree spondylolisthesis and spondylolysis. Acta Neurochir Suppl. 2005;92:87-92.
  27. Wu J, et al. A new technique for the treatment of lumbar facet joint syndrome using intra-articular injection with autologous platelet rich plasma. Pain Physician. 2016;19:617-625
  28. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical compared with nonoperative treatment for lumbar degenerative spondylolisthesis. four-year results in the Spine Patient Outcomes Research Trial (SPORT) randomized and observational cohorts. J Bone Joint Surg Am. 2009;91:1295-1304.
  29. Abdu WA, Lurie JD, Spratt KF, et al. Degenerative spondylolisthesis: does fusion method influence outcome? Four-year results of the spine patient outcomes research trial. Spine (Phila Pa 1976). 2009;34:2351-2360.

Original Version of the Topic

Michael B. Furman, MD, Jackson Liu, MD, Shounuck I. Patel, DO. Lumbar spondylolisthesis. 9/20/2013

Previous Revision(s) of the Topic

Michael B. Furman, MD, Jackson Liu, MD, Shounuck I. Patel, DO. Lumbar spondylolisthesis. 2/13/2018

Author Disclosure

Jackson Liu, MD
Nothing to Disclose

Michael Furman, MD
Nothing to Disclose