Jump to:

Disease/Disorder

Definition

Lumbar spondylolisthesis (LS) is the subluxation or slipping of one vertebral body relative to another. It is associated with back pain, neurological deficits, or may be asymptomatic.

Etiology

The widely accepted Wiltse classification scheme divides LS by etiology into the following 5 subtypes, listed here from most common to least common in adults.1-3

  • Degenerative: Most common in adults. Occurs due to age-related disc degeneration and zygapophysial joint (z-joint) arthropathy. Remodeling of facet joint orientation reduces resistance to shear forces, allowing slippage with an intact pars interarticularis (PI).
  • Isthmic: Caused by a defect in the PI, can be further divided into the following 3 subtypes
    • Subtype A (lytic): Fatigue or stress fracture with PI lysis, most frequently at L5-S1.
    • Subtype B: Elongation of the PI without separation due to healed chronic microfractures; also related to fatigue or stress fractures. 
    • Subtype C: The rarest subtype, caused by acute fracture of the PI.
  • 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 z-joint (facet joint) malformations.2
  • 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

Degenerative Spondylolisthesis (DS)

  • Key risk factors for DS include female sex, older age, higher pelvic incidence, increased lumbar lordosis, facet joint osteoarthritis, high BMI or obesity causing increased shear loading, family history, African American race, and occupational exposure including prolonged driving and heavy manual labor.1,2,4,5
  • Several studies have shown that LS is more prevalent in women, especially after the age of 50.4 Women have higher pelvic incidence and lumbar lordosis, which are independent predictors of LS.6 Women also have wider and more sagittally-oriented lower lumbar facet joints, which predispose to LS.7
  • Age-related disc desiccation and height loss reduce anterior column support, contributing to segmental shear and slippage.8
  • Degenerative changes of the facet joints, which support the vertebral joints, also lead to lumbar instability where the joint is unable to maintain proper alignment and control during movement and/or loading.8 One study by Zhang et al showed that facet joint osteoarthritis (Grade III or above) had an odds ratio of 2.465, the highest odds ratio of investigated risk factors, for LS.8 In other words, patients with facet joint osteoarthritis (Grade III or above) are approximately 2.5 times more likely to develop LS.8
  • Obesity is also associated with increased risk of LS due to the excess mechanical load on the lumbar spine.5
  • The incidence of LS is more common in African American women compared to white women, possibly due to higher frequency of L5 sacralization.9
  • Radiographic LS has been correlated with a history of occupational driving and intense manual activity in the agricultural fishing sector.10

 Isthmic Spondylolisthesis (IS)

  • The most clinically encountered non-degenerative subtype.
  • Incidence of 5-6% in the adult population and about 12% in the adolescent population.1,11
  • 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 weightlifting, underlying spondylolysis, and conditions affecting vertebral development such as Scheuermann’s disease.2,11
  • Athletic activities that involve repetitive lumbar hyperextension, such as gymnastics and weightlifting, have higher risk of lumbar spondylolysis, and although rare, could potentially progress to LS.12

Patho-anatomy/physiology

The natural lordotic curvature of the lumbar spine is characterized by anterior convexity, resulting in an anterior shift of the body’s center of gravity. This lordotic curvature increases shear forces in the lower lumbar segments.13 Z-joints are synovial joints located along the posterior aspect of each vertebra and articulate with the adjacent vertebra to provide stability to each spinal segment during load transmission with flexion, extension, and axial rotation.14 Compressive, axial forces are resisted by intervertebral discs located between each vertebral segment and are composed of an inner proteoglycan-dense nucleus pulposus (NP) and an outer collagen-rich annulus fibrosus (AF). A cartilaginous tissue called the vertebral end plate (CEP) contains the intervertebral discs between each vertebral segment.15

DS is characterized by loss of disc height and weakening of anterior column support, while facet arthropathy and sagittal joint orientation reduce posterior column resistance. Shear forces translate through the z-joints into the PIs and are accentuated with repeated lumbosacral extension.1 Reduced anatomical resistance to shear forces increase risk of anterior or posterior translation of vertebral bodies despite an intact PI.16

Isthmic LS is distinguished by a structural discontinuity in the pars interarticularis between the posterior and middle columns, which enables disruption of the posterior elements and allows for the forward translation of vertebral bodies under repetitive shear forces or extension loading at the level of the PI.12 Spinopelvic parameters are measurable, and patients with IS have been found to exhibit a higher pelvic incidence, sacral slope, pelvic tilt, and lumbar lordosis.17,18

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.15 Most adult LS is relatively stable, especially DS. Monitoring progression is typically unnecessary, unless there are new or worsening symptoms. If imaging is pursued, standing flexion/extension X-rays are first-line. MRI is indicated for neurological symptoms or sometimes prior to surgery. DS typically progresses slowly or not at all. It is more likely to progress when there is high pelvic incidence, increased slip angle, facet joint effusion, and moderate disc degeneration. Isthmic LS usually stabilizes after skeletal maturity, and adult progression is uncommon.

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).20

Specific secondary or associated conditions and complications

LS can cause compression of the cauda equina or conus medullaris, leading to cauda equina syndrome (CES). CES is a rare but serious complication associated with 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.21

Essentials of Assessment

History

LS is often asymptomatic.22 However, patients experiencing symptoms from LS typically complain of diffuse and dull axial lower back pain with or without lower limb radiation.1,23 Neurologic symptoms occur secondary to foraminal or central stenosis rather than the slip itself. System review should evaluate for symptoms indicating neurologic deficits, CES, or spinal 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.24 If sexual dysfunction is present, it typically reflects neurologic involvement. Spondylolysis is the most commonly identified cause of back pain in children and adolescents. Activity-related pain or a specific traumatic event should be queried, and a detailed sports-specific history should be obtained, especially in athletes.2

Physical examination

Inspection may reveal paraspinal hypertrophy, increased lumbar lordosis, or postural changes, such as a shortened waistline or flattening of the buttocks;1,23 however, neither are sensitive nor specific for LS. 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.18 Focal neurologic deficits, such as weakness, sensory loss, or diminished reflexes, may be seen secondary to radiculopathy. Hamstring contractures are common in children.23 If there is clinical concern for CES secondary to LS, perform a rectal exam for sensation and tone and to 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.17 These measures are not specific to LS and may be applied to other musculoskeletal conditions as well.

Imaging

Standing lumbar spine radiographs with anteroposterior and lateral views are the first-line studies for suspected LS. This allows assessment of the presence and grading of the slip, slip angle and spinopelvic parameters, degenerative changes such as disc height loss, osteophytes, facet arthropathy, and PI defects.

Flexion-extension radiographs are indicated when there is concern for instability, such as mechanical pain with positional changes or suspected dynamic slip progression. Flexion-extension imaging is particularly valuable in DS when determining whether a segment is suitable for decompression alone or requires fusion. 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.25 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.25

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.26 Oblique views may better visualize a PI fracture,2,23 although utility of oblique views in adolescents has been questioned by at least one study.27

CT is useful for evaluating PI defects, traumatic fractures, preoperative bony anatomy, and high-grade slips that require detailed osseous assessment. CT is more sensitive than radiographs for identifying lytic or elongated pars defects in adults with suspected isthmic spondylolisthesis. CT can also be utilized to rule out other pain-contributing factors, including tumors.

MRI is useful if there are neurological or radicular symptoms, if there is concern for CES, and with preoperative planning for neural compression1. Unlike plain radiographs and CT scans, MRI does not expose patients to radiation.

MRI findings that may be suggestive of instability include facet joint effusion, which is characterized by 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 spondylolisthesis on supine MRI.28 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 with more severe grade 5 disc degeneration. The degrees of MRI findings are significant, as the severity of low back pain is increased in patients with instability.28

Degenerative lumbar spondylolisthesis is often found incidentally on plain radiographs, and the majority of patients with DS are asymptomatic29 and do not require surgical intervention. Symptomatic DS is associated with mechanical low back pain that may include radicular or claudicating symptoms that are worsened with extension-based activities. This contrasts with degenerative disc disease, which is provoked symptomatically by lumbar flexion and sitting.

Early predictions of outcomes

Approximately 12-34% of patients with DS will have progression over 4-25 years.30 Of patients with DS who were managed nonoperatively, about 32% had progression, defined as >5% increase in slip percentage, after a 5 year follow-up.31 Risk factors for progression include age <60 years old, female sex, facet sagittalization, and presence of baseline slip.32 In addition to radiographic outcomes, there are several studies showing mixed association between progression of DS and back pain. For example, one study found no correlation between changes in clinical symptoms and progression of spondylolisthesis,33 while another reported that 32% of patients with slip progression had back pain compared to 19% of patients without progression.34

For isthmic spondylolisthesis, progression is similar to that of DS, with incidence of progression ranging from 9-30% over an average of 7 years.35

Growth periods appear to be a significant factor for slip progression in dysplastic lumbar spondylolisthesis.36 Patients with developmental and dysplastic slips have much higher rates of progression, particularly during skeletal growth periods.37 Specifically, most slippage progression was observed to occur in the cartilaginous or apophyseal stage of the lumbar skeletal age.36

Patients should be concerned about progression primarily when symptoms such as neurological deficits or pain develop or worsen. Monitoring should be based on both clinical symptoms and imaging rather than routine radiographic surveillance.30 For stable, asymptomatic patients, clinical follow-up is appropriate without routine imaging, whereas younger or symptomatic patients should be more closely monitored.30 Standing lateral radiographs are first-line for grading spondylolisthesis, while MRI is indicated for patients with new or changing neurological deficits.

Social role and social support system

As with any chronic low back pain condition, LS treatment requires a thorough understanding of the patient’s functional demands and social contexts. The clinician should consider whether individuals may be asymptomatic, if their symptoms can be reduced through conservative or interventional treatment, and how symptoms can affect their ability to work and perform daily activities. A full assessment should address their social support systems, physical demands of the workplace and general physical activity level, and the role of appropriate accommodations to optimize function and response to treatment.

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. The use of orthotics remains a controversial topic with literature recommending bracing for children or adolescents with acute isthmic spondylolysis to reduce PI stress25,28,38 and other studies showing no benefit.39 There are currently no recommendations to support the use of bracing in degenerative LS.40

At different disease stages

New Onset/Acute Management

  • Degenerative spondylolisthesis: initial management should emphasize activity modification with avoidance of hyperextension, physical therapy, medications (e.g. NSAIDs and acetaminophen), and epidural injections41 for short-term symptom relief. Surgery may be considered initially in patients presenting with neurological deficits or spinal instability.40
  • Isthmic spondylolisthesis: conservative management includes relative rest for 1-2 days post-injury with activity modifications to reduce extension-based activities, medications (e.g. NSAIDs and acetaminophen), and physical therapy (as described in the “Subacute management” section) with a focus on safe return to play for athletes, with consideration of epidural injections41 for intractable pain. Surgery can be considered for symptomatic high-grade spondylolisthesis with neurological deficits and/or instability.40

Subacute Management

  • Rehabilitation: spinal stabilization programs are recommended for short- and long-term benefit, with flexion-based exercises suggested over extension exercises to improve core strength and strengthen spinal stabilizers.40 Aggressive physical therapy provides significant short-term benefits and should include lower limb stretching and progressive abdominal, hip, and back muscle strengthening.
  • 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 inadequate 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 for 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, which incorporates manipulation, mobilization, and traction, has support for use in conjunction with physical therapy. However, other modalities such as traction, acupuncture and transcutaneous electric nerve stimulation have less support in the literature.40
  • Multidisciplinary 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 management. The treatment program should be tailored to the individual with close follow-up, communication with therapy staff, and tolerance and compliance monitoring. Any worsening of symptoms or development of new symptoms requires prompt clinical re-evaluation, with referral to a spine surgeon when indicated.

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.42 There is limited literature in support of prolotherapy43 and ozone44 injections for LS, as well as limited support of PRP as treatment for z-joint pain that can be associated with DS.45

Minimally invasive surgery, including transforaminal lumbar interbody fusion, oblique lumbar interbody fusion, and percutaneous endoscopic fusion have been shown to yield symptom relief, reduced blood loss, shorter hospital stays, and lower complication rates compares to open surgery, with comparable functional outcomes in patients with L4/L5 DS.46

Gaps in the Evidence-Based Knowledge

There is no consensus on the most effective conservative treatment, surgical timing, or surgical technique.47,48 Bracing has been used in conservative management, mostly in cases of spondylolysis and spondylolisthesis in adolescents and children. However, no clear guidelines exist for its use.47,48 There is evidence that surgical intervention is superior and more cost-effective to continued failed conservative management.49 However, these studies are often misinterpreted to discount individual nonoperative treatments, such as physical therapy or ESIs. 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.10 Recent studies show that in patients with DS, decompression alone was noninferior to decompression with fusion, although patients who had decompression alone had somewhat higher rates of re-operation.50

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. Alhosanie TN, Klaib AF, Al Hadidi FA, Kanaan T, Mohammad K, Al-Zurgan A, Yousef NT, Oweis L, Hasan SM, Eftiha M, Alkubaisi FA, Tarawneh MA, Altarazi A, Barakat M, AbuHijlah I, Al-Sabbag Q, Tarawneh E. Prevalence of lumbar spondylolisthesis in adults and elderly patients with low back pain in the Jordanian community: radiographic findings. Eur Spine J. 2025 Jul;34(7):2571-2579. doi: 10.1007/s00586-025-08963-1. Epub 2025 May 29. PMID: 40442514.
  5. Zhang Z, Tantai M, Ma H, Yu S, Chen B, Lu Z. Analysis of Risk Factors for Lumbar Spondylolisthesis: A Logistic Regression Study. World Neurosurg. 2025 May;197:123931. doi: 10.1016/j.wneu.2025.123931. Epub 2025 Mar 24. PMID: 40139497.
  6. Yoshihara T, Morimoto T, Tsukamoto M, Toda Y, Hirata H, Kobayashi T, Takashima S, Mawatari M. Analyzing lumbar vertebral shape and alignment in female patients with degenerative spondylolisthesis: Comparisons with spinal stenosis and risk factor exploration. PLoS One. 2024 Apr 16;19(4):e0301974. doi: 10.1371/journal.pone.0301974. PMID: 38626167; PMCID: PMC11020370.
  7. Abu-Leil S, Weisman A, Floman Y, Galbusera F, Masharawi Y. A morphological characterization of the lumbar neural arch in females and males with degenerative spondylolisthesis. BMC Musculoskelet Disord. 2021 Dec 8;22(1):1026. doi: 10.1186/s12891-021-04901-6. PMID: 34879825; PMCID: PMC8656081.
  8. Mazurek M, Kulesza B, Gołębiowska N, Tyzo B, Kura K, Szczepanek D. Factors Predisposing to The Formation of Degenerative Spondylolisthesis—A Narrative Review. Medicina. 2023; 59(8):1430. https://doi.org/10.3390/medicina59081430
  9. Vogt MT, Rubin DA, Palermo L, et al. Lumbar spine listhesis in older African American women. Spine J. 2003;3:255-261.
  10. Akkawi I, Zmerly H. Degenerative Spondylolisthesis: A Narrative Review. Acta Biomed. 2021; 92: 1-5.
  11. 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.
  12. Selected Issues for the Adolescent Athlete and the Team Physician: A Consensus Statement. Medicine & Science in Sports & Exercise 40(11):p 1997-2012, November 2008. | DOI: 10.1249/MSS.0b013e31818acdcb
  13. Wang W, Pei B, Pei Y, Li H, Lu S, Wu X, Wu N, Shi Z, Hao Y, Fan Y. Biomechanical effects of over lordotic curvature after spinal fusion on adjacent intervertebral discs under continuous compressive load. Clin Biomech (Bristol). 2020 Mar;73:149-156. doi: 10.1016/j.clinbiomech.2020.01.002. Epub 2020 Jan 24. PMID: 31986460.
  14. Almeer G, Azzopardi C, Kho J, Gupta H, James SL, Botchu R. Anatomy and pathology of facet joint. J Orthop. 2020 Apr 8;22:109-117. doi: 10.1016/j.jor.2020.03.058. PMID: 32322140; PMCID: PMC7163055.
  15. Mohd Isa IL, Teoh SL, Mohd Nor NH, Mokhtar SA. Discogenic Low Back Pain: Anatomy, Pathophysiology and Treatments of Intervertebral Disc Degeneration. Int J Mol Sci. 2022 Dec 22;24(1):208. doi: 10.3390/ijms24010208. PMID: 36613651; PMCID: PMC9820240.
  16. Saremi A, Goyal KK, Benzel EC, Orr RD. Evolution of lumbar degenerative spondylolisthesis with key radiographic features. Spine J. 2024 Jun;24(6):989-1000. doi: 10.1016/j.spinee.2024.01.001. Epub 2024 Jan 8. PMID: 38199449.
  17. Chaddha R, Keny SM. Current Concepts in the management of spondylolisthesis. Curr Orthop Pract. 2017;28(1):23-30.
  18. 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.
  19. Barr KP, Harrast MA. Low back pain. In: Braddom RL, ed. Physical Medicine & Rehabilitation. 4th ed. Philadelphia, PA: Saunders; 2011:897-898.
  20. 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.
  21. Yadla S, Lebude B, Tender GC, et al. Traumatic spondyloptosis of the thoracolumbar spine. J Neurosurg Spine. 2008;9:145-151.
  22. Li N, Scofield J, Mangham P, Cooper J, Sherman W, Kaye AD. Spondylolisthesis. Orthop Rev (Pavia). 2022 Jul 27;14(3):36917. doi: 10.52965/001c.36917. PMID: 35910544; PMCID: PMC9329062.
  23. Tallarico RA, Madom IA, Palumbo MA. Spondylolysis and spondylolisthesis in the athlete. Sports Med Arthrosc. 2008;16:32-38.
  24. Möller H, Sundin A, Hedlund R. Symptoms, signs, and functional disability in adult spondylolisthesis. Spine. 2000;25(6):683-690.
  25. Dvorak J, Panjabi M, et al. Functional radiographic diagnosis of the lumbar spine flexion-extension and lateral bending. Spine. 1991;16(5):562-571.
  26. 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.
  27. 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.
  28. 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.
  29. Evans N, McCarthy M. Management of symptomatic degenerative low-grade lumbar spondylolisthesis. EFORT Open Rev. 2018 Dec 19;3(12):620-631. doi: 10.1302/2058-5241.3.180020. PMID: 30697442; PMCID: PMC6335606.
  30. Atalay B, Gadjradj PS, Sommer FS, Wright D, Rawanduzy C, Ghogawala Z, Härtl R. Natural History of Degenerative Spondylolisthesis: A Systematic Review and Meta-analysis. World Neurosurg. 2023 Aug;176:e634-e643. doi: 10.1016/j.wneu.2023.05.112. Epub 2023 Jun 2. Erratum in: World Neurosurg. 2023 Nov;179:233. doi: 10.1016/j.wneu.2023.08.123. PMID: 37271258.
  31. Cushnie D, Johnstone R, Urquhart JC, Gurr KR, Bailey SI, Bailey CS. Quality of Life and Slip Progression in Degenerative Spondylolisthesis Treated Nonoperatively. Spine (Phila Pa 1976). 2018 May 15;43(10):E574-E579. doi: 10.1097/BRS.0000000000002429. PMID: 28953710.
  32. Enyo Y, Yoshimura N, Yamada H, Hashizume H, Yoshida M. Radiographic natural course of lumbar degenerative spondylolisthesis and its risk factors related to the progression and onset in a 15-year community-based cohort study: the Miyama study. J Orthop Sci. 2015 Nov;20(6):978-84. doi: 10.1007/s00776-015-0759-8. Epub 2015 Aug 21. PMID: 26293800.
  33. Matsunaga S, Ijiri K, Hayashi K. Nonsurgically managed patients with degenerative spondylolisthesis: a 10- to 18-year follow-up study. J Neurosurg. 2000 Oct;93(2 Suppl):194-8. doi: 10.3171/spi.2000.93.2.0194. PMID: 11012048.
  34. Kauppila, Leena I. MD, PhD*; Eustace, Stephen MD†; Kiel, Douglas P. MD, MPH‡; Felson, David T. MD, MPH§; Wright, Alexander M. MD∥. Degenerative Displacement of Lumbar Vertebrae: A 25-year Follow-up Study in Framingham. Spine 23(17):p 1868-1873, September 1, 1998.
  35. Floman Y. Progression of lumbosacral isthmic spondylolisthesis in adults. Spine (Phila Pa 1976). 2000 Feb 1;25(3):342-7. doi: 10.1097/00007632-200002010-00014. PMID: 10703107.
  36. Ikata T, Miyake R, Katoh S, Morita T, Murase M. Pathogenesis of sports-related spondylolisthesis in adolescents. Radiographic and magnetic resonance imaging study. Am J Sports Med. 1996 Jan-Feb;24(1):94-8. doi: 10.1177/036354659602400117. PMID: 8638762.
  37. Hammerberg KW. New concepts on the pathogenesis and classification of spondylolisthesis. Spine (Phila Pa 1976). 2005 Mar 15;30(6 Suppl):S4-11. doi: 10.1097/01.brs.0000155576.62159.1c. PMID: 15767885.
  38. Choi JH, Ochoa JK, Lubinus A, Timon S, Lee YP, Bhatia NN. Management of lumbar spondylolysis in the adolescent athlete: a review of over 200 cases. Spine J. 2022 Oct;22(10):1628-1633. doi: 10.1016/j.spinee.2022.04.011. Epub 2022 Apr 30. PMID: 35504566.
  39. Virkki E, Holstila M, Kolari T, Lastikka M, Mattila K, Malmi S, Pajulo O, Helenius I. Rigid Thoracolumbar Orthosis Does Not Improve Outcomes of Acute Adolescent Spondylolysis as Compared With Placebo. Bony Union Predicts Improved Health-Related Quality of Life Outcomes at 2-Year Follow-Up. Spine (Phila Pa 1976). 2025 Apr 1;50(7):454-462. doi: 10.1097/BRS.0000000000005120. Epub 2024 Aug 15. PMID: 39146215.
  40. Nedelea DG, Vulpe DE, Gherghiceanu F, Capitanu BS, Dragosloveanu S, Stoica IC. Surgical and non-surgical management of spondylolisthesis: a comprehensive review. J Med Life. 2025;18(3):196-207. doi:10.25122/jml-2025-0039. PMID: 40291940; PMCID: PMC12022737. 
  41. Sencan S, Ozcan-Eksi EE, Cil H, et al. The effect of transforaminal epidural steroid injections in patients with spondylolisthesis. Journal of Back and Musculoskeletal Rehabilitation. 2017;30(4):841-846. doi:10.3233/BMR-160543
  42. 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.
  43. Hsu C, Vu K, Borg-Stein J. Prolotherapy: A Narrative Review of Mechanisms, Techniques, and Protocols, and Evidence for Common Musculoskeletal Conditions. Phys Med Rehabil Clin N Am. 2023 Feb;34(1):165-180. doi: 10.1016/j.pmr.2022.08.011. Epub 2022 Oct 18. PMID: 36410881.
  44. Sconza C, Leonardi G, Kon E, Respizzi S, Massazza G, Marcacci M, Di Matteo B. Oxygen-ozone therapy for the treatment of low back pain: a systematic review of randomized controlled trials. Eur Rev Med Pharmacol Sci. 2021 Oct;25(19):6034-6046. doi: 10.26355/eurrev_202110_26881. PMID: 34661263.
  45. Yum JI, De Luigi AJ, Umphrey GL, Ganter BK, Yoo M. Platelet-Rich Plasma Treatment for the Lumbar Spine: A Review and Discussion of Existing Gaps. Pain Physician. 2024 Jul;27(5):283-302. PMID: 39087964.
  46. Song Z, Zhang Z, Zheng J, Zhang K, Wang F, Ran M, Luo J. Short-term and mid-term evaluation of three types of minimally invasive lumbar fusion surgery for treatment of L4/L5 degenerative spondylolisthesis. Sci Rep. 2024 Feb 21;14(1):4320. doi: 10.1038/s41598-024-54970-5. PMID: 38383595; PMCID: PMC10881486.
  47. Agabegi SS, Fischgrund JS. Contemporary management of isthmic spondylolisthesis: pediatric and adult. Spine J. 2010;10:530-543. 
  48. Bell DF, Ehrlich MG, Zaleske DJ. Brace treatment for symptomatic spondylolisthesis. Clin Orthop Relat Res. 1988;(236):192-198. 
  49. 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.
  50. Austevoll, I. M., Hermansen, E., Fagerland, M. W., Storheim, K., Brox, J. I., Solberg, T., Rekeland, F., … & Weber, C. (2021). Decompression with or without fusion in degenerative lumbar spondylolisthesis. The New England Journal of Medicine, 385(6), 526–538.

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

Jackson Liu, MD, Michael B. Furman, MD. Lumbar Spondylolisthesis. 6/22/2022

Author Disclosure

Annie Yang, MD
Nothing to Disclose

Jared Stowers, MD
Nothing to Disclose

Sandra de Mel, MD
Nothing to Disclose

Mohammed Emam, MD
Nothing to Disclose

Alexis Coslick, DO, MS
Nothing to Disclose