Secondary Logo

Treatment of Instability and Spondylolisthesis: Surgical versus Nonsurgical Treatment

Vibert, Brady, T; Sliva, Christopher, D; Herkowitz, Harry, N

Section Editor(s): Moskovich, Ronald MD, Guest Editor; Nordin, Margareta DrSci, Guest Editor

Clinical Orthopaedics and Related Research: February 2006 - Volume 443 - Issue - p 222-227
doi: 10.1097/01.blo.0000200233.99436.ea
SECTION I: SYMPOSIUM II: Surgical versus Nonsurgical Management of Spinal Disorders
Free
SDC

Spondylolisthesis is a common cause of lower-back pain, radiculopathy, and neurogenic claudication among the adult population. Treatment should begin with nonoperative measures that may include physical therapy, aerobic exercise, epidural steroid injections, and homeopathic remedies. If these treatments fail, surgical intervention may provide the patient pain relief and improvement in neurologic symptoms. The use of instrumentation for posterolateral fusions as well as interbody fusion may improve clinical outcomes for those having surgical intervention. We discuss the current nonoperative modalities and surgical techniques treating degenerative spondylolisthesis.

Level of Evidence: Level V: Expert Opinion. See the Guidelines for Authors for a complete description of the levels of evidence.

From the William Beaumont Hospital, Department of Orthopaedic Surgery and Division of Spine Surgery, Royal Oak, MI.

Each author certifies that he has no commercial associations that might pose a conflict of interest in connection with the submitted article. Correspondence to: Harry N. Herkowitz, MD, 3535 West 13 Mile Road Suite 604, Royal Oak, MI 48073. Phone: 248-551-0426; Fax: 248-551-5404; E-mail: cmusich@beaumont.edu.

Spondylolisthesis is a common cause for lower-back pain, radiculopathy, and neurogenic claudication among the adult population. Translated from Greek, spondylolisthesis literally means slipping of the spine. Spondylolisthesis can begin as a childhood disease or it may not develop until adulthood. Similarly, it may be congenital or acquired. Recognizing the multiple types of spondylolisthesis, Wiltse et al52 developed a classification system in 1976. Subtypes included congenital, isthmic, degenerative, pathologic, iatrogenic, and traumatic etiologies. Isthmic and degenerative causes are by far the most common in the adult population. Although we focus on degenerative spondylolisthesis, many of the treatment principles also may be applied to adults with spondylolisthesis resulting from other etiologies.

Although the nonoperative treatment modalities of degenerative spondylolisthesis have remained relatively unchanged during the past two decades, the number of surgical options has increased rapidly over that same period. The optimal surgical technique to treat symptomatic spondylolisthesis has not been determined. Although decompression for patients with stenosis is a well established intervention, controversy exists regarding whether or not to fuse patients electing surgical intervention.10,13,42 However, recent evidence suggests those patients in whom a solid fusion is obtained have better long-term outcomes than patients with pseudarthroses.29 Furthermore, current evidence suggests instrumentation, and more recently interbody fusion, may improve fusion rates5,12,23,32,55; however, these surgical techniques come at higher cost and morbidity to the patient.43,47

In this review, we explore the current methods and controversies of nonoperative and operative treatment of spondylolisthesis. This review reflects our selection of literature and opinions.

Back to Top | Article Outline

Epidemiology

The most commonly affected level of the spine in degenerative spondylolisthesis is L4-L5.7 Authors of an anatomic and clinical study of more 200 patients found spondylolisthesis was five to six times more likely to occur in women than men.42 This same study revealed black women have about a three times greater risk than white women for this condition. Authors of followup studies have postulated the increased risk in women primarily is because of their increased ligamentous laxity compared with that seen in men.3,24,45 Authors of previous studies have suggested the increased risk in black women stems from decreased lordosis in this population in conjunction with increased sacralization of L5, leading to greater force across the L4-L5 segment.42

Back to Top | Article Outline

Pathogenesis

The functions of the facet joints are to bear load and to allow motion, but also to restrict excessive motion. The lumbar facets burden 3% to 35% of the static compressive load at each motion segment and dynamically up to 33% of the axial load.54 Grobler et al19 subsequently critically examined facet joint morphology in patients with and without spondylolisthesis. They found significantly more sagittal orientation of the facets at L4-L5 in those patients with spondylolisthesis than in the control patients. Grobler et al19 suggested those patients with sagittal development of their L4-L5 facets are at increased risk for spondylolis-thesis because they lack normal resistance to shear forces. Facet joint morphology later was studied in living patients using computed tomography (CT) and plain radiographs.8 Cinotti et al8 corroborated the work of Grobler et al19 when they found increased sagittal orientation of the facets joints and hypermobility of the spondylolisthetic vertebra in patients with spondylolisthesis. The sagittal orientation of the L4-L5 segment combined with the more coronally situated L5-S1 results in hypermobility of the L4-L5 segment, particularly in the coronal plane. Combining this hypermobility with other risk factors such as generalized ligamentous laxity and disc degeneration, facet arthritis develops and subluxation of the superior vertebra occurs. The superior vertebra, or “ring,” then slides forward on the inferior “ring,” resulting in a narrowed canal and narrowed lateral recesses at the location of the slip. Subluxation with ligamentum flavum thickening may result in further central stenosis. Likewise, superior facet hypertrophy may contribute to lateral recess stenosis. The development of central and lateral recess stenosis lends to a wide range of clinical presentations.

Back to Top | Article Outline

Natural History

The natural history of degenerative spondylolisthesis generally is favorable. Only 10% to 15% of patients seeking treatment eventually will have surgery.40 The development of osteoarthritic spurs, hypertrophy and ossification of the intervertebral ligaments, and facet arthrosis may lead to secondary stabilization that prevents slip progression.33 This secondary stabilization may result in improvement or resolution of symptoms. Matsunaga et al33 initially reported a 30% rate of slip progression in 40 patients treated nonoperatively and they found the percent slip rarely exceed 30%. Of those who did not progress, there was disc space narrowing, endplate spurring, and sclerosis at presentation, suggesting physiologic stabilization of an unstable segment may occur. Matsunaga et al34 published a followup to their original study in which they followed up on 145 patients with degenerative spondylolisthesis who were treated nonoperatively for a minimum of 10 years. They found progressive spondylolisthesis in 34%, but no correlation between slip progression and clinical symptoms. Of the 110 patients who had no neurologic symptoms at presentation, 76% remained without neurologic deficit. Conversely, of the 35 patients presenting with neurologic claudication or vesicorectal disorder, 83% had worsening of their neurologic status.

Back to Top | Article Outline

Clinical Presentation

Patients presenting with degenerative spondylolisthesis generally are older than 50 years and may have any combination of lower-back pain, neurogenic claudication, vesicorectal disorder, and radiculopathy. The most common complaint is lower-back pain that has waxed and waned for many years. Lower-back symptoms often are exacerbated by activity and may worsen throughout the day. If radiculopathy is present, the L5 nerve root most often is affected. However, the L4 nerve root may be irritated in severe cases. Neurogenic claudication consists of unilateral or bilateral leg and buttock pain with activity and is improved with rest or lumbar spine flexion. Patients also may describe an unsteady gait or frequent falls. With severe stenosis, loss of bowel or bladder control may occur. Great care must be taken to differentiate neurogenic claudication from peripheral vascular disease or neuropathy. Furthermore, patients with atypical back pain, such as pain at rest or night pain, should be evaluated for tumor, infection, or other etiologies.

Back to Top | Article Outline

Physical Examination

On inspection, the patient may have a loss of lumbar lordosis as a result of his or her listhesis or a stooped posture if he or she is additionally stenotic. Hip flexion contractures may be found if the patient has been maintaining the forward flexed position for a long period. Muscle atrophy should be documented if present. Despite the degenerative nature of the disease, range of motion (ROM) usually is normal and occasionally hypermobility may exist. Some patients may be able to touch their toes on forward flexion as a result of the hypermobile segment or generalized ligamentous laxity. Palpation may, but often does not reveal a step-off at the listhetic level.

Neurologic examination is a crucial factor in determining the cause of the symptoms but often the examination results are normal or nonspecific. Lower motor neuron symptoms such as weakness, hyporeflexia, and sensory loss are most common in the L5 nerve root distribution but also may occur in the L4 nerve root distribution. Perianal sensation and rectal tone should be evaluated in all patients who have bowel or bladder incontinence. Peripheral pulses should always be checked as an initial evaluation for peripheral vascular disease. Similarly, careful hip and knee examinations can help rule out peripheral joint arthritis.

Back to Top | Article Outline

Imaging Studies

Initial radiographs of the lumbar spine should include anteroposterior (AP), lateral, lateral flexion and extension, and oblique views. An AP view of the pelvis also should be included with any lumbar series to help rule out pelvic etiologies for lower-back or leg pain. Although slips may be graded according to Meyerding's system, where Grade 1 is up to 25% displacement, Grade 2 is 50%, Grade 3 is 75%, and Grade 4 is 100% displacement or greater; a more descriptive technique is to describe the percent slip of the superior vertebra on the inferior vertebra calculated by the millimeters of displacement divided by the total width of the vertebral endplate.35 In degenerative arthritis, the percent slip rarely exceeds 25%. The flexion and extension views should be evaluated for motion at the olisthesed segment. Lack of motion may show secondary stabilization.

If neurologic symptoms are present, a magnetic resonance imaging (MRI) scan of the lumbosacral spine should be done. The MRI should be evaluated for thecal sac impingement, nerve root compression, disc pathology, and other etiologies for lower-back pain or radiculopathy. If the patient is incompatible with an MRI, a computed tomography (CT) myelogram can be obtained. The knowledge gained from the MRI or CT myelogram should be used in conjunction with signs, symptoms, and physical findings to determine the appropriate method of treatment.

Back to Top | Article Outline

Nonoperative Treatment

Lower-back pain is a ubiquitous finding among the United States population. Up to 80% of the population may have lower-back pain at some point, but the lifetime prevalence for lumbar spine surgery is only 1% to 3%.15 Furthermore, the natural history studies noted above reveal most patients with spondylolisthesis do not worsen with time and very rarely is there rapid deterioration.33 Therefore, nonoperative treatment is the mainstay of treatment for lower-back pain and should be the initial course of action in most cases of spondylolisthesis, with or without neurologic symptoms. There are, however, no prospective, randomized clinical trials establishing an optimal nonoperative treatment protocol. Most physicians begin with a 1-day to 2-day period of rest followed by a short course of anti-inflammatory medications, if they are not contraindicated for gastrointestinal reasons. If symptoms persist beyond 1 to 2 weeks, physical therapy consisting of aerobic conditioning should be instituted. Stationary bicycling is an excellent exercise because it promotes spine flexion, deconstriction of the thecal sac, and allows for more exercise before the development of neurogenic claudication if present. Furthermore, bicycling allows the patient to avoid the wear and tear associated with impact aerobic exercisesuch as running. Swimming, walking, and elliptical machines are other good alternatives for cardiovascular exercise.

The addition of strengthening exercises to physical therapy protocols was addressed by authors of two studies from the Mayo Clinic18,46 who evaluated flexion-only exercises versus extension-only exercises in patients with spondylolisthesis. After 3 months they found only 27% of patients had moderate or severe pain after flexion-only exercises, whereas 67% of patients had moderate or severe pain after extension-only exercises. At 3-year follow up, only 19% of the patients in the flexion-only exercise group experienced moderate or severe pain, compared with 67% of patients in the extension-only exercise group. These authors suggest flexion or isometric strengthening should be considered and extension exercises should be avoided. One limitation of this study, however, is that these two groups were not compared with a control (no exercise) group. Therefore, the overall effectiveness of flexion exercises versus no exercise at all has not been determined.

Physical therapy methods such as ultrasound, heat, and massage often are added to the therapy protocol. However, no study has yet shown their usefulness in patients with spondylolisthesis.

If patients fail a reasonable course of therapy (4-6 weeks), they may benefit in the short term from a course of epidural steroid injections. Benefits may include decreased lower-back pain and decreased pain related to radiculopathy. No authors have evaluated the effectiveness of epidural steroid injections in patients with spondylolis-thesis alone. However, authors of a long-term followup study of patients having a course of injections failed to reveal a lasting benefit (beyond 3 years) in patients with degenerative disc disease, herniated discs, or spinal stenosis.6,16,41,50

Spinal manipulation is an alternative treatment often pursued by the patient. No randomized clinical trials of patients with spondylolisthesis or spinal stenosis have been done. Authors of the only study involving patients with spondylolisthesis and manipulative therapy reviewed a group of 260 patients with spinal stenosis, 25 of whom had concomitant spondylolisthesis.36 All patients had spinal manipulative therapy. There was no difference in outcomes between the two groups. However, this study was limited in its power and by a lack of control group. Patients may have some short-term pain relief from chiropractic manipulation, but no long term benefit has been proven.

Back to Top | Article Outline

Surgical Treatment

The majority of patients with spinal stenosis will respond to nonoperative treatment and will not require surgery. Only 10% to 15% of patients with degenerative spondylolisthesis and spinal stenosis ultimately have surgery.40 Determining which patients should have surgical intervention often is simple, but for many patients the decision to have surgery may be difficult. Surgical goals include pain reduction, improvement of neurologic symptoms, and improvement in the quality of life. If attainment of these goals is unlikely, conservative treatment should be continued.

Relative indications for surgical intervention include the following: persistent radiculopathy despite conservative treatment, progressive neurologic deficit, persistent and unremitting lower-back pain for more than 6 months, and loss of quality of life because of neurogenic claudication. Absolute indications include progressive neurologic deficit or cauda equina syndrome.

Even after the decision for surgical intervention is made the choice of surgical technique may not be clear. Options include decompression with or without a posterolateral fusion, decompression with posterolateral fusion and instrumentation, and posterior spinal fusion combined with an anterior fusion, transforaminal lumbar interbody fusion, or anterior lumbar interbody fusion alone. All of these treatment methods are discussed independently.

Back to Top | Article Outline

Decompression Alone

The initial surgical treatment of degenerative spondylolis-thesis was based on a standard laminectomy.13,42 Laminectomy was the mainstay for many years until fusion procedures became more popular. Despite this, authors of relatively modern studies have upheld the usefulness of laminectomy without fusion. In 1998, Epstein10 reported on 290 patients with degenerative spondylolisthesis who had decompressive surgery without fusion (249 laminectomies, 41 hemilaminectomies). The majority of his patients (82%) had excellent or good outcomes. Only eight patients required fusion surgery at a later date.

One year later, Herron and Trippi22 published the results of laminectomies done on 20 patients with at least 10% slips. There were 20 good results, three fair results, and one poor result. However, these patients had no more than 2 mm of mobility on their lateral flexion-extension views. Therefore, fusion may not have been necessary because secondary stabilization may have already occurred.

An alternative, less invasive posterior decompressive surgery using a unilateral approach was recently described by Kinoshita et al28 in 2001. They found 78% of patients had good to excellent results and their tissue-sparing technique could be a possible treatment option that preserves the posterior ligamentous complex. However, more investigation is required before this technique can be recommended.

These authors show laminectomy alone may provide beneficial results in the treatment of degenerative spondylolisthesis with stenosis. We think laminectomy alone should be reserved for patients who have a “stiff” spinal segment.

Back to Top | Article Outline

Laminectomy and Posterior Spinal Fusion (without Interpedicled Instrumentation)

In the mid 1980s, the role of posterior fusion became a much studied topic. Dall and Rowe9 retrospectively reported on 17 patients who had laminectomy alone for degenerative spondylolisthesis. Only nine of the patients improved and eight had worsened at an average followup of 20 months. That same year, Feffer et al11 reported more favorable results when posterolateral fusion is added to laminectomy. In a prospective randomized study published in 1991, Herkowitz and Kurz21 compared decompression alone with decompression and posterolateral fusion in patients with single-level spondylolisthesis. They randomly assigned 50 patients into two groups. Patients in Group I had decompression alone whereas patients in Group II had decompression with posterolateral fusion. The patients who had posterolateral fusion all had good or excellent results, far exceeding the results for patients in Group I. Of note, however, was a 36% pseudarthrosis rate in the fusion group. Pseudarthrosis, however, did not affect outcome significantly. The authors postulated that even a pseudarthrosis restricted motion enough that the benefits of a solid fusion were obtained.

Kimura et al27 retrospectively reviewed 57 patients with L4-L5 degenerative spondylolisthesis who had decompression and posterolateral fusion with and without instrumentation. They found no difference in fusion rate or clinical results between the two groups at 2-year followup, once again suggesting instrumentation may not always be necessary.

Back to Top | Article Outline

Decompression with Posterolateral Instrumented Fusion

As evidence that fusion improved clinical outcomes was compiled, it was theorized interpedicled instrumentation would fix the spine more rigidly, increasing fusion rates and improving patient outcomes. In 1993, a prospective randomized study by Zdeblick55 demonstrated instrumented fusion procedures of the lumbar spine produced better fusion rates than uninstrumented fusion procedures did. In the same year, Bridwell et al5 reported increased fusion rates in patients with degenerative spondylolisthesis who had instrumented fusions compared with those who had uninstrumented fusions. Furthermore, there was greater slip progression in the uninstrumented group. Booth et al4 corroborated the argument for instrumentation when they reported on a 5-year retrospective followup study of 36 patients who had fusion with instrumentation for degenerative spondylolisthesis; patients reported an 83% satisfaction rate.4

In a progressive randomized study comparing decompression and posterolateral fusion with and without instrumentation, Fischgrund et al12 found an increased fusion rate patients who had instrumented fusion (82%) compared with patients who had fusion without instrumentation (45%). One peculiar finding was that there was no difference in clinical outcome between patients with solid fusions and patients with pseudarthroses. The authors theorized a fibrous union of a pseudarthrosis provided enough stability to prevent slip progression.

Kornblum et al29 analyzed a subset of the patients studied by Herkowitz and Kurz,21 and those of Fischgrund et al12: those patients who had intertransverse posterolateral fusion without instrumentation. At an average followup of 8 years, they found the early positive results of the patients with pseudarthroses did not hold up for the long term. Just more than 1½ (56%) of the patients with pseudarthroses had good or excellent outcomes compared with 86% good or excellent results in the patients who had solid fusion. They subsequently recommended the use of instrumentation in all patients having fusion for degenerative spondylolisthesis.

Authors of a meta-analysis who reviewed the literature pertaining to degenerative lumbar spondylolisthesis from 1970 to 1993 showed outcomes are improved when concomitant arthrodesis is achieved.32 Therefore, if one believes instrumentation does increase fusion rates, then instrumented fusions should be used to treat spondylolisthesis.

Back to Top | Article Outline

Decompression with Anterior and Posterior Spinal Fusion

As more evidence revealed increased fusion rates improved patient outcomes, the combined anterior and posterior spinal fusion (360°) fusion was gaining popularity. Conventional thought stated that increased fusion surface area would result in an increased rate of fusion and improved patient outcomes. Combined anterior lumbar inter-body fusion and posterolateral fusion as well as posterior lumbar interbody fusion have been used in the treatment of degenerative spondylolisthesis. However, these techniques have been supplanted by the newer transforaminal lumbar interbody fusion. The transforaminal lumbar interbody fusion has been shown to be effective in short-term studies with less morbidity and expense to the patient than a combined anterior-posterior spinal fusion or a posterior lumbar interbody fusion.20,23,43,44,51 Furthermore, interbody fusion combined with posterolateral fusion has shown increased mechanical strength compared with posterolateral fusion alone.30,47 Therefore, transforaminal lumbar inter-body fusion shows great promise in the treatment of degenerative spondylolisthesis. A prospective randomized study comparing decompression with transforaminal lumbar interbody fusion with decompression with instrumented posterior spinal fusion is necessary to determine its true efficacy.

Back to Top | Article Outline

DISCUSSION

Although many surgical options exist for the treatment of degenerative spondylolisthesis, it generally is agreed that in most cases nonoperative treatment should be attempted before surgical intervention is pursued. Most patients will not require surgery. Of the nonoperative options, none are conclusively superior to the others and all have a role in the treatment of symptomatic patients.

For the 15% of patients who do progress to surgery, each of the surgical techniques noted above have merit and quality studies supporting their use. Current literature supports decompression of stenotic areas if symptoms warrant surgery.10,13,22,42 Authors of more recent studies suggest less invasive decompression procedures may also provide symptomatic relief for patients.28 However, long-term prospective randomized trials involving minimally invasive decompression techniques are lacking. Decompression without fusion may be preferred if there is secondary stabilization at the slipped segment. However, there are conflicting studies in the literature regarding fusion surgery. Although some authors suggest good outcomes with decompression alone, others have found improved outcomes in patients with solid fusions over those not undergoing fusions or those with pseudarthroses.10,11,12,21,22,29,32,55

If fusion surgery is to be performed, the surgeon and patient must also consider anterior column fusion as a compliment to the traditional posterolateral fusion. Some studies suggest the addition of interbody fusion to postero-lateral fusion may improve fusion rates.43,44 Furthermore, transforaminal lumbar interbody fusion offers many advantages over combined anterior and posterior fusion surgery and may prove to be the procedure of choice for unstable slipped segments. However, a prospective randomized study comparing the transforaminal lumbar inter-body fusion with the traditional posterolateral fusion has not yet been published.

Back to Top | Article Outline

References

1. Bassewitz H, Herkowitz HN. Lumbar stenosis with spondylolisthesis: Current concepts of surgical treatment. Clin Orthop Relat Res. 2001;384:54-60.
2. Bednar DA. Surgical management of lumbar degenerative spinal stenosis with spondylolisthesis via posterior reduction with minimal laminectomy. J Spinal Disord Tech. 2002;15:105-109.
3. Bird HA, Eastmond CJ, Hudson A, Wright V. Is generalized ligamentous joint laxity a factor in spondylolisthesis? Scand J Rheumatol. 1980;9:203-205.
4. Booth KC, Bridwell KH, Eisenberg BA, Baldus CR, Lenke LG. Minimum 5 year results of degenerative spondylolisthesis treated with decompression and instrumented posterior fusion. Spine. 1999;24:1721-1727.
5. Bridwell KH, Sedgewick TA, O'Brien MF, Lenke LG, Baldus CR. The role of fusion and instrumentation in the treatment of degenerative spondylolisthesis with spinal stenosis. J Spinal Disord. 1993;6:461-472.
6. Butterman GR. Treatment of lumbar disk herniation: Epidural steroid injection compared with discectomy. A prospective, randomized study. J Bone Joint Surg. 2004;86A:670-679.
7. Cauchoix J, Benoist M, Chassaing V. Degenerative spondylolisthesis. Clin Orthop Relat Res. 1976;115:112-129.
8. Cinotti G, Postacchini F, Fassari F, Urso S. Predisposing factors in degenerative spondylolisthesis: A radiographic and CT study. Int Orthop. 1997;21:337-342.
9. Dall BE, Rowe DE. Degenerative spondylolisthesis: Its surgical management. Spine. 1985;10:668-672.
10. Epstein NE. Decompression in the surgical management of degenerative spondylolisthesis: Advantages of a conservative approach in 290 patients. J Spinal Disord. 1998;11:116-122.
11. Feffer HL, Wiesel SW, Cuckler JM, Rothman RH. Degenerative spondylolisthesis: To Fuse or not to fuse. Spine. 1985;10:287-289.
12. Fischgrund JS, Mackay M, Herkowitz HN, Brower R, Montgomery DM, Kurz LT. Volvo Award winner in clinical studies. Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine. 1997;22: 2807-2812.
13. Fitzgerald JAW, Newman PH. Degenerative spondylolisthesis. J Bone Joint Surg. 1976;58B:184-192.
14. Frymoyer JW. Degenerative spondylolisthesis: Diagnosis and treatment. J Am Acad Orthop Surg. 1994;2:9-15.
15. Frymoyer JW, Cats-Baril WL. Epidemiology and the impact of low back pain. Spine. 1991;222:263-271.
16. Fukusaki M, Kobayashi I, Hara T, Sumikawa K. Symptoms of spinal stenosis do not improve after epidural steroid injection. Clin J Pain. 1998;14:148-151.
17. Glaser JA, Bernhardt M, Found E, McDowell GS, Wetzel FT. Lumbar arthrodesis for degenerative conditions. Instr Course Lect. 2004;53:325-340.
18. Gramse RR, Sinaki M, Ilstrup DM. Lumbar spondylolisthesis: A rational approach to conservative treatment. Mayo Clin Proc. 1980;55:681-686.
19. Grobler LJ, Robertson PA, Novotny JE, Pope MH. Etiology of spondylolisthesis: Assessment of the role played by lumbar facet morphology. Spine. 1993;18:80-91.
20. Hee HT, Castro FP Jr, Majd ME, Holt RJ, Myers L. Anterior/posterior lumbar fusion versus transforaminal lumbar interbody fusion: Analysis of complications and predictive factors. J Spinal Disord. 2001;14:533-540.
21. Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective study comparing decompression with decompression and intertransverse arthrodesis. J Bone Joint Surg. 1991;74A:802-808.
22. Herron LD, Trippi AC. L4-5 degenerative spondylolisthesis: The results of treatment by decompressive laminectomy without fusion. Spine. 1989;14:534-538.
23. Humphreys SC, Hodges SD, Patwardhan AG, Eck JC, Murphy RB, Covington LA. Comparison of posterior and transforaminal approaches to lumbar interbody fusion. Spine. 2001;26:567-571.
24. Imada K, Matsui H, Tsuji H. Oophorectomy predisposes to degenerative spondylolisthesis. J Bone Joint Surg. 1995;77B:126-130.
25. Ishihara H, Osada R, Kanamori M, Kawaguchi Y, Ohmori K, Kimura T, Matsui H, Tsuji H. Minimum 10-year follow-up study of anterior lumbar interbody fusion for isthmic spondylolisthesis. J Spinal Disord. 2001;14:91-99.
26. Junghanns H. Spondylolisthesis ohne spalt in zwischengelenstuck. Archiv fur Orthopaedische und Unfall-Chirurgie. 1930;29:118-127.
    27. Kimura I, Shingu H, Murata M, Hashiguchi H. Lumbar posterolateral fusion alone or with transpedicular instrumentation in l4-l5 degenerative spondylolisthesis. J Spinal Disord. 2001;14:301-310.
    28. Kinoshita T, Ohki I, Roth KR, Amano K, Moriya H. Results of degenerative spondylolisthesis treated with posterior decompression alone via a new surgical approach. J Neurosurg Spine. 2001;95: 11-16.
    29. Kornblum MB, Fischgrund JS, Herkowitz HN, Abraham DA, Berkower DL, Kitkoff JS. Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective long-term study comparing fusion and pseudarthrosis. Spine. 2004;29:726-733.
    30. La Rosa G, Conti A, Cacciola F, Cardali S, La Torre D, Gambadauro NM, Tomasello F. Pedicle screw fixation for isthmic spondylolisthesis: Does posterior lumbar interbody fusion improve outcome over posterolateral fusion. J Neurosurg Spine. 2003;99:143-150.
    31. Magora A. Conservative treatment in spondylolisthesis. Clin Orthop Relat Res. 1976;117:74-79.
    32. Mardjetko SM, Connolly PJ, Shott S. Degenerative lumbar spondylolisthesis: A meta-analysis of the literature 1970-1993. Spine. 1994;19(20 Supp):2256S-2265S.
    33. Matsunaga S, Ijiri K, Hayashi K. Nonsurgically managed patients with degenerative spondylolisthesis: A 10 to 18 year follow-up study. J Neurosurg Spine. 2000;93:194-198.
    34. Matsunaga S, Sakou T, Morizono Y, Masuda A, Demirtas AM. Natural history of degenerative spondylolisthesis. Pathogenesis and natural course of the slippage. Spine. 1990;15:1204-1210.
    35. Meyerding HW. Spondylolisthesis. SurgGynecol Obstet. 1932;54: 371-379.
    36. Mierau D, Cassidy JD, McGregor M, Kirkaldy-Willis WH. A comparison of the effectiveness of spinal manipulative therapy for low back pain in patients with and without spondylolisthesis. Journal of Manipulative Physiologic Therapy. 1987;10:49-55.
    37. Moller H, Hedlund R. Instrumented and noninstrumented postero-lateral fusion in adult spondylolisthesis. A prospective randomized study: Part 1. Spine. 2000;25:1711-1715.
    38. Moller H, Hedlund R. Instrumented and noninstrumented postero-lateral fusion in adult spondylolisthesis. A prospective randomized study: Part 2. Spine. 2000;25:1716-1721.
    39. Osterman K, Schlenzka D, Poussa M, Seitsalo S, Virta L. Isthmic spondylolisthesis in symptomatic and asymptomatic subjects: Epidemiology and natural history with special reference to disk abnormality and mode of treatment. Clin Orthop Relat Res. 1993;297: 65-70.
    40. Postacchini F, Cinotti G,Perugia D. Degenerative Lumbar Spondylolisthesis II. Surgical Treatment. Ital J Orthop Traumatol. 1991;17:467-477.
    41. Rosen CD, Kahanovitz N, Bernstein R, Viola K. A retrospective analysis of the efficacy of epidural steroid injections. Clin Orthop Relat Res. 1988;228:270-272.
    42. Rosenberg NJ. Degenerative spondylolisthesis: Predisposing factors. J Bone Joint Surg. 1975;57A:467-474.
    43. Rosenberg WS, Mummaneni PV. Transforaminal lumbar interbody fusion: Technique, complications, and early results. Neurosurgery. 2001;48:569-574.
    44. Salehi SA, Tawk R, Ganju A, LaMarca F, Liu JC, Ondra SL. Transforaminal lumbar interbody fusion: Surgical technique and results in 24 patients. Neurosurgery. 2004;54:368-374.
    45. Sanderson PL, Fraser RD. The influence of pregnancy on the development of degenerative spondylolisthesis. J Bone Joint Surg. 1996;78B:951-954.
    46. Sinaki M, Lutness MP, Ilstrup DM, Chu CP, Gramse RR. Lumbar spondylolisthesis: A retrospective comparison and three year follow-up of two conservative treatment programs. Arch Phys Med Rehabil. 1989;70:594-598.
    47. Suk KS, Jeon CH, Park MS, Moon SH, Kim NH, Lee HM. Comparison between posterolateral fusion with pedicle screw fixation and anterior interbody fusion with pedicle screw fixation in adult spondylolytic spondylolisthesis. Yonsei Med J. 2001;42:316-323.
    48. Thomsen K, Christensen FB, Eiskjaer SP, Hansen ES, Fruensgaard S, Bunger CE. Volvo Award winner in clinical studies. The effect of pedicle screw instrumentation on functional outcome and fusion rates in posterolateral lumbar spinal fusion: A prospective, randomized clinical study. Spine. 1997;22:2813-2822.
    49. Vaccaro AR, Garfin SR. Degenerative lumbar spondylolisthesis with spinal stenosis: A Prospective study comparing decompression with decompression and intertransverse process arthrodesis: A critical analysis. Spine. 1997;22:368-369.
      50. Wang JC, Lin E, Brodke DS, Youssef JA. Epidural steroid injections for the treatment of symptomatic lumbar herniated discs. J Spinal Disord Tech. 2002;15:269-272.
      51. Whitecloud TS III, Roesch WW, Ricciardi JE. Transforaminal interbody fusion versus anterior-posterior interbody fusion of the lumbar spine: A financial analysis. J Spinal Disord. 2001;14:100-103.
      52. Wiltse LL, Newman PH, Macnab I. Classification of spondylolysis and spondylolisthesis. Clin Orthop Relat Res. 1976;117:23-29.
      53. Wood KB, Popp CA, Transfeldt EE, Geissele AE. Radiographic evaluation of instability in spondylolisthesis. Spine. 1994;19:1697-1703.
      54. Yang K, King A. Mechanism of Facet load transmission as a hypothesis for low back pain. Spine. 1984;9:557-565.
      55. Zdeblick TA. A prospective, randomized study of lumbar fusion: Preliminary results. Spine. 1993;18:983-991.
      © 2006 Lippincott Williams & Wilkins, Inc.