Javascript not enabled
SpineFocus On...

Understanding and Treating Spinal Stenosis

T. S. Rajagopal, R. W. Marshall
FocusOn_aug10_05.pdf4.22 MB


Lumbar spinal stenosis is narrowing of the central spinal canal, lateral recess or the neural foramen. After initial recognition of spinal stenosis in 1802, a gradual understanding evolved over the next 150 years.1-4 Harris and Macnab described the importance of disc degeneration in the pathogenesis of stenosis.5Macnab highlighted the lateral recess beneath the posterior facet joint.6Verbiest identified neurogenic claudication as a result of spinal canal stenosis. 7

Anatomical Considerations

The shape of the lumbar spinal canal varies and may be an oval, rounded triangular or trefoil configuration.8The trefoil configuration usually occurs at the fifth lumbar level, making L4-L5 the narrowest level 9(Fig. 1), and occurs in 25% of the population, only appearing in  adulthood.10The anteroposterior diameter of the lumbar spinal canal is critical in the pathogenesis and is affected by the length of the pedicles. 


Fig 1. View of the L5 vertebra showing the trefoil configuration of the spinal canal (Reprinted with permission from JBJS - Eisenstein S.M, The trefoil configuration of the lumbar vertebral canal; A study of South African skeletal material. J Bone Joint Surg [Br] : 62-B (1): 73-7).



Lumbar spinal stenosis is classified according to its aetiology (Table I).11Postacchini divided the stenosis into primary (congenital), secondary (acquired) or combined forms.12

The congenital type is rare. There are anatomical abnormalities such as short pedicles in achondroplasia. Other causes include hypochondroplasia, diastrophic dwarfism, Morquio’s syndrome, hereditary exostosis and cheirolumbar dysostosis. The majority of patients present with acquired stenosis because of degeneration in the fifth to seventh decades.

Anatomically, spinal stenosis can be central, within the lateral recess, or in the foramen. Central canal stenosis occurs at the level of the intervertebral disc with midline sagittal narrowing. Lateral recess stenosis occurs when the traversing nerve root is compressed beneath the superior articular process of the inferior vertebra, i.e. beneath the thickened facet joint.

Hansraj et al divided spinal stenosis into typical and complex lumbar spinal stenosis (Table II).13,14Typical cases were treated with decompressive surgery, while complex stenosis required decompression and fusion.


Kirkaldy-Willis et al described the sequence of degenerative changes which result in central or lateral recess stenosis.15

Central canal stenosis (Fig. 2) is mainly created by hypertrophy of the ligamentum flavum, facet joint osteophyte formation and degenerative spondylolisthesis (Fig. 3).


Fig 2. Sagittal and axial T2-weighted MRI scans showing central canal stenosis


Fig 3. Sagittal, axial and coronal T2-weighted MRI scans in an 80-year-old patient showing a degenerative spondylolisthesis at L4-L5. There is lateral recess stenosis but there is no compression of the exiting nerve root on the coronal images (arrowed)


Lateral recess stenosis results from compression between the medial aspect of a hypertrophic superior articular facet and posterior aspect of the vertebral body and disc (Fig. 4). Hypertrophy of the ligamentum flavum and/or facet joint capsule, vertebral body osteophyte and disc protrusion exacerbate the stenosis. The traversing nerve root is compressed in the lateral recess (i.e. the L5 nerve root in the L4-L5 lateral recess).


Fig 4. Sagittal and axial T2-weighted MRI scans in a 74-year-old patient showing lateral recess stenosis at L4-L5


Foraminal stenosis is rare and mainly occurs in isthmic spondylolisthesis, where the exiting nerve root (i.e. the L5 nerve root in L5-S1 isthmic spondylolisthesis) is compressed in the distorted foramen. It also occurs in far lateral disc herniation where the exiting nerve root is compressed in the foramen, or extraforaminal zone (Fig. 5).



Fig 5. Sagittal, coronal and axial T2-weighted MRI scans in a 62-year-old patient showing foraminal stenosis (arrow) caused by a far lateral disc prolapse at L4-L5


Lateral recess and foraminal stenosis are distinct entities with different clinical implications.16

Natural History

The course of spinal stenosis is chronic and benign. Johnsson, Rosen and Uden reported on 32 patients followed up for a mean of 49 months (10 to 103) without any treatment.17Of the 32 patients, 15% improved, 70% stayed the same and only 15% became worse. The majority of patients followed up for four years thus remained unchanged.

Despite a benign natural history, the long term is characterised by slow deterioration. A randomised study by Amundsen et al compared surgical and conservative treatment with a ten-year follow-up.18The outcome was more favourable for surgical treatment, but an initial conservative approach was recommended as late treatment still achieved a good result.

Clinical features


The symptoms are insidious, presenting in the sixth or seventh decade. There may be a long history of low back pain but the leg symptoms lead to presentation.

The patient with central canal stenosis has bilateral leg symptoms which are vague and often described as heaviness, soreness or weakness. The cardinal symptom is neurogenic claudication which presents as numbness, weakness or discomfort in the legs; this may come on with walking or prolonged standing and is relieved by sitting or rest. The patients are able to walk further when leaning on a shopping trolley or walking uphill because spinal flexion increases the space available for the cauda equina and unfolds the ligamentum flavum. The pain-free walking distance may vary.

Patients with lateral recess stenosis present with unilateral radicular symptoms of leg pain along with numbness, paraesthesiae or burning in a dermatomal distribution. Pain radiates from the buttock to the posterior thigh and lateral calf because most compression occurs at L4-L5. If there is a higher lumbar lesion then anterior thigh pain will be present. The symptoms may also be provoked by walking.

Cauda equina syndrome or major neurological deficits are very rare in the presence of canal stenosis.


Physical findings are limited. The diagnosis is made from the history and confirmed with imaging. There may be limitation of lumbar spinal extension, sensory deficit, muscle weakness, limited straight leg raise, absent knee reflexes and absent ankle reflexes.19 Neurological abnormalities are uncommon at rest. The “Shuttle walking test” has been suggested as a reliable objective assessment of walking distance.20 Loss of distal vibration sense may be present but is common in older patients anyway. Signs of cervical myelopathy may be detected, as lumbar spinal stenosis is associated with cervical canal narrowing in 5% of the patients (Tandem stenosis).21

Differential diagnosis

Peripheral Vascular Disease

Table III shows the differences between neurogenic and vascular claudication.

Hip Osteoarthritis

Anterior thigh pain can be present in hip arthritis as well as in spinal stenosis with involvement of the L3 or L4 nerve roots. However, pain on passive rotation of the hip should alert the clinician to the possibility of hip disease. The two conditions can coexist, so nerve root blocks and/or hip joint injections with local anaesthetic and steroid may be necessary to differentiate between them.

Peripheral Neuropathy

This diagnosis is determined more by neurological symptoms than pain, and produces a stocking pattern of numbness. Electrophysiological testing confirms the diagnosis.

Trochanteric Bursitis

Sometimes spinal stenosis patients are diagnosed as having trochanteric bursitis. Some have suggested a predisposition to this condition because of an  “altered pelvic balance”.22



Plain radiographs of the lumbosacral spine may show narrowing of the disc space, facet joint osteoarthritis, degenerative spondylolisthesis or degenerative scoliosis. Radiographs are also useful to exclude conditions such as tumour or infection. Dynamic instability can be demonstrated by lateral radiographs taken in the standing position with spinal flexion and extension.

Computed Tomography (CT) Myelography

CT or CT myelography is useful in patients who have a contraindication to magnetic resonance imaging (MRI) scan (pacemaker, metallic implants, etc.). On CT, midsagittal lumbar canal diameters of less than 10 mm are regarded as an absolute stenosis while less than 13 mm represents relative stenosis.23


MRI is the investigation of choice in confirming the diagnosis of spinal canal stenosis. Standard MRI examination includes T1- and T2-weighted sagittal and axial sequences. The typical findings in central or lateral recess stenosis include thickening of the ligamentum flavum, facet joint hypertrophy and synovial cysts, a trefoil appearance of the thecal sac, vertebral endplate osteophytes and obliteration of perineural fat in the neural foramina.

Parasagittal images can overdiagnose the incidence of foraminal stenosis. We recommend additional T2-weighted coronal and Short T1 Inverted Recovery (STIR) sequences which demonstrate the nerve roots very well and confirm that the incidence of foraminal stenosis is low in degenerative spondylolisthesis or spinal stenosis, but exists mainly in isthmic spondylolisthesis or extraforaminal disc protrusion.24


Peripheral neuropathy is a frequent concomitant finding or differential diagnosis in elderly patients with spinal stenosis. Neurophysiological assessments including electromyography and nerve conduction studies are useful in identifying peripheral neuropathy and in differentiating between radiculopathy and mononeuropathy (e.g. femoral neuropathy in diabetics).


Conservative treatment

Analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), weight loss and physiotherapy are used in the management of patients with spinal stenosis. Porter and Hibbert25 reported that nasal calcitonin improved the symptoms of neurogenic claudication but a further randomised controlled study in 2004 showed no benefit.26

There is conflicting evidence in the literature about the use of epidural steroids.27-29 However, they can provide temporary relief of symptoms. Nerve root blocks are useful in treating radicular pain due to lateral recess stenosis.30

Surgical treatment

Surgery is indicated when conservative measures fail and if moderate to severe leg symptoms interfere with the patient’s lifestyle. While these indications remain relative, progressive neurological deficit or cauda equina syndrome represent absolute indications for surgery.

The greater the degree of compression, the better the outcome of surgery. While the primary objective of surgery is to relieve the patient’s leg symptoms, it is important to consider the mechanical back pain and/or instability before deciding on the type of surgical procedure.

The surgical options include:

  • Decompressive laminotomy and partial facetectomy
  • Decompressive laminectomy and partial facetectomy
  • Micro-decompression
  • Decompression and non-instrumented fusion
  • Decompression and instrumented fusion
  • Decompression and flexible stabilisation
  • Inter-spinous spacer devices 

Decompressive Laminotomy and Laminectomy

The aim of decompression is to remove the pressure on the cauda equina and the individual nerve roots. The standard wide midline decompressive laminectomy involves the removal of the spinous processes, laminae, ligamentum flavum, medial part of the facet joints and the facet capsule at all involved vertebral levels. However, the potential for segmental instability has led to more conservative operations.

The popular technique of multiple laminotomies may preserve segmental spinal stability, but Postacchini et al  found that patients who had laminotomies had less back pain but a slightly higher incidence of nerve damage.31 Laminectomy was found to be better for tight stenosis, as it allowed safer neural decompression. Multiple laminotomies are recommended in developmental stenosis since the patients are younger, the stenosis is rarely severe and additional disc excision is often necessary.16

The results of surgical decompression for lumbar spinal stenosis vary from 57% to 81% excellent and good.32 The results for open31,33 or microsurgical laminotomy 34' 35 are similar. No difference between clinical outcome and spondylolisthesis progression was found when comparing laminectomy with laminotomy.36

While the initial results of decompressive laminectomy are favourable, they can deteriorate in the longer term. Jonsson et al reported on a prospective study of 108 patients who had laminectomy without fusion; 67% had excellent results at two years, but deteriorated to 50% at five years; 18% required re-operation.37

It has been suggested16, 37that the ideal surgical patient would have:

  • Severe osteoligamentous compression of the neural structures
  • Severe leg symptoms
  • Moderate or no neurological deficit
  • Little or no back pain
  • Symptoms for less than four years
  • No associated condition to impair mobility

Old age does not compromise the results of decompressive surgery.38


 “Microdecompression” minimises operative trauma by approaching and entering the canal from one side only. After decompressing the ipsilateral open side, the dissection crosses the midline beneath the overhanging spinous processes and contralateral laminae, allowing trimming of the facet joints and other compressive structures on the contralateral side from within the canal39(Fig. 6). Mayer et al. reported success in 275 patients at a mean of two years, with an improvement in back pain in 48% of patients and of leg pain in 51%.40


Fig 6. Post-operative axial CT scan showing the spinal canal to be opened up after microdecompression


In another study, with a longer follow-up of 100 patients, sciatica improved in 90% and back pain in 84%. For 82% of the patients their results were graded as good or excellent according to the Macnab criteria.39

Decompression and Fusion

Fusion is generally recommended in addition to decompression in the following circumstances:

  • Degenerative spondylolisthesis
  • Degenerative scoliosis
  • Concomitant moderate to severe back pain
  • Necessity for wide decompression with facet joint removal
  • Recurrent spinal stenosis

Herkowitz and Kurz prospectively compared decompression alone with decompression and fusion in 50 patients with spinal stenosis and degenerative spondylolisthesis with a follow-up of three years.41 The results were satisfactory (excellent or good) in 44% of the unfused and 96% in the fused group. Fischgrund et al prospectively randomised 76 patients and compared intertransverse non-instrumented fusion with pedicle screw fusion.42 Excellent or good results were obtained in 82% of the intertransverse group (45% fusion rate) and 76% of the pedicle screw group (82% fusion rate). The authors concluded that the use of instrumentation leads to a higher rate of fusion but there was no statistically significant clinical difference.

Kornblum et al later showed that the patients with a solid fusion had improved long-term clinical results after five to 14 years.43

We can thus conclude that an instrumented fusion should be performed in addition to decompression in the management of degenerative spondylolisthesis.

Decompression and Flexible stabilisation

In patients with spinal stenosis who have segmental instability or degenerative spondylolisthesis, spinal decompression and stabilisation with a flexible or dynamic stabilisation system (e.g. Dynesys (Zimmer Ltd, Swindon, Wilts)), is a controversial option, but Schnake, Schaeren and Jeanneret found clinical results similar to decompression and fusion with pedicle screws.44

Interspinous spacer devices

Interspinous spacer devices are inserted between the spinous processes to prevent extension of the symptomatic levels, but allow flexion, axial rotation and lateral bending.

Biomechanical studies have shown that in extension the implants increase the dimensions of the spinal canal.45 There are some favourable reports of outcome with interspinous devices;46-48 however, others report high failure rates for these implants and the need for further surgery.49 The evidence is thus still inconclusive. Interspinous spacer devices may have a place in elderly patients who are unfit for anaesthesia and more major surgery.

Degenerative Scoliosis

Spinal stenosis associated with degenerative scoliosis is a complex problem and its treatment is controversial. These patients have multilevel disease with varying combinations of central, lateral recess or foraminal stenosis. They have a mixed pattern of symptoms, which include stenotic, radicular and arthritic pain (Fig. 7). Nerve root compression is present more often on the concave side of the curve.50 True foraminal compression can occur due to lateral disc herniation, collapse of the disc and scoliosis. The incidence of complications is high after surgery51 as these are patients of advanced age who may have multiple medical comorbidities. Two types of deformity have been described.52 Type I is a lumbar scoliosis with no or minimal rotational deformity. Type II curves have degeneration superimposed on a pre-existing scoliosis with greater rotational deformity and loss of lordosis. Shorter segmental instrumentation is usually possible for type I deformities while longer instrumentation with sagittal plane reconstitution is necessary for type II curves (Fig. 8).52 The choice of surgical technique remains controversial but most would agree that decompression and instrumented fusion is necessary for a successful outcome.13


Fig 7.Sagittal, coronal and axial T2-weighted MRI Scans in an 89-year-old patient showing degenerative scoliosis and multilevel spinal stenosis 


Fig 8a. Pre-operative views. Anteroposterior and lateral radiograph of a 79-year-old patient with degenerative scoliosis, loss of lumbar lordosis and rotational deformity. The patient had persistent back pain after a single-level fusion that had been performed many years earlier.


Figure 8b. Post-operative views showing correction of the degenerative scoliosis and restoration of sagittal alignment. Anteroposterior and lateral radiograph of a 79-year-old patient with degenerative scoliosis, loss of lumbar lordosis and rotational deformity. The patient had persistent back pain after a single-level fusion that had been performed many years earlier.



1. Portal A, editor. Cours d'anatomie medicale au elements de l'anatomiede l'homme. Paris: Badoin, 1802.

2. Sachs B FV. Progressive and Kyphotic rigidity of the spine. J Nerv Ment Dis 1900;27(1).

3. Putti V. New Conception in the treatment of sciatic pain. Lancet 1927;2:53-60.

4. Hirsch C. On lumbar facetectomies. Acta Orthop Scand 1948;17:240-52.

5. Harris RI, Macnab I. Structural changes in the lumbar intervertebral discs; their relationship to low back pain and sciatica. J Bone Joint Surg [Br] 1954;36-B:304-22.

6. Macnab I. Negative disc exploration: an analysis of the causes of nerve-root involvement in sixty-eight patients. J Bone Joint Surg [Am] 1971;53-A:891-903.

7. Verbiest H. Fallacies of the present definition, nomenclature and classification of the stenoses ofthe vertebral canal. Spine 1976;1:217-25.

8. Porter RW. Variations in shape and size of the lumbar spinal canal. Paleopathol Newsl 1980;32:9-11.

9. Eisenstein S. Measurements of the lumbar spinal canal in 2 racial groups. Clin Orthop 1976;115:42-6.

10. Papp T, Porter RW, Aspden RM. Trefoil configuration and developmental stenosis of the lumbar vertebral canal. J Bone Joint Surg [Br] 1995;77(3):469-72.

11. Arnoldi CC, Brodsky AE, Cauchoix J, et al. Lumbar spinal stenosis and nerve root entrapment syndromes. Definition and classification. Clin Orthop 1976;115:4-5.

12. Postacchini F. Lumbar spinal stenosis and pseudostenosis. Definition and classification of pathology. Ital J Orthop Traumatol 1983;9:339-50.

13. Hansraj KK, O'Leary PF, Cammisa FP, et al. Decompression, fusion, and instrumentation surgery for complex lumbar spinal stenosis. Clin Orthop 2001;384:18-25.

14. Hansraj KK, Cammisa FP, Jr., O'Leary PF, et al. Decompressive surgery for typical lumbar spinal stenosis. Clin Orthop 2001;384:10-17.

15. Kirkaldy-Willis WH, Paine KW, Cauchoix J, McIvor G. Lumbar spinal stenosis. ClinOrthop 1974;99:30-50.

16. Postacchini F. Management of lumbar spinal stenosis. J Bone Joint Surg [Br] 1996;78-B:154-64.

17. Johnsson KE, Rosen I, Uden A. The natural course of lumbar spinal stenosis. Clin Orthop 1992;279:82-6.

18. Amundsen T, Weber H, Nordal HJ, Magnaes B, Abdelnoor M, Lilleas F. Lumbar spinal stenosis: conservative or surgical management?: A prospective 10-year study. Spine (Phila Pa 1976) 2000;25:1424-35; discussion 35-6.

19. Katz JN, Wright EA, Guadagnoli E, Liang MH, Karlson EW, Cleary PD. Differences between men and women undergoing major orthopedic surgery for degenerative arthritis. Arthritis Rheum 1994;37:687-94.

20. Spratt KF, Keller TS, Szpalski M, Vandeputte K, Gunzburg R. A predictive model for outcome after conservative decompression surgery for lumbar spinal stenosis. Eur Spine J 2004;13:14-21.

21. Epstein BS, Epstein JA, Jones MD. Anatomicoradiological correlations in cervical spine discal disease and stenosis. Clin Neurosurg 1978;25:148-73.

22. Wong DA, Transfeldt, E. Macnab's Backache. Fourth ed. Philadelphia: Lippincott Williams & Wilkins, 2007.

23. Verbiest H. The significance and principles of computerized axial tomography in idiopathic developmental stenosis of the bony lumbar vertebral canal. Spine (Phila Pa 1976) 1979;4:369-78.

24. Rajagopal TS, Marshall, R.W., McKenzie, J., Archibald, C. Improved diagnosis of spinal stenosis with coronal MRI, 2010 - Research in Progress.

25. Porter RW, Hibbert C. Calcitonin treatment for neurogenic claudication. Spine (Phila Pa 1976) 1983;8:585-92.

26. Podichetty VK, Segal AM, Lieber M, Mazanec DJ. Effectiveness of salmon calcitonin nasal spray in the treatment of lumbar canal stenosis: a double-blind, randomized, placebo-controlled, parallel group trial. Spine (Phila Pa 1976) 2004;29:2343-9.

27. Kraemer J, Ludwig J, Bickert U, Owczarek V, Traupe M. Lumbar epidural perineural injection: a new technique. Eur Spine J 1997;6:357-61.

28. Chou R, Atlas SJ, Stanos SP, Rosenquist RW. Nonsurgical interventional therapies for low back pain: a review of the evidence for an American Pain Society clinical practice guideline. Spine (Phila Pa 1976) 2009;34:1078-93.

29. Cuckler JM, Bernini PA, Wiesel SW, et al. The use of epidural steroids in the treatment of lumbar radicular pain. A prospective, randomized, double-blind study. J Bone Joint Surg [Am] 1985;67-A:63-6.

30. Datta S, Everett CR, Trescot AM, et al. An updated systematic review of the diagnostic utility of selective nerve root blocks. Pain Physician 2007;10:113-28.

31. Postacchini F, Cinotti G, Perugia D, Gumina S. The surgical treatment of central lumbar stenosis. Multiple laminotomy compared with total laminectomy. J Bone Joint Surg [Br] 1993;75:386-92.

32. Zingg PO, Boos N. Lumbar Spinal Stenosis. In: Boos N, Abei, M (eds). Spinal Disorders. Berlin Heidelberg: Springer-Verlag, 2008:513-37.

33. Aryanpur J, Ducker T. Multilevel lumbar laminotomies: an alternative to laminectomy in the treatment of lumbar stenosis. Neurosurgery 1990;26:429-32; discussion 33.

34. Khoo LT, Fessler RG. Microendoscopic decompressive laminotomy for the treatment of lumbar stenosis. Neurosurgery 2002;51(5 Suppl):S146-54.

35. Tsai RY, Yang RS, Bray RS, Jr. Microscopic laminotomies for degenerative lumbar spinal stenosis. J Spinal Disord 1998;11:389-94.

36. Thomas NW, Rea GL, Pikul BK, Mervis LJ, Irsik R, McGregor JM. Quantitative outcome and radiographic comparisons between laminectomy and laminotomy in the treatment of acquired lumbar stenosis. Neurosurgery 1997;41:567-74; discussion 74-5.

37. Jonsson B, Annertz M, Sjoberg C, Stromqvist B. A prospective and consecutive study of surgically treated lumbar spinal stenosis. Part I: Clinical features related to radiographic findings. Spine (Phila Pa 1976) 1997;22:2932-7.

38. Sanderson PL, Wood PL. Surgery for lumbar spinal stenosis in old people. J Bone Joint Surg [Br] 1993;75-B:393-7.

39. Orpen NM, Corner, JA, Shetty R, Marshall RW. Micro-decompression for lumbar spinal stenosis: the early outcome using a modified surgical technique. J Bone Joint Surg [Br] 2010;92- B:550-4.

40. Mayer HM, List J, Korge A, Wiechert K. [Microsurgery of acquired degenerative lumbar spinal stenosis. Bilateral over-the-top decompression through unilateral approach]. Orthopade 2003;32:889-95.

41. Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis. A prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg [Am] 1991;73-A:802-8.

42. Fischgrund JS, Mackay M, Herkowitz HN, Brower R, Montgomery DM, Kurz LT. 1997 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 (Phila Pa 1976) 1997;22:2807-12.

43. Kornblum MB, Fischgrund JS, Herkowitz HN, et al. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective long-term study comparing fusion and pseudarthrosis. Spine (Phila Pa 1976) 2004;29:726-33; discussion 33-4.

44. Schnake KJ, Schaeren S, Jeanneret B. Dynamic stabilization in addition to decompression for lumbar spinal stenosis with degenerative spondylolisthesis. Spine (Phila Pa 1976) 2006;31:442-9.

45. Siddiqui M, Karadimas E, Nicol M, Smith FW, Wardlaw D. Influence of X Stop on neural # foramina and spinal canal area in spinal stenosis. Spine (Phila Pa 1976) 2006;31:2958-62.

46. Kuchta J, Sobottke R, Eysel P, Simons P. Two-year results of interspinous spacer (X-Stop) implantation in 175 patients with neurologic intermittent claudication due to lumbar spinal stenosis. Eur Spine J 2009;18:823-9.

47. Kondrashov DG, Hannibal M, Hsu KY, Zucherman JF. Interspinous process decompression with the X-STOP device for lumbar spinal stenosis: a 4-year follow-up study. J Spinal Disord Tech 2006;19(5):323-7.

48. Zucherman JF, Hsu KY, Hartjen CA, et al. A multicenter, prospective, randomized trial evaluating the X STOP interspinous process decompression system for the treatment of neurogenic intermittent claudication: two-year follow-up results. Spine (Phila Pa 1976) 2005;30:1351-8.

49. Verhoof OJ, Bron JL, Wapstra FH, van Royen BJ. High failure rate of the interspinous distraction device (X-Stop) for the treatment of lumbar spinal stenosis caused by degenerative spondylolisthesis. Eur Spine J 2008;17:188-92.

50. Epstein JA, Epstein BS, Jones MD. Symptomatic lumbar scoliosis with degenerative changes in the elderly. Spine (Phila Pa 1976) 1979;4:542-7.

51. Cho KJ, Suk SI, Park SR, et al. Complications in posterior fusion and instrumentation for degenerative lumbar scoliosis. Spine (Phila Pa 1976) 2007;32:2232-7.

52. Simmons ED. Surgical treatment of patients with lumbar spinal stenosis with associated scoliosis. Clin Orthop 2001:45-53.