Degenerative Lumbar spinal stenosis

                                    Degenerative Lumbar spinal stenosis

                                                     Dr KS DHILLON

 

What is degenerative lumbar spinal stenosis?

A narrowing of the spinal canal, as a result of degenerative disease of the spine, which reduces the space available for the neural and vascular elements within the canal, is known as spinal stenosis. The narrowing of the canal can be symptomatic or asymptomatic. Clinical or symptomatic spinal stenosis is a syndrome which is characterised by the presence of ‘gluteal and/or lower extremity pain and/or fatigue which may occur with or without back pain’ (1). Classically the presentation is that of neurogenic claudication where the patient has pain, numbness and or weakness of the lower limb on standing and walking and the symptoms are relieved on sitting and lying down. They usually have relief of symptom on bending forward which increases the size of the lumbar canal and aggravation of symptoms on spinal extension.

Natural history of degenerative lumbar spinal stenosis

The North American Spine Society (NASS) evidence-based clinical guidelines committee (1) reviewed the literature to study the natural history of degenerative lumbar spinal stenosis. The question the committee posed was “What happens
to patients with symptomatic lumbar stenosis who do not receive treatment?” They identified 54 articles in the literature which broached the topic of the natural history of spinal stenosis and found that none of the publications answered the question because none of the studies had a cohort of patients who had no treatment. The workgroup concluded that there is insufficient evidence in the literature to define the natural history of degenerative spinal stenosis. Although there is no reliable evidence in the literature, the workgroup came to the following conclusions based on the available evidence:
1. The natural history of mild to moderate degenerative lumbar stenosis
may be favourable in one third to half the of patients.
2. In patients with mild to moderate lumbar spinal stenosis a ‘rapid or catastrophic
neurologic decline’ is unlikely.
3. The natural history of clinically or radiographically severe degenerative lumbar stenosis is unknown.

Diagnosis of lumbar spinal stenosis

 

Clinical diagnosis

Konno et al (2 and 3) developed a simple clinical diagnostic support tool to diagnose lumbar spinal stenosis (LSS) which has a sensitivity of 92.8% and a specificity of 72.0%. Patients who presented with back and leg symptoms were asked to fill up a simple questionnaire.  The questions included age, history of diabetes, presences and absences of intermittent claudication, aggravation of symptoms by standing and relief of symptoms on bending forward. This was followed by a short clinical examination consisting of checking for postural changes in their leg symptoms, Achilles' tendon reflex, SLR test and the measurement of ABI. With these measures, the diagnosis of LSS can be established with high sensitivity and specificity without imaging studies.
Classically patients with LSS will have numbness and or pain in the thighs down to the leg after walking or standing for a while and these symptoms will improve on bending forward and after sitting down. The physical examination usually includes ‘a gait-loading test to confirm neurogenic intermittent claudication’. The patient is asked to walk for a while till neurogenic symptoms develop and then the patient is examined for sensory and motor deficit and the knee and ankle reflexes are tested (2). The presences of peripheral vascular disease which can produce vascular claudication has to excluded.
Katz et al. (4) studied the diagnostic value of history and physical examination in the diagnosis of LSS.They used the opinions of several expert physicians including two orthopaedic surgeons to define the presence or absences of LSS. They found that the factors strongly associated with a diagnosis of LSS ‘were greater age,
severe lower-extremity pain, and absence of pain when seated’. The physical findings strongly associated with the diagnosis ‘were a wide-based gait, an abnormal Romberg test, thigh pain following 30 seconds of lumbar extension, and neuromuscular deficits’.
The clinical diagnosis can be confirmed with and correlated with radiological imaging.

Radiological imaging for spinal stenosis
The presences of spinal canal narrowing on radiological imaging does not indicate a diagnosis of spinal stenosis because degenerative changes in the spine are common in asymptomatic individuals. Brinjiki et al (5) did a systematic review of literature of imaging features of spinal degeneration in asymptomatic populations. They found that the prevalence of disk degeneration in asymptomatic individuals increased from 37% among 20-year-old individuals to 96% among 80-year-old individuals. The prevalence of disk bulge increased from 30% among 20 years old individuals to 84% among 80 years old individuals. The prevalence of disc protrusion increased from 29% of those 20 years of age to 43% of those 80 years of age.
Boden et al (6) did MRI scans in 67 individuals who never had back pain, sciatica and neurogenic claudication in the past. They found 21% of the individuals had radiological evidence of spinal stenosis.
Wiesel et al (7) did CT scans of the spine in asymptomatic individuals and found the presence of disc herniation, facet degeneration or spinal stenosis in about 50% of the subjects. They also found that there was no significant correlation between the area of the dural sac in axially loaded CT and the clinical symptoms of spinal stenosis.
False positive and false negative CT scan and MRI findings of nerve compression have been well documented, which makes radiological imaging as a sole means of diagnosing spinal stenosis untenable (6,7,8). There is also an element of significant variation of image interpretation of  MRI and CT scan in the diagnosis of spinal stenosis (9).
Therefore the diagnosis of spinal stenosis has to be clinical and it can be confirmed and correlated with imaging studies.
What are the most useful imaging studies? In patients where a clinical diagnosis of lumbar spinal stenosis has been made, an MRI of the lumbar spine would be the most appropriate non-invasive investigation to confirm spinal canal narrowing and nerve root compression (1).
Kent et al (10) did a systematic review of the literature to compare the usefulness of CT, MRI and myelography in the diagnosis of spinal stenosis. They found that the sensitivity of MRI in the diagnosis of adult spinal stenosis was 81-97%, the sensitivity of CT was between 70-100% and sensitivity of myelography was about 67-78%. The sensitivity of all three modes of imaging for diagnosis is about the same and no one mode is superior to the other.
There are several other studies in literature (11,12,13) which have compared the value of MRI, myelography and CT myelography in the diagnosis of LSS and they all showed that the accuracy of all three modalities is about equal in the diagnosis of spinal stenosis. MRI is widely used and accepted as a mode of investigation since it is non-invasive and it does not expose the patient to contrast media and ionizing radiations.
Barz et al (14) did a study to evaluate the usefulness of the nerve root sediment sign on MRI’s of the lumbar spine. The studied 100 patients with clinical lumbar stenosis and 100 patients who had low back pain and no clinical evidence of spinal stenosis. Ninety-four of the 100 patients with clinical spinal stenosis had a positive sediment sign whereas none of the patients with low back pain had a positive sign. The authors concluded that ‘a positive sedimentation sign exclusively and reliably occurs in patients with LSS, suggesting its usefulness in clinical practice’. However, critics have pointed out that the sign does not ‘discriminate between symptomatic and asymptomatic patients with Dural Sac Area (DSA)<80mm2,(patients with LSS) and hence is of limited clinical value. A positive sediment sign is expected with a DSA of less than 80mm2 (1).
In patients with a clinical diagnosis of LSS in whom an MRI is contraindicated, inconclusive or cannot be done, a CT myelogram would be the imaging study of choice (1). Several studies (11,13,15) have shown that MRI and CT myelograms are equally effective in confirming narrowing of spinal canal and root compression in LSS.
When an MRI or CT myelogram cannot be done, a CT scan would be an appropriate imaging modality, although the sensitivity is slightly lower with a CT scan in diagnosing spinal canal narrowing and nerve root compression (10).
The radiological criteria for defining the severity of spinal stenosis is unclear. The are several classifications for defining radiological spinal stenosis that has been published in the literature (16).
Lee et al. (17) have recently offered a more simple MRI based classification system for central stenosis. They described a 4-grade (0, 1, 2, and 3) system based on the degree of separation of the cauda equina on T2-weighted axial images. They did not measure the parameters. They defined grade 0 as no lumbar stenosis when there was no obliteration of the CSF space in front of the cauda equina; mild or grade 1 stenosis was present when there was no csf in front of the cauda equina and the cauda equina remained separated; grade 2 or moderate stenosis was present when there was  some cauda equina aggregation or bunching and grade 3 or severe stenosis was present when there was no space between the cauda equina elements and the roots cannot be visually separated. They found that with this classification the interobserver reliability was substantial to excellent for all levels and the intraobserver reliability was excellent. This classification system has been independently validated by Park et al (18) who showed that there was substantial interobserver reliability in the diagnosis of spinal stenosis with this classification. The authors also showed that none of the patients with grade 0 stenosis had neurological symptoms and almost all patients with grade 3 stenosis had neurological symptoms. The relevance of grade 1 and 2 stenosis remained unclear.
Lee et al (19) have also developed a grading system for foraminal stenosis. They divided the stenosis into 4 grades, from 0 to 3 based on sagittal MRI images of the lumbar spine. In this classification grade 0 refers to the absence of foraminal stenosis. In grade 1 stenosis there is mild foraminal stenosis with perineural fat obliteration in the two opposing directions, vertical or transverse. In grade 2  stenosis there is moderate foraminal stenosis with perineural fat obliteration in all four directions without morphologic change and grade 3 refers to a severe foraminal stenosis with nerve root collapse or morphologic change. The authors concluded that this ‘new grading system for foraminal stenosis of the lumbar spine showed nearly perfect interobserver and intraobserver agreement and would be helpful for clinical study and routine practice’.
Wildermuth et al (20) have similarly divided foraminal stenosis into four Grades (1-4) based on the presence of perineural fat as seen on MRI imaging. Grade 1 is the absences of stenosis with normal perineural fat. In grade 2 or slight stenosis, there is compression of perineural fat but the fat is still present all around the nerve root. In grade 3 or marked stenosis there is a loss of perineural fat on at least one side of the nerve and in grade 4 or advanced stenosis, there is a complete loss of perineural fat.
There are no universally accepted criteria for the radiological diagnosis of lateral canal stenosis. Steuer et al (21) did a systematic review of the literature and found that the height and the depth of the lateral recess and the lateral recess angle are the criteria used for describing lateral canal stenosis. The measurements are done on a CT scan or an MRI (axial T2 weighted) images of the lumbar spine. The depth refers to the measurement between the top of the pedicle and the superior articular facet. The height refers to the distance between the most anterior point of the superior articular facet and the posterior border of the vertebral body and the lateral recess angle as the angle between the lines parallel to the floor and the roof of the lateral recess. A lateral recess height ≤ 2 mm and/or lateral recess depth ≤ 3 mm or a lateral recess angle < 30° has been described as diagnostic for lateral recess stenosis.

Treatment of lumbar spinal stenosis

There is no evidence in the literature to show that the outcome of treatment of spinal stenosis is better as compared to the natural history of the disease (no treatment) (1).

Conservative treatment

Anti-inflammatory medications, physical therapy and conditioning is the usual mode of conservative treatment to relieve pain and improve function in patients with spinal stenosis (22). In the elderly population, the non-steroidal anti-inflammatory drugs (NSAIDs) have to be used with caution because of their potential gastrointestinal and cardiovascular adverse effects.
There is no credible evidence that other pharmaceutical agents such as methylcobalamin, gabapentin, prostaglandin E, intranasal calcitonin, and intramuscular calcitonin are of value in the treatment of spinal stenosis (1).
Unfortunately, there is insufficient evidence in literature ‘to make a recommendation for or against the use of pharmacological treatment in the management of spinal stenosis’ (1).
There is level II therapeutic evidence that an exercise program which includes stretching, strengthening and low-intensity cycling exercises, in the short term, improves pain and disability in patients with lumbar spinal stenosis (23).
Physical therapy has shown some improvement in physical function in patients with spinal stenosis although the evidence is not so robust (24,25).

Epidural steroid injections

Epidural steroid injections are widely used for the treatment of patients with spinal stenosis despite the absences of credible evidence regarding its efficacy and safety. Friedly et al (26) carried out a multisite, double-blind, randomised trial in 400 patients with spinal stenosis who had moderate to severe leg pain and disability. One group was given epidural injections of glucocorticoids plus lidocaine and the other group lidocaine alone. The epidural injections were fluoroscopically guided. At six weeks they found no difference between the two groups in the primary outcomes as measured by the Roland-Morris Disability Questionnaire (RMDQ) scores and the rating of the intensity of leg pain. Likewise, there was no difference between the subgroups who received interlaminar or foraminal injections. The authors concluded that ‘in the treatment of lumbar spinal stenosis, epidural injection of glucocorticoids plus lidocaine offered minimal or no short-term benefit as compared with epidural injection of lidocaine alone’.
Complications with epidural injections were not uncommon. The complication rate in the glucocorticoid–lidocaine group was 21.5% and in the lidocaine-alone Group was 15.5%. Complication rates were higher in the transforaminal injection group. Cortisol suppression was significantly higher in the glucocorticoid–lidocaine group.
In this study patients in both treatment groups had improvement in function and decreased pain probably due to a placebo effect, the natural history of spinal stenosis, and other factors present in both study groups. Unfortunately, this excellent study did not have a sham group.
Chou et al (27) in 2015 did a systematic review and meta-analysis of the published data on the use of epidural corticosteroids in the treatment of lumbar radiculopathy and spinal stenosis. They evaluated 30 placebo-controlled trials of epidural corticosteroid injections for radiculopathy, and 8 trials were for spinal stenosis. They found that with epidural corticosteroid injections for radiculopathy there was an immediate reduction in pain and function but the benefits were small and not sustained. There was also no effect on long-term surgical risk. There was some evidence to suggest that there are no benefits of epidural steroids in the treatment of spinal stenosis. They found that ‘serious harms were rare, but harms reporting was suboptimal’.
Nancy E. Epstein (28) in 2013 did a comprehensive review of the literature to assess the risks of epidural and transforaminal steroid injections in the spine. Epidural injections for the management of spinal conditions, though not approved by the FDA, is increasingly being used in the management of patients with spinal disorders. They are typically short-acting with no long-term benefit and their use can be associated with major risks/complications.
There have been reports of contaminated epidural steroid injections which had resulted in meningitis, stroke, paralysis, and even death. Though many of the complications go unreported, other reported complications include ‘life-threatening infections, spinal fluid leaks (0.4-6%), positional headaches (28%), adhesive arachnoiditis (6-16%), hydrocephalus, air embolism, urinary retention, allergic reactions, intravascular injections (7.9-11.6%), stroke, blindness, neurological deficits/paralysis, hematomas, seizures, and death’ (28).
In 2009 FDA started investigations into adverse events related to epidural injections and they found that between 1997 and 2014 there were 90 serious and sometimes fatal neurological complications associated with the use epidural glucocorticoid injections. The complications included paraplegia, quadriplegia, spinal cord infarction, and stroke. Following this investigations, in 2014, the FDA issued a mandatory requirement that ‘all injectable glucocorticoid product labels carry a warning stating that “serious neurologic events, some resulting in death, have been reported with epidural injection of corticosteroids” and that the “safety and effectiveness of epidural administration of corticosteroids have not been established and corticosteroids are not approved for this use” (29).

Ammendolia et al (30) in 2013 did a Cochrane database systematic review to evaluate the effectiveness of non-operative treatment of patients with spinal stenosis and neurogenic claudication. The review included pharmaceutical and physical therapy interventions, as well as epidural injections and they, found that ‘moderate and high-quality evidence for nonoperative treatment is lacking’. What about surgical treatment for spinal stenosis?

Surgical treatment of spinal stenosis

Spinal decompression

Since the symptoms of spinal stenosis are due to narrowing of the spinal canal, surgical decompression was considered to be the logical treatment for symptomatic spinal stenosis from time immemorial. However, over the years clinical experience showed that many patients did well without surgery.
There have been many reports in literature with variable outcome after surgical treatment for spinal stenosis. The outcome varied from 26% to 100% good results at 4 years (31 ), 77% good results at 8 years (32), and  68% good results at 12 years (33).
Johnsson et al (34) compared the outcome of surgical and conservative treatment of patients with spinal stenosis. They found that 60% of the patients treated surgically improved and 25% deteriorated at 53 months follow up and of those treated conservatively 30% improved and 60% remained unchanged at 31 months follow up.
Amundsen et al (35) did a long-term prospective study in 100 patients to compare the outcome of conservative and surgical treatment of spinal stenosis. In this study, there were 19 patients with severe symptoms who had surgical treatment and 50 patients with moderate symptoms had conservative treatment, and another 31 patients were randomized between the conservative treatment group (18 pts) and surgical treatment group (13 pts). All patients were followed up for 10 years.
In the conservative treatment group, good results were reported in 70% of the patients at 6 months, 64% at 1 year and 57% at 4 years. In the surgical group, good results were reported in 79% at 6 months, 89% at 1 year and 84% at 4 years. In patients who were randomly assigned to the conservative and surgical group, the results were much better in the surgical group as compared to the conservative group.
This study provides Level IV evidence that patients with severe symptoms at presentation, who undergo surgical decompression, the outcome will be good 80-90% of the time and in patients with moderate symptoms who undergo conservative treatment, the results will be good in about 70% of the time (1).
Mariconda et al (36) reported a prospective study, of 44 patients, which compared laminectomy with conservative treatment in patients with mild to moderate leg pain. At 4 years follow up they found that 68% of the surgical group had good results while 33% in the conservative group had good results. There was a 9 percent reoperation rate in the surgical group and 9% crossover rate. This study provides level IV evidence that surgical decompression gives good results in 68% of the patients (1).

Spinal fusion

Spinal fusion is often done after spinal decompression due to a belief that posterior spinal decompression can destabilize the spine. Spinal fusion prolongs the operating time and increases the blood loss and can be associated with more complications. Is spinal fusion necessary after posterior decompression?
 Grob et al (37) did a study to address this issue. They did a randomized, controlled trial of 45 patients with symptomatic lumbar stenosis with no spinal instability. The patients were randomly assigned to one of the three groups. Group 1 patients had laminotomy with medial facetectomy. In group 2 the patients had decompression with fusion of the most stenotic segment and in group 3 the patients had decompression with fusion of all decompressed segments. At an average follow up  28 months all groups showed an increase in walking ability and a decrease in pain and there was no difference in the outcome between the groups. This study provides Level II therapeutic evidence that there is no difference in the clinical outcome in patients, with spinal stenosis and no spinal instability, who had posterior decompression alone and in those who had decompression with fusion (1).
Patients with spinal instability as defined by Posner’s method generally do not do well if a laminectomy is done without fusion. Yone and Sakou (38) studied 60 patients who had surgery for spinal stenosis. Thirty-three of the 60 patients had spinal instability as defined by the Posner’s criteria. Of the 33 patients with instability 19 had laminectomy with fusion and the other 14 refused fusion and had laminectomy alone. Twenty-seven other patients without instability had laminectomy alone. Eighty percent of the patients without instability and 80% of those with instability and fusion had good outcome whereas only 43% of patients with instability and no fusion had a good outcome.This study provides Level II  evidence that in patients with spinal stenosis and spinal instability, decompression with fusion is more effective than decompression alone (1). There are other authors who believe that all patients with spinal stenosis can be treated by decompression alone without fusion.
Iguchi et al (39) studied the long-term outcome of posterior spinal decompression without fusion in patients with spinal stenosis. They did laminectomy with partial facetectomy without fusion in 122 patients with spinal stenosis. At a minimum of 10 years (average 13 years) follow up, 37 patients were available for evaluation. In 62.2% of the patients, there was no impairment in activities of daily living. The outcome was excellent in 13 (35.1%), good in 8 (21.6%), fair in 8 (21.6%) , and poor in 8 patients (21.6%). Three of the 8 patients (8.1%) required additional surgery. The outcome was the same in patients with preoperative spondylolisthesis and those without spondylolisthesis. Similarly, the outcome was the same in patients with preoperative scoliosis and those without scoliosis. At least 2 levels of laminectomy was performed in each patient. Preoperative sagittal rotation of more than 10° with multilevel laminectomy was thought to be a risk factor for poor outcome. The authors concluded that acceptable results can be obtained with a laminectomy without spinal fusion in patients with spinal stenosis on long-term follow-up.
Satisfactory long-term outcome (8 years to 13 years) of surgical treatment for spinal stenosis ranges from 55% (40), 56.7% (39) and  71% (35).

The risk factors for unsatisfactory outcome following surgery for spinal stenosis are numerous. Katz et al (41) found that poor long-term outcome, defined as severe pain or the need for a repeat operation, or both, included comorbidities such as osteoarthrosis, cardiac disease, rheumatoid arthritis, or chronic pulmonary disease, longer duration of follow-up, and laminectomy at a single level. However Iguchi et al (39) found that patients who had multilevel laminectomies and a 10° or more of sagittal rotation had a poorer outcome. Patients undergoing repeat spinal surgery has a poorer prognosis (42). Lower income, presences of anxiety and depression, the existence of compensation claims, absences of preoperative neurological deficit, less severe canal stenosis and absences of preoperative subjective difficulty in walking, are all associated with poorer outcome after surgery (43).
Despite the existence of a large number of publications in the scientific literature regarding the treatment of spinal stenosis, there appears to no consensus as to what is the best form of treatment for spinal stenosis. Zaina et al (44), in 2016, did a systematic review of the literature for the Cochrane group to compare conservative and surgical treatment for spinal stenosis. They were unable to conclude whether surgical treatment or a conservative approach is better for lumbar spinal stenosis. They, however, noted that there was a complication rate of between 10% to 24% in patients treated with surgery and there were no side effects of conservative treatment. There were no clear benefits of surgery when a comparison was made with conservative treatment. Their conclusion was that ‘clinicians should be very careful in informing patients about possible treatment options, especially given that conservative treatment options have resulted in no reported side effects’.
There is also no good evidence in the literature on the efficacy of surgery for spinal stenosis. Machado et al (45) in 2016 did a systematic review of literature for the Cochrane group to evaluate the outcome of surgical treatment for spinal stenosis. They found that there was very little literature on the efficacy of surgical treatment of spinal stenosis. There were no trials comparing ‘surgery with no treatment, placebo or sham surgery’ though ‘placebo-controlled trials in surgery are feasible and needed in the field of lumbar spinal stenosis’. They also found that decompression with fusion and interspinous process spacers were not superior to decompression alone.

Conclusions

Clinical or symptomatic spinal stenosis has been well defined with little ambiguity. Radiological narrowing of the spinal canal due to degenerative disease of the spine has been well studied and classified. However, the natural history of symptomatic spinal stenosis is not known because there no studies comparing treatment and no treatment. However, from the little evidence available it appears that the outcome is favourable in one third to half of the patients with mild to moderate spinal stenosis even without treatment.The natural history of patients with severe stenosis is unknown. Rapid neurological decline does not happen in patients with spinal stenosis.
The use of anti-inflammatory medications, physical therapy and conditioning remains the mainstay of conservative treatment of symptomatic spinal stenosis. There is no robust evidence to support the use of other pharmaceutical agents in the treatment of spinal stenosis.
 Epidural steroid injections are widely used for the treatment of patients with spinal stenosis despite the absences of credible evidence regarding its efficacy and safety. Complications are not uncommon with an epidural injection. Complication rates as high as 21.5% have been reported in the literature. Life-threatening infections, paralysis and even death have been reported.
Despite the presences of a large number of publications in the scientific literature regarding treatment of spinal stenosis, there appears to be no consensus as to what is the best form of treatment for spinal stenosis. There is no evidence in literature as to whether surgical or conservative treatment is better for treatment of spinal stenosis. Surgical treatment can be associated with up to 24% complication rate. Conservative treatment is not known to be associated with side effects. There is no good evidence on the efficacy of surgical treatment for spinal stenosis. Studies show that the outcome of spinal decompression alone is the same as that with decompression with fusion. Interspinous process spacers do not provide any additional benefits to patients in the treatment of spinal stenosis.
Till good evidence is available the treatment of patients has to be individualized and the least invasive treatment which will provide maximum relief with minimal or no side effects should be offered to the patient.

References

1. Kreiner DS, Shaffer WO, Baisden JL, et al; North American Spine Society: An evidence-based clinical guideline for the diagnosis and treatment of degenerative lumbar spinal stenosis (update). Spine J 2013;13(7):734-743.
2. Konno S, Kikuchi S, Tanaka Y, et al. A diagnostic support tool for lumbar spinal stenosis: a self-administered, self-reported history questionnaire. BMC Musculoskelet Disord. 2007 Oct 30; 8:102.
3. Konno S, Hayashino Y, Fukuhara S. Development of a clinical diagnosis support tool to identify patients with lumbar spinal stenosis. Eur Spine J. 2007;16(11):1951-7.
4. Katz JN, Dalgas M, Stucki G, et al. Degenerative lumbar spinal stenosis. Diagnostic value of the history and physical examination. Arthritis Rheum. 1995; 38(9): 1236-41.
5. Brinjiki W, Luetmer P, Comstock B, et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR American Journal of Neuroradiology. 2015;36(4):811-816.
6. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am. 1990;72:403–408.
7. Wiesel SW, Tsourmas N, Feffer HL, Citrin CM, Patronas N. A study of computer-assisted tomography. I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine. 1984;9:549–551.
8. Coulier B, Devyver B, Ghosez JP. Severe underestimation of lumbar spinal stenosis by supine imaging. Clin Radiol. 2003;58:167–169.
9. Stafira JS, Sonnad JR, Yuh WT, Huard DR, Acker RE, Nguyen DL, Maley JE, Ramji FG, Li WB, Loftus CM. Qualitative assessment of cervical spinal stenosis: observer variability on CT and MR images. AJNR Am J Neuroradiol. 2003;24:766–769.
10. Kent DL, Haynor DR, Larson EB, Deyo RA. Diagnosis of lumbar spinal stenosis in adults: a meta-analysis of the accuracy of CT, MR,and myelography. AJR Am J Roentgenol. 1992;158(5):1135-44.
11. Bischoff RJ, Rodriguez RP, Gupta K, et al. A comparison of computed tomography-myelography, magnetic resonance imaging,and myelography in the diagnosis of herniated nucleus pulposus and spinal stenosis. J Spinal Disord. 1993;6(4):289-95.
12.  Jia LS, Shi ZR. MRI and myelography in the diagnosis of lumbar canal stenosis and disc herniation. A comparative study. Chin Med J (Engl). 1991;104(4):303-6.
13. Modic MT, Masaryk T, Boumphrey F, Goormastic M, Bell G. Lumbar herniated disk disease and canal stenosis: prospective evaluation by surface coil MR, CT, and myelography. AJR Am J Roentgenol. 1986;147(4):757-65.
14. Barz T, Melloh M, Staub LP, et al. Nerve root sedimentation sign: Evaluation of a new radiological sign in lumbar spinal stenosis. Spine. 2010;5(8):892-897.
15. Schnebel B, Kingston S, Watkins R, Dillin W. Comparison of MRI to contrast CT in the diagnosis of spinal stenosis. Spine. 1989;14(3):332-7.
16. Schroeder GD, Kurd MF, Vaccaro AR. Lumbar Spinal Stenosis: How Is It Classified? J Am Acad Orthop Surg. 2016 Dec;24(12):843-852.
17. Lee GY, Lee JW, Choi HS, Oh KJ, Kang HS. A new grading system of lumbar central canal stenosis on MRI: an easy and reliable method. Skeletal Radiol. 2011 Aug;40(8):1033-9.
18. Park HJ, Kim SS, Lee YJ, et al: Clinical correlation of a new practical MRI method for assessing central lumbar spinal stenosis. Br J Radiol 2013;86 (1025):20120180.
19. Lee S, Lee JW, Yeom JS, et al: A practical MRI grading system for lumbar foraminal stenosis. AJR Am J Roentgenol 2010;194 (4):1095-1098.
20. Wildermuth S, Zanetti M, Duewell S, et al: Lumbar spine: Quantitative and qualitative assessment of positional (upright flexion and extension) MR imaging and myelography. Radiology 1998;207(2): 391-398.
21. Steurer J, Roner S, Gnannt R, Hodler J; LumbSten Research Collaboration: Quantitative radiologic criteria for the diagnosis of lumbar spinal stenosis: A systematic literature review. BMC Musculoskelet Disord 2011;12:175.
22. Covaro A, Vilà-Canet G, de Frutos AG, Ubierna MT, Ciccolo F, Caceres E. Management of degenerative lumbar spinal stenosis: an evidence-based review. EFORT Open Rev. 2017 Mar 13;1(7):267-274.
23. Goren A, Yildiz N, Topuz O, et al. Efficacy of exercise and ultrasound in patients with lumbar spinal stenosis: a prospective randomized controlled trial. Clin Rehabil. 2010;24(7):623-31.
24. Delitto A, Piva SR, Moore CG, et al. Surgery versus nonsurgical treatment of lumbar spinal stenosis: a randomized trial. Ann Intern Med 2015;162:465-73. 
25.  Fritz JM, Lurie JD, Zhao W, et al. Associations between physical therapy and long-term outcomes for individuals with lumbar spinal stenosis in the SPORT study. Spine J 2014;14:1611-21.
26. Friedly JL1, Comstock BA, Turner JA, Heagerty PJ, Deyo RA, Sullivan SD, Bauer Z, Bresnahan BW, Avins AL, Nedeljkovic SS, Nerenz DR, Standaert C, Kessler L, Akuthota V, Annaswamy T, Chen A, Diehn F, Firtch W, Gerges FJ, Gilligan C, Goldberg H, Kennedy DJ, Mandel S, Tyburski M, Sanders W, Sibell D, Smuck M, Wasan A, Won L, Jarvik JG. A randomized trial of epidural glucocorticoid injections for spinal stenosis. N Engl J Med. 2014 Jul 3;371(1):11-21. doi: 10.1056/NEJMoa1313265.
27. Chou R, Hashimoto R, Friedly J, Fu R, Bougatsos C, Dana T, Sullivan SD, Jarvik J. Epidural Corticosteroid Injections for Radiculopathy and Spinal Stenosis: A Systematic Review and Meta-analysis. Ann Intern Med. 2015 Sep 1;163(5):373-81. doi: 10.7326/M15-0934.
28. Nancy E. Epstein. The risks of epidural and transforaminal steroid injections in the Spine: Commentary and a comprehensive review of the literature. Surg Neurol Int. 2013; 4(Suppl 2): S74–S93.
29. Judith A. Racoosin, Sally M. Seymour, Laurelle Cascio, and Rajdeep Gill. Serious Neurologic Events after Epidural Glucocorticoid Injection — The FDA's Risk Assessment. N Engl J Med 2015; 373:2299-2301.
30. Ammendolia C, Stuber KJ, Rok E, Rampersaud R, Kennedy CA, Pennick V, Steenstra IA, de Bruin LK, Furlan AD. Nonoperative treatment for lumbar spinal stenosis with neurogenic claudication. Cochrane Database Syst Rev. 2013 Aug 30;(8):CD 010712. doi: 10.1002/14651858.CD 010712.
31. Turner JA, Ersek M, Herron L, Deyo R. Surgery for lumbar spinal stenosis:Attempted meta-analysis of the literature. Spine 1992;17:1–8.
32.  Postacchini F, Cinotti G, Gumina S, Perugia D. Long-term results of surgery in lumbar stenosis: 8-Year review of 64 patients. Acta Orthop Scand 1993; 64(Suppl 251):78–80.
33.  Herno A, Airaksinen O, Saari T. The long-term prognosis after operation for lumbar spinal stenosis. Scand J Rehabil Med 1993;25:167–71.
34.  Johnsson KE, Uden A, Rosen I. The effect of decompression on the natural course of spinal stenosis: A comparison of surgically treated and untreated patients. Spine 1991;16:615–19.
35. 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. 2000;25(11):1424-1435; discussion 1435-1426. Mariconda M, et al. Unilateral laminectomy for bilateral decompression of lumbar spinal stenosis: a prospective comparative
36. study with conservatively treated patients. J Spinal Disord Tech. 2002;15(1):39-46.
37. Grob D, Humke T, Dvorak J. Degenerative lumbar spinal stenosis. Decompression with and without arthrodesis. J Bone Joint Surg Am. 1995 Jul;77(7):1036-41.
38. Yone K, Sakou T. Usefulness of Posner’s definition of spinal instability for selection of surgical treatment for lumbar spinal stenosis. J Spinal Disord. 1999;12(1):40-4.
39. Tetsuhiro Iguchi, Akira Kurihara, Junichi Nakayama, Keizou Sato, Masahiro Kurosaka, and Kyoko Yamasaki. Minimum 10-Year Outcome of Decompressive Laminectomy for Degenerative Lumbar Spinal Stenosis. SPINE Volume 25, Number 14, pp 1754–1759. 
40. Atlas, S.J.,  Keller, R.B.,  Wu, Y.A.,  Deyo, R.A.,  Singer, D.E. Long-term outcomes of surgical and nonsurgical management of lumbar spinal stenosis: 8 to 10 year results from the Maine lumbar spine study. Spine Volume 30, Issue 8, 15 April 2005, Pages 936-943.
41. J N Katz; S J Lipson; M G Larson; J M McInnes; A H Fossel; M H Liang. The outcome of decompressive laminectomy for degenerative lumbar stenosis. J Bone Joint Surg Am. 1991 July; 73(6):809–816.
42. Herno,A.,Airaksinen, O., Saari, T., Sihvonen, T., 1995. Surgical results of lumbar spinal stenosis. A comparison of patients with or without previous back surgery. Spine (Phila Pa 1976) 20, 964–969.
43. E. Foulongne, S. Derrey , M. Ould Slimane, S. Levêque, A.-C. Tobenas , F. Dujardin, P. Fréger ,P. Chassagne, F. Proust. Lumbar spinal stenosis: Which predictive factors of favorable functional results after decompressive laminectomy? Neurochirurgie 59 (2013) 23–29.
44. Zaina F, Tomkins-Lane C, Carragee E, Negrini S. Surgical versus non-surgical treatment for lumbar spinal stenosis. Cochrane Database Syst Rev. 2016 Jan 29;(1):CD010264.
45. Machado GC, Ferreira PH, Yoo RI, Harris IA, Pinheiro MB, Koes BW, van Tulder MW, Rzewuska M, Maher CG, Ferreira ML. Surgical options for lumbar spinal stenosis. Cochrane Database Syst Rev. 2016 Nov 1;11:CD012421.