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Lumbar spinal stenosis (LSS) is a clinical syndrome resulting from narrowing of the spinal canal centrally, in the lateral recess, subarticular zone or neural foramen. The clinical syndrome is characterized by low back pain with neurogenic claudication, a forward inclined posture, progressive pain, weakness and paresthesia when ambulating, relieved by sitting or leaning forward and/or fatigue.


The most common etiology is spinal degeneration, ligamentum flavum hypertrophy, and spondylosis plus/minus chronic disc herniation. Other causes include sequelae of prior surgical intervention, local trauma, space occupying lesions (such as simple cysts, lipomas, epidural lipomatosis, tumors), Paget’s disease, ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, rheumatoid arthritis, congenital malformation such as spina bifida, achondroplasia, myelomengiocoele, spondylolisthesis, or congenitally short pedicles.

Epidemiology including risk factors and primary prevention

The prevalence of LSS is difficult to establish. Up to 47% of men aged >/= 65 meet the anatomical criteria for stenosis, with as high as 30% having symptoms of LSS.1 Data for the US in 2030 projects 24 million people will have symptoms suggestive of cervical or lumbar stenosis.2 LSS remains the leading preoperative diagnosis for adults older than 65 years who undergo spinal surgery.2


LSS most often occurs as the end stage of spondylosis. This can be simplified into 3 key phases.3 In phase I (Dysfunction Phase), repetitive microtrauma leads to the development of circumferential tears of the annulus fibrosis that coalesce to form radial tears. The disc nutrition supply is compromised and there is loss of ability of the disc to retain water, leading to loss of disc height, disc desiccation, and disc bulging. In phase II (Instability Phase), there is further loss of disc height, increasing the mechanical stress on the zygapophysial joints and resulting in zygapophysial joint degeneration, subluxation, and instability. In phase III (Stabilization Phase), continued disc space narrowing and fibrosis occurs with osteophyte formation. This cascade of lumbar degenerative changes, including osteophyte complexes on the vertebral bodies, degeneration of the facet joints, and hypertrophic ligamentum flavum, contributes to the narrowing of the spinal canal centrally, in the lateral recess, or in combination.

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

In one longitudinal observational study following 32 patients with LSS over a mean period of 49 months, 70% of the cases were unchanged, 15% showed improvement, and 15% worsened.4 For any individual patient, the course can be unpredictable with flare-ups and stable periods over time.

Specific secondary or associated conditions and complications

LSS may be complicated by the compression of the cauda equina or conus medularis. The Cauda Equina Syndrome is associated with symptoms of significant bilateral lower limb weakness, bowel, bladder, erectile dysfunction, and saddle anesthesia. This is considered a surgical emergency because immediate decompression may decrease the chances of long-term neurological dysfunction. The Conus Medularis Syndrome occurs when there is compression between T12 and L1 at the conus medullaris, producing a mixed picture of myelopathy and radiculopathy. It may present similarly to Cauda Equina Syndrome, but patients may have intact lower limb reflexes.



The most common presentation of LSS is low back pain, followed by intermittent neurogenic claudication, variably felt in the buttocks, posterior thigh, calf, and groin.5 Additionally, patients may have paresthesias, weakness, cramping, or fatigue affecting the lower limbs. Symptoms of a central stenosis are usually bilateral and worsen with lumbar extension and walking, especially downhill for progressively shorter distances. There may be improved pain while sitting or with lumbar flexion as when one leans on a shopping cart.6 Subarticular, lateral recess and foraminal stenosis present typically with a unilateral radiculopathy based on the affected level.

Physical examination

A complete lumbar spine examination should be performed, including: inspection, palpation, range of motion (ROM), muscle strength, sensation, reflexes, Romberg maneuver, and special tests (straight leg raise, crossed straight leg raise, slump test, femoral nerve stretch test, Kemp’s test). Neurological examination and straight leg raise test may be normal, or may demonstrate focal weakness, sensory loss, diminished muscle stretch reflexes or radiating leg pain. The patient may demonstrate a slow, wide-based gait or unsteadiness during the Romberg maneuver.7Peripheral pulses, skin and hair exam should be performed to assess for signs of vascular insufficiency. Lumbar extension may worsen pain.

Functional assessment

Diminished walking distance is a significant functional limitation in patients with lumbar stenosis and may be used as a functional outcome measure.8 In addition, functional assessment may be accomplished using functional tools (VAS score, Oswestry Disability Index, FIM score, Brief Pain Inventory, Medical Outcomes Survey 36-Item Short-Form Health Survey (SF-36), McGill Pain Questionnaire).

Laboratory studies

In patients age 50-69, LSS symptoms are closely associated with elevated hemoglobin A1c and hypertension.9


Plain x-rays may demonstrate evidence of spondylolisthesis, scoliosis, disc space narrowing, marginal osteophytes, facet arthropathy, vacuum sign, verterbal endplate changes or foraminal narrowing in LSS. The most commonly used magnetic resonance imaging (MRI) criteria define relative LSS as a central canal diameter between 10 and 12 mm, and absolute LSS is less than 10 mm.5 However, studies in asymptomatic populations have found that up to 20% of subjects had imaging findings consistent with LSS.5 Computed tomography (CT) preferentially images bone compared to MRI has similar diagnostic accuracy for LSS and diagnostic yield is improved when combined with myelography.

Supplemental assessment tools

Electrodiagnostic studies are not required but are recommended. Although the findings in LSS are often not diagnostic, central stenosis may present as a multilevel bilateral radiculopathy. Subarticular, lateral recess and foraminal stenosis may present with a unilateral radiculopathy, typical findings of abnormal spontaneous activity, and long duration, polyphasic motor unit action potentials in chronic compressions.

Early predictions of outcomes

A prospective, 17 medical center, longitudinal observation of 274 patients in Japan showed that 30% of patients did well with conservative management.10 These patients had only radicular symptoms for <1 year, and no listhetic segments or scoliosis. Predictors of a poor outcome from lumbar stenosis surgery include depression, cardiovascular comorbidity, ambulatory impairment, and scoliosis. Better walking ability, self-rated health, higher income, less overall comorbidity, and pronounced central stenosis predicted better subjective outcome.11


Environmental and occupational hazards that aggravate symptoms must be addressed. Adaptive equipment (e.g., lumbar support, cane, etc.) to assist the patients with mobility and activities of daily living should be considered. If a patient wishes to return to or remain at work, consider a referral to occupational therapy for an ergonomic evaluation and adaptive strategies and placing the patient in vocational rehabilitation, work hardening, and conditioning programs.

Social role and social support system

Patients may need assistance for basic activities of daily living and functional mobility, especially if they have had surgery. Adaptive devices such as canes, walkers and wheelchairs may create a social stigma and feelings of reduced independence.


Available or current treatment guidelines

In general, a trial of medical and rehabilitative treatment precedes surgical treatment unless the patient has an indication for emergent/urgent treatment (progressive neurologic deficits, cauda equina syndrome, neoplasm). Evidence-based guidelines from the North American Spine Society, revised in 2011, are accessible online at their website12 -http://www.spine.org/Pages/PracticePolicy/ClinicalCare/ClinicalGuidlines/Default.aspx .

At different disease stages

New onset/acute

  1. Activity modification – Avoid spinal extension in central or foraminal stenosis
  2. Medications – NSAIDs, short-acting opiates, neuropathic pain medications, muscle relaxants


  1. Rehabilitation – Lumbar stabilization program with focus on flexion-biased exercises (Williams exercises), pelvic posture correction, core strengthening, to prevent excessive lumbar extension and emphasize hamstring relaxation. These therapeutic exercises may include, but are not limited to: hip flexor, hamstring, lumbar paraspinal stretching, abdominal and gluteal strengthening exercises such as pelvic tilts, trunk raises, and bridging, conditioning exercises such as inclined treadmill, stationary bicycle, and aquatic exercises. Avoid exercise postures that may put nerve roots under excessive tension.
  2. Orthoses – Lumbar corsets maintain patients in a slightly flexed posture and provide mechanical support for the lumbar spine. Patients should wear them to minimize symptoms during lifting and upright activity; further, continual use should be limited as it may lead to weakness of core muscles.
  3. Epidural steroid injection – Interlaminar, caudal or transforaminal epidural steroid injections under fluoroscopic guidance are suggested to provide short-term symptomatic relief (2 weeks to 6 months) but there is conflicting evidence regarding efficacy.13,14
  4. Surgical consultation – Decompression of spinal canal and neural foramina: 80% of patients have some degree of symptomatic relief after surgery. Seven to 10 years later, at least one-third of patients report recurrent axial pain.2


  1. Alternative treatments – Acupuncture, manual therapy, TENS
  2. Medications – NSAIDs, extended release opiates (controversial), antiepileptics, SNRI’s, tricyclic antidepressants.

Coordination of care

An interdisciplinary team approach involving physiatrists, neurologists, physical therapists, occupational therapists and spine surgeons may be beneficial, even in the outpatient setting. Physiatrists write specific rehabilitation protocols based on their biomechanical assessment and obtain feedback from the therapists. The decision between medical or operative treatment may be enhanced by good communication between all providers and clear establishment of functional goals by the patient.

Patient & family education

Patients should be given a home exercise program to maintain mobility, strength and range of motion. Activity modifications should be discussed. Patients need to be informed regarding the risks, benefits and expected efficacy of various treatment options. Although patients may experience relief from epidural steroid injections, they must understand that these effects might be temporary and rehabilitation is essential. Patients should be advised regarding behavioral, environmental and occupational hazards.

Emerging/unique Interventions

Treatment outcomes may be assessed through VAS score, Oswestry Disability Index, FIM score, Brief Pain Inventory, Medical Outcomes Survey 36-Item Short-Form Health Survey (SF-36), McGill Pain Questionnaire, or other functional measures.

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

Alternative diagnosis for symptoms suggestive of LSS should be considered. Vascular claudication, such as Leriche syndrome, may present similarly to neurogenic claudication and should be ruled out.

The diagnosis of LSS should be based on the clinical presentation with support by radiologic studies, not based on imaging interpretations alone. This is because many individuals with anatomic spinal canal stenosis are asymptomatic.


Cutting edge concepts and practice

There are newer, less invasive percutaneous interventional treatments designed to decompress the spinal canal or increase vertebral body distraction, for example the MILD (minimally invasive lumbar decompression)procedure. Recent studies with the MILD procedure and as part of the MiDAS ENCORE protocol he shown safety, cost efficacy and better pain outcome than epidural steroid.15,16 The therapeutic application of intravenous prostaglandinE1 is reported to relieve symptoms of neurogenic claudication in patients without redundant nerve roots or intraradicular edema.17


Gaps in the evidence-based knowledge

Current data from randomized, controlled trials demonstrate mixed results regarding the efficacy of medical and surgical interventions including physical therapy, bracing, exercise regimens, medications, injections, decompression with or without fusion. A recent survey screened 12,966 citations, yielding a meta-analysis of 26 full-text articles and 5 randomized trials concluding surgical interventions have a higher rate of side effects than conservative treatment18More high quality clinical evidence is needed to assess the efficacy of both surgical and medical treatments. As noted in a commentary of the NASS guidelines, the process identifies major gaps in the overall understanding of degenerative lumbar stenosis.19


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  2. Ammendolia C, Cote P, Ramersaud YR, et al. The Boot Camp Program for Lumbar Spinal Stensosis: a protocol for a randomized controlled trial. Chiropr Man Therap. 2016; 24: 25-40.
  3. Middle K. Fish D., Lumbar Spondylosis: Clinical Presentation and Treatment Approaches. Current Review of Musculoskeletal Medicine. 2009;2(2): 94-104.
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  8. Whitman J, Flynn T, Fritz, J. Nonsurgical management of patients with lumbar spinal stenosis: a literature review and a case series of three patients managed with physical therapy. Phys Med Rehabil Clin N Am. 2003;14(1):77-101, vi-vii.
  9. Uesugi K, Sekiguchi M, Kikuchi S, et al. Relationship between lumbar spinal stenosis and lifestyle-related disorders: a cross-sectional multicenter observational study. Spine(Phila Pa 1976) 2013; Apr 20:38(9)E540-545.
  10. Matsudaira K, Nobuhiro H, Hiroyuki O, et al. Predictive factors for subjective improvement in lumbar spinal stenosis patients with nonsurgical treatment: a 3-year prospective cohort study. PLoS One. 2016;11(2):e0148584.
  11. Aalto TJ, Malmivaara A, et al. Preoperative predictors for postoperative clinical outcome in lumbar spinal stenosis: systematic review. Spine(Phila Pa 1976). 2006;31(18) E648-63.
  12. Diagnosis and Treatment of Degenerative Lumbar Spinal Stenosis. NASS Clinical Practice Guidelines. 2011. http://www.spine.org/Pages/PracticePolicy/ClinicalCare/ClinicalGuidlines/Default.aspx. Accessed May 13, 2012.
  13. Manchikanti L, Knezevic NN, et al. Epidural Injections for Lumbar Radiculopathy and Spinal Stenosis: A Comparative Systematic Review and Meta-Analysis. Pain Physician 2016;19:E365-E410.
  14. Meng H, Qi F, Bingglang W, et al. Epidural injections with or without steroids in managing chronic low back pain secondary to lumbar spinal stenosis: a meta-analysis of 13 randomized controlled trials. Drug Des Devel Ther. 2015; 9:4657-4667.
  15. Wang JJ, Bowden K, et al. Decrease in Health Care Resource Utilization with MILD. Pain Medicine 2013;14:657-61.
  16. Staats PS, Benyamin RM, et al. MiDAS ENCORE: Randomized Controlled Clinical Trial Report of 6-Month Results. Pain Physician 2016;19:25-37.
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  18. Zaina F, Tomkins-Lane C, et al. Surgical vs Nonsurgical Treatment for Lumbar Spinal Stenosis. Cochrane Database Syst Rev 2016;Jan 29;1:CD010264.
  19. Deyo RA. Commentary: Clinical practice guidelines: trust them or trash them? The Spine Journal. 2013; 17(7)744-746.

Original Version of the Topic:

Patricia W. Nance, MD, Hamilton Chen, MD. Lumbar stenosis. Publication Date: 2012/07/20.

Author Disclosure

Patricia W. Nance, MD
Receives consulting fees or other remuneration from the following organizations: Xenoport; Acorda Therapeutics; Allergan. Serves as an independent contractor and receives remuneration from Siemens, Athena, Elan.