Author(s): Thiru M. Annaswamy, MD, Zach Oberdoerster, DO
Originally published: July 20, 2012 Last updated: July 3, 2024
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Disease/Disorder

Definition

Lumbar spinal stenosis (LSS) is a clinical syndrome resulting from narrowing of the spinal canal with impingement on neurological and vascular structures, characterized by the classic symptom of neurogenic claudication (aka pseudoclaudication) defined as lower back pain with radiating pain down one or both hips and legs, aggravated by standing and/or walking, and relieved by forward flexion or sitting. Pain is often associated with weakness and paresthesia in the legs. In severe cases lack of symptom relief with rest and/or progressive neurological deficits such as weakness and incontinence may occur.

Etiology

Symptoms arise from a combination of lumbar spinal degenerative changes including spondylosis, facet hypertrophy, chronic disc herniation and ligamentum flavum thickening.  Other causes include sequelae of prior surgical intervention, local trauma, space occupying lesions (i.e., simple cysts, lipomas, epidural lipomatosis, tumors), Paget’s disease, ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, rheumatoid arthritis, congenital malformations (i.e., spina bifida, achondroplasia, myelomeningocele, spondylolisthesis, or congenitally short pedicles).

Epidemiology including risk factors and primary prevention

Although the exact prevalence of LSS is difficult to establish, it is estimated that symptomatic lumbar spinal stenosis affects some 103 million people worldwide.1 In 2014, there were more than 350,000 persons in the US age 45 or older who underwent decompressive laminectomy and 370,000 with lumbar fusion. The vast majority of these procedures were done for LSS.4 As of 2016, LSS remains the leading preoperative diagnosis for adults older than 65 years who undergo spinal surgery.2

Patho-anatomy/physiology

Lumbar spinal stenosis develops from the narrowing of the central lumbar spinal canal, lateral recess and/or the neural foramina resulting in mechanical compression of neurovascular structures. Symptomatically these compressive forces can present as radiculopathies, neurogenic claudication, or mechanical back pain depending on the location of whatever neurovascular structure affected.3,4

Typically, acquired lumbar spinal stenosis develops due to a variety of degenerative changes that happen with aging including disc protrusion, facet joint hypertrophy, ligamentous hypertrophy, and spondylolisthesis. Less common etiologies include congenital stenosis, Paget’s disease, and epidural lipomatosis. Furthermore, studies show that epidural venous varicosities may contribute to the neurologic symptoms seen in LSS via compressive forces transmitted onto the thecal sac and nerve root.33

When considering the pathophysiology of LSS, it is important to distinguish that not all patients with anatomical findings of spinal canal narrowing will develop symptomatic stenosis. The term LSS therefore refers specifically to the clinical syndrome that presents because of the mechanical compressive forces from this narrowing on neurovascular anatomy.3

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

Although there is limited literature available on disease progression, the disease process is slow, with mild to moderate degenerative lumbar spinal stenosis having 33-50% favorable natural history defined as rare rapid neurologic decline.31

Specific secondary or associated conditions and complications

LSS may be uncommonly complicated by the compression of the cauda equina or conus medullaris. Cauda Equina Syndrome is associated with symptoms of significant bilateral lower limb weakness, numbness, bowel, bladder, erectile dysfunction, and saddle anesthesia. This condition can be seen in the setting of a massive disc herniation at L5-S1 causing severe, bilateral nerve root compression. This is considered a surgical emergency because without immediate surgical decompression the chances of long-term neurological dysfunction remain high.  Conus Medullaris Syndrome occurs when there is severe compression between T12 and L1 spinal segments at the conus medullaris, producing a mixed picture of myelopathy and radiculopathy. It may present similarly to Cauda Equina Syndrome, but patients can have intact lower limb reflexes.

Essentials of Assessment

History

Often patients with lumbar spinal stenosis will present to their healthcare provider when symptoms have progressed to the point that it affects their daily activity.

Most commonly, patients will present with discomfort in their lower lumbar spine, with possible involvement in the buttocks, groin, thigh and in some cases extension to the legs and feet (neurogenic claudication). Accompanying symptoms may include either unilateral or bilateral lower extremity numbness, paresthesia, or weakness, which may be indicative of a radiculopathy stemming from nerve root compression at the lumbar level. Later in the clinical course, patients often report loss of balance with stance and ambulating.

It is typical for patients to report exacerbation of discomfort when walking or standing (lumbar extension) and relief when sitting/bending forward (lumbar flexion). Often patients will default to a forward flexion stance or walking posture commonly known as the “shopping cart sign.” Relief with a forward flexion is attributed to a widening of the central canal in this position, resulting in a decrease of mechanical compression on the nerve roots.4

A thorough history taking in a patient with suspected syndrome of LSS is essential in correlating symptoms with the overall clinical picture to narrow your differential diagnosis and steer further decision making. A fact further illustrated through the conclusion of a 2010 systematic review evaluating four studies that examined 741 patients which showed that the most useful symptoms for increasing the likelihood of the clinical syndrome of LSS included no pain when seated, improvement of symptoms when bending forward, the presence of bilateral buttock or leg pain, and neurogenic claudication.5

Physical examination

A complete lumbar spine examination should be performed including inspection, palpation, range of motion (ROM), muscle strength, sensation, reflexes, Romberg’s maneuver and special tests looking for nerve root irritation (i.e., straight leg raise, crossed straight leg raise, slump test, femoral nerve stretch test). Generally, palpation of the spine itself does not produce tenderness. With ROM in mind, lumbar extension may produce or exacerbate pain in the lumbosacral area, buttock and thighs. Lumbar flexion will generally result in pain relief. Any signs of focal weakness, sensory loss, diminished muscle stretch reflexes or radiating leg pain should be documented.

The patient may demonstrate a slow, wide-based gait and/or unsteadiness during Romberg’s maneuver, findings of which are associated with a specificity of more than 90%, but a sensitivity of approximately 40% for lumbar spinal stenosis.6

Peripheral pulses, skin and hair exam should be performed to assess for signs of vascular insufficiency.

Functional assessment

The Shuttle Walking Test (SWT) and Swiss Spinal Stenosis Questionnaire (SSS) are reliable assessment tools in LSS with the SSS being the most precise and condition specific.7 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 aged 50-69, LSS symptoms are strongly associated with elevated hemoglobin A1c levels and hypertension.8

Imaging

Imaging serves to confirm structural diagnosis with the additional utility of providing an anatomical map if injections or surgery will be considered with management.

Plain lumbar spine x-rays may demonstrate evidence of scoliosis, disc space height loss, marginal osteophytes, facet arthropathy or foraminal narrowing.  Lumbar flexion and extension x-rays may demonstrate segmental instability (i.e., mobile spondylolisthesis).  Cross-sectional imaging is indicated if there are concerns for neurologic involvement or when injections or surgery will be pursued in with management. Additionally cross-sectional imaging should be urgently done for concerns of cauda equina syndrome including urinary retention, fecal incontinence, rapidly progressing lower extremity weakness, or saddle anesthesia.

MRI is the favored means of cross-sectional imaging as it provides a high diagnostic accuracy owing to its delineation of soft tissues including muscle, disc, nerve roots and ligaments. For patients with contraindications to MRI, CT imaging can be pursued. As it stands there is no standardized criteria for defining relative LSS, and as such there exists a high degree of variability in current practice.9

Diagnosis of LSS should not be made on radiographic findings alone as studies showed approximately 80% of people aged 60 and older have imaging evidence of lumbar spinal stenosis, with 80% of whom are asymptomatic.10-12

Supplemental assessment tools

Electrodiagnostic studies are not required but are often used in conjunction with radiographic imaging in patients with LSS.31 The North American Spine Society (NASS) review concluded that electrodiagnostic paraspinal mapping is helpful when determining clinically relevant spinal levels, in addition to imaging findings in LSS.31  However, EMG is more useful in identifying other disease entities which may be contributing to symptoms such as diabetic polyneuropathy and is often negative in LSS, but single or polyradiculopathies can be seen.31

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.19 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. Electrophysiological abnormalities such as polyradiculopathy were predictive of worse outcomes.13 Better walking ability, self-rated health, higher income, less overall comorbidity, and pronounced central stenosis predicted better subjective outcome.20

Environmental

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.

Rehabilitation Management and Treatments

Available or current treatment guidelines

In general, a trial of medical and rehabilitative treatment precedes surgical treatment unless the patient indicates emergent/urgent treatment (progressive neurologic deficits, cauda equina syndrome or neoplasm). Evidence-based guidelines from the North American Spine Society, 2011, are accessible online at their website.31 Additionally, the SPORT trial provides guidance regarding non-operative versus operative intervention.32

As in any case, best practice dictates that a providing physician should strive to educate a patient regarding their diagnosis and establish a clear understanding of goals when approaching options for management.

At different disease stages

New onset/acute

  • Activity modification – Avoid spinal extension in central or foraminal stenosis. Suggestion of exercises that are typically performed with lumbar flexion position such as cycling or swimming side stroke.4
  • Medications 
    • NSAIDs, short-acting opiates (cautiously limited and restricted to short duration), muscle relaxants. Although studies have assessed the effectiveness of these and other medications on low back pain, there is little research on their effectiveness specific to LSS.4
    • Gabapentin may be effective in treating pain due to LSS. In a 2007 prospective randomized control trial, patients assigned to the Gabapentin treatment group produced significantly lower VAS scores (2.1 points on a 0-10 VAS) when compared to the control.34

Subacute and Chronic

  • Rehabilitation – Physical therapy can be effective in patients with LSS. In a 2018 clinical trial, 86 patients with LSS were assigned to either physical therapy or home exercises. At the 6-week mark, 63% of those patients assigned to supervised PT reported improvement in the Zurich Claudication Questionnaire symptom severity scale compared to those assigned home exercise.35 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. Multiple randomized controlled clinical trials have demonstrated how supervised and structured therapies incorporating the physical therapy modalities as illustrated above have resulted in improvement in pain and functional status in those patients with LSS.4
  • 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 long-term efficacy.14,15,16,31
  • Surgical consultation – Surgical consideration may be pursued for patients with intractable pain that is resistant to non-operative management, marked or progressing neurological deficits, or significant changes in lifestyle. The most common decompressive procedure is laminectomy.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 A sub-analysis of the SPORT trial, a randomized controlled trial of patients with lumbar spinal stenosis with neurogenic claudication or leg symptoms without lumbar instability who had previous conservation treatment (i.e., medications, physical therapy and epidural steroid injections) underwent surgical decompression with favorable outcomes at 4 and 8 years follow-up.32 Consideration for pursuing lumbar arthrodesis alongside decompression may be made in patients with increased instability with a concomitant spondylolisthesis or developing scoliosis.

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 honest communication between all providers and clear establishment of functional goals by the patient.

Patient and 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.

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

The diagnosis of LSS should be based on 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. Electrodiagnostic studies can be used to identify confounding pathologies.  Mild to moderate symptoms rarely progress to rapid neurologic decline and can be treated with medical/interventional therapies.  Moderate to severe symptoms may benefit from surgical decompression for long term improved outcomes. 

Cutting Edge/Emerging and Unique Concepts and Practice

There are newer, less invasive percutaneous interventional treatments designed to decompress the spinal canal or increase vertebral body distraction, such as with the MILD (minimally invasive lumbar decompression) procedure. Recent studies with the MILD procedure and, as part of the MiDAS ENCORE protocol, have shown safety, cost efficacy and better pain outcomes than with epidural steroids.24,25

Epidural venous congestion may be an essential factor precipitating circulatory disturbance in compressed nerve roots and inducing or contributing to neurogenic claudication symptoms. In such instances, venodilators have been used with variable success.26,27

Interspinous process spacing at 1 or 2 levels offers a minimally invasive intervention thought to increase central spinal canal size during weight bearing from indirect decompression.  This differs from the traditional surgical decompression via laminectomy. Zucherman et al performed a randomized trial and found favorable outcomes at 2 years with interspinous process spacing devices compared to medical/interventional treatment alone for mild to moderate LSS.31 A review and meta-analysis published in 2021 supported this finding of associated improvement in symptoms for patients with mild to moderate stenosis. However, reoperation rates proved to be higher than open decompression when followed up from the 2-year procedure mark.28

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 2018 survey screened 12,966 citations, yielding a meta-analysis of 26 full-text articles and 5 randomized trials concluding surgical interventions had 10-24% rate of complications versus conservative treatments not having any reported complications.29 More high-quality clinical evidence is needed to assess the efficacy of both surgical and medical/interventional treatments. As noted in a commentary of the NASS guidelines, the process identifies major gaps in the overall understanding of degenerative lumbar stenosis.30

References

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Original Version of the Topic

Patricia W. Nance, MD, Hamilton Chen, MD. Lumbar stenosis. Published 7/20/2012.

Previous Revision(s) of the Topic

Patricia W. Nance, MD. Lumbar stenosis. Published 8/25/2016.

Monika Patel, MD. Lumbar Stenosis. 12/15/2020

Author Disclosure

Thiru M. Annaswamy, MD
Nothing to Disclose

Zach Oberdoerster, DO
Nothing to Disclose