Acquired lumbar spinal stenosis : JAAPA

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CME: Orthopedics

Acquired lumbar spinal stenosis

Deasy, JoAnn PA-C, MPH, DFAAPA

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JAAPA 28(4):p 19-23, April 2015. | DOI: 10.1097/01.JAA.0000462052.47882.fd
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Box 1

Lumbar spinal stenosis is a common medical disorder in the aging population, and is characterized by the narrowing of the lumbar spinal canal and the nerve root canals, leading to compression of the neural and vascular structures in the canals. Neurogenic claudication, recognized as aching, cramping, or heaviness in the buttocks, thighs, or lower legs with standing or walking, is the classic clinical feature associated with lumbar spinal stenosis and causes diminished function and impaired quality of life.1,2 An estimated 1.2 million office visits in the United States are related to symptoms of lumbar spinal stenosis, which has become the most frequent cause for spinal surgery in patients over age 65 years.3,4 With the aging of the US population, an increasing number of patients will be diagnosed and treated for lumbar spinal stenosis by primary care providers, pain management specialists, and surgical specialists.


Acquired lumbar stenosis most often occurs from age-associated degenerative or arthritic changes that affect the complex that includes the lumbar vertebrae, facet joints, and adjoining intervertebral disk (Figure 1). The earliest changes occur in the disks, with desiccation and flattening that can lead to disk bulging and collapse.5 This loss of the structural integrity of the disks leads to stress on the facet joints and ligaments that connect the laminae of adjacent vertebrae (ligamentum flavum) resulting in the formation of osteophytes on facet joints and vertebral endplates and thickening of the ligamentum flavum. The central and lateral spinal canals become narrowed due to a combination of disk bulging, osteophyte formation, and ligamentum flavum hypertrophy. This results in less space for neural elements. Compression of the lower spinal cord or nerve roots branching out from that area leads to the characteristic symptoms of lumbar spinal stenosis.6 The spinal canal narrowing causes pain that is increased with lumbar extension (which narrows the canal) and eased with forward flexion (which increases the cross-sectional area of the neural foramina).7

Anatomy of the spine
Box 2

Compression of the neural elements alone does not fully explain the symptoms of neurogenic claudication. An abundant vascular system supplies the nerve roots in the cauda equina, spinal canal, and nerve root tunnels. Mechanical deformity of the cauda equina results in venous congestion and pressure on arteries with resultant ischemia that can impair nerve conduction.8,9


Patients with degenerative lumbar spinal stenosis generally are over age 50 years and have back or leg pain or a combination of both. The onset is usually insidious with the first symptoms often being low back pain and morning stiffness relieved by activity.10 Over time, patients frequently develop buttock, calf, and thigh pain described as a feeling of heaviness, deep aching pain, or cramping. Many patients will have bilateral leg pain. They may have associated numbness and tingling in the lower extremities. The most specific feature of lumbar spinal stenosis is neurogenic intermittent claudication—pain, heaviness, or cramping that occurs in the legs after starting to walk or with prolonged standing. These symptoms progress to the point at which the patient must stop walking or standing and change position. Sitting and leaning forward relieves the pain and lumbar extension aggravates it.11

Patients often have the “shopping cart sign”—their symptoms improve when they flex forward at the waist over a shopping cart. Although neurogenic intermittent claudication is the most characteristic presentation of lumbar spinal stenosis, some patients present with unilateral or bilateral radicular symptoms rather than claudication.6 Weakness is not a common symptom but may develop, most often as a partial foot drop or weakness in plantar flexion after prolonged walking or standing.12

Patients with lumbar spinal stenosis typically have a normal neurologic examination. A minority of patients have objective neurologic findings, including a wide-based gait, focal weakness, and/or sensory loss in the distribution of one or more spinal nerve roots, asymmetric deep tendon reflexes, or a positive Romberg sign (the nerve pathways for proprioception travel through the dorsal columns that can be affected by spinal stenosis).13 Motor findings are generally mild.


Many conditions can cause symptoms similar to those of lumbar spinal stenosis, including pain from soft tissues, joints, and bones.

Osteoarthritis of the knees or hips can cause pain exacerbated by walking and although the pain is usually localized over joints (rather than being diffuse as in lumbar spinal stenosis), it can radiate. Osteoarthritis of the hip, in particular, may mimic lumbar spinal stenosis. Hip arthritis is typically associated with pain in the groin reproduced by internal rotation of the hip. Lumbar spinal stenosis and hip osteoarthritis can present concurrently and can affect one another (hip-spine syndrome).14 Clinicians may need to prioritize management and the order in which to address these two problems.

Herniated lumbar disk with peripheral neuropathy is another consideration and also may coexist with lumbar spinal stenosis. A patient with a herniated lumbar disk is more likely to have a positive straight-leg raise along with a focal weakness or sensory loss following a dermatome or myotome. Pain in disk herniation also is more acute in onset than pain in lumbar spinal stenosis.

Trochanteric bursitis is associated with pain over the lateral greater trochanter that may radiate distally to the knees or ankles or proximally to the buttocks. The pain is worse when the patient first rises from sitting or lying down; the patient typically feels better after a few steps, which may help differentiate this condition from lumbar spinal stenosis.

Peripheral arterial disease (PAD) causes exertional calf pain and may be confused with lumbar spinal stenosis. The vascular claudication of PAD usually does not persist when resting in a standing position, unlike neurogenic intermittent claudications, which persist. Diminished distal pulses in the lower extremities suggest a vascular cause, as do changes in skin color and temperature of the patient's lower extremities. Auscultate for arterial bruits to help confirm the diagnosis.12 The ankle-brachial index (ABI) test can be performed for PAD. Using a handheld Doppler, obtain the occlusive systolic pressure of the ankle (posterior tibial and dorsalis pedis artery) and divide it by the highest systolic pressure measured in the patient's arm. An ABI of less than 0.9 indicates PAD.15

Peripheral neuropathy should be considered, especially in patients with diabetes, but usually has a stocking-glove distribution of pain or paresthesias.

Tumor and infection are rare causes of spinal pain, but should be considered in patients with back pain. Red-flag signs for these conditions include fever and weight loss.


The clinical diagnosis of lumbar spinal stenosis depends primarily on the patient's description of his or her symptoms and the physical examination. New-onset low back pain in patients over age 50 years or with a neurologic deficit consistent with lumbosacral spinal disease are indications for a neuroimaging study.16 MRI, CT, and CT/myelography have comparative effectiveness in detecting lumbar spinal stenosis.17 Based on its noninvasive nature and lack of radiation exposure, MRI is recommended as the most appropriate initial study in patients with suspected lumbar spinal stenosis.18

MRI findings must be interpreted in the context of the patient's clinical history and examination. Asymptomatic central canal stenosis on MRI increases in prevalence with age and occurs in about 25% of asymptomatic patients older than age 60 years.19,20 Plain radiographs are not routinely needed but may be ordered before MRI. Degenerative changes including disk space narrowing, osteophytes, spurs, endplate irregularities, and facet hypertrophy can be seen on radiographs. Lateral flexion and extension radiographs may reveal spinal instability.21


In patients who do not have severe or progressive nerve involvement, the usual initial management is analgesia and physical therapy to maximize the space in the canal by reversing tissue inflammation and edema, strengthening abdominal musculature, and avoiding lumbar extension. Patients whose symptoms persist despite this conservative therapy or who have severe symptoms are considered for surgery.

Nonsurgical management

Acetaminophen may be administered for the pain of lumbar spinal stenosis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed for their analgesic and anti-inflammatory properties, but must be used cautiously in older adults because of the risk of renal insufficiency and gastrointestinal bleeding. Opioids may be best used to control acute exacerbations of pain; providers should be aware of adverse reactions including constipation, sedation, and, in older adults, increased fall risk. None of these drugs have been tested in randomized, controlled trials designed to assess their use in patients with symptomatic spinal stenosis.11

Weight loss is recommended for obese patients. To reduce symptoms including pain, patients are generally advised to avoid activities that place mechanical stress on the lower back, particularly those that place the spine in extension.6 Riding a stationary bicycle increases calorie use and provides aerobic exercise without putting stress on the lumbar spine. At least one randomized clinical study has shown that physical therapy programs that provide leg strengthening and abdominal strengthening exercises improve function.22 The Spine Patient Outcomes Research Trial (SPORT), the largest trial to date comparing surgical and nonsurgical interventions for pain associated with lumbar spinal stenosis, reported in 2013 that physical therapy was associated with reduced likelihood of patients receiving surgery within 1 year. Results for other outcomes were mixed.23 Receiving physical therapy was associated with greater improvement in physical function and a patient self-rating of improvement. However, several outcome measures, including the Oswestry Disability Index (used to quantify disability related to low back pain) and the bodily pain Short Form Health Survey subscale showed no differences between patients who received physical therapy and those who did not. The nature of the analysis and lack of randomization to conservative treatment preclude conclusions about the more favorable outcomes.23

When oral drugs and physical therapy fail to provide relief of symptoms, epidural steroid injections may be used on the assumption that symptoms result from inflammation at the interface between the nerve root and compressing tissues. Data on efficacy of these injections are sparse and mixed. A Cochrane database systemic review of nonoperative treatments for patients with lumbar spinal stenosis and neurogenic intermittent claudication revealed low-quality evidence from a single trial that epidural steroid injections improved pain, function, and quality of life for up to 2 weeks, compared with home exercise or inpatient physical therapy.24 Limited observational data suggest that epidural injections may relieve leg pain for up to 3 months but do not influence functional status and thus are controversial.25


The goal of surgery is to decompress the central spinal canal and neural foramina to eliminate pressure on nerve roots. The SPORT study found that patients with symptomatic lumbar spinal stenosis who were treated surgically showed significantly greater improvement in pain and function through 4 years follow-up compared with patients treated without surgery.26 The standard surgical procedure is an open laminectomy with a single, larger incision to access the spine, as used in the SPORT study. This procedure involves removing the bone, bone spurs, and ligaments that are compressing the nerves at single or multiple levels. Depending on various factors, including spinal instability existing prior to surgery, fusion may be necessary. Complications of laminectomy include nerve root damage, bowel or bladder incontinence, cerebrospinal fluid leak, infection, and complications related to general anesthesia.

Alternatively, a minimally invasive laminectomy can be done using several smaller incisions. The limitation with this procedure is that less of the patient's anatomy will be visualized, and this approach may not be appropriate when the stenosis extends over a large area.

A newer surgical option, which is less invasive than a laminectomy, is to implant a device at one or two vertebral levels to relieve compression in patients without spondylolisthesis (when one of the vertebrae slips out of place onto the vertebra below it). The first approved implant in this class, the X Stop, is indicated for patients with mild-to-moderate neurogenic intermittent claudication.27,28 This device can be implanted under local anesthesia during an outpatient procedure. Other spacer devices are being evaluated. The effectiveness and long-term outcomes of these devices compared with standard laminectomy have not been determined. However, compression device implantation is a less-invasive option for patients who are unable or unwilling to undergo laminectomy, with its surgical risks and longer recovery time.


Although lumbar spinal stenosis is not life-threatening, it can cause chronic and substantial pain and can severely limit patient activity. In advanced cases of lumbar stenosis, patients are barely able to walk short distances without severe pain.

Cauda equina syndrome is a rare complication of lumbar spinal stenosis caused by compression of the thecal sac and nerve roots; this may occur in the absence of significant disk herniation. Patients should be evaluated for saddle-distribution anesthesia, bowel and bladder dysfunction, and diffuse leg weakness.29 Cauda equina syndrome usually requires emergency surgery.

A small number of patients with advanced lumbar spinal stenosis (who do not have cauda equina syndrome) develop symptoms of bladder involvement with incontinence and recurrent urinary infections.30 Bladder involvement may be due to impingement of sacral nerves and indicates advanced disease.


Patients with lumbar spinal stenosis typically have pain in the buttocks or legs on walking or standing; this pain improves or resolves with sitting or lumbar flexion. Lumbar spinal stenosis has a high prevalence in older adults and a strong negative influence on quality of life, preventing many older adults from maintaining an active, independent life. Nonsurgical treatment includes analgesics, NSAIDs, and physical therapy; however, recent prospective randomized studies have demonstrated that surgery is superior to nonsurgical treatment for improving pain and function. Symptoms may recur with either approach. Management involves shared decision making between the patient and medical provider, taking into account the severity of the patient's symptoms, comorbidities, tolerance for anesthesia, and the patient's personal preferences for treatment.


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lumbar spinal stenosis; back pain; leg pain; neurogenic claudication; spinal surgery; chronic pain

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