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Lumbar Spinal Stenosis: A Review of the Treatment Options and Modalities

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Lumbar stenosis is clearly a growing problem with the aging population. There are perhaps more treatment options for this diagnosis than any other spine pathology. Goldstein et al present a concise overview of the treatment options available today. In evaluating lumbar stenosis, it is important to realize discrepancies in the terminology and understanding of the disease process.

One common component of lumbar spinal stenosis is thickening of the ligamentum flavum. However, the etiology and pathophysiology of this finding is somewhat unclear. There has been tremendous debate as to whether the ligamentum flavum actually hypertrophies or simply buckles and becomes redundant. One large study based on measurements of disc herniation and aging found that buckling was the primary factor in thickened ligamentum flavum.1 An earlier National Institutes of Health (NIH)–sponsored study had similar findings.2 Other studies support the hypothesis that a facet degeneration alone without disc space narrowing can lead to physiologic ligament thickening.3 Furthermore, thickening occurs as a result of inflammation and fibrocartilaginous transformation can cause hypertrophy of the ligament.4 Consequently, the pathophysiology of ligament thickening is poorly understood.

Regarding the minimally invasive lumbar decompression (MILD) procedure, personally, I cannot attest to its efficacy. However, I have many trusted colleagues who perform the procedure with good results. The procedure is not without detractors, however. A recent study by a principal investigator and consultant raised serious doubts as to the long-term efficacy of the procedure.5 Wilkinson and Fourney questioned the long-term viability of results as early as 6 months post-procedure. My concerns regarding the procedure, for one, are that patients being selected for the procedure have likely not seen a surgeon. Secondly, I have yet to see a patient who medically is not a candidate for general anesthesia. Most anesthesiologists would argue it is better to intubate a patient with a controlled airway for a 30-minute procedure than to consciously sedate a patient for a similar-length percutaneous procedure like the MILD procedure without an attending anesthetist. Lastly, the long-term results and payor adaptation of this procedure remain to be seen.

Some clarification should be made regarding the authors’ description of surgical spinal decompression. The indications for laminectomy and discectomy are quite different. Laminectomies are typically reserved for relieving neurogenic claudication while discectomies are typically performed for radiculopathy. Gross total laminectomies are becoming rarer as the long-term consequences have been seen. The increased incidence of post-laminectomy kyphosis has led more surgeons to perform midline-sparing decompressions. These are done as hemilaminectomies or laminotomies, both of which can be done in a minimally invasive fashion.

Instrumented fusions are often done prophylactically to avoid instability. For example, a patient with severe facet arthropathy and stenosis may need to have the entire facet removed, which could render them unstable. Furthermore, bone-on-bone collapse of the disc space can benefit from an inter-body graft to distract the vertebrae bodies and provide indirect decompression. Finally, surgical fusion can often reduce a listhesis and gain additional indirect decompression.

With a paucity of Level 1 data, the most efficacious treatment for patients with lumbar stenosis remains somewhat elusive. As in most areas of medicine, a multidisciplinary approach to this pathology is the preferred course.

The incidence of lumbar spinal stenosis (LSS) in the United States has been estimated at 8% to 11% of the population.6 As the “baby boomers” age, an estimated 2.4 million Americans will be affected by LSS by 2021.7 As patients grow older, bony changes in the vertebrae—such as thickening of the pedicles, lamina, and facets—encroach on the space surrounding the nerve, causing loss of disc height and narrowing of the spinal canal and neural foramina. These degenerative spondylotic changes are usually associated with hyperplasia, fibrosis, and metaplasia of the surrounding ligamentous structures, including the intervertebral discs, causing LSS (Figures 1 and 2).8

People with LSS may or may not have back pain. Classic clinical findings of LSS include neurogenic claudication, sciatica, positional radicular pain, and weakness. The pain typically is exacerbated by standing and walking, and usually is decreased by positions that decrease lumbar spine lordosis (sitting and leaning forward). A key feature in the history of an LSS patient is the complaint of not having the ability to walk as far as one normally could without feeling symptoms, or without exacerbating already established symptoms.8

Another common cause of LSS is degenerative spondylolisthesis. This occurs when the vertebrae itself slips forward, causing a narrowing of the spinal canal. If the slip is moderate or severe, the emerging nerve roots get entrapped by the articular processes of the vertebra.9 The degree of slippage is also dependent on the patient’s anatomy. In patients with a wider spinal canal, then a mild slippage may be asymptomatic. If the spinal canal is normal width, then a mild or moderate slippage may produce symptomatology.9

LSS is a condition that affects many individuals, and can have a strong impact on activities of daily living, social aspects, physical stress, and the emotional status of a patient. The purpose of this article is to review the current therapies available for LSS, the indications for each one, and review the outcomes associated with each of the methods.

Non-surgical Management

The starting point for any pain management plan is conservative, non-surgical therapy. This includes physical therapy, anti-inflammatory medications, lumbar supports, opioid analgesics, steroid injections, and other modalities such as osteopathic manipulative treatment. Multiple studies have shown that conservative management is beneficial to patients suffering from LSS. Weinstein et al compared LSS and degenerative spondylolisthesis patients who received surgery to those who received conservative therapy. Although both patient groups showed that surgery was superior for treating these conditions, there was moderate improvement shown in the conservative treatment groups over time.10,11 In the Maine Lumbar Spine Study, 28% of the non-surgical group showed improvement with conservative therapy after 1 year of treatment (P=.003).12

When discussing conservative treatment, it is important to discuss the patient population who would benefit from such therapy. The goals of conservative management are slightly different than those of surgical therapy. With conservative management, the aim is to reduce inflammation, strengthen paravertebral and abdominal musculature, alleviate pain, and increase range of motion. It has been found that, despite these efforts, symptoms often recur, especially radiculopathy symptoms since these modalities typically have a temporizing effect.13

It is important to note that not all of these conservative treatments are benign. Initiation of NSAID therapy usually begins as a first-line treatment modality along with physical therapy. NSAIDs are contraindicated in patients with peptic ulcer disease, congestive heart failure, and renal disease due to the potential for serious adverse effects. When there is still inadequate pain control, opioid therapy may be initiated. Opioid therapy can cause constipation, dependence, and drowsiness. The side effects of medications always have to be discussed with patients, especially dependence on these agents, which is something to be seriously considered (Table 1).

Surgical Options

According to the American Academy of Orthopaedic Surgeons, “surgery for [LSS] is generally reserved for patients who have poor quality of life due to pain and weakness.” Each surgical procedure has its own special indications and requirements for the surgery to be successful.

Generally speaking, requirements for surgery include the following: patient must obtain medical clearance in order to tolerate the surgery, radiographic evidence must be present and match the clinical picture, and benefit must outweigh risk of surgery (Table 2). Here, we will examine some of the more popular and newer technologies available for spinal decompression surgery.

Interspinous Process Decompression Implant Device

Before considering the option of spinal decompression (laminectomy) surgery, and after failed conservative management, one may begin to think of smaller, less invasive operative procedures to alleviate LSS. One such option is an interspinous process decompression implant device, such as X STOP (Medtronic Spine LLC, Memphis, Tennessee). This device uses a titanium implant, which becomes fixated to the interspinous ligament between the symptomatic lumbar vertebrae, and decreases the extension of the spine at that level. When the vertebrae extend back, the spinal canal and neuronal foramina naturally become narrower, and in flexion, become significantly wider.14 This movement is a contributing pathophysiological cause of neurogenic intermittent claudication, which can be caused by lumbar spinal stenosis.

The premise of this device is to alleviate the narrowing of the spinal canal and foramina in extension, while preserving the dynamic changes experienced in flexion. This type of surgery would only be indicated for neurogenic intermittent claudication, which is significantly improved with flexion, and worsened by extension. In addition, other indications for this procedure are patients >50 years old, and candidates who have failed at least 6 months of nonsurgical treatment options.15 Also, radiological evidence of lumbar spinal stenosis, such as hypertrophied ligamentum flavum, narrowed lateral recesses, and central canal narrowing should be present for candidates of interspinous process implant devices.13

Several contraindications also exist for the X STOP device. They include allergy to titanium; spinal anatomy that prevents stable implantation, such as fracture and scoliosis with a Cobb angle greater than 25°; cauda equina syndrome; severe osteoporosis or osteoarthritis; systemic or localized infection at the implantation site; and spondylolisthesis greater than grade 1.15

Last updated on: June 1, 2015
First published on: July 1, 2013