BACKGROUND

Degenerative spondylolisthesis, spondylolisthesis with an intact neural arch, typically affects patients older than 40 years. The disorder is three times more common in people of African descent, and is four to six times more common in female than male individuals.¹ The cause of degenerative spondylolisthesis is thought to derive from a combination of degenerative disc disease and facet arthritis in the presence of ligamentous laxity. Degenerative spondylolisthesis most commonly affects the L4-L5 level. The natural history of degenerative spondylolisthesis was reviewed in Matsunaga and colleagues’² study, which followed a group of 40 patients over an average of 8.25 years (Level of Evidence 4). This study demonstrates that the conditions of only 10% of patients deteriorated clinically and were a subset of a group of patients who did not demonstrate progression of the spondylolisthesis. In this study, progression of the slip was found in 30% of patients, all of whom were asymptomatic. A majority of these of patients exhibited some improvement in their clinical symptoms over time. In Matsunaga and colleagues’³ long-term follow-up study, progressive slip was found in 34% of 145 nonsurgically managed patients at a minimum of 10 years (Level of Evidence 4). At the beginning of the study, 75% of patients were neurologically normal and remained so at final follow-up. Patients with neurologic symptoms comprised 34% of the patient population, and 84% of this group experienced neurologic deterioration with a resultant poor outcome.³ Several studies have demonstrated a lack of correlation between spondylolisthesis progression and clinical deterioration.^4,5

The clinical presentation of symptomatic degenerative spondylolisthesis is similar to spinal stenosis and includes axial back pain, leg pain, or both. The axial component of degenerative spondylolisthesis involves increasing back pain with extension, which distinguishes it from degenerative disc pain that involves increasing pain with flexion. The leg pain caused by degenerative spondylolisthesis may exhibit a radicular component or a neurogenic claudication component, or both. The radicular component exhibits a dermatomal pattern, is often unilateral, and more frequently involves the nerve root traversing the level of the spondylolisthesis. A degenerative spondylolisthesis at L4-L5 produces compression in the lateral recess, which can produce an L5 radiculopathy, manifested by sensory changes in the lateral thigh, lateral calf, and dorsum of foot, as well as extensor hallucis longus motor weakness. A degenerative spondylolisthesis will also anatomically narrow the neural foramen at the level of the slip, thereby compressing the exiting nerve root. As such, a degenerative spondylolisthesis at L4-L5 can also produce an L4 radiculopathy. This is manifested by sensory changes in the anterior thigh and knee extending to the anterior leg and tibialis anterior motor weakness. Neurogenic claudication involves weakness, paresthesias, or pain that typically extends from the thighs into the legs in a nondermatomal distribution and is secondary to central stenosis. The symptoms of neurogenic claudication increase with ambulation or standing because of decreased spinal canal cross-sectional area in lumbar extension leading to nerve root compression.⁶ The symptoms of neurogenic claudication are improved with lumbar flexion, which increases the canal cross-sectional area.⁷ Neurogenic claudication may be bilateral or unilateral with pain typically being the predominant symptom. Foraminal, lateral recess, and central stenosis leading to radicular pain or neurogenic claudication in the setting of spinal stenosis are exacerbated by concomitant degenerative spondylolisthesis, which contributes to the compressive effect. Physical examination of patients with a degenerative spondylolisthesis often de-monstrates normal or hypermobility of the lumbar spine. This has been suggested to be secondary to general ligamentous laxity thought to predispose these patients to degenerative spondylolisthesis.

The diagnosis of degenerative spondylolisthesis is confirmed with a radiographic examination of the lumbar spine that includes a standing lateral radiograph.⁸ A standing lateral radiograph will demonstrate the presence of a spondylolisthesis that is not detected in 15% of patients with supine films alone. Flexion/extension films of the lumbar spine may demonstrate dynamic instability at the level of spondylolisthesis. Computed tomography (CT), with or without myelography, has traditionally been used to further evaluate degenerative spondylolisthesis associated with spinal stenosis. CT gives excellent detail of the source of compression and the osseous pathology. Magnetic resonance imaging (MRI) has been used to further evaluate the source of nerve root compression including disc pathology, facet joint synovial cysts, and ligamentum flavum hypertrophy. An MRI scan may fail to demonstrate a degenerative spondylolisthesis that may be reduced with the patient supine. The “Open Facet Sign” on MRI involves increased T2 signal in the facet joints that are subluxed open. The “Open Facet Sign” may indicate instability in the absence of a visible spondylolisthesis, and ideally the MRI would have been preceded by a standing lateral radiograph of the lumbar spine. More recently, the upright MRI has been developed to further identify soft-tissue pathology with the patient in the standing position. Spondylolisthesis is typically measured in millimeters from the posterior inferior corner of the cephalad vertebra to the posterior superior corner of the caudal vertebra.⁹ The Meyerding classification of spondylolisthesis provides a simple quantification system for the degree of spondylolisthesis. The Meyerding classification of spondylolisthesis descri-bes the percentage of forward translation of the cephalad vertebral body relative to the end plate of the caudal vertebrae. A grade 1 slip is 0% to 25%, a grade 2 slip is 26% to 50%, a grade 3 slip is 51% to 75%, a grade 4 slip is 76% to 100%, and a grade 5 slip is greater than 100%.¹⁰ Although the Meyerding classification system was traditionally used to describe isthmic spondylolisthesis, it can also be applied to degenerative spondylolistheses. As such, translation secondary to degenerative spondylolisthesis can be objectively quantified on a standing lateral lumbar radiograph. Unfortunately, the radiographic differentiation between normal motion and symptomatic instability is more problematic. Clinically significant radiographic instability of the lumbar spine is difficult to distinguish from the reference range of translation seen between motion segments in the lumbar spine.^11,12 The importance of identifying clinically significant instability on an upright radiograph secondary to degenerative spondylolis-thesis is essential to selecting the appropriate treatment.

TREATMENT

The initial conservative management for symptomatic degenerative spondylolisthesis with associated low back and/or leg pain is limited rest, nonsteroidal anti-inflammatory medications, and physical therapy (Level of Evidence 5). Physical therapy should involve flexion-based exercises and back strengthening, and progress toward an aerobic regimen to maintain the patient’s weight within ideal parameters (Level of Evidence 5). Epidural steroid injections can also be used in the treatment of degenerative spondylolisthesis with the goal of relieving leg pain (Level of Evidence 5). After all conservative measures have failed an adequate trial, operative intervention may be considered if the patient continues to experience a significant reduction in quality of life.

The classic surgical indications as described by Herkowitz and Kurz¹³ for degenerative spondylolisthesis are persistent or recurrent leg pain despite a minimum of 3 months of conservative treatment, progressive neurologic deficit, significant reduction in the quality of life, and confirmatory imaging studies concordant with the clinical findings¹⁴ (Level of Evidence 5). The options for surgical intervention include decompression alone, decompression and posterolateral fusion with or without instrumentation, or anterior or posterior interbody fusion. The focus of this chapter is to review the literature and evidence available to answer the question, “Should patients undergoing decompression for a grade 1 degenerative spondylolisthesis also have an instrumented fusion?”

EVIDENCE

A meta-analysis of the role of decompression without fusion for the treatment of degenerative spondylolisthesis reviewed 11 articles published from 1970 to 1993.¹⁵ The studies reviewed included a nonrandomized retrospective study, two randomized prospective studies, and eight nonrandomized, retrospective, and uncontrolled studies¹⁶ (Level of Evidence 4). This study included 216 patients and found that 69% had a satisfactory result, 31% had an unsatisfactory result, and 31% had progression of the spondylolisthesis. This meta-analysis reviewed the literature regarding decompression without fusion only. Another retrospective study reviewed surgeon-reported outcomes of decompression without fusion for degenerative spondylolisthesis. This study examined a group of 290 patients with an average age of 67 years and suggested similar results.¹⁷