The term spondylolisthesis comes from the concatenation of two Greek words - spondylo (vertebra) and olisthesis (slipping). In the lumbar spine, spondylolisthesis is classified into several types according to the system of Wiltse.1
Table 1. The Modified Wiltse Classification of Lumbar Spondylolisthesis
|Type ||Name ||Description |
|I ||Dysplastic ||Congenital abnormalities in the posterior arch of L5 or S1|
|II ||Isthmic ||Also referred to as spondylolytic; a lesion in the pars interarticularis|
|III ||Degenerative ||Osteoarthritis of the facet joints and degenerative disk disease|
|IV ||Traumatic ||Acute fractures of the bony arch|
|V ||Pathological ||Weakening or absence of the normal bony restraints to motion|
|VI ||Iatrogenic ||Resection of the facet joints or disk material causing instability|
Etiology and Pathogenesis
Degenerative spondylolisthesis, also known as "senescent spondylolisthesis" or "spondylolisthesis with an intact neural arch," predominantly affects patients older than 40 years of age. Degenerative spondylolisthesis most often occurs at the L4-L5 level and is believed to be derived from a combination of facet arthritis and degenerative disk disease, as well as various other causes. This condition occurs five to six times more commonly in women and three times more often in patients of African descent.2 The reason for the female predominance may be due to the effects of estrogen on ligamentous laxity. It is known that women who have had an oophorectomy show a higher incidence, which also indicates a role for estrogen. In blacks, the higher incidence is explained by a higher rate of hemisacralization of L5, as well as less lumbosacral lordosis than other populations. These factors leave a relatively stiff segment below the L4-L5 disk space and are believed to be a major component of the pathogenesis of degenerative spondylolisthesis.3
Intervertebral disk degeneration also contributes to degenerative spondylolisthesis. As more load is carried by the posterior elements, they undergo progressive arthrosis and degeneration. This action, combined with abnormal stress concentration, causes breakdown of the facet joints.4 The facet angle contributes to this abnormal stress. A coronal orientation predominates in the upper lumbar spine and at L5-S1, which places a large load on the facets at L4-L5. Furthermore, in patients with degenerative slips, the facet angle at L4-L5 is more sagittal than in the average population.5 This angle prevents the facets from resisting forward flexion forces, increasing the tendency to slip and accelerating facet arthritis due to micromotion and microfractures. After disk degeneration occurs, the motion segment settles into an anterolisthesis. It is important to note that because the posterior arch of L5 is intact, this type of spondylolisthesis rarely progresses past grade II and it is usually of a lower grade than an isthmic spondylolisthesis.
Clinical Signs and Symptoms
The most common presentation of patients with degenerative spondylolisthesis is low back pain radiating down the buttocks into the anterolateral thighs. Other symptoms may include weakness and a limited capacity to stand or walk that is usually relieved by sitting. True radicular symptoms occur in less than 50% of patients6 and when present usually correspond to L5. Compression of L5 results from overgrowth of the facet at the L4-L5 level that causes compression of the nerve root posterolaterally between the superior facet and the posterosuperior border of the L5 vertebral body.
Clinically, the nonspecific neurogenic claudication symptoms of degenerative spondylolisthesis are related to spinal stenosis. The classic description is the relief of pain with leaning on something, such as a shopping cart or wheelchair, when walking. This maneuver opens up both the spinal canal and the intervertebral foramen, relieving the compression and venous congestion in the cauda equina and nerve roots. This description helps distinguish this disease from vascular claudication. In patients with vascular claudication, pain is brought on by walking a set distance and is usually relieved by standing still. Patients with spinal stenosis typically need to sit or lean forward to relieve their pain.
Examination of patients with degenerative slips often reveals normal or even hypermobility of the lumbar spine in flexion with a notable lack of stiffness. This is in contrast to the tight hamstrings and limited mobility of patients with isthmic spondylolisthesis. A generalized ligamentous laxity in patients is believed to predispose them to a slip.1 Extension maneuvers may exacerbate their pain due to narrowing of the canal and foramen. True symptoms of cauda equina are rare in this disorder, and their presence can be masked by symptoms related to the genitourinary system that are often thought to be part of the normal aging process. A history of symptoms indicating the presence of a cauda equina disturbance should be aggressively solicited because loss of function for an extended period of time portends a poor prognosis.
Plain radiographs taken with a patient in the standing position reveal a spondylolisthesis that was not detected on supine films in 15% of patients.7 Flexion and extension lateral radiographs may show a dynamic slip, but this is relatively rare and may not influence treatment. Anteroposterior radiographs may show hemisacralization of L5. Myelography, with or without computed tomography (CT), is traditionally the imaging modality of choice for the spinal stenosis associated with the slip (Slide 1). Axial CT images postmyelography provide information regarding canal diameter and neural compression regardless of the cause and give the best bony detail (Slide 2). Magnetic resonance imaging (MRI) is increasingly used for this disorder to further evaluate the soft tissue structures. MRI reveals nerve root compression, disk pathology, yellow ligament hypertrophy, and other soft tissue sources of compression. Facet joint synovial cysts are a pathognomonic sign of degenerative spondylolisthesis (Slide 3). MRI is noninvasive and prevents painful lumbar or cervical injections and their side effects including headache and nausea in 20% of patients.
Several studies on the natural history of degenerative spondylolisthesis conclude that many patients will experience a halt in the progression of their symptoms or even improvement.2,3,6,7 Approximately 25% to 30% of patients will experience progression of the slip, but the slip will rarely progress to more than 30% of the subjacent vertebra.2,6 Progression of the olisthesis does not correlate with clinical symptoms in patients who do not receive operative treatment.2,3,6,7
Nonoperative treatment should begin with rest for 1 to 2 days, nonsteroidal anti-inflammatory medications, and activity modification. This is supplemented by physiotherapy emphasizing flexion exercises and back strengthening, progressing to aerobic conditioning. Use of a stationary bicycle with the seat and handlebars set up to allow lumbar flexion is encouraged. This activity allows expansion of the spinal canal and neural foramen. If this initial nonoperative treatment fails, we advocate the use of epidural steroid injections or the selective nerve root injections for the symptoms of spinal stenosis. These injections are more effective for relief of radicular-type pain and less effective for back pain.
Indications for surgical treatment include persistent or recurrent leg pain despite conservative treatment, progressive neurological deficit, significant reduction in the quality of life, and confirmatory imaging studies consistent with the clinical findings.7 It is important to give the patient a long trial of conservative care, including the use of epidural steroids, before surgical intervention. If all reasonable methods fail, surgical options can be discussed. Surgical options include pedicle-to-pedicle decompression, decompression and posterolateral fusion, and decompression with interbody fusion. The role of instrumentation is controversial.
Poor results from several studies8,9 after decompression alone indicate that decompression additionally destabilizes the motion segments, which adversely affects outcome. Approximately 25% to 50% of patients who undergo decompression without fusion experience a progression of their slip, and this postoperative progression seems to correlate with outcome.10 Bone regrowth following decompressive laminectomy also contributes to recurrence of symptoms.11
Prospective, randomized trials examining the use of fusion and instrumentation in the treatment of degenerative spondylolisthesis have been performed. One such study demonstrated a statistically better fusion rate and clinical outcome in patients who underwent fusion.7 Zdeblik compared noninstrumented fusions to semirigid and rigid instrumented fusions in 56 patients with degenerative spondylolisthesis and found better fusion rates in the rigidly instrumented group, which corresponded to better clinical results.12 Bridwell reported on 44 patients divided into three groups: no fusion, noninstrumented posterolateral fusion, and instrumented posterolateral fusion using pedicle screws.13 Instrumentation significantly improved fusion rates, functional outcome, and sagittal alignment.
A meta-analysis of degenerative spondylolisthesis literature was performed in 199410 that examined the issues of fusion and instrumentation. In patients undergoing decompression without arthrodesis, 69% of patients had a satisfactory outcome. Progressive slipping after decompression was noted in most reports. The addition of arthrodesis increased the satisfactory outcome to 90%, with 86% achieving solid fusion. In this meta-analysis, the authors report a nonsignificant trend toward increased fusion with pedicle instrumentation but minimal difference in clinical outcome.
Recently, instrumentation as an adjunct to fusion in patients with degenerative spondylolisthesis was examined. The researchers found a significantly higher fusion rate in the instrumented group (82% versus 45%) but no significant difference in clinical outcomes with the use of instrumentation.14 With longer follow-up, however, the patients with a pseudarthrosis did not do as well as patients with a solid fusion. These findings prompted the researchers to advocate the routine use of instrumentation to increase the fusion rates.15 Another study of posterolateral spinal fusions for spondylolisthesis found that if neural decompression was performed, instrumentation significantly improved functional outcomes. The authors observed "significant symptoms related to misplacement of a screw" in 4.8% of patients and concluded that routine use of pedicle screw fixation alone is not justified as an adjunct to posterolateral lumbar fusion.16
Degenerative spondylolisthesis and its associated spinal stenosis are common clinical entities with a favorable outcome in the majority of patients. The persistent use of nonoperative treatment modalities can provide symptomatic relief in a large majority of patients. If surgical treatment becomes warranted, a decompression and stabilization with a posterolateral fusion is indicated to prevent progression of the deformity. The use of instrumentation carries the benefit of an added rate of fusion but must be weighed against the risks and costs of the procedure in the elderly patient population.
- Wiltse LL, Newman PH, MacNab I. Classification of spondylolisis and spondylolisthesis. Clin Orthop. 1976; 6:23-29.
- Rosenberg NJ. Degenerative spondylolisthesis. Predisposing factors. J Bone Joint Surg Am. 1975; 57:467-474.
- Frymoyer JW. Degenerative spondylolisthesis: Diagnosis and treatment. J Am Acad Orthop Surg. 1994; 2:9-15.
- Taillard WF. Etiology of spondylolisthesis. Clin Orthop. 1976; 6:30-39.
- Grobler LJ, Robertson PA, Novotny JE, Pope MH. Etiology of spondylolisthesis. Assessment of the role played by lumbar facet joint morphology. Spine. 1993; 18:80-91.
- Matsunaga S, Sakou T, Morizono Y, Masuda A, Demirtas AM. Natural history of degenerative spondylolisthesis. Pathogenesis and natural course of the slippage. Spine. 1990; 15:1204-1210.
- Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis. A prospective study comparing decompression with decompression and intertransverse progressive arthrodesis. J Bone Joint Surg Am. 1991; 73:802-808.
- Lombardi JS, Wiltse LL, Reynolds J, Widell EH, Spencer C 3rd. Treatment of degenerative spondylolisthesis. Spine. 1985; 10:821-827.
- Johnsson KE, Wilner S, Johnsson K. Postoperative instability after decompression for lumbar spinal stenosis. Spine. 1986; 11:107-110.
- Mardjetko SM, Connolly PJ, Schott S. Degenerative lumbar spondylolisthesis. A meta-analysis of the literature 1970-1993. Spine. 1994; 10(suppl 20):2256-2265.
- Postacchini F, Cinotti G. Bone regrowth after surgical decompression for lumbar spinal stenosis. J Bone Joint Surg Br. 1992; 74:862-869.
- Zdeblick T. A prospective, randomized study of lumbar fusion. Preliminary results. Spine. 1993; 18:983-991.
- Bridwell KH, Sedgewick TA, O'Brien MF, Lenke LG, Baldus C. The role of fusion and instrumentation in the treatment of degenerative spondylolisthesis with spinal stenosis. J Spinal Disord. 1993; 6:461-472.
- Fischgrund JS, Mackay M, Herkowitz HN, Brower R, Montgomery DM, Kurtz LT. Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine. 1997; 22:2807-2812.
- Bassewitz H, Herkowitz H. Lumbar stenosis with spondylolisthesis: Current concepts of surgical treatment. Clin Orthop. 2001; 3:54-60.
- Thomsen K, Christensen FB, Eiskjaer SP, Hansen ES, Fruensgaard S, Bunger CE. The effect of pedicle screw instrumentation on functional outcome and fusion rates in posterolateral lumbar spinal fusion: A prospective, randomized clinical study. Spine. 1997; 22:2813-2822.