Epidemiology and Biomechanics

DS is a condition of older people and rarely affects those younger than 40 years of age. It most commonly involves the L4-5 level, although other levels may be affected. It much less commonly involves the L5-S1 level, in contrast to isthmic spondylolisthesis, which most commonly occurs at L5-S1. Factors that have been reported to predispose to anterolisthesis at the lumbosacral junction include an L5 vertebral body that is less deeply seated within the pelvis, a more slender L5 transverse process, and increased sacral inclination, all of which are more common in women than men.⁶

DS is approximately four to five times more common in females than in males and is more common in black females than in white females.⁷ The female preponderance is thought to be due to greater ligamentous laxity and hormonal effects.^8–10 A significantly increased expression of estrogen receptors has been found in facet joints of postmenopausal women having severe facet arthritis associated with DS compared with those with spinal stenosis only. It was not clear whether the higher expression of estrogen receptors aggravated the degenerative facet changes or was a causative factor for DS.⁹

In an epidemiologic survey of 4151 patients, the Copenhagen Osteoarthritis Study found the incidence of DS was 2.7% in males and 8.4% in females.¹¹ The only factors associated with an increased risk of DS in women were elevated body mass index (BMI), increased age, and increased angle of lordosis. In men, only increased age was associated with a higher risk of degenerative spondylolisthesis. There was no association between DS and age at menopause, smoking, or occupational lifting exposure.

It is likely that the development of DS is multifactorial and dependent on anatomic factors such as intervertebral disc pathology, ligament laxity, posterior facet joint arthrosis, the amount of lumbar lordosis, hormonal factors, and prior pregnancy. Genetic factors are also a likely contributor to the development of spinal stenosis with DS in some patients. One study demonstrated that a type IX collagen gene polymorphism that introduced a tryptophan residue into the protein’s triple helix predisposed its carriers to development of spinal stenosis with DS.¹²

A cadaveric model investigating the relative contributions of disc integrity and anterior and posterior longitudinal ligament factors in the development of low-grade anterolisthesis found that integrity of the disc was more important than ligamentous factors, although disruption of both was necessary to produce significant destabilization.¹³ The effect of facet joint orientation has also been reported to be a potential factor in the development of DS. Specifically, more sagittally oriented L4-5 facet joints have been implicated as a cause of DS.^14–16 In one study, individuals in whom both L4-5 facet joint angles were sagittally oriented more than 45 degrees were 25 times more likely to have DS than those with less than 45 degrees of facet angulation.¹⁴ Whether the sagittal orientation is developmental or acquired is unclear and is a matter of debate. One study reported that sagittal orientation is a result of facet joint remodeling associated with arthrosis rather than the cause of anterior subluxation.¹⁶

A retrospective, age- and sex-matched, case-control radiographic study of middle-aged women found that decreased anterior disc height and increased lumbar index (lumbar index = posterior vertebral body height/anterior vertebral body height) were two independent predictors of DS.¹⁷

Natural History

The natural history of DS, like many other spinal conditions, is not well characterized.¹⁸ A meta-analysis of the literature on DS between 1970 and 1993 found that only 25 of the 152 studies reviewed, representing 889 patients, satisfied their inclusion criteria.¹⁹ Only three of these studies, encompassing 278 patients, described the natural history of DS.^20–22 Overall, 90 of these 278 patients (32%) achieved satisfactory results without treatment. The study by Matsunaga and colleagues²¹ represented the best of the three studies and was the only true natural history study. In that study 40 patients who received no treatment were followed from 5 to 14 years (mean, 8.25 years). Only 4 of 40 patients (10%) showed clinical deterioration over the course of the study, and all were in the group of 28 patients who exhibited no slip progression over the follow-up period. Progressive slip was noted in 12 patients (30%), although none of the 12 patients exhibited clinical deterioration. The majority of the patients in this study showed slight improvement in their clinical symptoms over time. In general, no correlation was noted between slip progression and clinical deterioration. No slip progression was noted in patients with intervertebral disc narrowing, spur formation, subcartilaginous sclerosis, or ligamentous ossification, suggesting that these anatomic factors were protective against further slip and represented a mechanism of spinal restabilization. The lack of correlation between slip progression and progression of symptoms has also been reported by other authors.^18,23,24 The generally favorable prognosis of DS was confirmed by a North American Spine Society (NASS) work group consensus statement that summarized evidence-based clinical guidelines on the diagnosis and treatment of DS.¹⁸ Although it did not distinguish between natural history and conservative care, that committee reported that most patients without neurologic deficits did well without surgery.

Clinical Features

The clinical features of DS are the same as those of spinal stenosis. DS, like spinal stenosis, may be either asymptomatic or may produce low back and/or leg pain. Back pain with DS is typically mechanical and may be aggravated by back extension or by arising from a bent posture. It is to be distinguished from discogenic back pain, which is typically provoked by flexion or sitting. Only a small percentage of patients with DS may experience low back pain (LBP). A recent report that investigated a small cohort of patients from the Framingham Heart Study concluded that there did not appear to be an association between LBP and DS, as diagnosed by computed tomography (CT).²⁵

Leg pain may be either radicular or referred in a characteristic pattern of neurogenic claudication. Neurogenic claudication, also known as pseudoclaudication, is a clinical condition consisting of leg pain associated with walking.²⁶ Neurogenic claudication must be distinguished from vascular claudication, which has slightly different clinical features, a different etiology, and completely different treatment (Table 65–1). Neurogenic claudication is defined as lower extremity pain, paresthesias, or weakness associated with walking or standing.^27,28 Pain is the predominant symptom, being present in up to 94% of patients with spinal stenosis, with numbness (63%) and weakness (43%) being less common.^27,28 Bilateral involvement is common. Patients with neurogenic claudication may present with either unilateral radicular pain or with diffuse, nondermatomal symptoms beginning in the buttocks and extending a variable distance into the legs. Radicular pain is typically dermatomal in distribution and is often unilateral. It is the presenting type of symptom in 6% to 13% of symptomatic patients with stenosis.²⁸ It is often seen with lateral recess stenosis, foraminal stenosis, or concomitant disc herniation. The clinical effects of spinal canal narrowing are magnified by the presence of a degenerative slip that further narrows the spinal canal.

TABLE 65–1 Characteristics of Vascular vs. Neurogenic Claudication

Typical neurogenic claudication is less dermatomal in character than is radicular pain. It is frequently bilateral and may have a radicular component to it. Symptoms are typically produced by standing or walking and are relieved by sitting or bending forward (see Table 65–1). Indeed, patients may preferentially assume a stooped-over posture when walking or standing to ameliorate symptoms (“grocery cart sign”). Other leg symptoms such as weakness or numbness may also occur in association with standing or walking. Night pain is an uncommon feature of spinal stenosis, although it has been described in patients with lateral stenosis (lateral recess stenosis or foraminal stenosis). Unusual symptoms of spinal stenosis such as priapism associated with intermittent claudication during walking have also been reported.

The relationship of symptoms to posture can be explained on the basis of variation in canal size with posture.^29,30 Cadaveric studies have demonstrated that spinal canal cross-sectional area, midsagittal diameter, subarticular sagittal diameter, and foraminal size are significantly reduced in extension and are increased with flexion.²⁹ Similarly, neural compression is greater in extension than in flexion. An association between posture and epidural pressure measurements has also been demonstrated. In vivo studies relating posture to epidural pressure measurements have shown that epidural pressures at the level of stenosis were higher in standing compared with lying and sitting and were increased with extension and decreased with flexion.²⁹

Neurogenic claudication should be distinguished from vascular claudication because their causes and treatments are different (see Table 65–1). Although both conditions may present as leg pain associated with walking, only patients with neurogenic claudication typically have leg pain with standing. Leg pain associated with neurogenic claudication is highly position dependent, whereas vascular claudication is unaffected by back flexion or extension. Leg pain with cycling in a sitting position is common with vascular claudication but is unaffected by neurogenic claudication.³¹ Patients with vascular claudication will typically have more leg pain produced by walking uphill than downhill, whereas patients with a neurogenic claudication will typically have less pain walking uphill, owing to the slightly flexed posture of the lumbar spine that results in neuroforaminal widening and reduced neural compression. Patients with neurogenic claudication may actually have increased leg pain when walking down an incline owing to associated lumbar lordosis and consequent neuroforaminal narrowing.

The radicular pattern of spinal stenosis with DS most commonly involves the L5 nerve root, which is usually compressed within the lateral recess. This radicular pain is typically located in the posterolateral thigh and extends into the lateral calf and occasionally into the dorsum of the foot. The presence of a degenerative slip also narrows the L4-5 neural foramen and can therefore result in L4 radicular pain from foraminal compression of the L4 nerve root. Pain in an L4 distribution is characteristically located in the anterior thigh to the knee and along the anterior shin. It can occasionally be confused with pain from a hip etiology, so careful attention must be given to the possibility of hip pathology as a cause for anterior thigh pain.

Radiographic Diagnosis

The diagnosis of DS is a radiographic diagnosis that is made on the lateral lumbar radiograph (Fig. 65–1). Although the slippage (anterolisthesis) may also be evident on a supine lateral radiograph, it is important that the lateral x-ray be performed in the standing position because there can be a dynamic component to the slip, causing it to reduce in the supine position and appear normal.³² It is not unusual for a patient to present with a normally aligned supine magnetic resonance imaging (MRI) study as the only radiographic study. Unless standing lumbar radiographs are obtained, however, the presence of a degenerative slip could be missed. In one recent study, 22% of L4-5 degenerative slips, as documented by standing lateral flexion-extension radiographs, were not detectable on supine MRI.³³ Other dynamic radiographic views such as sitting or standing flexion-extension views and distraction-compression radiography may also be considered.

FIGURE 65–1 Standing lateral lumbar radiograph showing the anterior slippage (arrow) of L4 on L5.

MRI may show increased signal within a facet joint at the level of the slip.^33,34 Large facet effusions greater than 1.5 mm were found to be highly predictive of L4-5 DS, even in the absence of a measurable slip on the supine MRI.³³ Therefore a patient who presents with only an MRI should be suspected of having a DS if a large facet effusion is detected, and standing lumbar radiographs should be obtained. Alternatively, the slip can be documented by upright or axial loaded MRI.^34,35

Although the actual measurement of translation is generally straightforward, the distinction between what is normal dynamic translation and abnormal segmental motion (instability) is not.^36,37 There is no consensus as to what constitutes clinically significant radiographic instability of the lumbar spine, nor even what is considered to be the normal range of translation between motion segments.^36,37 As with routine radiographs, there exists a spectrum of normal translation that can exist in the absence of symptoms.^36,37 One study showed that more than 90% of asymptomatic volunteers exhibited between 1 and 3 mm of translation on flexion-extension lateral lumbar radiographs and that a dynamic change of greater than 4 mm was therefore considered abnormal.³⁶

It is important not to base the decision for type of surgery on the MRI or myelography/CT (myelo/CT) findings without obtaining a preoperative standing lateral lumbar radiograph. Failure to identify a listhesis preoperatively could result in performing the wrong surgery, namely, decompression rather than decompression and fusion. Furthermore, unless preoperative standing lateral radiographs are obtained, it cannot be determined if the presence of postoperative spondylolisthesis in a patient with poor pain relief after surgery was the result of destabilization from the surgery or if it was a preexisting condition.

Treatment

As mentioned previously, both the natural history of DS and, until recently, its optimal treatment are incompletely understood. The well-publicized Spine Patient Outcomes Research Trial (SPORT) was a prospective evaluation of the 2-year³⁸ and 4-year^18,39 outcomes of 607 patients with DS. Half of the patients were enrolled in a randomized cohort and half in an observational cohort. Pre-enrollment nonoperative care was not specified, and the type of surgery or nonoperative treatment during the study period was left to the discretion of the treating physicians. This study was hampered by a significant cross-over and nonadherence to treatment between the two groups, leading to both an as-treated and an intent-to-treat analysis of the data. When both the randomized and observational cohorts were combined, the as-treated analysis revealed that the surgically treated patients had significantly better outcome for both pain and function at 2-year and 4-year follow-ups. This study did not allow comparison of types of treatments, so it did not answer the question of which surgical treatments provided better outcomes.

That same SPORT trial examined radiographic predictors of outcome in both surgically and nonoperatively treated patients.⁴⁰ Radiographic features examined included degree of slip (grade I vs. grade II), disc height (<5 mm vs. >5 mm), and mobility (stable vs. hypermobile). As noted previously, surgically treated patients had better outcomes than nonsurgically treated patients across all three radiographic parameters examined. For nonoperative patients, those with a grade I slip did better than those with a grade II slip, and those with a hypermobile slip did better than those with a stable slip.

In a long-term follow-up of patients with DS, progressive slip was noted in 34% of the 145 nonsurgically managed patients who were observed for a minimum of 10 years.⁴¹ This study was not a true natural history study because it included patients who had various nonsurgical interventions. Seventy-five percent of the patients were neurologically normal at the beginning of the study, and the majority (76%) remained so at final follow-up. Of the 34% who had neurologic symptoms, 83% experienced neurologic deterioration and had a poor outcome. There was no correlation between slip progression and clinical symptoms. This study suggested that conservative (nonsurgical) treatment in neurologically normal patients can result in satisfactory clinical outcome at an average of 10 years’ follow-up in the majority of patients.