Spondylolisthesis is an easily recognized deformity, yet confusion persists over its natural history and preferred treatment. Some spondylolistheses progress to severe deformity resulting in moderate pain and neurologic compromise. Other slips progress very little and but produce significant symptoms. Sometimes, spondylolisthesis is only discovered incidentally. Why does this apparent paradox exist? Thirty years ago, Dandy and Shannon recognized that confusion arose from the mistaken belief that all spondylolistheses must have a single cause.1 It should now be understood that each type of spondylolisthesis is the similar radiographic end result of different and distinct disease processes. These disparate pathologic conditions produce spondylolisthesis because of the common morphology and biomechanical forces applied to the lumbosacral junction.
The lumbosacral joint is the keystone of the axial skeleton. Its function is to provide stability by supporting physiologic loads, preventing nonphysiologic motion, and protecting the neural elements.
The spine can be conceptualized as a two-column structure. The anterior column of vertebral bodies and discs progressively enlarges in size and mass from cranial to caudal. The L5 vertebral body is the largest and is somewhat trapezoidal in shape in the sagittal profile. The sacrum provides a bony shelf to support the proximal spinal column. The orientation of the sacrum is interdependent on pelvic rotation, hip extension, and overall lordosis.2 The normal sacral inclination is between 40° and 60°. The intersegmental angulation between L5 and S1 is lordotic, and the lumbosacral angle ranges from −20° to −30°.3–5 The relationship between L5 and S1 is, in part, maintained by the intervening intervertebral disc. At this level, the disc is usually 10 to 15 mm in height, with a surface area of approximately 30 × 50 mm.6 The anulus fibrosus is composed of obliquely oriented fibers in concentric laminated bands.
The configuration of the lumbosacral anatomy in spondylolisthesis can be variable as demonstrated by Antonaides et al.7 The same forces that cause spondylolisthesis may also produce deformities of the sacrum in growing children. The relationships between sacral slope, pelvic inclination, and lumbar lordosis are dependent on the pelvic incidence. The pelvic incidence is unique to each individual and is the only fixed pelvic or spinal parameter. It increases with age but stabilizes after puberty, usually averaging 53° (range, 34°–77°).8 A high pelvic incidence results in high shear forces at the lumbosacral junction. Studies by Hanson et al10 and others2,9,11 have confirmed observations that spondylolisthesis is usually associated with a pelvic incidence greater than the mean and that a higher degree of slippage is associated with a higher pelvic incidence.
The posterior column is composed of bony and ligamentous structures. The bony elements include the zygapophysial joints, pars interarticularis, laminae, spinous processes, and transverse processes. The lumbosacral articulations are oriented at a 45° angle to the coronal and sagittal planes. The laterally situated superior facets of S1 are concave, and the medially situated inferior facets of L5 are convex. The lumbosacral facets are invested in a synovial lined capsule reinforced by insertions of the ligamentous structures.
The lamina, spinous process, and transverse process provide attachment for the erector spinae musculature as well as the posterior ligaments. The pars interarticularis acts as a bolt uniting the superior and inferior facets. The pedicle acts as a bridge between the anterior and posterior columns.
In static equipoise, stability of the spine requires very little muscular activity. Stability is rendered by the overall coronal and sagittal balance of the spinal column and the integrity of the osteo-discal-ligamentous complex. At the lumbosacral junction, stability is dependent on the spatial orientation of L5 to the sacrum, lumbosacral angle, sacral slope, and pelvic incidence as well as an intact osteo-discal-ligamentous complex. Because spinal parameters are dependent on pelvic parameters, alterations in local spatial orientation, such as spondylolisthesis, can produce global spinal imbalance (Figure 1).
Stability during dynamic function, in other words, with motion or load bearing, is dependent on the neuromuscular system as well as the osteo-distal-ligamentous complex. Motion is permitted through the disc because of its viscoelastic properties. Motion is passively restricted by the ligaments and posterior facets. Total combined flexion-extension at L5–S1 ranges from 14° to 20°.12–15 This is greater than the upper lumbar levels. Axial rotation ranges from 1.3° to 5°, the least of the lumbar spine. Lateral bending ranges from 1.5° to 5.5°.
Nachemson et al have shown that the contents of the nucleus pulposus are strongly hydrophilic with a resting internal hydrostatic pressure of 1.5 kg/cm2.16 The compressive loads on the lumbar disc in vivo under physiologic loads has been found to exceed 2,000 N.16,17 The ultimate strength of a lumbar motion unit is between 4,000 N and 10,000 N.18–20
The high loads experienced by the lumbosacral spine are well documented, but how are these loads distributed? Loads applied to the lumbosacral spine are usually shared between the disc and posterior articulations, hence the concept of load sharing.21 Cyron et al.22 and Troup23 presented a simplified two-dimensional analysis of the forces acting at the lumbosacral disc in the erect posture. Their analysis indicates that compression is resisted by the disc. Shear is resisted by both the disc, and the posterior elements in concert with the action of the sacrospinalis and multifidus muscles.24,25
Cadaver studies by Adams and Hutton show that the apophyseal joints resist 16% of intervertebral compressive forces in lordotic postures but resist very little in the flexed postures.26 These findings are similar to those of other investigators who suggest the facets carry 12% to 25% of the combined loads.27–29 The distribution of loads shared by the posterior elements and intervertebral disc varies with posture and the individual morphology of the trijoint complex.16,17,30
When an intact functional spinal unit is loaded, the facet joints resist the majority of the shear force, while the disc is primarily subjected to compression. If the facets are ablated, the disc will readily creep forward secondary to stress relaxation.31 Haher et al have identified an alternate path of loading of the lumbar spine.32 Ablation of the posterior facets led to transfer of axial loads to the anulus and anterior longitudinal ligaments. They concluded that the load transfer could conceivably accelerate disc degeneration.
Resistance to torsion depends primarily on the integrity of the facet joints, whereas resistance to lateral bending is dependent on the integrity of the disc and perhaps the iliolumbar ligaments.33 Resistance to flexion is primarily dependent on the capsular ligaments of the facet joints. The disc, supraspinous and intraspinous ligaments, and the ligamentum flavum constitute secondary restraints.31
The lumbosacral facet joints protect the intervertebral disc from excessive shear, flexion, and axial rotation. Clearly, when the posterior bony elements are dissociated from the anterior column, the disc experiences unusually high shear forces, which can lead to spondylolisthesis. The importance of the posterior bony hook acting as a tension band to protect the anterior column is reflected in its strength. Troup25 and Cyron and Hutton34 found that the strength of the L5 isthmus was in the order of 2,000 N. Lamy et al found the force for failure was about 50% higher or proportionally close to that of a femur.35
The mechanism of failure of a normal pars interarticularis is through a fatigue fracture. Stewart, from his observations of Eskimos, felt that repetitive flexion was responsible for the fractures.36 Lamy et al similarly implicated flexion.35 Jayson37 and Shah et al38 found the site of maximal strain under central compression loads was on the superficial and deep surfaces of the pars interarticularis. Under posterior offset loads simulating extension, the compressive and tensile strains were increased at the isthmus. Their findings suggest that hyperextension leads to spondylolysis.
Studies by Cyron et al22 and Cyron and Hutton34 suggest that alternate loading may be responsible for the development of pars interarticularis fatigue fractures. More recently, Green et al have demonstrated large stress reversals in cadaver pars secondary to alternate flexion and extension loading.39 They agree that alternate loading is the most likely etiology for the development of spondylolysis.
These findings corroborate clinical observations that people involved in repetitious alternate loading activities such as gymnastics, weight lifting, and football have higher incidences of spondylolysis. Cyron and Hutton suggest that young people are more likely to develop spondylolysis because they engage in more strenuous activity and that their discs retain sufficient viscoelasticity to accommodate the significant reversals in motion that are necessary to lead to a fatigue fracture.34
Marchetti and Bartolozzi have developed an etiology-based classification system that differentiates between the various pathologic processes leading to spondylolisthesis.40 Two main categories of spondylolisthesis are defined (Table 1). One primary category is identified by primary developmental deficiencies at the lumbosacral junction resulting in various degrees of dysplasia. The other main category, acquired spondylolisthesis, is a result of traumatic, iatrogenic, pathologic, or degenerative causes.
The term “isthmic” should be avoided because it is a nonspecific anatomic reference and does not differentiate between developmental and acquired forms of spondylolisthesis. Both types may have defects of the pars interarticularis, but they represent significantly different pathologic processes.
Developmental spondylolisthesis is analogous to developmental dysplasia of the hip, which can progress to a frank dislocation depending on the degree of dysplasia and other factors such as age, growth, weight bearing, and muscle imbalance. In developmental spondylolisthesis, posterior deficiencies in the bony hook, that is, in the lamina, pars interarticularis, and lumbosacral facets may predispose to slippage. In addition, inadequacies of the anterior column including the intervertebral disc, body of L5, and sacral shelf may increase the likelihood of slippage. In the growing child, bony remodeling as a result of adaptation to the altered biomechanical forces may contribute to the development of high-grade slippage. A major component of the progression observed in high dysplastic slips may be due to growth abnormalities.
The developmental forms of spondylolisthesis are further subdivided into high dysplastic and low dysplastic types. The high dysplastic form is usually at L5–S1 and becomes symptomatic in adolescents. Radiographically, they are characterized by a wedge L5 and a domed and vertical sacrum. The anterior translation of L5 is associated with angulation producing a true lumbosacral kyphosis. These slips have the potential to develop into spondyloptosis if untreated or mismanaged (Figure 2).
In the past, this type has been described as congenital, but it is not congenital in the true sense of the word as it is not present at birth. True congenital spondylolisthesis has been reported by Bradford et al as lumbosacral kyphosis.41 However, it is extremely rare, and like teratologic hip dislocation, is usually part of a more inclusive syndrome.
Patients with the low dysplastic forms of developmental spondylolisthesis usually present as young adults. Spina bifida occulta is frequently observed. The slippage is characterized by translation without the angulatory or kyphotic component. However, a patient at age 5 years with a low dysplastic form may, by the age 15 years, have a high dysplastic form secondary to growth, remodeling, and adaptive changes.
Many clinical and radiographic factors have been analyzed as predictors of slip progression. These include female gender, prepubescence, increased slip angle, trapezoidal L5, domed and vertical sacrum, and sagittal rotation.42 It is difficult to determine if these parameters are primary or secondary adaptive changes. Ikata et al proposed that L5 wedging and S1 doming are actually adaptive changes.43
Increasing evidence suggests that growth, or more specifically abnormal growth, is the most powerful influence on slip progression. Ikata et al observed that slippage occurred between the osseous and cartilaginous endplates during the apophyseal stage of lumbar skeletal grown.43 Takahashi et al reviewed the MRI scans of 13 patients with severe spondylolisthesis.44 They found a unique defect of the anterosuperior shelf of the sacrum, which appeared during progression and led to lumbosacral kyphosis. They termed the resulting deformity kyphospondylolisthesis, a high-grade slip. Investigations by Kajiura et al confirmed the role of a biomechanical weakness in the vertebral growth plate as an important mechanism in spondylolisthesis.45
An impairment of the vertebral growth plate as the basic lesion in producing slippage in immature spines was also demonstrated by Sakamaki et al.46 Pars defects were created in immature and mature rat spines. Slippage was observed in the immature rats but not in the adult rats. Histologic examinations showed growth plate injury in the immature rat apophyses and disc degeneration in the mature rat spines. These findings suggest that developmental spondylolisthesis may be the sacral equivalent of Blount’s disease of the tibia (Figure 3).
The degree of developmental dysplasia at the lumbosacral junction and the growth potential of the patient are the most important predictors of progression. The presence or absence of an isthmic defect is noted, but of secondary significance. Indeed, high-grade forms of developmental spondylolisthesis with intact posterior elements demand special caution. This situation may arise by elongation of the posterior elements secondary to repeated microfractures and subsequent healing as the disc bond slowly fails allowing ventral translation. These slips present a high risk of neurologic compromise, including cauda equina syndrome before or during surgical intervention (Figure 4).47
The acquired forms of spondylolisthesis include traumatic, postsurgical, pathologic, and degenerative etiologies. Traumatic spondylolisthesis can be the result of a single high-energy injury and is probably better considered as a fracture dislocation. The other type of acquired traumatic spondylolisthesis is secondary to stress or fatigue fracture through a normal pars interarticularis, termed spondylolytic in this discussion. Spondylolytic spondylolisthesis usually presents in young to middle-aged adults as low back pain. This injury is being seen more frequently in younger patients as emphasis on organized sports has increased. The morphology of the lumbar spine and sacrum is normal (Figure 5). The stress fracture is usually at L5 but may be higher and, in some cases, at multiple levels.48 A fracture observed through dysplastic posterior elements, as in spina bifida, is regarded as a developmental rather than an acquired spondylolisthesis. Frequently, a history of an activity requiring repetitive lumbar flexion and extension is elicited. Initially, an acute spondylolysis without slippage will be observed. However, as the involved disc undergoes degeneration secondary to increased shear forces, a low-grade slip will develop (Figure 6). This is termed a spondylolytic spondylolisthesis, reflecting the traumatic etiology of the slip.
A number of radiographic parameters have been used to describe the anatomic spatial relationship between L5 and the sacrum.48 The Meyerding classification divides a slip into four grades (I, II, III, IV) depending on the severity of translation. This is a simple method, easily understood, and the most widely used. A combination of the Marchetti-Bartolozzi classification system with an anatomic descriptor, such as the Meyerding classification, can convey an accurate image of the spondylolisthesis.
The postsurgical, pathologic, and degenerative types of spondylolisthesis are similar to those in Newman’s classification.49 Postsurgical spondylolisthesis is divided into direct and indirect. A direct postsurgical spondylolisthesis may result from posterior decompression or disc surgery at the level of subsequent slippage. An indirect slippage may occur at a level superior to previous surgery such as a short lumbosacral fusion; or distal to a long thoracolumbar fusion for scoliosis. Indirect postsurgical spondylolisthesis is observed as part of the so-called transition syndrome.
Pathologic spondylolisthesis is subdivided into local and systemic processes. Local pathologic spondylolisthesis is secondary to a focal process at the involved level. Systemic pathologic spondylolisthesis is the result of a generalized bone or connective tissue disorder such as osteogenesis imperfecta, Ehler-Danlos disease, or Marfan’s syndrome.
Degenerative spondylolisthesis is categorized as primary or secondary. The prototype for primary degenerative spondylolisthesis is the typical degenerative spondylolisthesis observed in a middle-aged woman. Secondary degenerative spondylolisthesis is found in patients with a predisposing factor for degenerative changes such as at the level above a congenital fusion.
The acute traumatic, postsurgical, pathologic, and degenerative types of spondylolisthesis are usually recognized as inherently different and treated accordingly. Unfortunately, developmental and spondylolytic, or “isthmic,” spondylolisthesis in adolescents and young adults have been grouped and discussed together. As a consequence, the natural histories of these processes have been obscured, resulting in confusion over the appropriate treatments. The two pathologies share a similar initial radiographic deformity, but the etiologies and natural histories are clearly different, necessitating different clinical expectations and treatments.
The natural history of high dysplastic developmental spondylolisthesis is much more progressive than the spondylolytic form. The Marchetti and Bartolozzi classification system makes the distinction between the two types, permitting early recognition and treatment.40 Certainly, all would agree that the surgical treatment of a low grade slip is preferable to any operative procedure for a spondyloptosis.
- The posterior elements play a key role in resisting the high shear forces at the lumbosacral junction. The loss of posterior restraint can result in spondylolisthesis.
- The spinopelvic relationships also have role in the development and progression of spondylolisthesis, although the exact nature is not yet clearly defined.
- The Marchetti-Bartolozzi classification system differentiates between developmental and acquired forms of spondylolisthesis. The system recognizes that, although both dysplastic slips and acquired pars stress fractures may demonstrate isthmic defects, the former are more disposed to severe progression.
- A growth deficiency of the anterosuperior sacrum may be an important factor in the progression of dysplastic spondylolisthesis.
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