eMedicine Specialties > Radiology > Musculoskeletal

Spondylolisthesis

Author: Zubin Irani, MD, MBBS, Resident Physician, Department of Radiology, Dotter Interventional Institute, Oregon Health and Science University School of Medicine
Coauthor(s): Jehangir J Patel, MD, Director, Musculoskeletal Radiology Service, Department of Radiology, Baystate Medical Center
Contributor Information and Disclosures

Updated: Sep 14, 2009

Introduction

Background

The word spondylolisthesis is derived from the Greek words spondylo, meaning spine, and listhesis, meaning to slip or slide. Spondylolisthesis is a descriptive term referring to slippage (usually forward) of a vertebra and the spine above it relative to the vertebra below.

A grading system of spondylolisthesis is shown in Image 1 .

Spondylolisthesis has many etiologies, all of which ultimately lead to a loss of the stability offered by the locking mechanism of the articular processes of the vertebrae that allow the superior vertebrae to slide forward over the inferior vertebrae (see Anatomy). The etiologies can be classified as congenital (dysplastic), spondylolytic (isthmic), degenerative, traumatic, pathologic, or iatrogenic (eg, postoperative).

The focus of this chapter is spondylolytic spondylolisthesis.¹

Recent studies

Lawhorne et al reviewed the exclusion and inclusion criteria in various dynamic stabilization studies and investigational drug exemption protocols and summarized the limitations for both pedicle- and intraspinous-based systems. They then conducted a retrospective chart and imaging review of 100 consecutive cases undergoing fusion for degenerative spondylolisthesis and estimated how many patients in that population would have been candidates for dynamic stabilization with either intraspinous or pedicle-based systems. They found that 34 patients had no exclusion criteria for intraspinous devices and 23 patients had none for pedicle screw-based dynamic stabilization. Therefore, they estimated that 34% and 23% of degenerative spondylolisthesis patients indicated for surgery could have been treated with either intraspinous or pedicle-based dynamic devices, respectively.²

Huang et al used axially loaded MRI to measure disability and physical function in 29 patients with degenerative lumbar spondylolisthesis. The findings were compared with those of unloaded MRI of the lumbosacral spine in supine position to measure disc height, sagittal translation, segmental angulation, dural sac cross-sectional area at L4-5, and lumbar lordotic angles at L1-5. The morphologies of the lumbar spine changed after axially loaded MRI, according to the authors. They suggest from their findings that the angular instability of the intervertebral disc may play a more important role than neurologic compression in the pathogenesis of disability in degenerative lumbar spondylolisthesis.³

Kalanithi et al performed a database study using the Nationwide Inpatient Sample data from 1993-2002 of 66,601 patients who underwent posterior lumbar fusion for acquired spondylolisthesis. The authors found that older patients (65-84 y) and those with more comorbidities (3 or more) had greater rates of in-hospital complications and complex disposition. Patients aged 65-84 years were almost 70% more likely to have complications and 5 times as likely to have complex disposition.⁴

Weinstein et al found that compared with patients treated nonoperatively for degenerative spondylolisthesis, patients in whom degenerative spondylolisthesis and associated spinal stenosis were treated surgically experienced substantially greater pain relief and improvement in function.⁵

Pathophysiology

A working knowledge of normal anatomy and the locking mechanism is helpful in understanding how and where the mechanism can fail.

In the healthy person, the facet joint in the lumbar spine is, for the most part, in the coronal plane, with the inferior articular process of the superior vertebra located posteriorly and the superior articular process of the inferior vertebra located anteriorly. This configuration prevents forward movement of the vertebrae relative to each other. It locks in the superior vertebra relative to the inferior vertebra. This mechanism is important because the center of gravity of the human body is located anterior to the spine and exerts a forward slipping force on the spine, especially at the L5-S1 level. Furthermore, the anteriorly located center of gravity causes a rotating movement, with the axis of rotation oriented transversely at the L5-S1 level. Thus, in severe spondylolisthesis, a kyphotic deformity also develops.

Simplistically, a vertebra (and the spine above it) may slip if abnormalities are present within the facets and facet joints, articular processes, or neural arch (ie, connection between the facet joints and the vertebral body). Various etiologies affect one or more locations.

Spondylolytic spondylolisthesis

The spondylolytic (isthmic) type is the most common cause of spondylolisthesis. It affects the region of the pars interarticularis, which is roughly the region of the junction of the pedicle and lamina, where the articular and transverse processes of the vertebrae arise. A defect at this point functionally separates the vertebral body, pedicle, and superior articular process from the inferior articular process and remainder of the vertebrae. Thus, the defect cleaves the vertebra into 2 parts (see Image 4). The portion of the vertebra posterior to the defect remains fixed, and the anterior portions are free to potentially slip forward relative to the posterior structures and spine below. Note that bilateral pars defects are needed to allow slippage.

Established observations and factors relating to the development of this disorder are as follows: Apart from 1 reported case, humans are not born with a pars interarticularis defect.⁶ A congenitally dysplastic pars interarticularis, coupled with the stresses placed on the lumbar spine by upright (bipedal) posture with extension loading, appear to cause spondylolysis.⁷ A family history of spondylolysis and/or spondylolisthesis is commonly found. Upright posture places a continual downward and forward thrust on the lower lumbar spine, with the forces concentrating on the pars interarticularis. High-risk activities include gymnastics, rowing, tennis, wrestling, weightlifting, and football; all of these create mechanical stresses that play an important role in the development of spondylolysis.^8,9,10

Placing such stresses on a weak pars results in a pars fracture.¹¹ These microfractures heal with a false joint, a bony bridge across this portion of the arch, or fibrous bridging of the fracture.

Most defects are believed to begin as a stress fracture that most likely persists because of continued motion (especially extension movements of gymnasts, which have been implicated in causing the fractures in the first place), which usually impairs bone healing. Some defects heal and may do so with elongation of the pars, representing healing of repeated microfractures. No diastatic defect is seen on radiographic imaging in such cases, but a spondylolisthesis does occur.

A study by Fredrickson and colleagues showed a 4.4% incidence of spondylolysis and a 2.6% incidence of spondylolisthesis at age 6 years and a 5.4% and 4.0% prevalence, respectively, in adulthood.¹² Note that once the pars defect has occurred, not all patients necessarily develop a spondylolisthesis. The largest degree of slippage occurred during the adolescent growth spurt. After skeletal maturity, slip progression usually is minimal and often is related to disk pathology, which more commonly occurs in patients with at least a grade 2 spondylolisthesis.

The affected population shows a 2:1 male-to-female predominance.¹³ White men are affected more commonly than black men, and white women are affected more often than black women.¹⁴ A near 50% prevalence is found in Eskimos. Although males more commonly have the pars defect, females are more likely to progress to higher degrees of spondylolisthesis.¹⁵

Degenerative spondylolisthesis

The pars interarticularis is not affected by degeneration. As such, a pars interarticularis defect is not present.

Long-standing intersegmental instability leads to degenerative spondylolisthesis. This may arise from other problems, such as disk degeneration or spondylolytic spondylolisthesis. Surgical laminectomy is another cause.²

Osteoarthritic changes develop in the facet joints. Eburnation and erosive changes occur, which may lead to abnormal alignment of the articular surfaces. Other factors include abnormalities of the ligamentous structures and intervertebral disk, such as loss of disk height. All of these combine to cause spondylolisthesis. Usually, the degree of spondylolisthesis is not great in this group. The L4-L5 vertebral space is affected 6-10 times more commonly than at other levels.

Retrolisthesis may result from the degenerative factors in some individuals. This is a slippage in the posterior direction (opposite to an anterolisthesis).

Black women are affected 3 times more commonly than white women. Degenerative spondylolisthesis usually occurs in patients older than 40 years.^16,17

Congenital spondylolisthesis

In the congenital (dysplastic) type, congenital anomalies of the vertebral arch and/or facets occur at the lumbosacral junction. Spondylolysis is excluded, as patients are not born with that lesion. Lesions in this category include dysplastic facets that may have an axial (horizontal) or sagittal orientation; lesions may occur as a result of the failure of vertebral body formation. The end result is that the facets do not lock in, and forward slippage is allowed. The pars may remain intact, develop poorly, elongate, or even lyse. Note that when an intact posterior arch accompanies forward slippage, potential exists for the arch to impinge on the cauda equina. Alternatively, spondylolisthesis of the L5 vertebra may cause S1 nerve root compression by the L5 vertebra inferior articular process.

The female-to-male predominance is 2:1.¹³ This type accounts for approximately 15-20% of cases of spondylolisthesis. Symptoms usually develop during the adolescent growth period.

The facet joint is a synovial joint and is subject to the same osteoarthritic changes that affect other synovial joints in the body. Thus, loss of hyaline cartilage (which is eburnation of the joint surface) and reactive hypertrophic bony changes can lead to altered alignment of the facet joint, allowing spondylolisthesis.¹⁸

Traumatic spondylolisthesis

Trauma in the development of a spondylolysis is discussed in Spondylolytic spondylolisthesis, above. Also, trauma can cause an acute fracture through a normal pars interarticularis and result in a diastatic defect that may lead to a spondylolisthesis. If immobilized, these should heal. Although fractures are also involved in the pathogenesis of the spondylolytic type, it is assumed that in the traumatic variety, pars is normal and that fractures occur as a result of excessive forces being applied upon the pars. In the spondylolytic variety, the pars fails under normal stresses (ie, sustains stress fractures).

Traumatic forces may affect other parts of the spine and result in a spondylolisthesis. For instance, fractures may be seen in the articular processes or through the facet joints. Subluxation or dislocation (eg, jumped facet) of the facet joint may occur. Associated ligamentous injury should always be considered; such injuries can occur if the traumatic force involves the disk, anterior and posterior longitudinal ligaments, interspinous ligament, supraspinous ligament, and the capsule and ligaments of the facet joints, causing facet-joint instability. Any 1 or more of these mechanisms may result in a spondylolisthesis.

Pathologic spondylolisthesis

Neoplasm or infection may involve the pars interarticularis, facets, or pedicles. Malignancy, such as metastasis from primary breast, prostate, and lung carcinoma, as well as myeloma, do occur in the posterior elements. Infections, such as blood-borne staphylococcal osteomyelitis, also occur.

Frequency

United States

With the exception of 1 reported case, spondylolysis is not present at birth.⁶ One study reported a prevalence of 4.4% in children aged 6 years, with prevalence increasing to 5.4% by adulthood. It is presumed that the increase is related to the adolescent growth spurt. In the same study, prevalence of spondylolisthesis was reported to be 2.6% and 4.0%, respectively.¹²

Dysplastic spondylolisthesis represents approximately 14-21% of all cases of spondylolisthesis.

International

Eskimos have a reported incidence of spondylolysis in adults of almost 50%, which is presumed to result from a combination of genetic and environmental factors.

Mortality/Morbidity

• Mortality has never been reported in spondylolisthesis.
• Morbidity is not uncommon, since back pain and neural involvement, if severe enough, can affect activities of daily living.

Race

Studies from the United States demonstrate that the white population is affected more frequently with spondylolysis than is the black population. Eskimos also have a high incidence. The degenerative form has a higher prevalence in the black population.

Sex

Spondylolysis has a 2:1 male-to-female predominance; the congenital and degenerative forms of spondylolisthesis have a female-to-male predominance of 2:1 and 5:1, respectively.^17,19

Age

Spondylolysis, with the exception of 1 reported case, is not present at birth. Its appearance develops with increasing age, in keeping with the presumed pathogenesis relating to increasing activity and spinal loading. At age 6 years, a 4.4% prevalence is reported; a 5.4% prevalence is reported in adulthood. Consequent spondylolisthesis has a reported prevalence of 2.4% and 4.0%, respectively. Congenital spondylolisthesis may be seen in early life, but patients usually present with symptoms during the adolescent growth spurt.^12,17,19

Anatomy

Presentation

Symptoms and signs in patients depend on the severity of the condition.

Pain is the most common symptom of spondylolysis and spondylolisthesis. Pain may originate in the area of lysis or may arise from other structures that have been affected by secondary changes of lysis or spondylolisthesis, such as degenerative change in the disk, facet-joint arthropathy, and ligamentous sprain or strain.

In addition, pain may arise from neural involvement, which may be from the spinal canal stenosis that can occur in high grades of spondylolisthesis. In this situation, an intact neural arch slides forward, narrowing the spinal canal and compressing the cauda equina. Clinical features of spinal claudication may ensue.

Alternatively, as the neural arch slides forward, the inferior articular process of the slipping vertebra can impinge on the nerve roots in the lateral recess of the spinal canal and cause clinical findings of radiculopathy. Typically, this may involve the L5 or S1 nerve roots.

These pain mechanisms are common to all etiologies of spondylolisthesis. However, studies show that patients with spondylolysis are relatively asymptomatic. When a symptomatic adolescent is evaluated, other causes of pain should be considered; these include infection, neoplasm, osteoid osteoma, and disk herniation. Indeed, the same findings may hold true for mild grades of spondylolisthesis.

Preferred Examination

Lateral and anteroposterior plain radiographs of the lumbar spine should be obtained in patients with complaints of back pain. The lateral view is useful in detecting spondylolisthesis. The lateral view may demonstrate the pars defect; bilateral oblique views are especially useful to visualize the pars interarticularis defect, which has the appearance of a Scottie dog with a collar. An elongated pars also may be seen.

Plain radiographs also may demonstrate congenital types and the changes of spondylosis. In the setting of trauma, fractures may be apparent. Note that other causes of the patient's symptoms may be demonstrated, such as an osteoid osteoma, Paget disease, and osteolytic lesions. The grade of spondylolisthesis can be measured by using the lateral view (see Image 2).

Cross-sectional imaging should be considered next.

In patients with back pain and no clinical findings of nerve root involvement, CT scan of the lumbar spine yields information regarding spondylolisthesis and its cause, along with other possible conditions, such as disk disease, disk herniations, spondylosis, and spinal canal stenosis. Other associations, such as spina bifida, may be seen. In patients with radiculopathy, CT myelography can yield information regarding nerve-root impingement and its etiology, such as disk herniation, abscess, or neoplasm.

CT of the spine can be performed with or without intrathecal contrast enhancement. Axial images are obtained in a plane parallel to the disk spaces at each level imaged. Sagittal reconstruction images are obtained by using post-acquisition processing software. Bone window (eg, 1500/300 HU) and soft-tissue window (eg, 300/30 HU) settings are used.

Section-thickness selection is important to avoid problems, such as volume averaging, and thin sections should be used. Contiguous images also reduce such problems. Indeed, if the sections are too thick and if a gap is present between sections, spondylolysis can be missed. In such cases, sagittal reconstructions may be of help.

With spondylolysis, CT is performed as close as possible to 90° to the level of interest. CT scans typically demonstrate a horizontally oriented defect in the pars, which interrupts the normally complete bony ring of the posterior elements (see Images 7-8). Sagittal reconstruction images also show the spondylolysis (see Images 9-11).

Spondylolisthesis is evaluated best on lateral topogram but can be suggested in patients with spinal stenosis in the absence of disk pathology, posterior hypertrophic changes, or a congenitally narrow spinal canal. One typically looks for an elongated spinal canal (see Images 7-8).

CT scans can also demonstrate findings of congenital/dysplastic and degenerative types of spondylolisthesis. Abnormalities of the vertebral body or articular processes may be present (see Pathophysiology).

Changes of spondylosis deformans (degenerative changes) are apparent on CT scans. Degenerative disease of the spine has a characteristic appearance involving a loss of disk space height with or without the presence of vacuum phenomenon, narrowing of the facet joint space, subchondral sclerosis, osteophyte formation, and subchondral cysts. Some or all of the changes may be present and cause altered alignment of the facet-joint articular surface, leading to slippage. Spinal canal and/or intervertebral neural foraminal stenosis may be present.

In traumatic spondylolisthesis, findings may include jumped facets and fractures of the articular processes and/or lamina that result in spondylolisthesis.

MRI has the distinct advantage of being able to image the spine in any plane without exposure to radiation. Typically, the axial and sagittal planes are used, but images in the coronal plane can also be acquired easily, if needed.

Spin-echo and fast spin-echo sequences are used for image acquisition in these planes. A fat-saturation technique can be applied to minimize signal from fat and to bring out signal from fluid structures (eg, bone edema). Gradient-echo sequences can also be used and have the advantage of faster image acquisition, limiting problems related to motion. In a postoperative patient, consideration should be given to gadolinium enhancement with T1-weighted spin-echo sequences in the sagittal and axial planes.

MRIs should be scrutinized for the presence of a spondylolisthesis and for any abnormality of the pars interarticularis, pedicles, or facet joints. Nervous structures, including exiting neural foramina and spinal canal, should be evaluated.

A spondylolisthesis is best assessed on median sagittal images of the spine. The levels involved and the grade can be seen.

A spondylolysis pathologically can be a fibrous bridge or a pseudarthrosis, both of which have corticated/sclerotic margins in the adjacent portions of the bony ring. The bony sclerosis and fibrous tissue appear as an area of low signal intensity in the region of the pars interarticularis on images obtained with all sequences. This finding may not be easily seen and is a limitation of the use of MRI for spondylolysis.

Similar signal-intensity changes in these areas may be seen with bony sclerosis, volume averaging with adjacent osteoarthritic facet joints, osteoblastic metastases, and even involvement of the pedicles with Paget disease. Even if one sees normal bone signal extending from vertebral body to pedicle into the lamina, it is not possible to exclude a spondylolysis because there may be minimal sclerosis in the bone and because its signal intensity is similar to that of posterior element bone. This is a limitation of MRI in detecting spondylolysis.

High signal intensity may be seen in the pars interarticularis with T2-weighted sequences. This finding indicates the presence of fluid, a pseudarthrosis, or bone edema from infection.

Degenerative disease can also be seen. Narrowed disk space, with disk desiccation (low T2 signal intensity), should be sought. This disk narrowing allows for superoinferior subluxation at the facet joint at the level of disease, which allows for anterolisthesis or retrolisthesis. Reactive marrow changes should also be sought; such changes may occur in portions of vertebral body adjacent to disks and also in marrow adjacent to facet joints, resulting in abnormal signal intensity in the pars interarticularis.

Neoplastic disease involving the pars interarticularis or other parts of the vertebra typically yields low marrow signal intensity with all sequences. Infection may be evidenced by fluid signal intensity (appearing bright on T2-weighted MRIs) from bone edema. Both disease processes show enhancement with a gadolinium-based contrast agent. Other diseases causing a sclerotic response (eg, Paget disease) result in low signal intensity with all sequences.

MRI is not appropriate in every patient, as the presence of metal hardware and claustrophobia may preclude its use. In addition, some pediatric patients may need sedation to undergo MRI, which poses some risk.

Limitations of Techniques

If present, spondylolisthesis usually is detected on plain radiographs. A spondylolysis may not always be visible.

CT scanning is more sensitive for detecting spondylolysis, but occasionally this can be missed, since scanning occurs in the plane of the spondylolysis or from volume averaging. Sagittal reconstruction images are of help in patients with these findings.

MRI reveals spondylolisthesis on sagittal views. Spondylolysis may not be readily apparent on MRIs, especially if there is a mild degree of bony sclerosis. Other sclerotic lesions, such as osteoblastic metastases, in the pars interarticularis may give similar appearances.

Differential Diagnoses

Other Problems to Be Considered

If spondylolisthesis is confirmed using lateral radiographs, the differential diagnosis involves ascertaining the etiology of the spondylolisthesis. In this regard, the patient's age and all imaging information is considered.

A pars defect has a typical appearance, but other causes of bone lysis, such as neoplasm and infection, need to be entertained on rare occasions.

Degenerative disease of the spine has a characteristic appearance, including loss of disk space height with or without the presence of vacuum phenomenon, narrowing of the facet joint space, subchondral sclerosis, osteophyte formation, and subchondral cysts. Some or all of these changes may be present and cause altered alignment of the facet-joint articular margins, leading to slippage. Spinal-canal or neural foraminal stenosis also may be present and are viewed best on CT (with sagittal reconstructions); MRI can also display spinal stenoses and neural foraminal narrowing.

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