Lumbar Spondylolysis and Spondylolisthesis

Spondylolysis is a defect in the pars interarticularis that may or may not be accompanied by forward translation of one vertebra relative to another (spondylolisthesis). See the image below.

Axial computed tomography (CT) scan shows bilateral spondylolysis. Note elongation of the spinal canal at this level.

Wiltse, Macnab, and Newman developed a classification to help outline causes of vertebral translation in an anterior direction.[3, 4] Their categories include the following:

• Type I: Congenital spondylolisthesis

• Type II: Isthmic spondylolisthesis

• Type III: Degenerative spondylolisthesis

• Type IV: Traumatic spondylolisthesis

• Type V: Pathologic spondylolisthesis

Type I: Congenital spondylolisthesis is characterized by the presence of dysplastic sacral facet joints, allowing forward translation of one vertebra relative to another. Orientation of facets in an axial or sagittal plane may allow for forward translation, producing undue stress on the pars, resulting in a fracture.

Type II: Isthmic spondylolisthesis is caused by the development of a stress fracture of the pars interarticularis.

Type III: Degenerative spondylolisthesis is commonly caused by intersegmental instability produced by facet arthropathy. This variation usually occurs in the adult population and, in most cases, does not progress beyond a grade I spondylolisthesis (see grading system below).[5]

Type IV: Traumatic spondylolisthesis can, in rare instances, result from acute stresses (trauma) to the facet or pars.

Type V: Any bone disorder may destabilize the facet mechanism producing pathologic spondylolisthesis. Iatrogenic spondylolisthesis, lastly, may occur if an overzealous surgeon performs too great of a facetectomy.

The most commonly used grading system for spondylolisthesis is the one proposed by Meyerding in 1947. The degree of slippage is measured as the percentage of distance the anteriorly translated vertebral body has moved forward relative to the superior end plate of the vertebra below. Classifications use the following grading system:

• Grade 1: 1- 25% slippage

• Grade 2: 26-50% slippage

• Grade 3: 51-75% slippage

• Grade 4: 76-100% slippage (see the image below)

  Grade 4 traumatic spondylolisthesis.

• Grade 5: Greater than 100% slippage

Frequency

United States

Wiltse and Beutler each reported an incidence of 6-7% for isthmic spondylolysis.[3, 6] Up to 5% of children aged 5-7 years have been found to have spondylolysis, many of whom are asymptomatic. The incidence increases up to the 7% by age 18. Athletic activities requiring repetitive hyperextension and rotation or repetitive combined flexion-extension predispose some athletes to developing pars defects.[7, 8, 9, 10] Gymnasts, linemen in college football, weight lifters, javelin throwers, pole-vaulters, and judoists are most commonly affected.[11, 12] Approximately 82% of cases of isthmic spondylolisthesis occur at L5-S1.[13] Another 11.3% occur at L4-L5. Congenital defects, including spina bifida occulta, have been linked to occurrence of isthmic spondylolisthesis. Scoliosis has been found to occur along with spondylolysis as well.[14] Roughly 50% of all cases of spondylolysis are not associated with spondylolisthesis.

Degenerative spondylolisthesis occurs more frequently with increasing age. The L4-L5 interspace is affected 6-10 more times than any other level. Sacralization of L5 is frequently seen with L4-5 degenerative spondylolisthesis.

Mortality/Morbidity

See the list below:

• Increased mortality is not associated with spondylolisthesis. While some patients may have persistent low back pain, significant disability is rare unless the patient has severe neurologic compromise that has not been addressed.

• The most common morbidity is persistent low back pain or nerve impingement. Because disk degeneration is accelerated at the sight of level of the spondylolysis, diskogenic pain may occur. Degenerative spondylolisthesis produces characteristic arthritic symptoms that may worsen with age.

Race

See the list below:

• Isthmic spondylolytic defects affect roughly 1.1% of black females. The most commonly affected group is the white male with an incidence of 6.4%. Arkara Plains Indians and Aleut people groups have a very high incidence of spondylolytic defects, due to a combination of genetic and environmental factors.

• Degenerative spondylolisthesis affects black females more commonly than white females (and females are more commonly affected than men).

Sex

Beutler et al noted a 2:1 male-to-female ratio of occurrence in asymptomatic patients with spondylolysis.[6]

• Females with isthmic spondylolytic lesions appear to be more prone to progressive displacement and may need surgical intervention more often than males.

• Congenital spondylolisthesis (dysplastic type) occurs with a 2:1 female-to-male ratio with symptoms beginning around the adolescent growth spurt. These comprise about 14-21% of all cases of spondylolisthesis.

• Degenerative spondylolisthesis occurs more commonly in females with a 5:1 female-to-male ratio. The incidence increases after age 40 years.

Age

See the list below:

• Acute isthmic spondylolysis often occurs during the first and second decades of life. Most cases occur before the patient reaches age 15 years. In rare cases, acute spondylolysis may be seen in early adulthood. Younger patients are at higher risk than older patients for developing progressive spondylolisthesis. The risk for progression in adults is rare when the lesion is at L5. In contrast, lesions at L4-5 may progress into adulthood because of increased sagittal rotation, shear translation, and axial rotation at this segment.

• Congenital/dysplastic spondylolisthesis has been documented in children as young as 3.5 months. More commonly, congenital spondylolistheses go undiagnosed until later in life after an individual has been ambulating for quite some time.

• Degenerative spondylolisthesis occurs most commonly after age 40 years.

See the list below:

• Isthmic spondylolisthesis

  • Symptoms often occur around the time of an adolescent growth spurt.

  • Some report acute onset of focal low back pain during activity, while others have more insidious onset.

  • Radiating pain may extend to the buttocks or thigh. Pain may be more significant and have mechanical characteristics with higher grades of spondylolisthesis.

  • In most cases, patients do not complain of symptoms suggesting neurologic deficit with lower grades of spondylolisthesis. Radicular pain becomes more common with larger slips. Complaints of radiating pain below the level of the knee associated with numbness and tingling in a dermatomal distribution would suggest the presence a radiculopathy resulting from either the foraminal stenosis that occurs with spondylolisthesis or a concomitant herniated disk. Nerve root impingement from the fibrocartilaginous bar that forms at the sight of the lysis may occur. High degrees of spondylolisthesis may present with neurogenic claudication or symptoms suggesting cauda equina impingement.

  • The patient's pain usually is provoked by activity, particularly back extension activities.

  • Patients with acute spondylolysis tend to demonstrate poor tolerance of activities requiring excessive spine loading, including running and jumping. Sitting usually is better tolerated.

  • A large percentage of patients with spondylolysis are asymptomatic. Progression of a spondylolisthesis also may occur without symptoms.

• Degenerative spondylolisthesis

  • The pain begins insidiously and may be achy in character. Pain is located in the low back and posterior thighs.

  • Neurogenic claudication may be present as well, with lower extremity symptoms being made worse with activity and better with rest.

  • Symptoms are often chronic and progressive, although patients may experience periods of remission.

• Dysplastic spondylolisthesis: Symptoms present much like isthmic spondylolisthesis, but neurologic compromise is more likely.

• Traumatic spondylolisthesis

  • Patients present with acute pain associated with trauma.

  • If a slip is severe enough, cauda equina compression may occur and present with classic symptoms including bowel and bladder dysfunction, radicular symptoms, or neurogenic claudication.

• Pathologic spondylolisthesis: Symptoms may be insidious in onset and associated with radicular pain/claudication.

See the list below:

• Isthmic spondylolisthesis

  • Hamstring tightness is observed almost universally, even in low-grade spondylolisthesis.

  • Lumbar spasm may be present.

  • A palpable step-off is noted with slips equal to or greater than grade 2.

  • With higher degrees of spondylolisthesis, an increased lumbosacral kyphosis is seen (50% or greater), along with a compensatory thoracolumbar lordosis. Truncal shortening may be present. With severe slips, the rib cage may rest on the iliac crest.

  • Dermatomal weakness may be present if a radiculopathy or an element of stenosis is present.

  • A waddling gait may be noted secondary to hamstring tightness producing a shortened stride length.

  • If spondylolisthesis is not present, spondylolysis presents with paraspinal spasm, pain provocation with lumbar spine extension, and tight hamstrings.

• Degenerative spondylolisthesis

  • These patients present with less prominent physical findings. Pain often is provoked with lumbar spine extension.

  • If lumbar stenosis is present, then reflexes may be diminished. Radicular findings also may be present.

• Congenital/dysplastic spondylolisthesis: Physical findings are similar to those described above for isthmic spondylolisthesis.

• Traumatic and pathologic spondylolisthesis

  • These patients also present with similar findings.

  • A good neurologic evaluation is important.

A genetic predisposition to isthmic spondylolisthesis is believed to be linked with patients having a thin pars or subtle hypoplastic facet joints. Family members have a reported incidence of 28-69%. Activities requiring lumbar extension stress increase the risk. Patients with spina bifida occulta are known to have a higher occurrence.[15]

Degenerative spondylolisthesis is caused by facet degeneration accompanied by disk degeneration most commonly at the level of L4-L5. Some studies identify sagittally oriented facets as more prone to arthritic change.

Congenital spondylolisthesis is due to dysplastic sacral or lower lumbar segments. Dysplastic facets or abnormal orientation of the facet joints are the cause for spondylolisthesis.

Traumatic spondylolisthesis is rare. In theory, severe hyperextension stress placed on the pars could produce fracture and instability. One should keep in mind that hyperflexion-distraction forces can cause facet dislocation and spondylolisthesis.

Pathologic spondylolisthesis can occur as a result of any bone lesion that might weaken the posterior elements. Generalized skeletal diseases including osteomalacia, syphilitic disease, and Von Recklinghausen disease are some reported causes. Bony destructive lesions, including tumor or infection, are other potential causes.

A study by Sakai et al suggested that male patients with L5 spondylolysis may be congenitally predisposed to the condition. The report involved 36 patients (37 vertebrae) with terminal-stage spondylolysis that was not diagnosed until adulthood, with 33 of the vertebrae (89.2%) having L5 spondylolysis, 14 of the patients (38.9%) having neither a history of athletic activity nor the occurrence of low back pain during their growth period, and nine patients (25%), eight of whom were men, having spina bifida occulta concurrently with L5 spondylolysis.[16]

Laboratory studies do not help in diagnosing spondylolytic spondylolisthesis. Workup is radiographic in nature.

Radiography

Initial workup includes anteroposterior, lateral (done while standing), and spot view radiographs of the lumbar spine and lumbosacral junction. Oblique views may provide additional information but are not obligatory. Flexion/extension views increase the sensitivity of radiographic studies and give the clinician some idea of the degree of instability that may be present. Percentage of slip and slip angle (calculated by measuring the angle formed by a line drawn from superior endplate inferiorly and the inferior endplate at the segment of involvement) are clinically valuable.

Radiographic studies allow visualization and grading of spondylolisthesis but may not always reveal the presence of an isolated spondylolysis (without spondylolisthesis). The 'Scottie dog' whose neck is broken can be seen on the oblique films when there is a classic spondylolysis. See the images below.

Lumbar oblique radiograph showing the "Scottie Dog." A pars defect is seen at L5.

Diagram in the oblique projection shows the components of the vertebrae that result in the appearance of a Scottie dog with a collar.

Bone scan

Bone scan with single-photon emission computed tomography (SPECT) imaging is helpful and often helps to direct management. See the image below.

Bone scan with single-photon emission computed tomography (SPECT) imaging showing acute spondylolysis

If the bone scan is positive, then the lesion is metabolically active. The physician may consider bracing, since healing is still in progress. A cold scan in the context of documented spondylolysis indicates that healing is complete; therefore, bracing is of limited utility.

Computed tomography (CT) scan[17, 18]

CT scanning performed with 1 mm sections, including coronal and sagittal reconstructions, allows for better visualization of the spondylolytic defect.

CT scanning not only documents the presence and severity of spondylolysis but can help to rule out more serious causes for a positive bone scan.

Myelogram/CT studies are helpful in delineating the severity of central stenosis. Nerve root cut-off often is observed in the presence of radiculopathy.

Magnetic resonance imaging (MRI)[17]

MRI may visualize edema in the marrow around the sight of an acute spondylolytic defect. MRI also is helpful in identifying the presence of nerve root compression as a result of foraminal or central canal stenosis.

In a study of adolescent athletes suffering from low back pain who had no neurologic symptoms or findings, Yokoe et al determined that male sex and a “ratio of the interfacet distance of the L1 vertebra to that of the L5 vertebra” of greater than 65% independently predicted whether lumbar spondylosis would be revealed on magnetic resonance imaging (MRI). The odds ratios for these predictors were 4.66 and 3.48, respectively.[19]

See the list below:

• Electromyography may provide 1 more modality for identifying a concomitant radiculopathy or polyradiculopathy (ie, stenosis), which may be present as a result of spondylolisthesis.

Histologic studies completed at the sight of the spondylolisthesis reveal a fibrocartilaginous mesh that often bridges the gap between the edges of the fracture sight if actual healing does not occur.

Physical Therapy

Most patients with low-grade isthmic spondylolisthesis and degenerative spondylolisthesis can be treated conservatively. If an isthmic lesion is acute, the patient should be restricted from provocative activities or sports until they are asymptomatic. Physical therapy is an integral part of the patient's rehabilitation process. The most accepted protocol includes activity and exercise that reduces extension stress.

The goals of exercise are to improve abdominal strength and increase flexibility. Since tight hamstrings are almost always part of the clinical picture, appropriate hamstring stretching is important. Instruction in pelvic tilt exercises may help to reduce any postural component causing increased lumbar lordosis. Myofascial release may play a role in reducing pain from the surrounding soft tissues.

If conservative treatment is indicated for congenital spondylolisthesis, the above principles apply. Adequate work up must be completed for pathologic causes of spondylolisthesis prior to treating with conservative means. Traumatic spondylolisthesis most often requires surgical stabilization.

Younger patients have a higher risk for progression of isthmic or congenital spondylolisthesis. Serial radiographic studies (standing lateral films only) should be performed every 6 months to follow these patients. Progression rarely occurs after adolescence. Patients with a unilateral pars defect may be prone to developing a contralateral pars defect with extension stress. Patients with degenerative spondylolisthesis are often older and have coexisting medical issues that must be taken into consideration when deciding appropriate treatment.

Surgical treatment is indicated when any type of spondylolisthesis is accompanied by a neurologic deficit. Persistent disabling back pain after conservative management may be considered an indication. High-grade slips (greater than 50%) more commonly require surgical intervention. Traumatic spondylolisthesis is rare but almost always requires surgical stabilization.[2]

A literature review by Longo et al suggested that in patients with high-grade spondylolisthesis, surgical treatment with reduction followed by arthrodesis may be more beneficial than arthrodesis in situ. The report was based on eight studies, involving a total of 165 operations in which reduction was performed prior to arthrodesis and 101 surgeries in which patients underwent arthrodesis in situ, with no reduction performed. The investigators found that in the patients treated first with reduction, the percentage of slippage and slip angle and the frequency of pseudarthrosis were significantly lower than in the arthrodesis in situ patients. Moreover, there was no significant difference between the two groups with regard to the prevalence of neurologic deficits.[20]

Bracing for acute isthmic spondylolysis/spondylolisthesis is controversial, but it has been shown in some studies to reduce symptoms and to facilitate healing. Most sources discuss use of a thoracolumbosacral spinal orthosis or modified Boston Brace for low-grade slips or for isolated spondylolytic lesions (without spondylolisthesis). Some sources advocate more extensive bracing with inclusion of most of the thorax (to the nipple line) and the thighs. Recommend use of the device for 3-6 months.[21]

Steroid injections for pars pain have been advocated by some physicians. Epidural steroid injections may help radicular pain or neurogenic claudication.

Matsudaira et al tested the effectiveness of limaprost, an oral prostaglandin E1 derivative, against that of etodolac, a nonsteroidal anti-inflammatory drug (NSAID), in improving the health-related quality of life in patients with symptomatic lumbar spinal stenosis.[22] In a randomized, controlled trial, 66 patients suffering from central stenosis with acquired, degenerative lumbar spinal stenosis, along with neurogenic intermittent claudication and bilateral leg numbness related to the cauda equina, were administered a daily dose of limaprost (15 μg) or etodolac (400 mg) for 8 weeks. The results indicated that limaprost was more effective than etodolac in improving patients' physical functioning, vitality, and mental health, and in reducing pain and leg numbness.

Treatment for degenerative spondylolisthesis may include bracing and facet or epidural steroid injections, along with the above-mentioned physical therapy approach.

The goal of medication in care of spondylolysis or spondylolisthesis of any type is to mitigate pain. NSAIDs are used most commonly while narcotic analgesics are used for breakthrough pain.

Class Summary

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Ibuprofen (Ibuprin, Motrin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Naprosyn, Naprelan, Anaprox, Aleve)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.

Etodolac (Lodine, Lodine XL)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclo-oxygenase, which results in decreased formation of prostaglandin precursors, which in turn results in reduced inflammation.

Sulindac (Clinoril)

Decreases activity of cyclo-oxygenase and in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain.

Acetaminophen (Tylenol, Feverall, Tempra, Aspirin Free Anacin)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Hydrocodone and acetaminophen (Vicodin, Lortab, Norcet, Lorcet-HD)

Drug combination indicated for moderate to severe pain.

See the list below:

• Because risk of progression exists in younger patients with isthmic or congenital spondylolisthesis, obtain serial radiographs on a semiannual basis to rule out the possibility of progression if symptoms are persistent.

See the list below:

• Anti-inflammatories and other analgesics are the only medications used in the care of patients with spondylolysis or spondylolisthesis.

See the list below:

• Prevention of isthmic spondylolisthesis may be difficult in athletes who must perform repetitive activities requiring hyperextension.[12] The best prevention is to avoid repetitive hyperextension if at all possible, since this activity appears to place athletes at the greatest risk.

See the list below:

• The most common complication of spondylolisthesis of any type is nerve root impingement/radiculopathy at the level of spondylolisthesis. Spinal stenosis and cauda equina syndrome may occur when a significant slip has occurred.

• Disk degeneration occurs at the level of the spondylolisthesis faster than at other levels of the spine, increasing the risk of diskogenic low back pain.

In general, patients with grade 1 or grade 2 isthmic slips do quite well with conservative management. Patients may return to play once they are asymptomatic. A flexion-based home exercise protocol is vital. Overall long-term outcome is quite favorable, specifically with lower grades of listhesis not accompanied by neurologic impairment.

A literature review by Overley et al found that among adolescent athletes with symptomatic spondylolysis but without spondylolisthesis, rate of return to play after nonoperative treatment was 92.2%, compared with 90.3% after surgical management.[23]

A study by Tatsumura et al found that in patients of high school age or below with lumbar spondylolysis who underwent conservative treatment, the vertebral lesions had a 76.2% union rate. More specifically, in unilateral cases, in which only one side of the vertebra was affected, the union rate was higher than in bilateral cases, at 95.8% versus 75.5%, respectively.[24]

A study by Yamazaki et al indicated that in pediatric and adolescent athletes with spondylolysis, the likelihood of bone healing is negatively impacted by a high defect stage, a high contralateral pars interarticularis defect stage, and poor flexibility. For example, for very early stage contralateral pars interarticularis defect, the bony-union rate was 84.2%, compared with 37.1% for the progressive stage.[25]

Higher grades of isthmic spondylolisthesis have a variable prognosis with regard to persistent low back pain. Surgical intervention does provide nice improvement in claudication or radicular symptoms. Diskogenic pain may produce more persistent lower lumbar discomfort.

Patients with degenerative spondylolisthesis seem to have persistent waxing and waning pain originating from the facet joints. Surgical decompression for neurologic compromise has a high rate of success in relieving lower extremity symptoms. A literature review by Joaquim et al indicated that in degenerative lumbar spondylolisthesis, decompression alone, without instrumented fusion, may be a useful treatment in some patients. The data suggested, however, that long-term outcomes may be better with fusion. The investigators suggested that isolated fusion may not be suitable in patients with a facet angle of greater than 50°, a disk space of greater than 6.5 mm, low back pain (in contrast to lower extremity symptoms), hypermobility at the listhetic level (>1.25-2 mm) on dynamic radiographs, and resection of the posterior elements.[26]

A prospective, randomized, controlled trial by Inose et al reported that for low-grade (< 30%) degenerative lumbar spondylolisthesis, outcomes for decompression plus fusion or decompression plus stabilization were no better at 1- and 5-year follow-up than for decompression alone.[27]

However, a study by Haddas et al indicated that in patients with degenerative lumbar spondylolisthesis, decompression plus fusion surgery significantly improves stance stability. The investigators reported that following treatment, range of sway for the center of mass and head were reduced in the sagittal, coronal, and axial planes, with total sway for the center of mass and head also decreased. Nonetheless, total sway did not shrink to the levels of normal controls, and range of sway in the sagittal head was also greater than in controls.[28]

See the list below:

• Athletes involved in higher risk sports should be educated about the risk of developing a spondylolysis.[7, 8, 9, 11, 12, 10]

• Instruction regarding an appropriate home exercise program, including a flexion-based spine exercise protocol and hamstring stretching, should be a part of treatment.