eMedicine Specialties > Physical Medicine and Rehabilitation > Lumbar Spine Disorders

Lumbar Spondylolysis and Spondylolisthesis

Author: Beth B Froese, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Orthopaedic Associates of DuPage Ltd
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Updated: Jul 5, 2009

Introduction

Background

Kilian, Robert, and Lambl first described spondylolysis accompanied by spondylolisthesis in the literature in the mid 1800s. The number of different spinal abnormalities contributing to development of spondylolisthesis was appreciated only after Naugebauer's anatomic studies in the late 1800s. (See image below and Image 1.)

Pathophysiology

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 image below and Image 4.) Wiltse, Macnab, and Newman developed a classification to help outline causes of vertebral translation in an anterior direction.^1,2 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 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).³

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 image below and Image 5.)
• Grade 5: Greater than 100% slippage

Frequency

United States

Wiltse and Beutler each reported an incidence of 6-7% for isthmic spondylolysis.^1,4 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.^5,6,7,8 Gymnasts, linemen in college football, weight lifters, javelin throwers, pole-vaulters, and judoists are most commonly affected.^9,10  Approximately 82% of cases of isthmic spondylolisthesis occur at L5-S1. 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.¹¹ 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

• 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

• 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.⁴

• 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

• 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.

Clinical

History

• 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.

Physical

• 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.

Causes

• 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.¹²
• 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.

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