Lumbar Spondylolysis and Spondylolisthesis Clinical Presentation

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]