Spondylolysis and Spondylolisthesis

“False facts are highly injurious to progress of science, for they often endure long; but false views, if supported by some evidence do little harm, for everyone takes a salutary pleasure in proving their falseness.”

—Charles Darwin

Spondylolysis

With the significant increase in sporting effort in high school athletes (“My son is the best linebacker in his high school’s history!”), there is an epidemic of spondylolysis. Up until recently, we have considered this condition a routine problem. More recently, with the use of computed tomography (CT) scanning and single photon emission computed tomography (SPECT) scanning, it has been found that the condition is far from routine, and it is difficult to be dogmatic with regard to the criteria for diagnosis and treatment.

Etiology of Spondylolysis

The classic teaching of causation for spondylolysis has been that an individual is born with a weakness in the pars interarticularis, and at approximately age 6, a fatigue injury occurs that breaks the pars (7). Later, in high school, with the weightlifting and contact stresses of football or the extension stresses of gymnastics or wrestling, the latent fracture is irritated and becomes symptomatic.

Another group of teenagers exists who present with an acute lesion. They have no history of injury, and they suffer a significant hyperextension injury or compressive force to their lumbar spine, which is followed by the immediate and sudden onset of very severe low back pain. Radiographs reveal a fresh fracture, and these patients have a very hot bone scan (Fig. 6-1) (10). These patients are in the minority and represent a special treatment situation.

Finally, remember that 5% of the general population walks around with a spondylolysis that is completely asymptomatic (10). Spondylolysis may be unilateral in up to one third of these patients.

Clinical Presentation

A wide spectrum of presentations exists in these young patients, ranging from an acute disabling episode of back pain to mild low back discomfort when the patient engages in certain activities. The back pain may be dominant to one side, but more often is across the lumbosacral junction. Radiating leg pain is rare in spondylolysis, but hamstring tightness on straight leg raising testing is common. Neurologic symptoms and signs are absent.

FIGURE 6-1 A: Axial CT of spondylolysis, L5. B: Bone scan in same patient showing bilateral “hot” pars interarticularis (arrow).

FIGURE 6-2 A: Schematic of oblique view of spondylolysis (arrow). B: Note how lesion looks like a collar on a Scottish terrier.

Radiographic Findings

The radiographic findings have no set pattern. Although most teenagers will have a defect that is seen on oblique radiographs (Fig. 6-2), enough negative oblique radiographs occur (Fig. 6-3) to require additional radiologic investigation in a young patient with unexplained mechanical back pain.

Additional investigative steps include a SPECT scan (Fig. 6-4) and a CT scan (Fig. 6-5). Experience has shown us that there is no pattern to the findings in these three tests (oblique lumbar radiographs, SPECT scan, and CT scan). You can almost pick whichever combination you wish: for example, positive oblique radiographs/negative SPECT and CT; negative oblique radiographs and SPECT/positive CT; positive oblique radiographs, SPECT, CT; and so on. In addition, the CT scan findings are by no means uniform (Fig. 6-6).

Level of Lysis

The majority of spondylolytic lesions occur at L5, but a few will be present at higher lumbar levels.

Treatment

After many years of programmed treatment (e.g., a hot bone scan means a fresh fracture that must be immobilized), we have reduced our advice to two rules for two different groups of patients:

If the patient has low back pain and any one of the three tests is positive, take the patient out of the sport, put them in exercise physical therapy, and brace them. When they become asymptomatic, they join Group 2.
If the patient has no symptoms, do not restrict activities and do not brace them (or take them out of a brace), despite the results of radiographs, bone scan, and CT scan.

Unfortunately, many young persons fall between these two groups and require some form of activity restriction, therapeutic exercise, and bracing. The real problem comes when trying to determine the duration of treatment. Remember, “my son is the best linebacker in his high school’s history,” which is a statement usually associated with an important game in the near future at which all the college scouts will be in attendance! In this pressure situation of having to treat the patient/parent team, do what is best for the patient. If the patient is asymptomatic, let them play regardless of the investigation results. If the patient is symptomatic, restrict activities (regardless of the investigation results).

FIGURE 6-3 A: An oblique radiograph of an adolescent who, after a football injury, developed low back pain; there is no apparent fracture. B: CT scan done at the same time showing bilateral pars defects (arrows). C. The reverse gantry angle technique used to show defect in B.

FIGURE 6-4 SPECT of spondylolysis (arrow)

FIGURE 6-5 A CT scan of an old lysis (L5 bilateral).

FIGURE 6-6 Compare this CT of spondylolysis to Figures 6-5 and 6-3; each scan shows a different fracture pattern.

Specific Treatment of Spondylolysis

Conservative Treatment

Patients are treated with modalities and a flexion exercise program. Once symptoms start to improve, a generalized conditioning program and specific equipment-based exercises are instituted to strengthen the low back. During this program, the patient is abstaining from the aggravating activity (sport), which in itself may be the most important treatment step.

On relief of symptoms, the patients gradually return to sports. The most difficult aspect of judging the rate of return to sports is to balance what a stoical teenager who wants to “mix it up” with his or her peers is telling you about ongoing symptoms with what you, the treating physician, observe on examination.

Surgical Treatment

It is rare that a young patient cannot improve with conservative treatment. In these situations, direct surgical repair of the defect can be considered. Figure 6-7 shows the various ways of accomplishing this repair.

FIGURE 6-7 A: Axial view of repair of spondylolysis with wire around spinous process and transverse processes. B: Sagittal view of the same repair.

FIGURE 6-8 This is the CT scan of the same patient in Figure 6-3, 5 months later; the patient experienced no pain and was playing sports. The pars interarticularis fractures are still obvious.

Follow-Up

On follow-up, plain radiograph, and CT scan, we have seen a minority of these lesions heal despite the patient becoming asymptomatic (Fig. 6-8). We simply follow up these patients every 6 months to a year with a standing lateral lumbar spine radiograph. If they start to develop a slip (spondylolisthesis), we become more aggressive with treatment intervention.

Spondylolisthesis

Forward slip of the fifth vertebra is resisted by the bony locking of the posterior facets, the intact neural arch and pedicle, normal bone plasticity preventing stretch of the pedicle, and the intervertebral discs bonding the vertebral bodies together (Fig. 6-9). Breakdown of this normal locking mechanism occurs with articular defects and defects in the neural arch. These pathologic defects produce five recognizable clinical groups of spondylolisthesis (6) (Tables 6-1 and 6-2): dysplastic, isthmic, degenerative, traumatic, and pathologic.

Description of Spondylolisthesis on Radiograph

Before describing the various types of spondylolisthesis, it is best to understand the terms used to measure the extent of the vertebral body slip.

The classic measurement of the slip degree has been that of Myerding (4), an obstetrician who described four degrees of slip (Fig. 6-10) (Grade 1 = 25%, Grade 2 = 25% to 50%, Grade 3 = 50% to 75%, and Grade 4 = 75% to 100% slip). A complete dislocation of L5 on S1 (Fig. 6-25) was called a spondyloptosis.

Wiltse and Winter (8) proposed a more sophisticated group of measurements (Fig. 6-11). The reason for this was to separate the tangential movement in the low-grade slips (Grades I and II) from the angular/tangential slips that occurred in the higher levels of slip. In fact, this more complete classification has served to point out that the low-grade slips behave like degenerative disc disease, and the high-grade slips are more like a spinal deformity that requires a whole new set of management principles. This distinction is covered in the following sections.

FIGURE 6-9 The normal locking mechanisms resisting forward displacement of the fifth lumbar vertebral body. (From Macnab I. Backache. Baltimore: Williams & Wilkins; 1977:45 with permission.)

TABLE 6-1 Working Classification of Spondylolisthesis

	Etiology
Bony Location of Defect	Congenital	Acquired
Pars	Isthmic (fatigue fracture)	Traumatic fracture
Facet joint	Congenital absence or dysplasia	Degeneration of facet joint
Bone	0	Weak or ‘plastic’ bone

TABLE 6-2 Commonly Accepted Clinical Classification of Spondylolisthesis

Type	Classification	Description
I	Dysplastic	Congenital abnormalities of upper sacrum or arch at L5
II	Isthmic	Lesion in pars interarticularis Lytic—fatigue fracture Elongated but intact pars Acute fracture
III	Degenerative	Facet joint degeneration
IV	Traumatic	Fractures in areas of arch other than pars
V	Pathologic	Secondary to generalized or localized bone disease

FIGURE 6-10 Myerding (4) classification of slip grades, which divides the sacrum into “quarters.” This is a drawing of a Grade II slip.

Type I Congenital or Dysplastic Spondylolisthesis

Congenital spondylolisthesis with forward displacement of a vertebral body at birth is a clinical curiosity. The spinal defect is usually only one of multiple congenital anomalies, and the clinical problem presented is not the management of the spondylolisthesis but the management of the associated congenital scoliosis.

In a true dysplastic spondylolisthesis, the lesion may be either dysplasia of the upper sacrum, specifically in the facet joints (Fig. 6-12), or an attenuation of the pars interarticularis that gets pulled out and thinned as though it were made of a malleable plastic (Fig. 6-13). As the slip increases, and as the pars interarticularis becomes increasingly stretched, it may eventually break, but this break is secondary to the slip and is not the cause of the slip. This concept represents a slight deviation from the Wiltse-Newman-Macnab classification (6), the reason for which is explained in the

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