and Spondylolisthesis in Athletes

Fig. 17.1

Three cases of spondylolysis from one family

In 1978, Haukipuro et al. reviewed the pedigrees of spondylolysis families and concluded that inheritance of lumbar spondylolysis is autosomal dominant [6]. Finally, Cai et al. [7] found a possible gene associated with spondylolysis. Future studies are likely to identify specific genetic alleles that predispose patients to pars fractures.

CT Stage Classification

A key component to the diagnosis and treatment of lumbar spondylolysis in our practice relies on CT stage classification . Figure 17.2 demonstrates the CT stages of lumbar spondylolysis [8, 9]. The heart of this classification relies on a baseline understanding of fracture healing. As the pars fracture develops, it will ultimately undergo changes that will lead to union or non-union. These unique stages in healing will lead to varying clinical presentations and treatments in patients with spondylolysis. Bone absorption is seen in the early stage and is demonstrated as an incomplete fracture on sagittal reconstruction CT scan. The progressive stage shows evidence of a complete fracture of the pars without sclerotic fracture margins. The terminal stage is equivalent to a pseudoarthrosis and demonstrates sclerotic fracture margins and blunting of the fracture edges.

../images/468535_1_En_17_Chapter/468535_1_En_17_Fig2_HTML.jpg — Fig. 17.2

CT stages of the pars fracture

In our classification schematic early- and progressive-stage defects are designated as acute pars fractures. These acute fractures still have the opportunity to form a bone union under the correct biomechanical circumstances. The terminal CT stage is classified as a chronic pars fracture, since it is a pseudoarthrosis. Once a fracture is in this stage, it will never progress to a union, and this influences management.

Early Diagnosis of the Pars Fracture

It is very difficult to diagnose the early stage using plain radiographs. For the accurate diagnosis of the early-stage defects, we have proposed two hallmark findings: bone marrow edema of the adjoining pedicle on MRI [3] and bone absorption at the caudal aspect on the sagittal reconstructed CT scan [10]. Figure 17.3 demonstrates a CT scan and T2-weighted MRI for a patient with the early-stage defect. Even though the fracture is not clear on CT (left panel), bone marrow edema in the adjoining pedicle is clear on MRI (right panel). We have found that assessment of these early-stage defects on CT scan is more readily identifiable on the sagittal reconstructed CT scan. In Fig. 17.4, we present three cases of the early-stage defects. As you can see, the pars fracture is most identifiable at the caudal aspect of the pars interarticularis. This area should be scrutinized on an adolescent presenting with back pain and a CT scan. This inferior aspect of the pars is especially vulnerable to stress fracture development due to the high concentration of mechanical stress during lumbar motion, which has been proven using the finite element analysis [10]. Technetium (Tc-99 m) single-photon emission CT often is used to identify acute lesions in athletes for whom the clinician has a high suspicion for spondylolysis in the setting of negative results on plain radiography, but this imaging modality can expose patients to high levels of radiation.

../images/468535_1_En_17_Chapter/468535_1_En_17_Fig3_HTML.jpg — Fig. 17.3

Early-stage defects with pedicle marrow edema

../images/468535_1_En_17_Chapter/468535_1_En_17_Fig4_HTML.jpg — Fig. 17.4

Sagittal reconstructed CT scans in the early-stage defect

Although MRI historically has not been recommended for detecting pars defects, more recent evidence suggests that specific sequences can enable successful detection in up to 98% of patients with pars defects. In totality, this information has led us to recommend MRI as the first-line imaging in a patient suspected of spondylolysis. Diagnosis of progressive and terminal stages of pars fractures is readily identified on advanced imaging, either MRI or CT scan. If the suspicion is still high for a pars fracture after a negative MRI, then a bone scan should be ordered.

Pain Mechanism

For each stage, the pain mechanism is different. Therefore, the goal of conservative treatment is also different. For the early and progressive stages, pain is due to an acute fracture, which is obvious on STIR-MRI as marrow edema and/or extra-osseous bleeding (edema) (see Fig. 17.3).

Figure 17.5 presents two cases that plainly illustrate the difference in the stage of fracture healing and therefore pain mechanism . The left pars in Case 1 and right pars in Case 2 can both be classified as the progressive stage. The CT scan shows a complete fracture without overt blunting of the fracture margins. The associated MRI findings are in the right panels. Once again, the left pars in Case 1 and right pars in Case 2 demonstrate marrow edema and extra-osseous edema consistent with the progressive stage. This is in direct contrast to the right pars in Case 1 and the left pars in Case 2 which demonstrate the radiographic characteristics of the terminal stage. In these pars, the fracture edges are clearly blunted on CT scan, and there is no marrow edema or extra-osseous bleeding. These images clearly show that although each patient has bilateral spondylolysis, the classification of each particular pars fracture can be unique. In the progressive stage, the edema indicates a more acute fracture that stands a chance at union. In the acute fracture, inflammation is the pain generator. The terminal stage has no edema, and the pain generator is communicating synovitis from pseudoarthrosis [13].

../images/468535_1_En_17_Chapter/468535_1_En_17_Fig5_HTML.jpg — Fig. 17.5

Painful defects on STIR-MRI [11, 12]

Figure 17.6 demonstrates the typical MRI findings of communicating synovitis in terminal-stage spondylolysis. Effusion is obvious in the defect and adjoining facet joints (yellow arrows). With conservative management , low back pain can be decreased, and the effusion due to synovitis can subside. The decreased effusion is obvious in the STIR-MRI taken 3 months after conservative treatment.

../images/468535_1_En_17_Chapter/468535_1_En_17_Fig6_HTML.png — Fig. 17.6

Communicating synovitis of facet joint (14-year-old soccer player, male)

Slippage Mechanism

Regarding slippage in spondylolytic spines (spondylolisthesis), it has been well reported that slippage is very common in children and adolescents and very rare after the skeletal maturation [14–16]. Seitsalo et al. followed 272 children with spondylolysis and found that in age groups of early puberty (girls, 9–12 years; boys, 11–14 years), slippage was likely to progress [15]. Our data is in good agreement with them [16]. We followed 46 pediatric patients aged under 18 years. The mean follow-up period was 6 years. We evaluated correlation between their skeletal age and progression of slip. As shown in Fig. 17.7, skeletal age of the spine can be evaluated by the condition of the secondary ossification center (SOC) of the vertebral body. In the cartilaginous (C) stage of the spine (Fig. 17.7, left panel), SOC is cartilage and cannot be seen on a plain radiograph. The SOC is ossified and is visible at the apophyseal (A) stage (Fig. 17.7, middle panel). Finally, the ossified SOC is fused to the vertebral body; and this defines the epiphyseal stage (Fig. 17.7, right panel). We reviewed the progression of spondylolisthesis to skeletal maturation. The most prevalent stage regarding slippage was found to be the C stage. From stage C to A, 80% of patients showed slip progression. On the contrary, after maturation, there were no slip progressions. Thus, surgeons should be cautious of slip progression in patients in the cartilaginous stage; this corresponds roughly to elementary school age.

../images/468535_1_En_17_Chapter/468535_1_En_17_Fig7_HTML.jpg — Fig. 17.7

Slippage with the skeletal age

The pathomechanism associated with slippage in the immature spine was analyzed by Sairyo and co-workers using calf [17, 18] and rat models [19, 20]. The growth plate in the immature spine is located between the vertebral body and the SOC. This area is a weak point and fails under the biomechanical stress experienced after spondylolysis. Figure 17.8 demonstrates the separation of the growth plate and the location of pediatric spondylolisthesis pathoanatomy. This explains why progression of the slip is common in children and adolescents. After skeletal maturation, the growth plate disappears; and the weak point for slippage also disappears.