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Isthmic Spondylolisthesis
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Starting from August 2007, we are performing all pedicle screw surgeries with the use of Inomed special instrumentation for pedicular screw monitoring.



A working knowledge of normal anatomy and the locking mechanism is helpful in understanding how and where the mechanism can fail. In the healthy person, the facet joint in the lumbar spine is, for the most part, in the coronal plane, with the inferior articular process of the superior vertebra located posteriorly and the superior articular process of the inferior vertebra located anteriorly. This configuration prevents forward movement of the vertebrae relative to each other. It locks in the superior vertebra relative to the inferior vertebra. This mechanism is important because the center of gravity of the human body is located anterior to the spine and exerts a forward slipping force on the spine, especially at the L5-S1 level. Furthermore, the anteriorly located center of gravity causes a rotating movement, with the axis of rotation oriented transversely at the L5-S1 level. Thus, in severe spondylolisthesis, a kyphotic deformity also develops. Simplistically, a vertebra (and the spine above it) may slip if abnormalities are present within the facets and facet joints, articular processes, or neural arch (i.e., connection between the facet joints and the vertebral body).
Various etiologies affect one or more locations.

Isthmic Spondylolisthesis

Earlier theories that isthmic defects were the result of separate ossification centres have been largely discredited. These theories were based primarily on irreproducible work that claimed the existence of two ossification centres for each side of the posterior vertebral ring. More recent findings support the theory that spondylolysis and isthmic spondylolisthesis probably result from a combination of genetic and mechanical factors. The increased prevalence of spondylolysis among  first-degree relatives of patients with isthmic spondylolysis or spondylolisthesis  strongly supports an inherited predisposition, although a definite pattern of transmission has not been identified. Similarly, the observation that spondylolysis is found more frequently among female gymnasts and college football players suggests that mechanical factors also play a significant role. The impact of mechanical factors is further supported by the failure of a review of non ambulatory patients to find cases of spondylolysis. Furthermore, photoelectric modelling experiments demonstrate that the peak mechanical stress of the lumbar spine is centered at the isthmus. Therefore, it is now generally accepted that these isthmic defects are the result of successive fatigue fractures that occur more easily in patients with a genetic predisposition.

These fatigue fractures lead to pathologic changes of the isthmus, facet joints, and intervertebral disc. The isthmic defect is usually surrounded by an acellular and avascular band of coarse fibrous tissue that resembles normal ligamentum but may incorporate zones of fibrocartilage, hyaline cartilage, or endochondral bone formation. Hypertrophy of the facet joints and alterations in the chemical composition of the intervertebral disc, specifically a reduction in proteoglycans and collagen types I and III occur secondarily. These factors operating between the L5 and SI vertebral segments contribute to symptomatology by encroaching on the intervertebral foramen on one or both sides and directly compressing the L5 nerve root or tethering the L5 nerve root by anchoring it to the anteriorly displaced vertebra.

The spondylolytic (isthmic) type is the most common cause of spondylolisthesis. It affects the region of the pars interarticularis, which is roughly the region of the junction of the pedicle and lamina, where the articular and transverse processes of the vertebrae arise. A defect at this point functionally separates the vertebral body, pedicle, and superior articular process from the inferior articular process and remainder of the vertebrae. Thus, the defect cleaves the vertebra into 2 parts. The portion of the vertebra posterior to the defect remains fixed, and the anterior portions are free to potentially slip forward relative to the posterior structures and spine below. Bilateral pars defects are needed to allow slippage.

Oblique projection radiograph usually shows the presence of bilateral pars defects (arrows), with an appearance resembling a Scottie dog with a collar. (The collar is the pars defect.) Established observations and factors relating to the development of this disorder are as follows: Apart from 1 reported case, humans are not born with a pars interarticularis defect. A congenitally dysplastic pars interarticularis, coupled with the stresses placed on the lumbar spine by upright (bipedal) posture with extension loading, appear to cause spondylolysis. A family history of spondylolysis and/or spondylolisthesis is commonly found. Upright posture places a continual downward and forward thrust on the lower lumbar spine, with the forces concentrating on the pars interarticularis. High-risk activities include gymnastics, rowing, tennis, wrestling, weightlifting, and football; all of these create mechanical stresses that play an important role in the development of spondylolysis. Placing such stresses on a weak pars results in a pars fracture. These microfractures heal with a false joint, a bony bridge across this portion of the arch, or fibrous bridging of the fracture. Most defects are believed to begin as a stress fracture that most likely persists because of continued motion (especially extension movements of gymnasts, which have been implicated in causing the fractures in the first place), which usually impairs bone healing. Some defects heal and may do so with elongation of the pars, representing healing of repeated microfractures. No diastatic defect is seen on radiographic imaging in such cases, but a spondylolisthesis does occur. A study by Fredrickson and colleagues showed a 4.4% incidence of spondylolysis and a 2.6% incidence of spondylolisthesis at age 6 years and a 5.4% and 4.0% prevalence, respectively, in adulthood. Note that once the pars defect has occurred, not all patients necessarily develop a spondylolisthesis. The largest degree of slippage occurred during the adolescent growth spurt. After skeletal maturity, slip progression usually is minimal and often is related to disk pathology, which more commonly occurs in patients with at least a grade 2 spondylolisthesis. The affected population shows a 2:1 male-to-female predominance. White men are affected more commonly than black men, and white women are affected more often than black women. A near 50% prevalence is found in Eskimos. Although males more commonly have the pars defect, females are more likely to progress to higher degrees of spondylolisthesis

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Degenerative Spondylolisthesis

Degenerative spondylolisthesis occurs in patients with chronic intersegmental spinal instability and underlying degenerative joint disease and is most frequently observed between the L4 and L5 vertebral segments. A number of anatomic variants thought to predispose to this instability have been identified. These variants include hypolordosis, sacralization of the L5 vertebral body, a rectangular L5 vertebral body, narrow L4 inferior articular processes, a low position of the iliac crests relative to the spine, and Sagittally oriented facet articulations. These variants are thought to secure the lumbosacral junction while amplifying the forces of body weight at the junction between the L4 and L5 vertebrae. Such forces result in degenerative changes at the articular facet joints that include joint capsular laxity, synovitis, cartilage fibrillation and degeneration, osteophyte growth, and fractures of the articular processes. Similarly, the intervertebral disc becomes dehydrated and fibrotic. Such changes lead to disc space narrowing and hypertrophic changes at the facet joints and vertebral endplates.

As with isthmic spondylolisthesis the L5 nerve root is most frequently injured. The pathologic process is now operating between the L4 and L5 vertebral segments, however. It may be compromised by a herniation of the L4- L5 intervertebral disc, by compression within the narrowed lateral recess, or by tethering across the posterior border of the L5 vertebral body with progressive anterolisthesis. With progressive anterolisthesis, the intact isthmus of the superior vertebra eventually comes to rest on the superior articular process of the lower vertebra, however, and slippage is generally limited to 30 percent.

The pars interarticularis is not affected by degeneration. As such, a pars interarticularis defect is not present. Long-standing intersegmental instability leads to degenerative spondylolisthesis. This may arise from other problems, such as disk degeneration or spondylolytic spondylolisthesis. Surgical laminectomy is another cause. Osteoarthritic changes develop in the facet joints. Eburnation and erosive changes occur, which may lead to abnormal alignment of the articular surfaces. Other factors include abnormalities of the ligamentous structures and intervertebral disk, such as loss of disk height. All of these combine to cause spondylolisthesis. Usually, the degree of spondylolisthesis is not great in this group. The L4-L5 vertebral space is affected 6-10 times more commonly than at other levels. Retrolisthesis may result from the degenerative factors in some individuals. This is a slippage in the posterior direction (opposite to an anterolisthesis). Black women are affected 3 times more commonly than white women. Degenerative spondylolisthesis usually occurs in patients older than 40 years.

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Congenital Spondylolisthesis

In the congenital (dysplastic) type, congenital anomalies of the vertebral arch and/or facets occur at the lumbosacral junction. Spondylolysis is excluded, as patients are not born with that lesion. Lesions in this category include dysplastic facets that may have an axial (horizontal) or sagittal orientation; lesions may occur as a result of the failure of vertebral body formation. The end result is that the facets do not lock in, and forward slippage is allowed. The pars may remain intact, develop poorly, elongate, or even lyse. Note that when an intact posterior arch accompanies forward slippage, potential exists for the arch to impinge on the cauda equina. Alternatively, spondylolisthesis of the L5 vertebra may cause S1 nerve root compression by the L5 vertebra inferior articular process.

The female-to-male predominance is 2:1.13 This type accounts for approximately 15-20% of cases of spondylolisthesis. Symptoms usually develop during the adolescent growth period. The facet joint is a synovial joint and is subject to the same osteoarthritic changes that affect other synovial joints in the body. Thus, loss of hyaline cartilage (which is eburnation of the joint surface) and reactive hypertrophic bony changes can lead to altered alignment of the facet joint, allowing spondylolisthesis.


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Traumatic Spondylolisthesis

Trauma in the development of a spondylolysis is discussed in Spondylolytic spondylolisthesis, above. Also, trauma can cause an acute fracture through a normal pars interarticularis and result in a diastatic defect that may lead to a spondylolisthesis. If immobilized, these should heal. Although fractures are also involved in the pathogenesis of the spondylolytic type, it is assumed that in the traumatic variety, pars is normal and that fractures occur as a result of excessive forces being applied upon the pars. In the spondylolytic variety, the pars fails under normal stresses (i.e., sustains stress fractures).

Traumatic forces may affect other parts of the spine and result in a spondylolisthesis. For instance, fractures may be seen in the articular processes or through the facet joints. Subluxation or dislocation (e.g., jumped facet) of the facet joint may occur. Associated ligamentous injury should always be considered; such injuries can occur if the traumatic force involves the disk, anterior and posterior longitudinal ligaments, interspinous ligament, supraspinous ligament, and the capsule and ligaments of the facet joints, causing facet-joint instability. Any one or more of these mechanisms may result in a spondylolisthesis.


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Pathologic Spondylolisthesis

Neoplasm or infection may involve the pars interarticularis, facets, or pedicles. Malignancy, such as metastasis from primary breast, prostate, and lung carcinoma, as well as myeloma, do occur in the posterior elements. Infections, such as blood-borne staphylococcal osteomyelitis, also occur.



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