Summary of Key Points
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Degenerative thoracolumbar scoliosis is the most common etiology of adult spinal deformity and is caused by asymmetric disc degeneration and displacement of anatomic axial load distribution.
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Indications for spinal deformity correction include (1) refractory mechanical back pain, (2) rapid curve progression, (3) decompensation and loss of sagittal and coronal balance, (4) neurologic deficit, (5) gait disturbance, and (6) inability to perform activities of daily living.
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Goals of surgical deformity correction include (1) restoration of coronal and sagittal balance to reduce mechanical back pain, (2) elimination of pathologic motion by segmental fusion, (3) decompression of the neurologic elements to address neurogenic claudication and radicular pain, (4) prevention of deformity progression or replication of spinal deformity, and (5) restoration of cosmesis.
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Coupling (whereby one movement of the spine about or along an axis obligates another, compensatory movement about another Cartesian axis) contributes to the rotational deformity often encountered in multiplanar thoracolumbar spinal deformities.
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Cantilever forces created by modern, posterior-only pedicle screw-rod constructs with apical derotation maneuvers allow for correction of a multiplanar deformity that respects both the anatomic sagittal and coronal planes and restores harmony among the spinopelvic parameters all the while largely obviating the need for a ventral release.
Degenerative scoliosis is the most common cause of scoliosis in the adult. It develops de novo during and is largely due to asymmetric disc degeneration; the resultant curve has even been referred to as a “discogenic curve.” Additionally, osteoporosis and associated compression fractures may alter a patient’s overall spinal biomechanics and accelerate the degenerative processes, particularly in the thoracolumbar spine, often observed in cases of adult spinal deformity. The apex of degenerative scoliosis curve is most often present at either L2-3 or L3-4. Its extent, as discussed in detail later and as documented by radiographic imaging studies, does not necessarily correlate with symptoms or neurologic deficits, a fact that presents a significant dilemma to the treating physician. Management options are complicated by the wide variety of treatment strategies; algorithms to assist spine surgeons in clinical decision making are only recently taking shape.
When operative intervention is considered, the goals of surgery must be clearly delineated and based on all relevant clinical factors: overall spinal balance, bone health, neurologic symptoms, and medical comorbidities. Surgery is indicated in lumbar degenerative rotatory scoliosis for one of three reasons: segmental instability, neural compression, or spinal imbalance.
Instability can take many forms, ranging from mechanical low back pain to overt deformity or frank pathologic motion under normal physiologic loads. Instability usually manifests through pain of a mechanical nature—pain that is deep and agonizing and is worsened by activity (loading) and improved by rest (unloading). Loss of integrity of the lumbar spinal motion segment to tolerate physiologic loads affects the spine in all planes, which explains the common finding of multiple contributing pathologies being present in a single patient. These deformities are coupled by the asymmetric degeneration of the intervertebral disc and may manifest as spondylolisthesis, oligolisthesis, and fixed sagittal imbalance in addition to the scoliosis.
The treatment for neural compression is often surgical decompression; the treatment for instability is joint immobilization; and the treatment for imbalance is deformity correction. Neurogenic claudication (a neurologic syndrome) does not respond to spinal fusion alone. Conversely, mechanical low back pain does not respond to laminectomy alone. One must separate these clinical manifestations carefully so that surgical management can be tailored specifically to the patient’s complaints and to his or her structural pathology.
As we age, our spines “loosen” somewhat until midlife. Then, at about the age of 55, the degenerative process accelerates, and spinal stiffening occurs (i.e., spine re-stabilization). This stiffening process, although associated with spinal degeneration and spinal deformity, leads typically to a progressively more stable spine. Therefore, this scenario, which is the rule rather than the exception, should mandate a conservative, nonsurgical, approach in the majority of patients. For example, even with significant spinal deformity, a patient with neurogenic claudication may be best managed by a focal, technically sound, pedicle-to-pedicle decompressive operation as opposed to an instrumented deformity correction.
Finally, methods of deformity correction are described in this chapter. Adjuncts to this aspect of the management of degenerative rotatory scoliosis—such as ventral “release” procedures or orthotic management—are not. In the clinical scenarios presented in this chapter, it is assumed that the patient has a symptomatic and mechanically unstable spinal deformity and that adjuncts to surgical intervention have been undertaken when appropriate.
Pathophysiology of Disc Degeneration and the Spondylotic Process
Lumbar spondylosis is not a pathologic process; it is but a manifestation of the wear and tear associated with aging and, more specifically, is the consequence of repetitive axial and translational loading. It is defined as vertebral osteophytosis secondary to degenerative disc disease and is not an inflammatory process. Noninfectious inflammatory processes are grouped together as arthritides and are excluded from this discussion.
Spondylosis and associated osteophytosis are universally accompanied by degeneration of the intervertebral disc. The intervertebral disc is an amphiarthrodial joint (no synovial membrane) with particular traits that result in a characteristic degenerative pattern. Conversely, arthritides classically involve the synovial membranes of diarthrodial joints (joints lined with synovium and lubricated with synovial fluid, such as facet joints). Facet joints, however, are also affected by the spondylotic process.
The degenerative process primarily involves the disc interspace and alters intradiscal dynamics that result in spinal deformity. The resultant excessive motion and stresses cause extradiscal soft tissue proliferation. Finally, focal spinal deformity predisposes to more extensive regional and global deformity (see the section titled “ Osteoporosis ”). Osteoporosis contributes to the latter process, with its resultant asymmetric vertebral body collapse.
Intradiscal Dynamics
Chronically elevated intradiscal pressure causes disc interspace narrowing (collapse), distorting the anulus fibrosus and the facet joint capsule. This in turn accelerates the degenerative process. If disc space degeneration progresses asymmetrically in the coronal plane, then the precursor to a scoliotic deformity takes shape.
The water content of the disc interspace gradually decreases throughout life, which contributes to alterations in the chemical and anatomic makeup of the disc. Fibroblasts become defective, and the desiccated disc is less effective as a cushion. Fissures then develop in the cartilaginous end plates. Schmorl nodes are manifestations of this pathologic process. Gas may accumulate in the disc (the vacuum phenomenon). An in-growth of fibrocartilage (mucoid degeneration) with obliteration of the nucleus fibrosus ensues. Relative incompetence of the disc itself and relative instability result, and anulus fibrosus bulging occurs as a result of this process.
Disc Deformation
Bulging of the anulus fibrosus results in periosteal elevation and subperiosteal bone formation. Spondylotic ridges (osteophytes) are laid down, and this can result in spinal canal encroachment. These ridges occur most commonly on the concave side of a curvature. Therefore, natural cervical and lumbar lordosis predisposes the spine to osteophyte formation toward the spinal canal, causing spinal canal encroachment. The thoracic region, by virtue of its intrinsic kyphotic posture, is relatively spared this process.
Form follows function, even during the process of degeneration. Therefore, osteophyte formation occurs predominantly on the concave side of a scoliotic curvature (where anulus fibrosus bulging is most significant), whereas disc herniation occurs commonly on the convex side of a spinal bend. The thin dorsal anulus fibrosus and relatively weak lateral aspect of the posterior longitudinal ligament combine with the migratory tendencies of the nucleus pulposus to encourage dorsolateral disc herniation.
In the laboratory, three mechanical forces are required for the creation of a herniated lumbar disc: (1) flexion (causing dorsal nucleus pulposus migration), (2) lateral bending away from the side of disc herniation (causing lateral nucleus pulposus migration), and (3) application of an axial load (causing an increase in intradiscal pressure). A degenerated disc is also necessary as a predisposing factor. This complex loading pattern results in the application of tension on the weakest portion of the anulus fibrosus (the dorsolateral position, the location of the herniation), migration of the nucleus pulposus toward this position, and an asymmetric increase in intradiscal pressure. The age-related increased frequency of anulus fibrosus tears and a peaking of nucleus fibrosus pressures in people 35 to 55 years of age also predispose to an increased incidence of disc herniation. Asymmetric collapse of the disc interspace is often a result of the disc degeneration process and places asymmetric focal stresses on portions of the spine.
Extradiscal Soft Tissue Involvement
Hypertrophy and buckling of the ligamentum flavum, as well as other soft tissue proliferative processes, can result in spinal canal encroachment. Excessive pathologic segmental motion predisposes to this process and is a major factor related to the development of spinal stenosis.
Osteoporosis
Osteoporosis leads to a decrease in bony integrity, and this in turn leads to vertebral body collapse. The presence of thoracic kyphosis predisposes the thoracic spine to ventral vertebral body collapse, whereas asymmetric disc interspace collapse (which is commonly associated with degenerative disc disease) predisposes to lateral vertebral body collapse. As the overall coronal and sagittal spinal balance worsens, the load shifts to more lateral and ventral supporting elements of the spine, respectively. This load displacement is progressive, subjecting the spine to progressively longer moment arms. Therefore, deformity begets deformity and creates a vicious cycle that perpetuates more regional and global spinal deformity. Patients will often seek medical attention when the compensatory spondylotic processes have narrowed the spinal canal or the spine has become so immobile that the patient can no longer compensate for the spinal imbalance.
Spinal Configuration
All aspects of spinal alignment should be considered prior to determining the appropriate surgical approach. The thoracic and lumbar regions are affected differently in this regard. Thoracic disc interspace height loss occurs predominantly in the ventral aspect of the disc resulting in progression of the natural kyphotic deformity as the degenerative process ensues. The rib cage, however, substantially stabilizes the thoracic spine. Pathologic thoracic instability is rarely observed and is usually associated with either spinal metastases or trauma.
The coupling phenomenon (whereby one movement of the spine about or along an axis obligates another movement about or along another axis) plays a significant role in the development of degenerative spinal deformity in the lumbar region (whereas it is of minimal significance regarding degenerative deformities in the thoracic region). This is because thoracic degenerative deformities are often oriented in the sagittal plane, whereas degenerative lumbar deformities are usually oriented in the coronal plane (excluding degenerative lumbar spondylolisthesis). The absence of uncovertebral joints (in contrast to the cervical region) and the sagittal orientation of the facet joints (in contrast to the cervical and thoracic regions) create a situation that causes obligatory rotation of the spine in response to lateral bending (coupling) and, commonly, a loss of normal lumbar lordosis. The progression of lateral bending deformities in the lumbar spine (scoliosis) thus predisposes to rotation of the spine ( Fig. 153-1 ), and the influence of an uncompensated thoracic kyphosis predisposes the lumbar spine to greater “flattening” or loss of the normal lordotic curve.
Not all scoliotic curves are symptomatic, as patients may be able to compensate for these deformities by “rebalancing” the spine through other skeletal structures, such as increasing their pelvic tilt. When one’s pelvis is maximally retroverted and can no longer compensate for a progressive deformity, then the subsequent displacement of the load causes worsening of the curve that caused it in the first place. Therefore, lateral bending deformation predisposes to lateral bending deformity progression in the lumbar spine, as the presence of kyphotic deformation predisposes to the progression of kyphotic deformity in the thoracic spine. As described previously, asymmetric loss of height of the lumbar intervertebral disc may progress to an asymmetric collapse of the vertebral body. As this scoliotic deformity progresses, it is necessarily associated with spinal rotation, with the spinous processes rotating toward the concave side of the curve (coupling). The obligatory association of rotation and loss of lordosis with lateral bending (coupling) complicates lumbar corrective and spinal instrumentation surgery. Transverse process exposure and dissection can cause injury to underlying nerve roots because of the relative dorsal migration of the root with respect to the transverse processes. Neuroforamina are considerably smaller on the concavity, and the neural structures within the spinal canal will naturally “hug” the lateral wall of the concave curve. This heightens the risk of neurologic injury during placement of instrumentation along the concavity. Therefore, care must be taken both during surgical exposure of the lumbar transverse processes and during placement of spinal instrumentation and subsequent correction.
Operative Treatment
The operative treatment of scoliosis is reserved for patients with refractory pain due to their scoliosis curve, significant curve progression, gait disturbance, and neurologic deficit all leading to a significant limitation of activities of daily living. Preoperative surgical planning should include adequate imaging, as was already mentioned.
All surgical candidates should not only undergo detailed radiographic spine imaging, but also should obtain a variety of complementary studies. A dual-energy x-ray absorptiometry scan (DEXA) can provide useful information about bone quality that may affect surgical planning. Patients with suspected pulmonary compromise should be sent for pulmonary function testing, although pulmonary compromise is rare in patients with Cobb angles of less than 80 degrees. Medical and cardiac risk stratification should be obtained. It should be noted that occult cardiac disease can be seen in adult scoliotic patients owing to severe deconditioning and the patient’s inability to experience exercise-related stress. Smoking cessation should be pursued and, given the increased risk of pseudarthrosis, it is not unreasonable only to pursue elective spinal deformity correction surgery in those patients who have quit smoking.
The current approach to the surgical treatment of scoliosis is primarily segmental pedicle screw and rod constructs. One report comparing hook-rod constructs and pedicle screw-rod constructs found that no pedicle screw patient required revision surgery for instrumentation-related complications and, overall, pedicle screw patients were 89% less likely to require revision surgery. These patients were also found to have better radiographic curve correction with maintenance of thoracic kyphosis, and pedicle screw-rod constructs often negated the need for ventral release surgery. However, hooks remain a valuable alternative when pedicle screws are contraindicated.
Goals of surgical correction of scoliosis are correction of coronal and sagittal balance to decrease pain, decompression of the neurologic elements, correction of balance so as to improve function, and restoration of cosmesis.
Deformity Correction
A variety of techniques can be used to correct lumbar spinal deformities. Deformity correction is accomplished via the application of rotatory or translational forces to the spine along one or a combination of the three axes of the Cartesian coordinate system. It is tempting to use distraction to reduce a compressive deformity, but this maneuver, particularly when undertaken in the lumbar spine, invariably introduces a kyphotic force that can be deleterious to maintaining the patient’s sagittal balance. Compression is preferable because of its favorable effects on sagittal contour and is especially useful when combined with interbody devices. Similarly, three- or four-point bending forces can be applied. Finally, bending moments can be applied in either the coronal or sagittal plane to correct spinal curvatures. Complex bending moment forces are often applied.
Methods of deformity reduction and maintenance of anatomic spinal alignment are discussed in this chapter. When indicated, ventral release procedures can provide the “relaxation” necessary to achieve the desired reduction. There is a growing sense that relatively minor curves in the well-balanced patient may be corrected through ventrolaterally placed interbody devices. Excessive deformity reduction for degenerative lumbar rotatory scoliosis is seldom necessary. Alleviation of symptoms (both for the short and the long term), not necessarily the attainment of a perfectly reduced spine deformity, is the goal of any surgical management scheme. Additionally, except for the presence of the surgical implant and minor residual curve, the spine should appear relatively normal and well balanced in both the coronal and sagittal planes.