Anatomy, Pathophysiology, and Biomechanics

Lumbar and thoracic spondylosis, which can be broadly defined as degenerative destruction or remodeling of the bony elements of the spine, intervertebral discs, facet joints, and/or spinal ligaments, is a progressive age-related disorder. This degeneration secondarily affects the neural structures that are normally protected and supported by the ligamentous and bony elements of the spine as those same elements compress the spinal nerves and thecal sac. The anatomy of the thoracic and lumbar spine as it relates to this process is important not only for understanding the pathophysiology and clinical presentation but also for anatomically sound operative planning and execution. While an exhaustive review of thoracolumbar anatomy is beyond the scope of this chapter, certain anatomic relationships must be emphasized.

The progression of spondylosis in the thoracic and lumbar spine essentially occurs at three points anatomically: the intervertebral disc, the facet joints, and the ligamentum flavum. Each of these structures has its own contribution in a biomechanically intact spine. Therefore, subsequent spondylotic degeneration produces varying clinical pictures depending on the specific structure or combination of structures most involved.

The intervertebral disc is bound ventrally by the anterior longitudinal ligament, dorsally by the posterior longitudinal ligament, and rostrally and caudally by cartilaginous end plates that abut the vertebral bodies. The anulus fibrosus forms the outer ring of the disc and provides most of the structural integrity. A softer, notochord-derived nucleus pulposus forms the center portion of the disc and, although not as strong as the anulus, provides cushioning and some resistance, mainly to axial loads. With aging, the disc progressively desiccates and becomes less elastic, a process that has been termed disc degeneration. In the case of spondylosis, disc degeneration contributes to the overall pathology in several different ways. As the disc desiccates, a process that is demonstrable on MRI by loss of T2 signal (so-called dark disc disease) (Fig. 83-1), it has the potential, by virtue of its innervation by the recurrent sinuvertebral nerve, ventral rami, and rami communicantes, to contribute to back pain.¹ With the loss of hydration, the disc may become incapable of resisting physiologic biomechanical forces, resulting in failure by herniation through a defect in the anulus. This herniation may result in neurologic deficit and/or pain. Even in the absence of true herniation, a broad-based bulge may compress the neural elements, causing symptoms. Apart from symptomatology, the desiccated disc is no longer able to perform a portion of its biomechanical function in the normal movement of the spine. Other elements of the spine must therefore bear the resultant biomechanical stresses, potentially accelerating their degeneration.

FIGURE 83-1 Sagittal T2-weighted MRI of the lumbar spine illustrating advanced disc degeneration at L5-S1.

Facet joints in the thoracic spine and the lumbar spine are alternatively referred to as zygapophyseal or apophyseal joints. Because they oppose the neural elements, degeneration and hypertrophy may cause compression of spinal roots, the spinal cord, and the thecal sac of the lumbar spine. Each joint is composed of the superior articular process of the caudal vertebra and the inferior articular process of the rostral vertebra. The opposing surfaces are covered with synovium, while the outer surface is covered by fibrous capsule. The joints of the thoracic spine from the C7-T1 joint to the T9-10 joint are typically oriented in the coronal plane and assume a configuration not unlike that of shingles on a roof. The T10-11 joint is often a transition area where the joint orientation becomes slightly tangential to the coronal plane. The portion of the joint that is visible dorsally in the lumbar spine is mostly composed of the inferior articular process of the rostral vertebra; this is readily demonstrated with removal of the joint capsule. The superior articular process of the inferior vertebra forms the ventral and lateral portion of the joint. Because of its location directly adjacent to the exit point of the nerve root laterally and the thecal sac medially, the superior facet process often comprises the point of maximal compression when joint hypertrophy leads to neural compromise. Because innervation of the facets themselves is via medial branches of the dorsal primary rami, degeneration of the facets may produce back pain by this mechanism.^2–4

Signs and Symptoms

Radiculopathy

As was mentioned earlier in this chapter, thoracolumbar spondylosis may cause neural compromise by virtue of the location of both the thecal sac and nerve roots adjacent to structures that bear the brunt of the degenerative process. When nerve roots are compromised, radiculopathy may result.

The underlying pathophysiology of radiculopathy is most likely multifactorial. Direct mechanical compression of a nerve root certainly plays some role in the generation of radiculopathy, particularly as removal of the offending lesion frequently results in marked improvement in symptoms. In the lumbar spine, this compression most commonly occurs in the lateral recess and affects the nerve root exiting the next most caudal neural foramen (Fig. 83-2). Thus, a paracentral herniation at L4-5 most commonly affects the L5 nerve root exiting the L5-S1 neural foramen. However, while it is intuitive that a herniated thoracic or lumbar disc causes pain by direct mechanical compression or stretch on the nerve root, many patients have disc pathology that abuts or compresses the neural elements without associated radicular symptoms. Disc material is both immunogenic and inflammatory.^5,6 Animal models have demonstrated that nucleus pulposus material causes an inflammatory reaction and a demonstrable increase in reactive cytokines. Tumor necrosis factor alpha has been proposed as a possible underlying inflammatory factor.^7–10 Both processes have been implicated in symptom generation.

FIGURE 83-2 Axial T2-weighted MRI of the lumbar spine illustrating a left paracentral disc herniation at L4-5, causing compression of the left L5 nerve root.

Radiculopathy is not always the result of disc pathology. As the thoracolumbar facet joints hypertrophy as the degenerative process progresses, compression of the ventrally lying nerve roots may occur. This compression generally occurs in the aforementioned region directly adjacent to the exit point of the nerve root laterally and the thecal sac medially, termed the lateral recess (Fig. 83-3). The ligamentum flavum may also hypertrophy, contributing to this compression.

FIGURE 83-3 Axial T2-weighted MRI of the lumbar spine illustrating narrowing of the lateral recesses (arrows) due to facet and ligamentum flavum hypertrophy.

Correlative Diagnostics

In general, back pain in the absence of trauma, infection, or possible malignancy, without neurologic symptoms, does not require imaging. The presence of myelopathy, radiculopathy, or claudication symptoms merits diagnostic workup in most instances. Often, in the current era, the first test ordered is MRI without contrast. In the thoracic spine, findings of spinal cord compression are often associated with intervertebral disc herniation. This produces narrowing of the spinal canal and in more advanced disease may demonstrate hyperintensity within the parenchyma of the spinal cord on T2-weighted images. High signal on T2-weighted images is associated with spinal cord injury in the acute care setting; in the outpatient setting, this finding is associated with myelopathy. Ligamentum flavum hypertrophy and facet joint arthropathy that commonly appear on lumbar spine imaging in the setting of spondylosis are often absent in the spondylotic thoracic spine. This may be due to the fact that the thoracic spine is far less mobile than the lumbar spine. Thus, a desiccated thoracic disc does not necessarily cause a reactive hypertrophy of ligaments or joints.

MRI findings in lumbar spondylosis generally differ from those in thoracic spondylosis. Degeneration, as was mentioned earlier in the chapter, may be associated with disc herniation, ligamentum flavum hypertrophy, and facet joint hypertrophy. The summation of these pathologic tissue responses may cause stenosis of the spinal canal in the midline or lateral recesses of the canal (Figs. 83-4 and 83-5). Facet hypertrophy, ligamentum flavum hypertrophy, or broad-based disc bulges (Fig. 83-6) may also contribute to stenosis of the central canal, lateral recesses, or foramina. Extraforaminal disc herniations may cause compression of the exiting nerve root lateral to the neural foramen (Fig. 83-7). As spondylosis progresses and joint arthropathy worsens, increased fluid within the facet capsule itself or the presence of synovial cysts associated with the joints may contribute to compression of the thecal sac and/or nerve roots (Fig. 83-8). In the absence of frank instability, these findings may also portend the development of instability following surgical decompression without stabilization.

FIGURE 83-4 Sagittal T2-weighted MRI of the lumbar spine illustrating central stenosis at L2-3, L3-4, and L4-5.

FIGURE 83-5 Axial T2-weighted MRI of the lumbar spine illustrating central and lateral stenosis.

FIGURE 83-6 Axial T2-weighted MRI of the lumbar spine illustrating central stenosis secondary to a large midline disc herniation.

FIGURE 83-7 Axial T2-weighted MRI of the lumbar spine demonstrating an extraforaminal disc herniation at L4-5 on the left (arrow).

FIGURE 83-8 Axial T2-weighted MRI of the lumbar spine demonstrating a large synovial cyst at L4-5 on the right (arrow).

Typically, patients with lumbar spondylosis will undergo plain radiographic imaging of the affected area prior to or as a part of their initial evaluation. Most often, anteroposterior (AP), lateral, flexion, extension, and oblique images are obtained. Findings on AP and lateral radiographs include loss of disc space height, osteophyte formation, and possibly spondylolisthesis (Fig. 83-9). Flexion-extension films are used to assess the movement of the spine in sagittal plane rotation and AP translation, typically to evaluate for excessive translation. In the presence of a defect in the pars interarticularis, oblique radiographs demonstrate discontinuity of the pars (Fig. 83-10). In the presence of lumbar or thoracic spondylosis, attention should also be paid to the alignment of the spinal column as a whole, specifically regarding the presence of scoliosis, kyphosis, or any associated aberration of coronal or sagittal balance.

FIGURE 83-9 Lateral radiograph of the lumbar spine demonstrating a degenerative spondylolisthesis at L4-5 with disc degeneration at L5-S1.

FIGURE 83-10 Oblique radiograph of the lumbar spine demonstrating a fracture of the pars interarticularis of L5 (arrows).

CT may also be a valuable adjunctive imaging modality in the presence of spondylosis. In patients with questionable bony anatomy, CT may help to define difficult or otherwise obscured anatomic relationships (Fig. 83-11). CT combined with myelography may be particularly helpful when metallic implants from prior surgical procedures obscure the relevant anatomy on MRI or when implanted medical devices prevent the safe acquisition of MRI. CT may also provide invaluable information about pedicle diameters and angles when the placement of spine instrumentation is under consideration. This is particularly important in the thoracic spine, where midthoracic and upper thoracic pedicles may be so small as to prohibit the safe placement of transpedicular instrumentation. It is likewise important in patients with known spondylolysis and spondylolisthesis, in whom CT may demonstrate very small pedicles at the affected level, especially if the listhesis is high grade and long-standing.

FIGURE 83-11 Axial CT of the lumbar spine demonstrating bilateral fractures of the pars interarticularis of L5 (arrows).

Treatment

The management of lumbar spondylosis must be individualized, as many patients have some combination of disc disease, facet hypertrophy, and ligamentum flavum hypertrophy, with or without spondylolisthesis. In many instances, however, treatment may be based on the predominant pathology.

In patients with radiculopathy and minimal weakness from a lumbar disc herniation, a course of medical management including physical therapy, muscle relaxants, nonsteroidal anti-inflammatory medications, and neuropathic pain medication can provide relief. Some patients may obtain relief from epidural steroid injections as well, although data are conflicting and this therapy does not work as well for back pain.^14–16 Patients with acute intractable pain, cauda equina syndrome, or progressive neurologic deficit should be treated with surgery. Surgical treatment of disc herniation with radiculopathy has been the subject of much debate. The well-publicized Spine Patient Outcomes Research Trial was hailed as a definitive study demonstrating similar outcomes for surgical and nonsurgical treatment of lumbar disc herniation causing radiculopathy. However, statistical analysis did not account for crossover and other factors that decreased its validity and the weight of its findings.^17–19 Therefore, while the statistically robust intent to treat analysis showed no advantage of surgical treatment over nonsurgical treatment, the as-treated analysis showed a substantial advantage of surgical treatment over nonsurgical treatment.

In the case of lumbar spinal stenosis, oral agents have not been found to be effective in treating the typically present claudication symptoms, and insufficient evidence exists regarding physical therapy.²⁰ Epidural steroids may be of benefit for temporary relief.²⁰ Although the data are limited, patients who are treated nonsurgically with these measures may require surgery 20% to 40% of the time. Of those who do not require surgery, 50% to 70% can expect to have improvement in their pain symptoms with time.²⁰ Further study that was performed as a part of the aforementioned Spine Patient Outcomes Research Trial demonstrated an improvement in outcome for surgical treatment of symptomatic lumbar stenosis when compared to standard nonsurgical treatment.²¹

Regarding the management of lumbar spondylolisthesis with resultant stenosis, surgical treatment is indicated in patients with instability on flexion and extension radiographs or symptoms of stenosis that are recalcitrant to the previously mentioned nonsurgical treatments. Decompression with fusion with or without instrumentation is currently recommended.²² The need to reduce the listhesis to normal alignment is not supported in the literature, provided that adequate decompression has been accomplished.²²

The indications for fusion in patients with lumbar spondylosis in the absence of spondylolisthesis are less well defined. There is some class I evidence to support lumbar fusion in carefully selected patients who have failed conservative therapy, albeit with a moderate amount of benefit over conservative therapy alone.^23,24 There are also data to support the addition of transpedicular instrumentation to aid in fusion.²⁵ In general, the addition of fusion to simple discectomy should be considered for patients with instability or other structural anomaly or in recurrent herniations with chronic intractable back pain.²⁶ There are no convincing data to suggest that fusion in addition to decompression for lumbar stenosis conveys any benefit, except in cases of preoperative instability or spondylolisthesis.^27,28

Consideration must also be given to the possibility of iatrogenic postlaminectomy instability that may be predicted prior to decompression. Postlaminectomy instability is a theoretical risk in all patients, but this risk is increased in patients with marked preoperative instability or deformity.^29,30 If the preoperative imaging suggests that wide (i.e., more than one third of the joint) facetectomy or concomitant laminectomy and discectomy are required for adequate decompression, consideration should be given to adding fusion supplemented with transpedicular instrumentation.²⁷

Technique

While a detailed discussion of spine instrumentation techniques as an adjunct to decompression is beyond the scope of this chapter, this section describes the general techniques for spine decompression in the presence of spondylosis. The most important step in decompression of the lumbar spine, however, is the determination of surgical goals, specifically which nerve roots and levels are affected and what the surgical target will be.

Following induction of anesthesia, surgery begins with proper position of the patient in the prone position. Many surgeons prefer the Wilson (Mizuho OSI, Union City, CA) or similar frame when the goal of surgery is decompression, as the frame provides a degree of flexion that can open up the posterior elements of the spine and allow for safer dissection. Once the patient has been positioned, all pressure points must be assessed and appropriately padded. The arms are generally placed on arm boards and abducted no more than 90 degrees. At this point, particularly if the surgery involves only one segment or is a discectomy, many surgeons prefer to obtain radiographs to tailor the location of the incision. Antibiotics and deep venous prophylaxis are instituted prior to the skin incision, and local anesthetic may be injected prior to standard surgical prep.

After standard prepping and draping, an incision is made to the level of the thoracolumbar fascia, which is opened sharply or with electrocautery. A subperiosteal dissection is carried out of the appropriate spinous processes, laminae, and facet joints. For unilateral foraminal decompression or discectomy, unilateral exposure is usually sufficient, while bilateral exposure is usually required for other disease processes. For decompression alone, care is taken to preserve the facet joint capsules. If concurrent transverse process fusion is to be performed, exposure of the corresponding transverse processes is carried out. Attention should be paid to the location and orientation of the pars at each level.

After exposure, radiographic confirmation of the operative level is performed by using plain radiographs or fluoroscopy. It is imperative that an unambiguous and easily identified structure be used as a landmark. The pedicle or transverse process may serve this purpose. Usually, a lateral radiograph is used, though this may be supplemented by AP radiographs in the thoracic region. If an AP radiograph is used to identify a thoracic vertebral level, it is mandatory that the number of ribs be counted on a preoperative radiograph, as variations in the normal number are relatively frequent. Once this has been done, the remaining soft tissue in the area of interest should carefully be removed to expose the intralaminar space. It is here that the techniques for discectomy and laminectomy diverge.

In performing a discectomy, the rostral lamina at the level of interest is undermined by using a curette. This allows safe passage of rongeurs, which are used to accomplish a partial hemilaminotomy. In the case of unusually hard or thick bone, a drill may be used to thin the bone prior to the use of a rongeur. The laminotomy begins on the caudal surface of the more rostral lamina and should be continued to the rostral border of the ligamentum flavum. Care must be taken to avoid excessive thinning or transection of the pars interarticularis. The rongeur or a nerve hook can then be placed under the ligamentum and turned caudally in the epidural space to begin clearing the ligamentum flavum. This is continued until the rostral margin of the inferior lamina is encountered. Variable amounts of this lamina may need to be removed to achieve adequate exposure. More lateral exposure may be obtained by medial facetectomy. Up to one third of the medial portion of the facet may be removed with no increased theoretical risk to the stability of the joint. Removal of bone flush with the superior medial surface of the lower pedicle facilitates positive identification and mobilization of the crossing nerve root. Once the disc space has been identified, epidural veins are coagulated by using bipolar electrocautery. After the disc space has been opened, the herniated fragment can typically be removed with a pituitary rongeur. Calcified or adherent fragments may be delivered into the disc space by using specialized instruments. Care must be taken with the medial portion of the dissection, as a ventral durotomy may prove very difficult to repair. Blind dissection is to be avoided. After all fragments and easily obtainable disc pieces have been removed, the wound is copiously irrigated and closed.

For laminectomy, the exposure must demonstrate the medial facet joints, lamina, and pars interarticularis at each level. Generally, the procedure begins by removal of the spinous processes at each affected level and often the inferior aspect of the next most rostral spinous process, to facilitate exposure. It is typically easiest and safest to approach the target area from the caudal aspect, owing to the angle of the lamina. Ligamentous attachments are dissected free by using curettes to clear the epidural plane. Bony resection is carried out by using rongeurs until the laminae are removed in a caudal-to-rostral fashion. The lateral border of resection is defined by the facet joints and pars interarticularis. As in the discectomy approach described earlier in the chapter, the medial one third of the facet can be removed safely without effect on the biomechanics of the spine. Ligament and bone are removed until the thecal sac is relaxed and the lateral recesses are decompressed. Anatomically, lateral recess decompression includes resection of the medial superior facet process of the caudal vertebra at any given segment until the pedicle and lower exiting nerve root can be visualized. Each foramen should be probed to assess the degree of decompression, and further foraminal decompression should be done as indicated. This must be done with care, as the nerve root is susceptible to injury at this stage. It must also be remembered that complete facetectomy will result in at least the potential for resultant instability.

Expected Outcomes

Following lumbar discectomy, varying degrees of success have been reported. Resolution of both back pain and radicular pain was found in 62% of patients in one large study.³¹ Overall satisfaction with the procedure ranges from 69% to 96%, the higher percentage being observed in a 5-year study.^31,32 Up to 3% to 5% of patients may have worsening of motor symptoms, and up to 12% to 15% may have worsening of sensory findings after discectomy.³³ Comparison of technical variations has also yielded conflicting data. While some authors have advocated the so-called sequestrectomy (removal of only the herniated fragment without curettage of the disc space), an analysis of the published literature from 1980 to 2007 showed varying results.^34–37 While patients who had undergone aggressive discectomy demonstrated a lower incidence of recurrent disc herniation than did those with less aggressive removal (3.5% vs. 7%, respectively), they also demonstrated an increase in recurrent back and leg pain (27.8% vs. 11.6%, respectively) when compared with patients who had undergone limited discectomy.³⁵ Some researchers have suggested that microdiscectomy through minimally invasive tubular systems may be less effective, but results in this study were measured at 1 year postoperatively.³²

In patients for whom conservative therapy has failed, surgical decompression for lumbar stenosis can improve pain and claudication in up to 80% of cases.²⁰ Patients who are treated with decompression and fusion for lumbar stenosis with spondylolisthesis may experience relief in back and leg symptoms in up to 86% of cases.³⁸ Patients with solid fusion have also been shown to do better than those with pseudarthrosis, although this might not achieve true statistical significance.³⁹

Outcomes after surgery for spondylosis and related conditions may be influenced by other factors. In general, patients with multilevel disease do worse than those with single-level disease. Patients with underlying mental illness or other psychological impairment might also not do as well, and in the case of psychological impairment, unrealistic expectations must be addressed. Patients with preoperative drug dependency may also have worse outcomes secondary to increased drug tolerance or modified pain responses.

Complications can also arise after surgical treatment for spondylosis. Standard surgical complications such as nonimprovement, bleeding, infection, durotomy, nerve root injury, and, in the case of fusion, nonunion all occur with a finite frequency. Medical complications may also occur. By far the most common complication, however, is incomplete symptom relief. All patients who are being treated with surgery for conditions that arise from spondylotic processes must be counseled that partial relief and failure to improve are possible. Irreversible presurgical damage may preclude complete recovery. In some cases, the purpose of surgery is to stop the progression of disease. Relief of pain or weakness to the premorbid state in patients with long-standing nonprogressive symptoms is in some cases an unrealistic goal.

The importance of identifying coexisting nonspinal conditions that may contribute to the patient’s symptoms cannot be overstated. Underlying hip, knee, and vascular pathology may coexist with or even mimic the symptoms of thoracolumbar spondylosis. Peripheral nerve pathology, particularly peroneal nerve pathology, must be distinguished from radiculopathy. Finally, herpes zoster or postherpetic neuralgia may be mistaken for radiculopathy, especially in the thoracic region and especially in the absence of active skin lesions.

Conclusion

Thoracolumbar spondylosis is essentially a disease of repetitive trauma combined with aging effects on the human spine. It is a common condition with a variety of symptoms that may present a nonlinear decision tree with regard to treatment. For much of the treatment, there is a paucity of class I data, underscoring the importance of not only a careful history and physical examination but also a detailed discussion of surgical and nonsurgical options with the patient.