Indications for Spine Fusion for Axial Pain

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Chapter 58 Indications for Spine Fusion for Axial Pain

Low back pain (LBP) is among the leading reasons for individuals to seek medical attention. One out of 17 patients seen by a family practitioner presents primarily with LBP, with approximately 31 million patient visits for back pain occurring in the United States annually.1 It is estimated that 70% to 85% of individuals will suffer an acute episode of LBP in their lifetime. Most people experience a benign course with near complete resolution of symptoms within a few months of onset.2 Unfortunately, a small percentage, approximately 5% to 10%, continue to develop persistent or chronic LBP.3

Persistent LBP is often a significant source of personal anxiety, distress, and disability. In addition, chronic LBP weighs heavily on society. It is estimated that 28% of the working population in the United States will be disabled by LBP at some time during their professional lives, with approximately 8% of the entire work force disabled in a given year.3 Acute LBP occurs across a wide range of ages. Chronic LBP, however, is the primary cause of disability in individuals less than 50 years of age, when most people expect to be at their peak productivity. The total socioeconomic burden of LBP, including both health-care costs and lost wages, is estimated at $100 billion to $200 billion annually, with two thirds of this cost due to work-related disability.4 Of alarming concern is that while the incidence of diagnosed chronic LBP has been stable for 30 years, the rate of LBP-related disability claims has increased by 14 times that of population growth.5

These individual and socioeconomic problems are further compounded by a lack of consensus in the health-care community regarding the appropriate diagnosis and management of chronic LBP. LBP is a generalized somatic complaint that may be the manifestation of one or a combination of various processes. The underlying pathophysiologic mechanisms may be inherent to the spinal column or nerves or may be referred from various supporting musculotendinous structures. Furthermore, which anatomic structures, whether internal or external to the spine, are the actual source of pain for a given individual is often unclear. Potential LBP etiologies include the intervertebral discs, facet joints, bony vertebral column, neural elements, muscles, ligaments, tendons, and fascia. While these various structures are associated with certain LBP syndromes, such as “axial low back pain,” “discogenic pain,” “facetogenic pain,” “mechanical back pain,” and “myofascial pain,” the true relationship between an anatomic structure, pathophysiologic process, and pain transmission remains difficult to confirm. As a result, definitive diagnosis and appropriate treatment intervention remain challenging at best.

Of these LBP syndromes, axial LBP has undergone the most intense scrutiny by the health-care, scientific, and general communities. Axial LBP is described as a pain disorder of the lumbosacral region that is theorized to be secondary to advanced degeneration of the intervertebral discs. The term axial LBP is often used interchangeably with other, more anatomically directed terms such as discogenic pain, degenerative disc disease, internal disc disruption, black disc disease, and disc prolapse. The presumed pathophysiology of axial back pain is that accelerated disc degeneration results in abnormal alterations in the mechanical and chemical nature of the disc. Pain generation is believed to be due to the ensuing change in segmental biomechanics as it leads to instability, abnormal motion, or loss of stiffness. Alternatively, pain may be transmitted by changes in the biochemical environment through release of inflammatory cytokines or nociceptive neurotransmitters.

Controversy regarding axial LBP is due to a number of factors. First, there is a lack of definitive scientific evidence identifying the disc as the pathoanatomic source of pain. The validity and reliability of current diagnostic modalities for discerning which disc or discs are the primary pain generators are unresolved. Second, general medical journals and popular media have generated controversy by suggesting that surgeons are overtreating axial LBP without any proven basis for diagnosis and intervention. Subsequently, many people have made the claim that current trends for operative management of axial LBP have been propagated by ulterior interests from the surgical community and medical device industry. In fact, survey and national inpatient data sample results have indicated that lumbar fusion surgery for degenerative spinal conditions has been steadily increasing. Approximately 300,000 spine fusions are performed annually in the United States, which is a relative increase of 220% between 1990 and 2001. Of these fusion operations, about 75% are performed for degenerative disc disorders and spinal stenosis. A national inpatient data sample identifies degenerative disc disease as the diagnosis that accounts for the largest increase in the number of lumbar fusions during this period.6

Spine fusion for axial LBP is predicated on the theory that pain is related to the degenerated disc’s causing abnormal movement across a motion segment. Painful disc degeneration may be analogous to other arthritic joint pathology involving the hips or knees, in which the degenerated joint causes altered local mechanical and chemical processes that generate pain. Arthrodesis across these degenerated joints in the appendicular skeleton is known to eliminate pain successfully. Spine surgeons have adopted fusion across a degenerated disc as a method for stabilizing the abnormal motion segment to similarly relieve pain.

Unfortunately, the spine surgical literature has failed to demonstrate consistent successful clinical outcomes after fusion surgery in patients with axial LBP. Critics of fusion surgery for axial LBP again raise the issue that current imaging and functional diagnostic modalities do not accurately identify the source of LBP in most patients that lack evidence of nerve compression or neurologic deficit.7 Therefore, difficulties with patient selection and determining which levels to fuse may account for suboptimal rates of clinical success. Furthermore, the relationship between solid arthrodesis and LBP relief remains equivocal. This uncertainty is accentuated by an overall lack of improvement in successful outcomes despite increasing fusion rates with advancing surgical technique, fixation devices, and osteobiologic agents.

Alternatively, proponents of fusion surgery argue that patients with axial LBP who ultimately undergo surgery are unlike other lumbar spine surgery patients. Often, these patients have had debilitating pain for years with failure of multiple nonsurgical therapies. Axial LBP patients often suffer from psychosocial disorders, chronic narcotic use, and prolonged disability, which negatively affect outcome with any intervention. Even a modest rate of improvement in pain, narcotic use, or ability to return to work represents a positive result for an otherwise desperate patient population that has frequently exhausted all other therapeutic resources.

The controversy regarding fusion surgery for axial LBP continues today. In 1989, Nachemson issued an editorial stating that for the majority of patients, basic science has yet to demonstrate the true origin of back pain.8 He further stated that our present-day treatments are mostly ineffective, as evidenced by the epidemic increase in back pain related disability in all industrialized societies. Twenty years later, these issues remain subjects for debate, and several recent highly contested studies suggest that there is a lack of clinical evidence to support the surgical treatment for a number of degenerative lumbar disorders.6,9 To gain a better understanding of axial LBP and the indications for spine fusion, this chapter provides an overview of the pathophysiology and current literature with regard to diagnosis, surgical treatment, and outcomes for axial LBP.

Pathophysiology

The normal lumbar intervertebral disc consists of fibrocartilaginous tissue designed to absorb and dissipate load applied to the spinal column. The two components of the disc are the nucleus pulposus and the anulus fibrosus. The nucleus pulposus is composed of proteoglycan aggrecan molecules with 70% to 80% water content. Absorption of water into the nucleus provides disc height and resistance to compression. With loading, water defuses out of the disc, and subsequent reabsorption occurs with unloading. The anulus is an interlacing collagen network that provides tensile strength in axial rotation. With bending or compression of two adjacent vertebrae, the nucleus pulposus changes volumetrically, causing bulging of the disc away from the internal axis of rotation. The anulus also functions to limit and contain expansion or herniation of the nucleus.

With aging, the disc gradually becomes less hydrated, and the concentration of proteoglycans decreases. Normal disc metabolism shifts toward catabolic processes, which further deplete proteoglycans and lead to increasing matrix degeneration. As a result, the disc becomes progressively dysfunctional as the nuclear material is replaced by desiccated fibrocartilaginous material. Loss of fluid results in decreased hydrostatic pressure as a mechanism for effective load transference. Thinning or microfracture of the end plates can occur, and subsequent loss of end-plate vascularity reduces transport of nutrients and waste products out of the disc. Eventually, with cyclic loading of the degenerated disc, radial fissures or cracks propagate through the anulus, with migration of nuclear material peripherally. With complete anular disruption, disc material can herniate into the central canal, lateral recess, or foramen. These degenerative processes are estimated to occur in 90% of normal individuals by 50 years of age.10

In 1970, Crock first associated back pain with the pathophysiologic process of disc desiccation and subsequent radial fissure formation of the anulus.11,12 He termed this entity internal disc disruption, which was characterized by the progressive disruption of the internal architecture of the disc while essentially maintaining the external shape such that nerve root compression did not occur. Crock hypothesized that pain is generated when degradation of the disc matrix causes release of inflammatory cytokines, which then migrate through the disrupted inner anular fibers to irritate the high concentration of sensory nerve endings in the outer anulus. His conclusion was supported radiographically by the relative absence of any nerve root compression but the high correlation of concordant pain in discs that exhibited severe radial fissures with intradiscal contrast injection.

Since then, several theories regarding the relationship between degenerative disc disease and pain generation have developed. The mechanical theory suggests that degeneration results in alteration in the biomechanical properties of the disc. As the disc degenerates and the anulus becomes disrupted, increasing instability occurs at the motion segment. Therefore, with normal physiologic loading, the motion segment responds with excessive compression, bending, or rotation, which can trigger pain transmission in surrounding nociceptors. CT and MRI studies have quantified the response of the lumbar spine to rotatory torque and have correlated increased axial rotation in degenerated discs with pain provocation on discography.13,14 Also as the disc desiccates, it loses hydrostatic pressure, so with normal physiologic loading, more stress is transferred to the anulus and the end plate, where pain-sensitive nerve fibers are in high concentration. Increased stress to the end plate can lead to end-plate fracture and disc herniation into the vertebral body, which may further propagate pain generation.

The chemical theory suggests that catabolism of the disc results in release of proinflammatory chemical mediators. Nitric oxide, phospholipase A2, prostaglandin E, matrix metalloproteinases, and other cytokines have been implicated as chemical agents that infiltrate through radial fissures to irritate nociceptors that are present in the outer aspect of the anulus and the end plate. Proteoglycan breakdown is known to have a high concentration of the neurotransmitter glutamate, which may in turn stimulate glutamate-specific receptors in the dorsal root ganglion, resulting in back or radicular pain in the absence of nerve root compression. Nociceptors are also known to be present in high concentrations elsewhere within the spinal canal, such as the posterior longitudinal ligament, dura, and blood vessels.

Alternatively, although the disc may demonstrate signs of degeneration, pain may arise from other associated structures. The facet joints, ligaments, fascia, nerve roots, and dura are capable of transmitting pain. While disc degeneration may be the initial inciting pathology, one or more of these structures may in fact be the source of pain. Progressive disc disease results in increased load transference to surrounding structures such as the facet joints, ligaments, and paraspinal muscles, which may eventually exceed their capacity for resistance. Cyclic loading to these structures can lead to increased arthropathy, ligamentous hypertrophy, and muscle fatigue, which may contribute to pain. The medial branch of the dorsal primary rami courses around the facet and innervates the joint capsule and may be a particularly pain-sensitive fiber signaling back pain with increased stress. Diagnostic blockade of various spinal and paraspinal structures with injected anesthetic may be performed to evaluate certain areas as potential pain generators. Studies performed in patients with similar presentations of LBP have demonstrated a wide range of sources of pain, including the disc, facet joints, and sacroiliac joints. Therefore, while the degenerated disc may be implicated in the pathophysiology of LBP, it remains unclear whether the disc itself or other surrounding structures are the actual source of pain.

Diagnosis

Patients with axial LBP generally present with a deep, aching pain localized to the lower back, sacral, or gluteal region. The pain is characteristically worsened with mechanical activities such as bending, twisting, or lifting and is relieved with recumbency. Pain is also increased with lumbar flexion, such as when ascending stairs, and is presumed to be secondary to increased ventral loading on the degenerated discs. Also, patients often describe increased pain with prolonged sitting. Interestingly, patients may also describe buttock or leg pain (generally limited to above the knee) that is not radicular in nature but may be referred sclerotomal pain.

Physical examination rarely provides information in facilitating the diagnosis of axial LBP or the level of disease. Often, the physical and neurologic assessment is normal. The clinical history and the physical and neurologic examination, however, are critical in evaluating other potential etiologies of LBP such as nerve root compression, spinal deformity, fracture, spinal instability, spondylolisthesis, tumor, or infection. Masqueraders that closely mimic axial LBP symptomatology and that can be assessed on physical examination include myofascial pain, sacroiliac joint pain, piriformis syndrome, and hip osteoarthritis.

In light of a normal physical examination and relatively ubiquitous symptomatology, the diagnosis of axial LBP is made clinically using various radiologic studies. Because of the overt dependence on imaging for determining the source of pain, there has been intense scrutiny of radiologic criteria for identifying which discs are painful and which patients may ultimately benefit from fusion surgery.

Plain Radiographs

Plain radiographic findings in patients with axial LBP may demonstrate characteristics consistent with degenerative disc disease. While radiography does not visualize the soft tissue disc, plain films may reveal decreased disc height consistent with a collapsed or dehydrated disc (Fig. 58-1A). Sclerotic end plates or bone-on-bone appearance are commonly seen with severely degenerated discs (Fig. 58-1B). Plain radiographs can be performed with patients in weight bearing, flexion, or extension to demonstrate the alignment of the spine and the nature of the motion segments under normal physiologic loading. The presence of hypermobility or malalignment under such stresses may help to identify which levels are symptomatic or may suggest other pathologic processes.

In evaluating lumbar plain radiography in symptomatic patients, Scavone et al. observed that radiographs alone were uniquely diagnostic in only 2.4% of patients.15 Liang and Komaroff found that lumbar radiographs did not provide diagnostic value in differentiating patients with acute versus chronic LBP.16 Coste et al. reported that there was a high degree of variability in interpretation of plain films performed in LBP patients, underscoring the poor diagnostic value of these studies for this condition.17 Many clinicians conclude that the degenerative findings that are seen on lumbar plain radiographs may in fact represent normal age-related changes and as such provide little information with regard to differentiating symptomatic degenerated discs from asymptomatic age-appropriate discs. Plain radiographs, however, are useful in the assessment of axial LBP for effectively ruling out other etiologies of back pain. Fractures, osteomyelitis, tumor, spondylolisthesis, and deformity can often be quickly assessed with lumbar weight-bearing or 36-inch standing plain films. Therefore, plain radiographs are indicated in LBP patients who are of pediatric age, are at high risk for osteoporosis, have a history of prior surgery, present with neurologic deficit or gross deformity, or have clinical signs suggestive of trauma, infection, or malignancy.

Discography

The ability of discography to diagnose degenerated disc disease and identify painful symptomatic discs has been the subject of ongoing debate. Discography is an invasive procedure by which a needle is placed percutaneously into the nucleus pulposus under fluoroscopic or CT guidance. Contrast is injected into the nucleus, and images are generated on plain radiographs and/or axial CT images. The flow of contrast within the disc provides information regarding disc morphology and the integrity of the anulus. Contrast filling of a degenerated, desiccated disc may highlight a collapsed narrow disc space. Radial fissures may be revealed by contrast leakage from the nucleus into the periphery and, in the case of anular disruption, spilling of contrast into the canal or foramen. The integrity of the anulus can be inferred from the resistance or volume of injection, normal discs having a high resistance and smaller volume of injection. Low resistance or a high volume of injection suggests disruption or a possible tear in the anulus.

One unique feature of discography, in contrast to other conventional passive imaging modalities, is the behavioral component of the diagnostic procedure. Essential to discography is the evaluation of both the suspected symptomatic disc and control or asymptomatic discs. With injection of contrast into an abnormal disc, the discographer assesses for provocation of concordant pain. Pain with disc injection is likely due to either an increase in intradiscal pressure or the displacement of biochemical agents. With pressurized contrast injection, stretching of pain-sensitive nerve endings in the anulus may be stimulated, or stress may be transmitted to the end plates or vertebral body. Alternatively, contrast injection into the nucleus may cause displacement of inflammatory cytokines, which then diffuse through radial fissures to the periphery, where they may stimulate nociceptors in the outer anulus or the surrounding environment. Ideally, the provoked pain is similar to or an exact reproduction of the patient’s presenting back pain. Otherwise, the injection provokes dissimilar pain or does not produce pain, and the discogram is inconclusive or negative for that level. The gold standard for diagnostic discography is exact reproduction of pain at the morphologically abnormal level with no pain provocation at control or normal discs.

Several studies provide evidence to support discography as an effective method for identifying degenerated, symptomatic discs. Cadaveric studies have shown a strong correlation between discographic contrast distribution and the severity of degeneration on gross examination. There is also a good correlation between disc morphology on discography and intraoperative findings of disc protrusions and herniations. Importantly, studies have identified morphologic findings on discography that correlate with concordant pain provocation. As expected, pain provocation is most commonly observed in discs that demonstrate dorsal anular tears (65.3%) as compared to simply degenerated discs (36.6%), internal anular disruption (20%), or intraosseous disc herniations (0%).18 The use of axial CT imaging provides even further morphologic assessment of the disc. Using the Dallas Discogram Description (DDD) for CT-based discography, severe and moderately graded degenerated discs show a strong correlation with exact reproduction of pain, anular disruption being the best predictor of concordant pain.19 McCutcheon and Thomas found that contrast tracking to the periphery of the anulus suggesting radial fissures and anular disruption has an 87% correlation with concordant pain.20

Subsequent studies, however, have failed to consistently reproduce these positive correlations. Several studies have demonstrated pain production with discography in otherwise normal-appearing discs in asymptomatic individuals. Carragee et al. studied discography in a group of patients who did not have back pain but had chronic pain related to iliac crest bone harvest for non–lumbar spine surgery. Of these patients, 37.5% had similar or exact reproduction of donor site pain with lumbar discography. Some have proposed that high-pressure injection is responsible for false-positive pain production in normal discs. However, even with low-pressure discography, pain was produced in the same number of asymptomatic volunteers as LBP patients.21 Vanharanta et al. found that morphologically normal discs on DDD grading still provoked some pain response in 24% of individuals.22 Also, they observed that severely degenerated discs resulted in exact reproduction of pain in only 22% of individuals. In their study, even discs with severe anular disruption had exact pain reproduction in only 36% of subjects. The reverse association demonstrated slightly better correlation. Patients who had a positive pain response were also more likely to have evidence of disc degeneration. However, discs with exact reproduction of pain were distributed among a range of DDD grades from slight (20%) to moderate (39%) to severe (37%). The best correlation among patients with exact reproduced pain was for severe anular disruption (77%). Overall, the investigators found that painful discs tend to have higher degrees of degeneration and anular disruption compared to painless discs. However, all discs as they deteriorated were more likely to provoke pain, although often the pain was not similar to the presenting back pain and therefore the degenerating disc could not be conclusively diagnosed as the symptomatic disc. Further adding to diagnostic uncertainty, studies have shown that nonspinal factors such as abnormal psychometric findings, chronic pain states, and disputed compensation claims also strongly correlate with positive discography.21

Despite these conflicting studies, many clinicians have adopted discography as an instrument for presurgical screening and patient selection, with the presumption that positive discography can reliably predict which patients and levels will respond favorably to fusion. Specifically, discs that demonstrate abnormal morphology and/or concordant pain provocation are likely the symptomatic levels. Therefore, fusion across the positive discographic motion segment will result in alleviation of pain. Conversely, discs with normal morphology or discs that do not reproduce similar pain can be reasonably excluded from surgery or the fusion construct. As a result, for many surgeons, discography is assigned a critical role in selecting which patients with chronic back pain are surgical candidates and ultimately in determining which levels to fuse.

Certain studies have demonstrated that positive discography reliably predicts good surgical outcomes. Simmons and Segil studied patients who had discography prior to undergoing lumbar discectomy, discectomy and fusion, or fusion alone. They found that preoperative discography demonstrated 82% diagnostic accuracy in identifying the symptomatic level.23 This study, however, represented a heterogeneous patient population that included not only back pain patients, but also those suffering from herniated discs and nerve root compression. Colhoun et al. found that among patients undergoing lumbar fusion, 89% of those with a positive preoperative discogram had significant improvement postoperatively, including decreased pain, return to work, and cessation of analgesics.18 Patients with nondiagnostic preoperative discography had a lower rate of success after lumbar fusion, only 52% of patients reporting a similar satisfactory postoperative outcome.

Varying degrees of success with preoperative discography have been observed. Good clinical outcomes have been demonstrated in 64% to 86% of patients with positive discography who undergo anterior lumbar interbody fusion (ALIF).2426 Other studies have shown that more than 90% of patients with positive discography improve after posterior lumbar fusion.27,28 Derby et al. argue that better correlation is observed when chemically sensitive discs are identified on preoperative discography.29 Chemically sensitive discs provoke concordant pain under particularly low-pressure injection, suggesting that pain is generated by the displacement of biochemical agents that then stimulate sensory nerve endings in the outer anulus. Therefore, Derby et al. hypothesize that patients with chemically sensitive discs require complete discectomy with thorough removal of the offending disc for pain relief. Among patients with chemically sensitive discs, successful clinical outcome was observed in 89% of patients who underwent discectomy and interbody fusion, compared to only 20% of patients who underwent dorsolateral fusion alone and 12% of patients who were treated nonoperatively. Similarly, Weatherly et al. used discography to identify painful, symptomatic discs within a fused segment in patients with persistent LBP after posterior lumbar fusion.30 Subsequent ventral discectomy and interbody fusion of the positive discographic levels resulted in complete resolution of pain.

The positive predictive value of discography for success after lumbar fusion, however, has not been borne out through multiple repeated studies. Of particular concern is that the potential for a high false-positive rate may lead to an inappropriate rise in fusion surgery and consequently an unacceptable rate of unsatisfactory outcomes. Carragee et al. evaluated patients with positive single-level discography using low-pressure injection who then underwent lumbar fusion of the abnormal disc.31 They observed that only 27% of patients had a highly effective outcome as defined by a visual analogue score (VAS) of 2 or less, Oswestry Disability Index (ODI) of 15 or less, full return to work, and cessation of narcotics and analgesics. A minimal acceptable outcome of VAS of 4 or less, ODI of 30 or less, no narcotic use, and at least some gainful employment was reached in only 43% of patients. The authors concluded that in the best case calculation, the adjusted positive predictive value for a minimal acceptable outcome was only 55%. Other studies have similarly found less promising results, with successful outcomes in only 35% to 46% of patients who had undergone lumbar fusion with discography as the primary diagnostic tool.32 It should be noted, however, that in one of these studies, a particularly low arthrodesis rate was observed (47.9%), which may account for the unexpected poor outcomes.

Overall, discography remains an imperfect instrument for diagnosing and localizing discogenic pain. Particularly, discography has come into doubt as a reliable measure for predicting which patients and what levels will respond well to fusion surgery. Much of this lack of accuracy and consistency may be dependent on discography technique and reporting of pertinent positive and negative findings. Furthermore, patient, discographer, and surgeon expectations may bias toward false-positive results, potentially leading to increasing the number of surgeries or creating unrealistic prospects for successful results. Ultimately, the degree to which discography plays a role in surgical decision making largely depends on the surgeon’s prior experience in drawing upon this diagnostic modality and also establishing clear communication with the patient with regard to reasonable expectations for outcome. Given the available data, discography is best indicated for correlating concordant pain in discs that are morphologically abnormal, as the finding of pain provocation in otherwise normal-appearing discs appears to be clinically irrelevant. Discography may also facilitate assessing prior to fusion whether levels adjacent to the symptomatic level are also abnormal and may be included in the fusion construct. Last, in certain circumstances, discography may play a role in evaluating patients who have persistent back pain after posterior lumbar fusion to assess for a painful pseudarthrosis or the presence of a symptomatic disc within the fused segments.

Magnetic Resonance Imaging

MRI is the radiologic study of choice for visualizing the soft tissue structures of the spine, including the discs, ligaments, joints, and neural elements. As a result, MRI is the preferred test for nerve root compression from disc herniation or lumbar stenosis. MRI is also well equipped for clearly visualizing the intervertebral disc. Besides the ability to image in multiple planes, MRI, with good-quality spin-echo T2-weighted images, provides excellent characterization of the morphology of the disc and superb differentiation between the nucleus pulposus and anulus. The signal intensity within the nucleus is related to the concentration of water in the proteoglycan matrix. Therefore, a reduction in signal intensity correlates with matrix degradation and disc degeneration (Fig. 58-2A). The ability of MRI to detect loss of water content and disc desiccation has prompted consideration of MRI as a sensitive measure of degenerative disc disease.

MRI also well characterizes the effect of disc degeneration on the adjacent end plates and vertebral bodies. With advanced degeneration of the discs, greater load is transferred to the end plates. In the early phase, the normal vertebral body bone marrow is replaced with vascularized fibrous tissue as a reparative response to injury.33 This appears on T1-weighted MRI as decreased signal (Fig. 58-2B), and conversely increased signal on T2-weighted images. With chronic degeneration, the normally red bone marrow is converted to yellow marrow as the marrow elements are replaced by fat cells, a situation that appears to represent a chronic, stable state. The prevalence of fat is represented by increased signal on T1-weighted MRI.

Because MRI adeptly characterizes the various stages of disc degeneration and its effects on the discovertebral complex, it is often performed as the initial study in evaluating patients who present with axial LBP. However, it is unclear whether findings of disc degeneration on MRI are in fact age-related changes or abnormal processes that are related to pain generation. Several studies have evaluated MRI in asymptomatic volunteers and found that more than 30% of individuals without back pain have evidence of degenerated lumbar discs.5,34 These include significant findings of herniated discs (24%) and anular defects (14%) in individuals who are asymptomatic. Boden et al. observed that 28% of asymptomatic individuals had an MRI of the lumbar spine that was characterized as abnormal.34 The most common finding was bulging discs, which appeared in 79% of individuals older than 60 years of age and in 54% of those younger than 60 years of age. Degenerated discs were seen in all but one subject older than 60 years of age, many having multiple degenerated discs. Boden et al. concluded that given the high incidence of bulging and degenerated discs in asymptomatic subjects, these findings in part represent the normal process of aging.

Several studies, however, have shown that MRI findings correlate well with abnormal discography that is suggestive of symptomatic degenerative disc disease.35 Horton et al. performed both MRI and lumbar discography in 25 patients presenting with discogenic LBP.36 They observed that normal-appearing discs on MRI with a high fluid content rarely had concordant pain or abnormal morphology on discography. Alternatively, discs that demonstrated a dark nuclear pattern on MRI, suggesting severe disc dehydration and anular disruption, strongly correlated with pain provocation on discography. The more common finding, however, of a dark or speckled nucleus on MRI, which was interpreted as some degree of disc degeneration, had poor correlation with discographic findings. Subsequent studies observed that painful discs on discography tend to show more evidence of degeneration such as anular fissures, disc prolapse, and decreased disc height on MRI. However, there is no significant difference in pattern or frequency of these degenerative findings between asymptomatic individuals and those with LBP to suggest that MRI can effectively screen for painful, symptomatic discs.37

Aprill and Bogduk describe a specific finding on MRI that appears to correlate particularly well with concordant pain on discography.38

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