Chapter 8 Arthrodesis and Fusion for the Treatment of Discogenic Neck and Back Pain

Evidence-Based Effectiveness and Controversies

John H. Shin, Daniel J. Hoh, Michael P. Steinmetz

Chapter Synopsis: Discogenic pain presents enormous challenges to both patient and pain clinician. Not only is the condition difficult to diagnose, but few of the limited treatment options provide unequivocally positive outcomes. Spinal fusion surgeries in particular have increased dramatically in recent decades, but evidence for their efficacy has been called into question. It is clear by now that discs are legitimate pain generators; but, even with evidence of a diseased or degenerated disc, other pain generators may include the surrounding muscles, tendons, and fascia. This chapter examines the literature to determine under which circumstances surgical fusion may be indicated for discogenic pain. The results are intertwined with the controversial diagnostic tool discography. In some cases, provocation discography predicts a positive outcome for fusion surgery; but in others it may produce false positives, leading to unnecessary fusion surgery with poor results. The diversity of spinal fusion techniques available further complicates the matter. As with any chronic pain condition, psychosocial factors and co-morbid conditions should be carefully considered in patient selection for any treatment.

Important Points: Discogenic pain is difficult to diagnose and treat. Current diagnostic tests, including imaging studies, do not reliably and accurately identify the source of pain in most patients. This contributes to the wealth of conflicting data in the literature. With many variables to consider, including psychosocial factors and medical co-morbidities, the identification of a pain-generating disc is often difficult. The lack of standardization of non-operative therapeutics for discogenic back pain is a major confounding variable in most prospective clinical trials.

Clinical Pearls:

A careful and detailed patient history and physical are key to understanding the mechanism and physiology of pain.

Fusion for discogenic pain is controversial.

There is little evidence to suggest that fusion is associated with better clinical outcomes.

Clinical Pitfalls:

Determining the discs responsible for pain based on imaging studies alone is inaccurate, as degeneration of multiple levels is common with age.

Discography results should be interpreted with caution if used as a test to determine the number of symptomatic discs.

Introduction

Neck and back pain are common conditions that affect millions of people each year. Neck pain is reported to occur in as many as 66% of individuals at some point during their lifetime.¹ With the widespread use of magnetic resonance imaging (MRI), patients are increasingly being diagnosed with degenerative disc disease, prompting referrals to surgeons and pain management physicians. The clinical significance of these degenerative findings is often overstated by physicians and patients alike, leading to a cascade of interventions and treatments that may not improve their symptoms.

In the absence of radiculopathy or myelopathy, controversy exists overt the clinical significance of degenerative disc disease and its correlation with pain. Numerous diagnostic tests such as computed tomography (CT), MRI, and discography have been developed to help elucidate the etiology of nonradicular spinal pain; however, none has been shown to reliably and accurately identify the source of pain. Just as the reliability and validity of these interventions are questioned by the scientific community, so are the indications for surgery and the potential benefit of fusion for treating neck pain without any symptoms of neural compression.

Similarly, low back pain is among the leading reasons for individuals to seek medical attention. One out of 17 patients seen by general practitioners presents with low back pain, and approximately 31 million patient visits for back pain occur in the United States annually.² It is estimated that 70% to 85% of individuals will suffer an acute episode of low back pain in their lifetime. Although most experience near complete resolution of symptoms within several weeks, a small percentage continue to experience persistent or chronic low back pain.³

Persistent low back pain is a significant source of anxiety, distress, depression, and disability that affects not only the individual, but society. It is estimated that 28% of the working population in the United States will be disabled by back pain at some time during their professional life, with approximately 8% of the entire work force disabled in a given year.³ This is a troublesome statistic since back pain is the primary cause of disability in persons less than 50 years of age, often the most productive years in a lifetime. The total socioeconomic burden of back pain, including both health care costs and lost wages, is estimated at $100 to $200 billion annually, with two thirds of this cost the result of work-related disability.⁴ Of alarming concern is that, although the incidence of diagnosed chronic back pain has been stable for 30 years, the rate of disability claims has increased by 14 times that of population growth.⁵

The surgical treatment of discogenic pain is controversial, and there is no consensus from the medical literature regarding the management of these patients. In fact, there are limited data comparing nonsurgical vs. surgical treatment for discogenic neck or back pain. Because the fundamental concept of discogenic pain is debatable, the evidence comparing surgery to medical therapies for this condition is more speculative than definitive.

Spinal fusion for discogenic pain is based on the theory that pain is related to a degenerative disc causing abnormal movement across a motion segment. This has been compared to abnormal movement across other degenerative joints such as hips or knees, where degeneration causes local mechanical and chemical processes. Arthrodesis across these degenerated joints is known to successfully eliminate pain. Spine surgeons have adopted this concept and applied it toward fusing across a degenerative, abnormal motion segment to relieve pain.

Despite the lack of evidence, fusion for discogenic pain is being performed more often, and reports of successful outcomes stem mostly from small retrospective case series.⁶^–⁹ Approximately 300,000 spinal fusions are performed annually in the United States, an increase of 220% between 1990 and 2001. Of these fusion operations, approximately 75% are performed for degenerative disc disorders. National inpatient data sample identifies degenerative disc disease as the diagnosis accounting for the largest increase in lumbar fusions during this period.⁵

Critics of fusion surgery argue that current imaging and functional diagnostic modalities do not accurately identify the source of pain in most patients who lack evidence of nerve compression or neurological deficit.¹⁰ Further, the relationship between arthrodesis and pain relief remains equivocal. Despite advancements in surgical technology, instrumentation, and osteobiologics, clinical outcomes continue to lag behind fusion rates. This lack of correlation between rates of arthrodesis and pain improvement is an argument against arthrodesis for discogenic pain.

Conversely, proponents of fusion surgery argue that patients with discogenic pain are unlike patients with radiculopathy, myelopathy, or stenosis. It is argued that patients with discogenic pain suffer from psychosocial disorders, chronic narcotic use, and prolonged disability, which negatively impact surgical outcomes. Even a modest rate of improvement in pain, narcotic use, or ability to return to work may represent a positive result for an otherwise desperate patient population that has frequently exhausted all other therapeutic resources.

This chapter reviews the current evidence for fusion and the treatment of discogenic neck and back pain. After a brief discussion regarding the pathophysiology of discogenic pain, the best available evidence on outcomes is reviewed herein.

Pathophysiology of Discogenic Pain

Discogenic pain is a controversial concept and is defined as axial spine pain without neural compression secondary to a degenerative disc. Although the exact pathophysiology is unknown, several theories have been proposed.

The two components of the intervertebral disc are the nucleus pulposus and the annulus 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 diffuses out of the disc, and subsequent resorption occurs with unloading. The annulus 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 annulus 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 that further deplete proteoglycans and lead to increased 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 endplates can occur, and subsequent loss of endplate vascularity reduces transport of nutrients and waste products out of the disc. With cyclical loading of the degenerated disc, radial fissures or cracks propagate through the annulus with migration of nuclear material peripherally (Fig. 8-1, A). With complete annular disruption, disc material can herniate into the central canal or foramen (Fig. 8-1, B). These degenerative processes are estimated to occur in 90% of normal individuals by 50 years of age.¹⁰

Fig. 8-1 A, T2 weighted sagittal magnetic resonance image (MRI) of a degenerated disc with a high intensity zone in the dorsal annulus (arrow) suggestive of annular disruption. B, T2 weighted axial MRI of a degenerated disc with a high intensity zone in the dorsal annulus (arrow) suggestive of annular disruption.

In 1970 Crock ^11,¹² first associated back pain with the pathophysiological process of disc desiccation and subsequent radial fissure formation of the annulus. He termed this entity internal disc disruption. It 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 was generated when degradation of the disc matrix causes release of inflammatory cytokines, which then migrate through the disrupted inner annular fibers to irritate the high concentration of sensory nerve endings in the outer annulus. His conclusion was supported radiographically by the relative absence of any nerve root compression and 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 been developed. The mechanical theory suggests that degeneration results in alteration in the biomechanical properties of the disc. As the disc degenerates and the annulus becomes disrupted, increasing instability occurs at the motion segment. Therefore with normal physiological 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

As the disc desiccates, it loses hydrostatic pressure, and more stress is transferred to the annulus and endplate, where pain sensitive nerve fibers are in high concentration. Increased stress to the endplate can lead to endplate 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 pro-inflammatory 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 present in the outer aspect of the annulus and the endplate. Proteoglycan breakdown is known to have a high concentration of the neurotransmitter glutamate, which may stimulate specific receptors in the dorsal root ganglion, resulting in pain in the absence of nerve root compression. Nociceptors are also known to be present in high concentration elsewhere within the spinal canal such as the posterior longitudinal ligament, dura, and blood vessels.

Although disc degeneration may produce pain, other structures may also produce pain, confounding the precise identification of the symptomatic pain generator. The facet joints, ligaments, fascia, nerve roots, and dura are capable of transmitting pain. Although 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. Cyclical loading to these structures can lead to increased arthropathy, ligamentous hypertrophy, and muscle fatigue, which may contribute to pain. Studies performed in patients with similar presentations of low back pain have demonstrated a wide range of sources of pain, including the disc, facet joints, and sacroiliac joints. Therefore, although the degenerated disc may be implicated in the pathophysiology of low back pain, it remains unclear whether the disc itself or other surrounding structures are the actual source of pain.

Diagnostic Controversies

Neck Pain

In patients who have discogenic neck pain refractory to conservative therapy, surgery is rarely indicated. In cases in which surgical intervention is considered, identifying a pain generator is critical yet not often possible for reasons discussed earlier.

Although imaging studies often reveal degenerative changes, including disc desiccation, loss of disc space height, and osteophyte formation, these findings usually involve multiple levels and do not localize to a single disc. Moreover, as many as 85% of asymptomatic individuals over 60 years of age exhibit degenerative changes in their cervical discs on MRI.^15,¹⁶

Controversy regarding the validity of diagnostic testing techniques, including MRI and discography, for cervical discogenic pain continues to appear in the literature.^17,¹⁸ Cervical discography has been used by clinical practitioners in select cases as a provocative study to evaluate suspected discogenic pain.^19,²⁰ Despite its enthusiasts, many have questioned the validity of discography for this application.¹⁷ It has been argued that the specificity of discography is dramatically affected by the psychological profile of the patient.^17,²¹ Some propose that discography is not helpful in identifying the pain source or determining the predictive value of surgery.²²^–²⁵

Conversely, there are authors who argue that discography can be used effectively in determining the source of a patient’s pain.²⁶^–²⁸ Grubb and Kelly²⁸ reviewed their experience with cervical discography during a 12-year period and suggested that a reliable pattern of pain was produced by stimulation of each cervical disc. They reported a high percentage of patients who demonstrated multiple discs responsible for their axial neck pain.

Back Pain

Imaging findings are also generally nonspecific. Plain radiographs may show decreased disc height and sclerotic endplates (Fig. 8-2, A). Sclerotic endplates or bone-on-bone appearance is commonly seen with severely degenerated discs (Fig. 8-2, B). MRI may demonstrate dehydrated, desiccated, or collapsed discs (Fig. 8-3, A). However, these changes may occur in multiple discs, making it difficult to determine which level is symptomatic. Because of its sensitivity for visualizing soft tissue structures of the spine, including the discs, ligaments, joints, and neural elements, MRI is the preferred test to evaluate for nerve root compression from degenerative disc disease. The ability of MRI to detect loss of water content and disc desiccation has led to widespread use of this imaging modality. It also characterizes the effect of disc degeneration on the adjacent endplates and vertebral bodies. In the early phase the normal vertebral body bone marrow is replaced with vascularized fibrous tissue as a reparative response to injury (Fig. 8-3, B). With chronic degeneration the normally red bone marrow is converted to yellow marrow as the marrow elements are replaced by fat cells, which appears to represent a chronic, stable state. Despite these findings, these changes commonly occur in asymptomatic individuals, calling into question their clinical relevance.

Fig. 8-2 A, Lateral radiograph demonstrating a degenerated, collapsed L5-S1 intervertebral disc space. B, Lateral radiograph demonstrating a degenerated L3-L4 intervertebral disc space with sclerotic endplates.

Fig. 8-3 A, T2 weighted sagittal magnetic resonance image demonstrating a severely degenerated L5-S1 disc with abnormal signal changes in the adjacent vertebral body bone marrow. B, T1 weighted sagittal magnetic resonance image demonstrating decreased signal in the adjacent vertebral bone marrow consistent with vascularized, fibrous tissue.

Despite conflicting evidence, many 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. Advocates of discography argue that discs demonstrating abnormal morphology and/or concordant pain provocation are likely the symptomatic levels. Therefore it is assumed that fusion across the positive discographic motion segment results in alleviation of pain. Conversely, discs with normal morphology or that do not reproduce similar pain can be reasonably excluded from surgery. As a result, many surgeons use discography not only to determine candidates for surgery but to assess how many levels to fuse.

Certain studies have demonstrated that positive discography reliably predicts positive surgical outcomes. Simmons and Segil ²⁷ studied patients who had discography before undergoing lumbar discectomy, discectomy and fusion, or fusion alone. They found that preoperative discography demonstrated 82% diagnostic accuracy in identifying the symptomatic level. However, this study represented a heterogenous patient population, including not only patients with back pain, but those suffering from herniated discs and nerve root compression. Colhoun and associates²⁹ found that, among patients undergoing lumbar fusion, 89% of those with a positive preoperative discogram had significant improvement after surgery, including decreased pain, return to work, and cessation of analgesics.²⁹ Alternatively, patients with nondiagnostic preoperative discography had a lower rate of success after lumbar fusion, with only 52% of patients reporting a similar satisfactory postoperative outcome.

Varying degrees of success with preoperative discography have been observed. Positive clinical outcomes have been demonstrated in 64% to 86% of patients with positive discography who undergo anterior lumbar interbody fusion (ALIF).³⁰^–³²

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