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 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 defuses out of the disc, and subsequent reabsorption 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, which is limited or contained by the annulus.

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 promote 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 annulus with peripheral migration of nuclear material. With complete annular disruption, disc material can herniate into the central canal, lateral recess, or foramen. These degenerative processes occur in approximately 90% of healthy individuals by age 50.

Numerous theories attempt to describe the relationship between DDD and development of pain. The mechanical theory suggests that degeneration alters the biomechanical properties of the disc. Disc degeneration disrupts the annulus, thereby increasing instability of the motion segment. During normal physiologic loading, the motion segment compensates with excessive compression, bending, or rotation, which can trigger pain perception by nociceptors. Computed tomography (CT) and magnetic resonance imaging (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. Also, as the disc desiccates and loses hydrostatic pressure, normal physiologic loading transfers more stress to the annulus 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 exacerbate the pain.

The chemical theory suggests that catabolism within 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 radial fissures to irritate nociceptors that are present in the outer aspect of the annulus and the end plate. Proteoglycan breakdown is concentrated with the neurotransmitter glutamate, which may stimulate glutamate-specific receptors in the dorsal root ganglion, resulting in back or radicular pain in the absence of nerve root compression.

A combination of both theories may be the most accurate depiction of discogenic pain. In human and animal models of disc degeneration, the number of nerve fibers innervating the disc increases and can follow an unusual course extending into inner aspect of the annulus and even into the nucleus. In addition to the sensory nerve fibers, there is growing evidence that sympathetic afferents are also increased in degenerated discs, playing a significant role in low back pain. Subsequently, mechanical stimuli normally innocuous to disc nociceptors can generate an amplified response, which is termed peripheral sensitization . Nociceptors that are sensitized by the activity of sensory and sympathetic fibers may initiate a pain impulse in response to ischemia, pressure changes, or inflammatory irritation. Nociceptors are located in the posterior longitudinal ligament, dura, and blood vessels as well.

Although disc degeneration may be the initial inciting pathology, facet joints, ligaments, fascia, nerve roots, and dura may contribute to pain. Progressive disc disease increases 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 leads to increased arthropathy, ligamentous hypertrophy, and muscle fatigue, which can exacerbate pain. The medial branch of the dorsal primary rami courses around the facet and innervates the joint capsule. Furthermore, it may be a particularly pain-sensitive fiber signaling back pain in the setting of increased stress. Diagnostic blockade of various spinal and paraspinal structures with injection of anesthetic agents 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, although 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

The diagnosis of axial LBP is clinical, with the accompanying use of a variety of radiographic studies. 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, prolonged sitting, or lifting and is relieved by recumbency. With increased lumbar flexion during daily activities there is increased ventral loading on the degenerated discs resulting in amplified pain. Interestingly, patients may also describe buttock or leg pain, which is generally limited to above the knee and is not radicular in nature but may be referred sclerotomal non-neurogenic pain.

The physical and neurologic assessment is often normal, limiting the diagnosis of axial LBP and the level of disease. Still the clinical history and the physical examination are critical in evaluating other potential etiologies of LBP such as nerve root compression, spinal deformity, fracture, spinal instability, spondylolisthesis, tumor, or infection. Physical examination is also important in ruling out similar conditions that closely mimic axial LBP symptomatology including myofascial pain, sacroiliac joint pain, piriformis syndrome, and hip osteoarthritis.

Because of the overt dependence on imaging for determining the source of pain, there has been intense scrutiny of radiologic criteria to identify which discs are painful and which patients may ultimately benefit from fusion. The Joint Section of the American Association of Neurological Surgeons/Congress of Neurological Surgeons published guidelines for fusion to treat lumbar degenerative conditions and made recommendations regarding the diagnostic evaluation of axial LBP. MRI allows for the assessment of multiple levels simultaneously and noninvasively. Therefore, one can gain an appreciation of the disease pattern of the discs and determine which discs may have evidence of advanced degeneration, disc prolapse, annular disruption, or disc herniation. Once the degenerated levels have been identified on MRI, discography can be performed to further subselect which discs demonstrate abnormal morphology and concordant pain provocation. In their assessment of MRI and discography in 2005, the organization recommended that MRI be performed initially instead of discography in the evaluation of chronic LBP. It also recommended that normal-appearing discs on MRI should not undergo fusion. Updated guidelines in 2014 again stated evidence that the predictive value of discography is controversial, and based on the literature, discography should not be used as an independent predictor of success following lumbar fusion for low back pain or as a stand-alone test on which treatment decisions are based. In addition, a new diagnostic technique called “discoblock” may have improved the potential, compared to discography, for predicting success following lumbar fusion. The lack of a gold standard in imaging techniques for diagnosing axial LBP makes identifying the pain generator difficult. This section provides an overview of the various imaging methods available and their clinical applications.

Plain Radiographs

Plain radiographic findings in patients with axial LBP may demonstrate characteristics consistent with DDD. Although 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 a 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.

A, Lateral radiograph demonstrating a degenerated, collapsed L5-S1 intervertebral disc space. B, Lateral radiograph demonstrating a degenerated L3-4 intervertebral disc space with sclerotic end plates.

In evaluating lumbar plain radiography in symptomatic patients, Scavone and colleagues observed that radiographs alone were uniquely diagnostic in only 2.4% of patients. Liang and Komaroff found that lumbar radiographs did not provide diagnostic value in differentiating patients with acute versus chronic LBP. Moreover, Coste and colleagues reported that there was a high degree of variability in interpretation of plain films performed in patients presenting with LBP, underscoring the poor diagnostic value of these studies for this condition. The degenerative findings evident on lumbar plain radiographs may represent normal age-related changes and fail to distinguish symptomatic degenerated discs from asymptomatic age-appropriate discs. Plain radiographs, however, are useful in the initial assessment of axial LBP, effectively ruling out other etiologies of back pain including fractures, osteomyelitis, tumor, spondylolisthesis, and deformity. In conclusion, plain radiographs are indicated in patients with LBP 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 of trauma, infection, or malignancy.

Discography

The use of discography to diagnose DDD and identify painful symptomatic discs has been controversial. Discography is an invasive procedure in 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 or axial CT images. The flow of contrast within the disc provides information regarding disc morphology and the integrity of the annulus. Contrast filling of a degenerated and 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 annular disruption, spilling of contrast into the canal or foramen. The integrity of the annulus 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 annulus.

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 the 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 annulus 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 annulus 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 and symptomatic discs. Cadaveric studies have shown a strong correlation between discographic contrast distribution and the severity of degeneration on gross examination. Also, there is a good correlation between disc morphology on discography and intraoperative findings of disc protrusions and herniations. Importantly, studies have revealed morphologic findings on discography correlate with elicited pain. As expected, the onset of pain is most commonly associated with discs that demonstrate dorsal annular tears (65.3%) as compared to simply degenerated discs (36.6%), internal annular disruption (20%), or intraosseous disc herniations (0%). The use of axial CT imaging provides even further morphologic assessment of the disc. Using the Dallas Discogram Description for CT-based discography, severe and moderately graded degenerated discs show a strong correlation with exact reproduction of pain, annular disruption being the best predictor of concordant pain. McCutcheon and Thomas found that contrast tracking to the periphery of the annulus suggesting radial fissures and annular disruption has an 87% correlation with concordant pain.

Subsequent studies, however, have failed to consistently reproduce these positive correlations. Several authors have demonstrated pain production with discography in other­wise normal-appearing discs in asymptomatic individuals. Carragee and coworkers 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 a 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. Yet, even with low-pressure discography, pain was produced in the same number of asymptomatic volunteers as LBP patients. Vanharanta and colleagues found that morphologically normal discs on DDD grading still provoked some pain response in 24% of individuals. Furthermore, severely degenerated discs resulted in exact reproduction of pain in only 22% of individuals and even discs with severe annular disruption had exact pain reproduction in only 36% of subjects. The reverse association demonstrated a slightly better correlation. Patients who had a positive pain response were also more likely to have evidence of disc degeneration. Overall, the investigators found that painful discs tend to have higher degrees of degeneration and annular 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.

Despite these conflicting studies, some clinicians have not dismissed discography due to lack of alternatives for accurately diagnosing discogenic LBP. Discography is also used 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 or concordant pain provocation are likely at the symptomatic levels. Therefore, fusion across the positive discographic motion segment will alleviate pain, and 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 some 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.

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). Other studies have shown that more than 90% of patients with positive discography improve after posterior lumbar fusion. Derby and coworkers have argued that better correlation is observed when chemically sensitive discs are identified on preoperative discography. Chemically sensitive discs provoke concordant pain under particularly low-pressure injection, suggesting that pain is generated by the displacement of biochemical agents that stimulate sensory nerve endings in the outer annulus. Therefore, Derby and coworkers hypothesized 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 and associates used discography to identify painful and symptomatic discs within a fused segment in patients with persistent LBP after posterior lumbar fusion. Subsequent ventral discectomy and interbody fusion of the positive discographic levels completely resolved pain.

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. Much of this lack of accuracy and consistency may depend 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 planning largely depends on the surgeon’s prior experience with this diagnostic modality as well as discussion with the patient regarding realistic postoperative expectations.

More recently, data show that discography may cause iatrogenic injury to the disc and further accelerate the rate of disc degeneration. Over a 10-year period, Carragee and associates followed patients with and without a history of discography, and MRI was used to evaluate disc degeneration. They found progression of disc degeneration, occurrence of new disc herniations, loss of disc height, and loss of disc signal intensity in patients who underwent previous discography. Unfortunately, a significant portion of patients were lost to follow up, limiting the scope of this study. 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. According to the 2014 guidelines by the Joint Section of the American Association of Neurological Surgeons/Congress of Neurological Surgeons for fusion in management of lumbar degenerative conditions, discography should not be used as an independent predictor of success following lumbar fusion for low back pain or as a stand-alone test on which treatment decisions are based.

Lastly, as previously mentioned, “discoblock” is an alternative to traditional discography and involves injecting the intervertebral disc with an anesthetic agent, rather than contrast, which alleviates pain instead of reproducing pain. In 2009, Ohtori and associates compared discography to discoblock in 42 patients undergoing noninstrumented ALIF in a randomized trial. All patients achieved bony fusion, but significantly improved pain and disability were associated with a positive discoblock and not positive discography (p < 0.05). More studies are needed to further assess discoblock as a diagnostic tool for axial LBP and a predictor of fusion outcomes.

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. Besides its ability to image in multiple planes, MRI with good-quality spin-echo T2-weighted images accurately characterizes the morphology of the disc and differentiates between the nucleus pulposus and annulus, making MRI a sensitive measure of DDD and an initial study of choice in axial low back pain. 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 and disc degeneration ( Fig. 58-2A ).

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

Moreover, with advanced degeneration of the discs, greater load is transferred to the end plates, causing characteristic changes on MRI. Initially the normal vertebral body bone marrow is replaced with vascularized fibrous tissue as a reparative response to injury, which appears on T1-weighted and T2-weighted MRI as decreased ( Fig. 58-2B ) and increased signal, respectively. With chronic degeneration, the normally red bone marrow is converted to yellow marrow as fat cells enter the marrow, which increases the signal on T1-weighted MRI.

Although MRI adequately characterizes the various stages of disc degeneration and its effects on the discovertebral complex, the clinical relevance of disc degeneration on MRI remains unclear. In fact, several studies have shown evidence of degenerated lumbar disc on MRI in 30% of asymptomatic volunteers. In a study by Boden and coworkers, degenerated discs were seen in all but one symptomatic subject older than 60 years of age with many having multiple degenerated discs. The authors concluded the high incidence of bulging and degenerated discs in asymptomatic subjects was likely to represent the normal process of aging.

Still, several studies have shown that MRI findings correlate well with abnormal discography suggestive of symptomatic degenerative disc disease. Painful discs on discography have also been observed to show more evidence of degeneration such as annular fissures, disc prolapse, and decreased disc height on MRI. Moreover, the high-intensity zone (HIZ) is an area in the annulus fibrosus that can appear on T2-weighted MRI and has high signal intensity in a degenerated dark-appearing disc, which has been correlated well with concordant pain on discography. Subsequently, HIZ shown on MRI may suggest annular disruption and reliably correlate with pain provocation on discography. On the other hand, 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 symptomatic discs ( Fig. 58-3 ). Modic and colleagues also found that MRI does not appear to have any measurable value in terms of management and outcome of patients with acute LBP. Ultimately there is no clearly defined relationship between degenerative changes seen on MRI and axial LBP. Contributing MRI findings to clinical symptoms is not straightforward and requires a thorough evaluation, especially when considering surgery.

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