The Black Disc: Diagnosis and Treatment of Discogenic Back Pain

Summary of Key Points

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Studies have substantiated the existence of discogenic back pain associated with discrete annular tears and diffuse annular degeneration. Discogenic back pain is clinically characterized by sitting intolerance, pain on forward flexion, and pain relief with recumbency.
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Diagnosis of discogenic back pain lies in the prudent use of imaging correlates to support a clinical diagnosis. Discography is a controversial tool that may be used to clarify a suspicious disc’s contribution to the patient’s symptoms in ambiguous situations.
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Surgical treatment of discogenic back pain should be reserved for patients who were refractory to conservative management, as most patients will note slow resolution of pain with conservative therapies within 6 months.
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Studies have substantiated the efficacy of lumbar fusion for the treatment of discogenic pain in carefully selected patients. Total disc replacement has emerged as an alternative to fusion, with the benefit of removing and replacing the painful intervertebral disc and the added advantage of preserving spinal mobility.
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Novel molecular or cellular therapies focusing on the prevention of disc degeneration or disc regeneration are attractive. Significant work remains to be done before these treatments are widely accepted.

Black disc disease is the common term for the degenerative processes of intervertebral disc dehydration that correlate with imaging changes from a normal white nucleus to a black nucleus on magnetic resonance imaging (MRI). Despite the intriguing name of its MRI appearance, this condition is commonly observed incidentally and does not necessarily indicate the presence of disease that results in clinical symptoms.

Nevertheless, there are likely distinct situations in which disc degeneration alone can cause significant symptoms and, with appropriate screening, may benefit from surgical intervention. The diagnosis and treatment of patients with low back pain from disc degeneration, referred to as discogenic back pain , are the focus of this chapter.

The degenerative process of disc dehydration resulting in the “black disc” is common to all disc spaces in the body and is the earliest sign of normal aging and osteoarthritis in the spine. Degenerative disc disease must be distinguished as symptomatic or asymptomatic. The symptomatic “black disc” reflects intrinsic changes in the disc itself that can result in primary joint pain without compression of the traversing spinal nerve roots or spinal cord. Discogenic back pain, therefore, is the clinical presentation of lumbosacral pain in the absence of radicular pain or neurogenic claudication.

The fact that intractable axial back pain may be associated with degenerative changes in the lumbar discs has been recognized since the 1960s. Discography was introduced by Lindblom in 1948 to evaluate the disc anatomy for disc herniation. Four years later, Hirsh and Schazowicz described the provocation and localization of axial back pain with discography despite a normal myelographic study. Since the 1960s, in spite of a general understanding of the condition, a consensus definition of discogenic back pain has not been achieved.

The lack of consistent terminology to describe symptomatic disc degeneration has added to the controversy. In 1970, Crock used the term internal disc disruption as an alternative to describe this process. More recently, the term symptomatic annular tear has been used because of subtle findings on high-resolution MRI and lumbar discography. For consistency in this chapter, we will use the terms discogenic back pain , annular tear , and annular degeneration in reference to symptomatic disc degeneration. Less specific terms such as black disc disease , dark disc disease, postlaminectomy syndrome , and failed back syndrome should be avoided in favor of more specific terminology.

Because of inconsistent terminology and nonstandardized definitions for low back pain, the various causes of back pain have been difficult to differentiate in clinical studies. Furthermore, although axial back pain can occur independently of radicular pain, clinical studies have not routinely distinguished between the causes and treatments of axial back pain as compared to radicular leg pain. Consequently, accurate or reasonable epidemiologic estimates for the incidence, prevalence, or natural history of discogenic back pain as compared with radiculopathy with or without axial back pain are sparse.

Causes of Discogenic Pain

Although the most common source of midline axial back pain is muscular or ligamentous strain, chronic pain associated with specific postural changes can be attributed to either facet joints or intervertebral discs. More specifically, discogenic pain is classically associated with sitting intolerance and flexion of the spine, as compared with pain with spinal extension in cases of facet syndrome. As the body’s largest avascular structure, the intervertebral disc is prone to decreased nutritional uptake and subsequent degeneration. Repetitive motions in the spine from activities of daily life can create shear forces, resulting in microtrauma to the disc. Breakdown of proteoglycans and hydrophilic proteins in the nucleus pulposus leads to disc desiccation, which in turn initiates a cascade of disc height loss, progressive disc collapse, and immobility of the functional spinal unit. This decreased motion may actually lead to mechanical stability through the formation of osteophyte across the affected disc space and gradual resolution of pain, despite continued or progressive degeneration. The natural history and time course of symptoms can vary widely, and a small number of patients remain chronically symptomatic. The dilemma in diagnosis and treatment lies in our lack of understanding of why intervertebral discs with nearly identical morphology can behave differently, some causing patients’ chronic pain while others remain asymptomatic.

Progress has been made, however, in understanding the pathophysiology of the lumbar disc as a cause of discogenic pain. The lumbar disc is supplied by a network of pain fibers from the sympathetic chain arising from the sinuvertebral nerve, which innervates the outer layers of the annulus fibrosus. With progressive disc collapse, the annulus bulges and tears. Activation of annular nociceptive C-fibers then occurs from direct mechanical stimulation from disc material extending into the outer region of the disc. In addition to causing direct pain, annular tears decrease disc integrity and can cause pathologic loading of the facet joints and end plates, with resultant inflammation. Sprouting of pain fibers into the site of annular injury has also been observed and may be a factor in causing symptoms.

Pressure changes within the disc provide yet another mechanical factor that causes discogenic pain. Intradiscal pressures have been shown to be greatest in the sitting position and correlate with the symptomatic pattern of discogenic pain, which worsens with sitting and resolves with recumbency. Clinically, a lumbar disc herniation can present with an initial history of acute back pain prior to the development of radicular leg pain. Some patients report the resolution of this initial back pain with simultaneous acute new onset of radicular leg pain. Although cause and effect are difficult to prove, it has been postulated that the initial pain from a symptomatic annular tear resolves as internal pressure on the annular pain fibers decreases with herniation of nuclear material into the spinal canal.

In addition to mechanical sources of pain, a wide variety of putative inflammatory agents, such as phospholipase A2, metallomatrix proteinases, and prostaglandins have been reported to occur in the nucleus pulposus as part of the degenerative process ( Fig. 104-1 ). Leakage of these substances into the outer annulus fibrosus may be another mechanism of pain generation in degenerative disc disease. Exposure of the dorsal root ganglion to these same noxious agents has also been shown to result in histologic damage to the myelin sheaths and ganglion. This inflammatory process may be the basis of neuropathic pain, which may accompany discogenic pain.

Clinical Presentation

The hallmark of discogenic back pain is the pattern of activity-related back pain that is characterized by sitting intolerance and significant relief with recumbency. This chronic lumbosacral pain is usually described as a deep midline aching discomfort, not tender to the touch, which frequently extends into the gluteal region and occasionally radiates into the lower extremities. Patients may report an abrupt onset of symptoms with acute annular tears, which typically occur while the person is bent over to lift, and are described as a “pop” in the spine followed by severe pain. Activities that increase intradiscal pressure (e.g., coughing, sneezing, and bending forward) or increase axial loading (e.g., running) can also exacerbate symptoms. Ascending stairs and prolonged periods of driving, which require flexing the spine and loading the disc space, are often reported to significantly aggravate the patient’s pain.

The leg pain arising from a symptomatic annular tear typically extends into the dorsal thigh but only rarely extends below the knee and may be mistaken for true radiculopathy. Occasionally, pain may present extending distally into the foot but in the absence of nerve root compression on MRI; this pattern would signify referred pain that would best be described as pseudoradiculitis.

Despite the description of significant pain, the physical examination is usually normal; by definition, the diagnosis of discogenic back pain excludes findings associated with nerve compression. On close observation, the patient may exhibit a tendency for frequent position changes, a relative intolerance to sitting, and pain on forward flexion. The absence of physical findings may prompt the diagnosis of malingering or psychogenic pain. The presence of Waddell signs may indicate a nonorganic source of pain and prompt further psychological assessment. Waddell signs are a group of physical findings divided into five categories, the presence of which has been thought to indicate the possibility of a nonorganic cause for painful complaints. Formal psychometric testing should be used liberally to rule out potential psychosocial issues and to quantify the effect of long-standing pain on coping mechanisms. Abnormal psychological factors, in addition to the presence of active litigation, tobacco use, and disability, are predictive of a poor outcome with surgical treatment. Close observation of the patient at the time of discography can be helpful in further substantiating the presence or absence of psychological risk factors, and some institutions use video recordings for accurate recording of the patient’s response at the time of testing.

In addition to pain of discogenic origin, there are alternative sources of activity-related back pain. Myofascial and ligamentous pain tend to be more superficial, diffuse, and sharp; often have significant local tenderness; and are less associated with sitting intolerance. Pain from facet arthropathy typically occurs with extension maneuvers of the spine and improves with flexion. Tumors may present with vague back pain symptoms but are rarely missed with current MRI capabilities. Osteoporotic or pathologic fractures frequently present with isolated back pain but are easily recognized with standard radiographs and computed tomography (CT) and with MRI scans in the acute setting. Isthmic spondylolisthesis can result in chronic back pain or be asymptomatic and may present with acute back pain in adolescent patients, whereas older patients more often present with radiculopathy. An incomplete transitional vertebra syndrome with unilateral or bilateral pseudojoint formation between the enlarged L5 transverse process and sacral ala can also be a potential source of pain and can be easily missed without an angled anteroposterior (Ferguson’s) plain radiograph of the lumbosacral junction.

Diagnostic Imaging

Although imaging technology has advanced dramatically, there remains no technology capable of definitively diagnosing discogenic back pain. Rather, diagnosis lies in the prudent use of imaging correlates to support a clinical diagnosis. Typical radiographic findings include loss of disc space height, end-plate sclerosis, osteophyte formation, and disc bulge, consistent with spondylosis, which may also be found in asymptomatic patients. Standard spine radiographs are warranted to rule out spinal instability but are otherwise unhelpful in the diagnosis of symptomatic annular tear. With the advent of MRI, the entire spine can be screened for degenerative processes. Although the so-called black disc features nonspecific imaging changes that are consistent with loss of water content (and the disc therefore appears hypointense on T2-weighted imaging), a unique finding referred to as a high-intensity zone (HIZ) in the dorsal annulus has been described on MRI consisting of a discrete hyperintensity within the dorsal annulus. The HIZ lesion has been thought to represent either disc material visualized within an annular tear or edema fluid located within the dorsal annulus ( Figs. 104-2 and 104-3 ). Although this finding may be suggestive and helpful in localizing the site of pain, it may also be asymptomatic. In one study of 36 volunteers without low back pain or sciatica, the prevalence of disc bulging was 81%, and focal disc protrusion was 33%. Fifty-six percent of the volunteers had annular tears, the majority of which showed contrast enhancement on MRI.

Additional MRI findings have been characterized by Modic and colleagues, who described signal changes in the vertebral bodies adjacent to the affected disc space that may have clinical implications correlating with discogenic disease. Modic type I changes are hypointense on T1 and hyperintense on T2 sequences and signify bone marrow edema. These findings are indicative of acute changes in the vertebral body, have a high specificity for discogenic back pain, and may warrant further workup for the possibility of treatment. Modic type II changes indicate marrow replacement by fat, are hyperintense on both T1 and T2 sequences, and signify chronic degenerative changes involving the vertebral body and intervertebral disc that are less likely to be associated with discogenic pain. Modic type III changes are hypointense on both T1 and T2 sequences, indicating sclerotic vertebral end plates that are clinically insignificant. Pfirrmann and coworkers developed a grading system for lumbar disc degeneration based on T2 MRI sequences. Grade I discs are homogeneous, with bright hyperintense white signal intensity and normal disc height. Grade II discs are inhomogeneous, with a hyperintense white signal. The distinction between nucleus and annulus is clear, and the disc height is normal, with or without horizontal gray bands. Grade III discs are inhomogeneous, with an intermediate gray signal intensity. The distinction between nucleus and annulus is unclear, and the disc height is normal or slightly decreased. Grade IV discs are inhomogeneous, with a hypointense dark gray signal intensity. The distinction between nucleus and annulus is lost, and the disc height is normal or moderately decreased. Grade V discs are inhomogeneous, with a hypointense black signal intensity. The distinction between nucleus and annulus is lost, and the disc space is collapsed.

Although these imaging correlates may help to identify the disc as a pain generator, the predictability of a surgical response based on these findings and physical examination remains suboptimal. Discography is a tool that may be used to better clarify a suspicious disc’s contribution to the patient’s symptomatology in ambiguous situations. However, discography itself is controversial, as its use has not been definitely linked with improved surgical outcomes, and the test itself may cause accelerated disc degeneration at otherwise healthy levels over time. In a 10-year cohort study, 35% of the discs that had been exposed to discography puncture and injection had degenerative findings, compared to 14% of control discs.

Discography Technique and Interpretation

Discography involves the injection of water-soluble iodine contrast into the disc with observation of the contrast pattern, volume of injection, effect of pressure, and, most important, the patient’s pain response ( Figs. 104-4 and 104-5 ). The diagnosis of discogenic pain is made if the patient’s pain is identically and consistently reproduced when the contrast is injected into the disc. Although the development of concordant pain is key, equally important is the absence of significant pain from a control level. If lateralizing symptoms are described in the history, reproduction of these lateralizing symptoms at the time of discography help to determine the level of concordance. The patient’s typical referred pain should not be confused with radiculopathy.

The technique for discography requires the use of fluoroscopy for localization but does not necessarily require a biplane facility. With an anteroposterior view, a paramedian entry point 8 to 10 cm from the midline aligned with the disc of interest is chosen. A more lateral insertion may be required for obese patients. The needle is directed 45 degrees in the axial plane lateral to the superior articular process, at the midpoint between the two end plates, and medial to the exiting nerve root, which is known as the Kambin triangle. When large facets are encountered, a more lateral entry point may be needed.

A two-needle technique is typically utilized, which minimizes the potential for iatrogenic discitis. A standard-length 18-gauge spinal needle is first inserted through the skin following the trajectory toward the disc space but without entrance into the disc. The stylet is then removed, and a 6- to 7-inch 22-gauge spinal needle is placed coaxially through the 18-gauge spinal needle to avoid potential contamination with skin flora bacteria. Placement of the needle tip into the center of the disc space is confirmed with fluoroscopy. Peripheral placement of the needle must be avoided, as an injection into the annular region can result in either a false-positive result or negative pain responses. At L5-S1, entry into the disc space can be difficult because of the limitation of the iliac crests combined with the larger facet joints. Placing a gentle curve in the tip of the 22-gauge needle is usually sufficient for overcoming these anatomic obstacles. Occasionally, a midline transdural approach may be required at L5-S1.

Contrast agent should be injected until a firm pressure resistance is felt, and the volume should be recorded. Typically, 1.5 to 3 mL of contrast can be injected into the lumbar disc spaces. The use of manometry may help to standardize the injection procedure. Between 60 and 80 psi, pressure resistance is typically met, and injection of additional contrast agent becomes difficult and potentially painful. Degenerative discs acting as pain generators are often sensitive and may be symptomatic at the time of provocative testing even with lower pressures. These discs that develop concordant pain with relatively small volumes of contrast have been termed chemically sensitive discs and may have a higher rate of response to surgical treatment.

Close observation and recording of the pattern and intensity of the pain response must be done during the discography procedure. The reliability of this information is intimately related to the level and clarity of communication between the patient and physician. Sedation during the test should therefore be minimized and even avoided if possible. A discogram should not be considered positive or concordant without exact reproduction of the patient’s typical pain, and the patient must remain blind to the disc that is tested during the procedure for an accurate assessment of results. Injecting local anesthetic into the disc at the end of the procedure may relieve pain, further increasing the diagnostic sensitivity. With the addition of intradiscal steroids, there can occasionally be a therapeutic advantage. Because of this need for clinical correlation, the operating surgeon may be in the best position to assess the validity of the test, whether through direct performance of the procedure or by review of a video recording of the procedure.

The various radiographic appearances of the degenerated disc space containing contrast material have been described, and grading systems have been devised. The observed contrast patterns have not, however, been shown to consistently result in clinical symptoms. CT is usually obtained within a few hours after the injection and may help with operative planning by providing information regarding the internal architecture of the disc, localizing annular tears, and offering guidance for minimally invasive surgeries ( Fig. 104-6 ). Postprocedure CT images are especially important in cases with planned percutaneous approaches that involve direct treatment of a demonstrated annular tear.