ESSENTIALS OF DIAGNOSIS
Results from damage to the intervertebral disc with associated morphologic changes.
Produces axial low back pain with or without radicular pain.
Pain is provoked with activities that increase intradiscal pressure.
Discogenic low back pain is the cause of pain for almost 40% of chronic low back pain sufferers. The term discogenic means that the disc is the source of the patient’s pain. In some cases, anatomic changes occur that cause the disc to compress adjacent neural structures, causing pain (radiculitis) or loss of function (radiculopathy). In other cases, the anatomic changes allow for ingrowth of the neurovascular supply, causing the disc itself to be painful and results in nonradiating low back pain.
Discogenic pain usually falls into one of the following categories: (1) degenerative disc disease, (2) intervertebral disc displacement or internal disc disruption, and (3) disc herniation.
A. Degenerative Disc Disease
Degenerative disc disease starts as a result of the normal aging process, or by excessive or repetitive trauma, leading to disc dehydration and an increase in the collagen concentration. Disc degeneration can begin as early as the third decade of life. Aging, obesity, smoking, and excessive axial loads can accelerate the degeneration of the intervertebral discs, with age being the strongest association. Degenerative changes in the lumbar intervertebral discs are a common finding on imaging and may have little correlation with back pain. However, in patients with chronic low back pain, studies have found that disc degeneration was one of the main reasons for their pain.
B. Internal Disc Disruption
Internal disc disruption is breakdown of the internal architecture of the disc that can lead to back as well as limb pain without signs of disc degeneration and disc protrusion, and without nerve root compression on imaging. Internal disc disruption is characterized by the presence of isolated radial fissures penetrating from the nucleus pulposus into the annulus fibrosis. The morphologic and biophysical features of internal disc disruption correlate strongly with back pain, as do certain MRI features. The presence of a single fissure distinguishes an affected disc from a normal disc. These fissures can be graded according to the extent to which they penetrate the annulus.
A disc herniation, also known as slipped disc, prolapsed disc, bulging disc, or herniation of the nucleus pulposus, is a broad term that includes three specific types of disc abnormalities. These abnormalities are differentiated based on the integrity of the posterior longitudinal ligament that reinforces the back of the disc as follows: protrusion, extrusion, and sequestration.
In a disc protrusion the posterior part of the disc is focally or eccentrically pushing backward into the anterior epidural space and has contacted, and even somewhat compressed, the traversing nerve root and front of the thecal sac. The posterior longitudinal ligament is still intact. Disc protrusions without nerve root compression are seen in about 30% of the normal nonsymptomatic population (Figure 31–6).
Sagittal MRI scan of the lumbar spine showing degenerative disc disease at L4–5, as demonstrated by loss of signal intensity within the nucleus pulposus, creating the “dark disc.” At L3–4 a contained disc protrusion is seen.
A disc extrusion is defined by the rupture of the posterior longitudinal ligament, allowing for further migration of the nucleus pulposus into the anterior epidural space. A disc extrusion is not typically seen in the asymptomatic person (Figure 31–7).
Sagittal MRI scan of the lumbar spine showing L4–5 disc extrusion. Note the persistence of high signal intensity within the center of the disc and herniation.
The final type of disc herniation, known as a sequestration, occurs when a fragment of nuclear material detaches itself from the main body of the disc and resides loosely in the epidural space. Sequestration-type disc herniations can be excruciatingly painful and, if centrally located, occasionally cause neurologic deficits requiring prompt intervention.
Most patients present with a complaint of axial low back pain with or without radiation to the limb related to the level of the affected disc. The pain may be progressive and longstanding, in the case of degenerative disc disease, or acute, in the case of internal disc displacement. Occupational factors, such as exposure to vibrational energy or heavy lifting, may be present. Particular positions or activities can trigger the pain by increasing intradiscal pressure, particularly jumping, coughing, twisting, or flexing the spine.
Physical hallmarks include tenderness over the spinous processes and paraspinal muscles. Pain is often exacerbated with trunk flexion and relieved with extension of the spine. Maneuvers such as sustained hip flexion and the pelvic rock test are often provocative; however, neurologic examination is often normal unless there is compression of the neural structures.
Plain radiographs cannot specifically evaluate the disc, but they can show structural changes, such as loss of disc height, that could be suggestive of a herniated or degenerative disc. MRI is the test of choice in evaluating intervertebral disc pathology and also provides excellent imaging of the surrounding soft tissues. CT scan with or without myelography is used when MRI is not available or is contraindicated. Imaging must be carefully correlated with history and physical examination, as studies can often be falsely positive or falsely negative. MRI and CT scans detect disc herniation 20–36% of the time within an asymptomatic patient population.
Provocation discography with postdiscography CT remains the gold standard for confirming the diagnosis of discogenic low back pain. In this procedure, pain is reproduced by pressurizing the affected disc with a contrast material. Unfortunately, provocation discography may actually produce more damage to the disc or trigger a degenerative disc disease; therefore, it should be performed only in cases when further intervention is being seriously contemplated. The presence of “red flags” (see Table 31–1) in the patient’s history or physical examination should prompt an early imaging study.
Bed rest should be limited to acute and severe cases and last no longer than 2–3 days as inactivity can potentiate prolonged disability and produce even more pain. Treatment goals focus on restoring strength, flexibility, and function previously lost because of immobility. The physical therapy prescription should include stabilization of core muscles, emphasizing neutral to extension bias. Physical modalities may be helpful in alleviating localized back pain.
Proper spinal bracing can help relieve pain by preventing painful movement or further spinal deformities but does not alter the natural course of the disease. Traction is commonly recommended to increase the foraminal dimensions, reduce intradiscal pressure, and, thus, relieve radicular pain caused by a herniated disc. Manipulative therapy is designed to maximize motion and decrease pain, but long-term studies of efficacy are lacking.
NSAIDs are first-line agents in the treatment of discogenic low back pain but may be contraindicated in some cases because of their side effects (ie, gastrointestinal bleeding, allergic reactions, and renal or liver impairment). Opiates and muscles relaxants are frequently prescribed for severe pain but often have concomitant sedatives effects, and their long-term efficacy for discogenic back pain has not been established.
Epidural steroids injections are effective in providing symptomatic relief of radicular pain and are offered to patients who have not responded to conservative measures. Surgery is indicated for progressive or worsening neurologic symptoms. Standard open discectomy is the most common surgical approach unless there are signs of instability, for which fusion would be necessary.
Regenerative treatment strategies designed to reverse or inhibit disc degeneration include the administration of growth factors, autologous or allogenic cells, gene therapy, and the introduction of biomaterials, and are undergoing clinical trials.
C: Molecular pathogenic factors in symptomatic disc degeneration. Spine J 2005;5:260S–266S.
N: Degenerative joint disease of the spine. Radiol Clin North Am 2012;50:613–628.
et al.: Chemical radiculitis. Pain 2007;127:11–16.
L: Association between the -1562 C/T polymorphism of matrix metal proteinase-9 gene and lumbar disc disease in the young adult population in North China. Connect Tissue Res 2009;50:181–185.
et al.: Lumbosacral radicular pain. Pain Pract 2010;10:339–358.
et al.: Features of intervertebral disc degeneration in rat’s aging process. J Zhejiang Univ Sci B 2009;10:522–527.
et al.: Clinical diagnosis for discogenic low back pain. Int J Biol Sci 2009;5:647–658.