Lumbar Disk Disease and Low Back Pain

Brian C. Werner and Adam L. Shimer

Lumbar degenerative disk disease (DDD) and low back pain (LBP) are common conditions, with more than 12 million Americans diagnosed each year, and 70% to 85% of adults affected by LBP at some point during their lifetimes. The sequelae of DDD are among the leading causes of functional incapacity and a common source of chronic disability in the working years. Diagnostic options and surgical interventions for LBP due to lumbar DDD without radicular symptoms are controversial, and clinicians are left without clear evidence as to the best avenues for accurately diagnosing and effectively managing this common and debilitating condition. This chapter reviews the workup of the patient with discogenic LBP, including physical examination, imaging, and special diagnostic studies, and presents available treatment options for the condition, including current nonsurgical and surgical interventions as well as future biologic options.

Natural History

LBP due to DDD is believed to be a result of the loss of normal structure and function of the intervertebral disk. Although lumbar DDD is a recognized cause of LBP, it is important to note that disk degeneration can occur in the absence of back pain or other symptoms in over 30% of individuals by age 30, in 50% of individuals by age 50, and nearly 100% of 80-year-old individuals.1 The etiology of degenerative disk changes is multifactorial and can be related to aging, wear and tear, environmental factors, such as nutrition and cigarette use, or even genetics. In a degenerating disk, over time, the collagen structure of the annulus fibrosus weakens and the proteoglycan content decreases. These physiologic changes lead to a decrease in the water content of, and nutritional supply to, the disk, making it more susceptible to mechanical stresses. This progresses to altered spinal biomechanics, which, combined with release of neural mediators and neurovascular ingrowth into the disk, generate LBP.2 Continued degeneration of an affected disk can lead to secondary problems, such as degenerative spondylolisthesis, lumbar stenosis, and facet arthrosis, which are not the focus of this chapter.

Workup

History and Clinical Presentation

The clinical presentation of a patient with discogenic LBP is variable. An acute or insidious onset can be described, and a variety of alleviating and aggravating factors are often implicated. Differentiating between acute and chronic LBP is important because the natural history, treatment, and prognosis are different. Lower-extremity radicular symptoms are typically absent, unless there is an associated disk herniation or foraminal stenosis. Claudication symptoms are likewise generally absent unless concomitant spinal stenosis is also present. It is imperative to differentiate discogenic LBP from the aforementioned entities before proceeding with diagnostic and therapeutic measures.³ Screening for secondary gain issues and inconsistencies is also important. The goal of the history and exam in a patient with LBP is to determine a likely etiology, evaluate treatments already rendered, and rule out serious pathology (“red flags”), such as neural compromise, trauma, neoplasm, and infection.

Physical Examination

Patients with primarily discogenic LBP usually have an unremarkable physical examination. Regardless, a thorough exam should still be performed. The patient should be observed closely while walking and during movement to and from the examination table, which may reveal an antalgic gait and guarding during transfers. A meticulous neurological exam usually will not reveal any focal findings. Provocative tests, such as the straight leg raise and femoral stretch test, are usually negative. There may be limited range of motion of the lumbar spine, with greater pain typically in flexion. “Red flag” symptoms, such as bowel or bladder changes, fevers, night sweats, or unexplained weight loss, should be absent with this diagnosis.

Radiographic Imaging

Upright plain anteroposterior (AP) and lateral radiographs, including flexion and extension views, should be the first study used in the evaluation of the lumbar spine. These radiographs should be evaluated for coronal and sagittal alignment, as well as for the presence of degenerative changes, including osteophyte formation, foraminal narrowing, disk space narrowing, endplate sclerosis, and vacuum phenomenon within the disk.

Magnetic resonance imaging (MRI) is the imaging modality of choice for evaluation of spinal soft tissues and disk detail. MRI must be used carefully as an adjunct to the clinical presentation, history, and physical examination, as 30% of asymptomatic individuals show degenerative disk changes on MRI.1 MRI, however, is not initially indicated in the majority of patients presenting with LBP due to DDD. If there is concern for malignancy, infection, or if red flag or neurologic symptoms are present, MRI should be obtained. For LBP due to DDD that is unresponsive to reliable nonsurgical intervention after 3 to 6 months, MRI can be a useful diagnostic adjunct. Signs of degeneration, endplate changes, presence or absence of annular tears, Modic changes, or the presence of high-intensity zones all can be evaluated on an MRI.⁴ Unfortunately, the low sensitivity and specificity of these MRI findings limit their usefulness.

Other Diagnostic Studies

Diskography is a potentially helpful adjunct in the diagnostic algorithm for LBP due to DDD, as it is the only diagnostic modality that involves direct stimulation of the potentially offending disk. Diskography must involve a low-pressure injection, must involve abnormal morphology (extravasation), must reproduce the patient’s usual pain, and should be nonpainful at control levels to be considered a reliable test. As diskography relies on the patients’ subjective reporting of their pain, it is limited in its diagnostic reliability, leading to significant debate and controversy over its effectiveness. Furthermore, it has been demonstrated that abnormal psychometric testing further skews diskographic results.⁵ Accordingly, diskography is largely considered an available diagnostic tool but not an initial or confirmatory diagnostic test.

Treatment

Nonsurgical

The mainstay of treatment for patients with chronic LBP due to DDD is nonsurgical management. After an appropriate diagnostic workup ruling out serious pathology, including neoplasm, trauma, and infection, and in the absence of any neurologic or motor deficits, a 6-month regimen of active physical therapy, behavioral modification (i.e., smoking cessation), weight loss, and nonsteroidal anti-inflammatory drugs (NSAIDs) should be instituted.⁶ Care should be taken to evaluate imaging studies for correlative pathology that could account for the pain, such as segmental instability, pars interarticularis defects, or deformity, rather than just generalized DDD. Approximately 90% of individuals with LBP due to generalized DDD will have resolution of their symptoms within 3 months with or without treatment, the majority of cases resolving in as little as 6 weeks.

Interventional

Interventional procedures such as spinal epidural steroid injections (ESIs) have long been used to treat discogenic LBP. Although no studies support the use of ESIs in the treatment of LBP, their success in selected patients warrants consideration as an alternative to surgical intervention.7 The use of intradiskal electrothermal therapy (IDET) in the treatment of discogenic back pain remains controversial. There are no good long-term studies demonstrating conclusive benefit, and the procedure is not recommended for general use.⁸

Surgical

Surgical intervention for LBP due to DDD that has failed extensive conservative measures can be divided into two broad categories: arthrodesis (fusion) and non-fusion options. Unfortunately, all surgical interventions for discogenic back pain provide inconsistent results and are the subject of significant controversy.

Arthrodesis can be approached in an open or a minimally invasive fashion, and includes posterolateral, posterior lumbar interbody fusion (PLIF), transforaminal interbody fusion (TLIF), or anterior lumbar interbody fusion (ALIF). None of these forms of arthrodesis have been demonstrated to be superior to the others in the surgical management of discogenic LBP, and conflicting data exists as to the benefit of arthrodesis compared with nonsurgical management.

A well-established complication of spine fusion surgery is adjacent segment disease.³ This has led to the development of non-fusion options for the treatment of LBP due to DDD, which allow motion to be preserved at the diseased spinal segment, theoretically slowing the degeneration at adjacent segments. The efficacy of this broad class of interventions, including soft-tissue stabilization procedures, interspinous spacers, and dynamic stabilization systems, has not been validated in the literature for the treatment of LBP.

Finally, total disk arthroplasty (TDA) is being studied as an alternative to fusion for the treatment of symptomatic DDD. Much as with other motion-sparing non-fusion technologies, the major advantage of TDA is the preservation of motion at the diseased level and prevention of adjacent-level degeneration and disease. TDA has been approved in the United States for the treatment of single-level back pain without instability.⁹ TDA has been shown to preserve motion at the surgical level; however, it has not been demonstrated to reduce the incidence of adjacent-level disease. Current randomized controlled clinical trials demonstrate that single-level TDA is equivalent to lumbar fusion in reducing back pain.

Summary

LBP due to lumbar DDD is a commonly encountered problem that is challenging to treat. Initial diagnostic imaging should include plain radiographs, and, in the absence of any neurologic findings or “red flags,” initial management should be nonoperative. For the select population of patients who fail extensive conservative management, available surgical interventions include both fusion and non-fusion options.