Low back pain, presumably due to degenerative disease, is ubiquitous. Eighty percent of people experience an episode of low back pain at some point in their lives of sufficient severity to cause 48 hours or more of disability. This sort of axial back pain is frequently referred to as “nonspecific” low back pain. Unfortunately, the practical scientific and clinical utility of this term is quite limited as it has effectively resulted in investigator’s focusing on symptoms with many possible etiologies, as opposed to making a more precise diagnosis and investigating specific treatments for that diagnosis. As such, despite the existence of many well-designed studies, including numerous prospective, randomized controlled trials, the literature is surprisingly lacking in strong recommendations for either nonoperative or operative intervention. One of the major factors contributing to this is that the selection criteria for many studies are quite broad, heterogeneous, and there are numerous uncontrolled variables. Regardless of optimal study design, such shortcomings in study group selection severely limit the value of resultant data.

Typically there are five lumbar intervertebral disks. In many instances, reports of diagnostic imaging will number vestigial disks, resulting in “extra” lumbar vertebra. The key is to be certain that identification of the level is precise, particularly in a surgical setting. Strictly speaking, the characterization of a transitional segment or additional vertebra may be anatomically inaccurate.

The osseous anatomy includes the spinal canal, transverse processes, the vertebral body, pedicles, posterior laminar arch, and inferior and posterior zygapophyseal (facet) joints. Additional dynamic stabilization is provided by the following ligaments: anterior longitudinal ligament, posterior longitudinal ligament, and the ligamentum flavum. The ligamentum flavum is the only pre-stressed ligament in the body due to its high content of elastin and stretches posteriorly in the spinal canal between adjacent laminae. Paired facet capsules are true synovial joints with cartilage, joint capsules, and sensory innervation predominantly via the medial branch of the posterior primary ramus. Finally, the major check to excessive flexion, the supraspinous and interspinous ligaments run between the spinous processes at adjacent levels.

The degenerative cascade typically begins in the third decade of life with desiccation of the intervertebral disk (Fig. 18.1). As the nucleus loses water content, disk height decreases and radial fissuring in the annulus results. When such fissures reach the outer 50% of the annulus, back pain may result due to the innervation of this area by nociceptive fibers. Any activities which increase intradiscal pressure such as flexion, axial loading, or exposure to repetitive vibration may be expected to increase back pain due to disk degeneration.

As the disk space continues to narrow, there is secondary subluxation of the facet joints in a rostral caudal direction. This results in stress on the facet capsular ligaments, disrupted synovial nutrition, and cartilage degradation. The ligamentum flavum begins to enfold and frequently, as it stiffens, will become ossified or calcified. The net effect of this, aside from painful structural processes, is a narrowing of the spinal canal resulting in central stenosis. As the facet capsules continue to contract and degenerative changes (e.g., osteophytes) develop, lateral recess and foraminal stenosis also results. These lead to the clinical symptoms of claudication or radiculopathy; consequences of the degenerative cascade; but, not the cause of axial back pain per se.

Arguably, the most common source of degenerative low back pain is the intervertebral disk. As noted, the disk degeneration occurs first and begins quite early in life. The secondary disk space narrowing with resultant disk prolapse and secondary foraminal narrowing as noted above is, in the sense of back pain, irrelevant as the degenerative changes may be the main drivers of axial pain. As annular fissures propagate and begin to involve the innervated area in the outer annulus, back pain can result. From a clinical point of view, one of the most reliable sources of low back pain has been shown to be the posterior annulus, which when stimulated frequently produces back pain.

When secondary changes occur in the lumbar facets (in the absence of trauma or other structural issues as spondylosis or spondylolisthesis), facet-mediated symptoms may in fact be primary, again resulting in low back pain, which typically is improved with sitting or in flexion as compared to standing, walking, or lumbar extension. Aside from the customary degenerative changes such as joint space narrowing and osteophytes, magnetic resonance imaging may demonstrate a so-called “loaded facet,” in essence a facet effusion (Fig. 18.2). Effusions >1.5 mm on MRI are associated frequently with spondylolisthesis at that level, and should be investigated with plain films including flexion extension views.

Ninety-five percent of normal flexion and extension occur at L4–L5 and L5–S1. The L5–S1 segment is stabilized additionally by the iliolumbar ligament. As a result, during the degenerative cascade sagittal translation, specifically spondylolisthesis frequently occurs at L4–L5 as the degenerative process proceeds and ligamentous laxity increases. Spondylolisthesis is extremely common, with sagittal translations of 3 to 5 mm seen in up to 60% of the population by the seventh decade.

Low back pain is the leading cause of disability worldwide. In the assessment of the state of Health of the United States, 1990–2010, low back pain was the disease responsible for the largest number of years lived with disability. The 1-year incidence of a first ever episode of low back pain ranges between 6.3% and 15.4% with an episode remission rate at 1-year ranging from 54% to 90%. Estimates of recurrence at 1 year range from 24%
to 80%. In general, the incidence of low back pain is highest in the third decade, with the overall prevalence increasing until ages 60 to 65.