Indications for Spine Fusion for Axial Pain

Pathophysiology

The normal lumbar intervertebral disc consists of fibrocartilaginous tissue designed to absorb and dissipate loads 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 diffuses 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.

The disc gradually becomes less hydrated with aging, and the concentration of proteoglycans decreases. 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. These degenerative processes occur in approximately 90% of healthy individuals by age 50 years.

Numerous theories have evolved to link DDD and back 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 physiological 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 physiological loading transfers more stress to the annulus and the end plate, where there is a high concentration of pain-sensitive nerve fibers. 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 leads to a high concentration of 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 the inner aspect of the annulus and even the nucleus. In addition to the sensory nerve fibers, there is growing evidence that sympathetic afferents are also increased in degenerated discs, playing a role in LBP. 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.

Although disc degeneration may be the initial inciting pathology, additional structures, including the 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 ramus courses around the facet and innervates the joint capsule. 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 primary source of pain.

Diagnosis

The diagnosis of axial LBP is primarily clinical, with supplementary radiological studies. Patients with axial LBP generally present with a deep, aching pain localized to the lower back, sacral region, or gluteal region. Pain is characteristically worsened with bending, twisting, or axial loading, such as climbing stairs, lifting, or prolonged sitting. Relief typically occurs with changing position or resting. Patients may also describe buttock or leg pain generally limited to above the knee. The distribution pattern is not typically radicular in nature, but may be referred sclerotomal pain.

Physical examination and neurological assessment are usually normal. The clinical history and physical examination are critical, however, for ruling out 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 evaluating conditions that closely mimic axial LBP symptomatology, including myofascial pain, sacroiliac joint pain, piriformis syndrome, and hip osteoarthritis.

There has been intense scrutiny of imaging modalities for diagnosing axial LBP, including methods for identifying potentially symptomatic discs and which levels may respond to surgical intervention. This prompted the Joint Section of the American Association of Neurological Surgeons/Congress of Neurological Surgeons to publish guidelines for fusion surgery in the treatment of lumbar degenerative conditions, with specific recommendations regarding the diagnostic evaluation of axial LBP. ^, In summary, 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. Discography may have utility 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 that the predictive value of discography is controversial, and that, based on the literature, discography should not be used as an independent predictor of success following lumbar fusion for LBP or as a stand-alone test on which treatment decisions are based.

Plain Radiographs

Plain radiographs in patients with axial LBP typically 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. 135.1A ). Sclerotic end plates or bone-on-bone appearance are commonly seen with severely degenerated discs (see Fig. 135.1B ). Plain radiographs can be performed with patients in weightbearing, flexion, or extension to demonstrate the alignment of the spine and the nature of the motion segments under normal physiological loading. The presence of hypermobility or malalignment under such stresses may help to identify which levels are symptomatic or may suggest other pathological processes.

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. 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 for ruling out other etiologies of back pain, including fractures, osteomyelitis, tumor, spondylolisthesis, and deformity.