Adjacent Segment Disease After Fusion

Definitions

Adjacent segment disease (ASD) has been broadly and inconsistently defined in the literature. Other terms that have been used to describe ASD include junctional disease, junctional stenosis, or a transitional lesion. ASD has been applied to a plethora of radiographic findings suggestive of degeneration in a motion segment immediately adjacent to a spinal fusion construct with or without symptoms. Although the many symptoms included in studies range from minor symptoms to those necessitating surgical intervention, definitions generally do not include axial pain, numbness, or muscle spasms from the index operation. For the purposes of this chapter, we will define ASD as radiographic findings of adjacent segment degeneration with accompanying and correlative symptoms. We will define adjacent segment degeneration (ASDeg) as radiographic evidence of pathology in the adjacent segment without clinical sequelae.

Several imaging findings are consistently associated with ASDeg. On plain radiographs, one can observe disc height collapse, end-plate sclerosis, osteophyte formation, or spondylolisthesis. On computed tomography (CT) scanning and magnetic resonance imaging (MRI), the most common finding is disc degeneration, although facet hypertrophy and central or foraminal stenosis are also seen. There are two systems in the literature to describe ASD in the cervical spine, but there is no such accepted scale for ASD of the lumbar spine. The radiographic cervical ASD grading system proposed by Hilibrand and colleagues ranges from 1 to 4, with the higher numbers reflecting the increasing severity of adjacent disc and end-plate changes, as well as neural element compression on MRI, CT, and plain radiographs. The radiographic system proposed by Park and colleagues ranges from 0 to 3, with the higher numbers reflecting increasing degrees of ossification across the adjacent disc space. ASD in the lumbar spine has sometimes been described using scales designed for degenerative disc disease, such as the Pfirrmann or UCLA disc degeneration grades, although this is far from uniform. Unfortunately, our current conceptualization of ASD includes a heterogeneous group of patients, which makes it difficult to thoroughly, yet succinctly, encapsulate their radiographic patterns.

Biomechanical Pathogenesis of Adjacent Segment Disease

ASD can be viewed as an accelerated version of age-related lumbar spondylosis, which is briefly reviewed here. Most of the axial loading in the spine is transmitted through the disc space, which is comprised of the annulus fibrosus and nucleus pulposus. Through the aging process, the hydrated proteoglycan matrix of the nucleus desiccates, leading to the loss of disc height and increasing the load transmitted to the facet joints. Under supraphysiological loads, the facets degenerate, resulting in abnormal motion that can accelerate disc degeneration and spondylolisthesis. Disc herniation, reactive osteophyte formation, and buckling and hypertrophy of the ligamentum flavum can lead to neural element compression and clinical symptoms.

Lumbar arthrodesis alters physiological biomechanics and is thought to lead to ASD by transferring motion to adjacent mobile segments. A canine in vivo study by Dekutoski and colleagues found increased facet loading and motion at levels proximal to a fusion construct. Bastian and colleagues fused human cadaveric spines from T12 to L2 and found that the range of motion for the adjacent levels increased following fixation. Other human cadaveric studies not only corroborated these findings of increased motion but also found evidence of increased intradiscal pressure in adjacent segments. Although there may be contributions from the normal progression of degenerative disease, these biomechanical studies support the iatrogenic hypothesis in the pathogenesis of ASD.

Minimally invasive techniques probably represent the most studied attempt at preventing ASD, the prevailing theory being that reduced soft tissue disruption leads to less iatrogenic instability. Older studies, however, contend that the scar tissue formed from open surgery leads to less stability through the increased stiffness from scar tissue formation. There have been several attempts to study how traditional open surgery versus minimally invasive spine surgery affects the risk of developing ASD. One study by Yee et al. reported a trend toward a decreased risk of ASD in minimally invasive transforaminal lumbar interbody fusion (TLIF) compared with an open approach, although this trend was not statistically significant. Other studies, however, have failed to demonstrate any difference in ASD related to the surgical technique. A prospective study by Ekman and colleagues randomized 111 patients with isthmic spondylolisthesis to exercise or posterolateral fusion, and although there was an increased rate of radiographic ASDeg, there was no difference in the clinical outcome or reoperation rate, with a mean follow-up of 12.6 years.

Incidence

Describing the natural history of ASD is confounded by expected age-related degeneration of the spine. Data are conflicting and definitions are heterogeneous across studies. In a study of asymptomatic individuals, Boden and colleagues found degenerative changes in 57% of adults over 60 years of age. Rates of ASD range from 2% to 100% depending on the series. The exact timeline for ASD versus ASDeg has not been well established in the literature. In general, ASDeg that is symptomatic and that appears faster than the natural history of ASDeg is considered ASD. Of course, the length of time that is considered faster than expected is ambiguous and subjective. Cheh et al. found that 43% of their patients had ASDeg, but only 24% had clinical symptoms. Conversely, 6.3% had clinical symptoms without a radiographic correlation. A review of the literature by Park and colleagues found that the rate of ASDeg was significantly higher than the rate of ASD, suggesting that not all radiographic progression is clinically symptomatic or meaningful. When narrowing the focus to symptomatic patients, a review by Radcliff et al. and the retrospective study by Lee et al. both found an approximately 2% to 3% risk per year of developing ASD. Again, a similar result was reported in the retrospective series of Ghiselli and colleagues, who demonstrated an ASD risk of 16% at 5 years and 36% at 10 years. The time course for ASD has been studied both retrospectively and prospectively but, again, data are conflicting. The average duration from index operation to reoperation for ASD ranges from 6 months to 5 years.