Adjacent Segment Degeneration and Disease of the Lumbar Spine

Summary of Key Points

Adjacent segment degeneration (ASDeg) refers to the development of asymptomatic degenerative changes on radiographic imaging adjacent to a fused spinal segment.
Adjacent segment disease (ASD) describes the development of clinical symptoms associated with these radiographic changes.
The etiology of ASD is unknown.
Multiple risk factors have been described as possibly associated with the development of ASD, including sagittal imbalance, preexisting degeneration, fusion method and length, iatrogenic injury to the posterior elements, and patient-related factors, such as age and body mass index.
Dynamic stabilization, topping off, tethering, interbody fusion, and total disc replacement may be beneficial for preventing the development of ASD.
Extended posterior fusion, interbody fusion, and minimally invasive discectomy are reasonable approaches for management of ASD.
High-quality studies are necessary for developing a better understanding of ASD, as well as treatment strategies to both prevent and manage ASD.

Decompression and arthrodesis has been used to achieve symptom relief and stabilization in patients with degenerative disease of the lumbar spine. There is growing concern that this treatment method poses risk for developing further degenerative changes adjacent to fused segments. There are no universally accepted criteria for both the diagnosis and evaluation of adjacent segment degeneration (ASDeg) and adjacent segment disease (ASD). The general consensus is that ASDeg refers to the development of asymptomatic degenerative changes on radiographic imaging. The development of clinical symptoms associated with these radiographic changes, such as neurogenic claudication or radiculopathy, has been termed ASD. The purpose of this chapter is to discuss ASDeg and ASD in the lumbar spine, including etiology, risk factors, and proposed strategies for prevention and management.

Pathophysiology

The etiology of pathology adjacent to a lumbar fusion is unknown. Whether ASDeg or ASD is the consequence of altered spinal mechanics following arthrodesis or a natural progression of degenerative spine disease is debated. In vitro biomechanical studies have demonstrated that multilevel lumbar fusion increases force on neighboring intervertebral discs and facets up to 45%, and is accompanied by a 41% to 55% decrease in pressure at the level of fusion. These results have been further supported by in vivo studies that compared lumbar fusion to sham operation in rabbits and found significant radiographic and histological degeneration of the neighboring discs with fusion after 9 months. These studies suggest that fusion acts as a lever arm, increasing the loading forces acting on the adjacent spinal level and leading to premature degeneration. Nevertheless, it remains unclear if ASDeg or ASD occur because of altered biomechanics or if these processes represent progression of chronic degenerative changes.

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