Adjacent Segment Disease: Factors and Impact of Minimally Invasive Surgery

Amandeep Bhalla

Christopher M. Bono

FACTORS RELATED TO ADJACENT SEGMENT DISEASE

Spinal fusion has been established as the gold standard for the treatment of a number of spinal conditions. With this, however, resultant stresses or alterations on the adjacent segment have been caused degeneration at adjacent levels. In discussing this topic, it is important to delineate degenerative radiographic changes from clinically significant adjacent level changes. Adjacent segment degeneration is defined as radiographic changes seen at levels adjacent to a fusion, though these do not necessarily correlate with clinical symptoms. Adjacent segment disease (ASD) refers to the development of clinical symptoms associated with radiographic degenerative changes at an adjacent level (Fig. 34.1).

Epidemiology

The incidence and prevalence of adjacent segment degeneration and ASD have been reported extensively. Ghiselli and colleagues reported a rate of ASD warranting surgery after posterior lumbar arthrodesis to be 16.5% at 5 years, and 36.1% at 10 years.¹ In a large metaanalysis by Xia et al.² examining 94 papers, the prevalence of radiographic adjacent segment degeneration and ASD in the lumbar spine was 26.6% and 8.5%, respectively. A systematic review by Lawrence et al.³ found the mean annual incidence of clinically symptomatic ASD ranged from 0.6% to 3.9%. A challenge inherent to the study of ASD is differentiating the causality of the fusion surgery from the natural history of disk degeneration. Fan et al.,⁴ in a prospective study of patients with lumbar pathology treated operatively or nonoperatively, found that fusion had an independent effect on the natural history of adjacent segment degeneration. The natural history of disk degeneration progresses in 41% of asymptomatic patients,⁵ which confounds analysis of degeneration as a result of adjacent level fusion. The risk factors for ASD and ways to mitigate its development are still not clearly understood. Symptomatic ASD that occurs after lumbar fusion surgery can often benefit from further fusion and/or decompression.⁶

Factors Influencing Fusion

It is worthwhile to identify patient or surgical factors that have an effect on ASD. Further understanding could help guide patient expectations, inform patient selection, and influence surgical decision making.

Surgical Factors

Some authors have explored surgical variables that may be protective against the development of ASD. Min et al.⁷ retrospectively reviewed patients who underwent lumbar fusion surgery with minimal adjacent segment degeneration preoperatively and found that the restoration of lumbar lordosis may have a protective effect against the development of ASD. In a retrospective case-controlled study, Djurasovic et al.⁸ reported that fusion of the lumbar spine in abnormal sagittal alignment, with loss of lumbar lordosis, predisposed patients to the development of
ASD. Interestingly, the group found that, while maintenance of lumbar lordosis mitigated the risk of ASD, preexisting degeneration did not influence its development. Disch et al. performed a 14-year follow up of 102 patients who underwent single- or two-level fusion surgery between L4 and S1. The authors reported those patients with ASD had statistically significantly reduced sacral inclination and lumbar lordosis angles.⁹ From these data, a correlation between sagittal alignment and the risk for ASD seems to exist.

Figure 34.1 Anteroposterior (AP) (A) and lateral (B) views of a patient who underwent an L4-L5 laminectomy and fusion from L3 to L5. After 4 years of substantial pain relief, she developed increasing back and leg pain. An MRI at that time demonstrated adjacent level stenosis at the L3-L4 level (C and D). She preferred to hold off on surgery at that time, but developed much worse symptoms 6 months later. An MRI at this time demonstrated that she developed a superimposed disk herniation (arrow) at that level as well, descending behind the L4 vertebral body (E and F).

Some studies have sought to examine the effect of fusion length on the development of ASD, hypothesizing that the greater stress imparted by a longer rigid construct would result in higher incidence of ASD. Sears et al., in a retrospective cohort study of 912 patients and 1,000 consecutive posterior interbody lumbar procedures, with a mean follow up of 63 months, found that patients who underwent single-level fusions were at low risk for developing ASD. However, patients who underwent fusion of three or four levels had a threefold increased risk of further surgery compared with single-level fusions and had a 10-year ASD prevalence of 40%.¹⁰ This was greater than the 22.2% 10-year prevalence reported for the whole study cohort. In a study of patients with degenerative spondylolisthesis who underwent either an L4-L5 spinal fusion or L4-S1 fusion, there was an increased rate of L3-L4 ASD with the latter procedure.¹¹ These data are somewhat suggestive that the risk of ASD increases with more levels fused.

The influence of decompressive laminectomy has also been studied. A systematic review by Radcliff et al.¹² found that laminectomy adjacent to a fusion and sagittal imbalance were risk factors for ASD. Interestingly, 1- or 2-level laminectomy in the absence of fusion has been reported to have an incidence of ASD requiring reoperation of 10% over a mean of 4 years.¹³ These data suggest that laminectomy, with or without fusion surgery, contributes to the
pathogenesis of adjacent segment degeneration. The removal of posterior bony elements and supportive musculature can lead to greater stress on the adjacent segment. In a retrospective study by Bydon and colleagues, half of patients with ASD were treated with a fusion surgery.

Alternative decompressive techniques with less dissection and potential for iatrogenic destabilization have been proposed to address the challenge of ASD. Kawaguchi et al.¹⁴ retrospectively examined ASD following expansive lumbar laminoplasty. With an average follow up of 5.4 years, the authors reported an ASD rate of 11% with this procedure.

Host Factors

A multinational research project, the Twin Spine Study, reported a substantial influence of heredity on lumbar spine degeneration.¹⁵ Despite significant variance in lifestyle and occupation, high degrees of similarities were noted between twin siblings. Since heredity influences disk degeneration, it is reasonable to extrapolate that genetics similarly influences the risk for adjacent segment degeneration.

Attention has also been given to predisposing demographic associations with ASD. Cho et al.,¹⁶ in a retrospective study with 5.5 year follow up, found that age over 50 was a risk factor for the development of ASD. In a retrospective study of 109 patients who underwent posterior lumbar interbody fusion for degenerative instability, Chen et al.¹⁷ found that age was the significant difference between those who developed ASD at the cranial segment at a minimum 2 year follow up. In fact, the study did not find preoperative radiographic evidence of degenerative disease or sagittal alignment to be significant factors, the latter of which conflicts with other data. Lawrence et al.³ noted that age over 60 was associated with an increased risk for developing symptomatic ASD. The study also notes that the risk of developing symptomatic ASD is higher after multilevel fusions, fusions adjacent to but not including the L5-S1 level, and may increase when performing a laminectomy next to a fusion. A prospective study of 74 patients by Anandjiwala et al.¹⁸ did not find age to be a significant risk factor, but rather found existing preoperative degenerative disease to be an important prognostic factor for the development of ASD.

Anatomic risk factors for ASD have also been examined. From a surgeon’s perspective, identifiable anatomic risk factors for ASD could aid in setting patient expectations, and possibly influence surgical options or patient selection. Okuda et al.¹⁹ found that lamina horizontalization, with inclination greater than 130 degrees at the cranial segment, and facet tropism greater than 10 degrees were associated with accelerated ASD after posterior lumbar interbody fusion.

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