Lumbar Spinal Fusion as a Risk Factor for Adjacent Segment Degeneration - Results of a Randomized Controlled Trial
Podium presentation at EuroSpine 2016
Berlin, October 7th 2016
Berlin, October 7th 2016
Abstract
Background
Lumbar spinal fusion may be followed by degeneration at levels adjacent to the fusion. Despite in vitro evidence of increased mechanical burden on motion segments adjacent to simulated fusions, it remains controversial as to whether fusion is a causative factor in adjacent segment degeneration (ASD).
Aims
The current study aims to resolve this issue by further analysis of X-ray data sourced from a U.S. FDA Investigational Device Exemption (IDE) randomized control trial (RCT) comparing decompression and interlaminar-stabilization with decompression and instrumented postero-lateral fusion, for spinal stenosis and low-grade degenerative spondylolisthesis. Methodology Pre-operative through 5-year post-operative imaging was subjected to secondary radiographic analysis in the 55 investigational and 27 fusion control subjects from the two-level arm of the interlaminar-stabilization IDE RCT. Angular range-of-motion (ROM) and disc-space heights were measured at the index, 1st and 2nd adjacent segments using Quantitative Motion Analysis® (Medical Metrics Inc, TX).
Results
At 24-months post-op, mean angular ROM had increased in the fusion control patients, at the 1st superior adjacent level, from 3.9° (±2.7°) pre-op to 6.3° (±4.7°) (P=0.007). ROM remained unchanged, in the interlaminar-stabilizer patients, at both the index and adjacent levels. By 60-months, ROM in the fusion patients had returned to 3.9° (±2.6°). At 60-months, mean disc-space heights at the 1st adjacent level had decreased in both the fusion control & investigational groups. However, the loss of height was significantly greater in the fusion controls than in the investigational patients: 2.15±2.2mm (30.1%) versus 1.06±1.5mm (13.7%), respectively (P=0.007). The estimated difference between treatment cohorts in the mean reduction in disc height was 1.06mm (95%CI: 0.26 to 1.86). Analysis of covariance (ANCOVA) was used to statistically control for between-group baseline differences in disc height, age & patient height, the estimated difference in loss of disc space height between treatment groups was 0.92mm (95%CI: 0.01-1.09, p=0.046). Amongst the dynamic stabilization patients, fifty-five percent lost less than ten percent of their pre-operative, adjacent level disc-space height compared with thirty-two percent of fusion patients. Mean disc space heights decreased at the 2nd adjacent level, in both cohorts, by 1.0mm (±1.5mm) and 0.5mm (±0.8mm), respectively (P=0.03).
Conclusion
Based on accurately measured post-operative changes in disc-space height, the current study provides high-level in vivo evidence that lumbar spinal fusion is a risk factor for ASD. The increased degeneration may be associated with the temporary increase in adjacent level angular ROM, observed post-fusion in the fusion patients. The finding of less severe ASDegen at 2nd adjacent levels and in patients randomized to motion preservation surgery suggests that factors other than fusion also play a role in ASD.
Background
Lumbar spinal fusion may be followed by degeneration at levels adjacent to the fusion. Despite in vitro evidence of increased mechanical burden on motion segments adjacent to simulated fusions, it remains controversial as to whether fusion is a causative factor in adjacent segment degeneration (ASD).
Aims
The current study aims to resolve this issue by further analysis of X-ray data sourced from a U.S. FDA Investigational Device Exemption (IDE) randomized control trial (RCT) comparing decompression and interlaminar-stabilization with decompression and instrumented postero-lateral fusion, for spinal stenosis and low-grade degenerative spondylolisthesis. Methodology Pre-operative through 5-year post-operative imaging was subjected to secondary radiographic analysis in the 55 investigational and 27 fusion control subjects from the two-level arm of the interlaminar-stabilization IDE RCT. Angular range-of-motion (ROM) and disc-space heights were measured at the index, 1st and 2nd adjacent segments using Quantitative Motion Analysis® (Medical Metrics Inc, TX).
Results
At 24-months post-op, mean angular ROM had increased in the fusion control patients, at the 1st superior adjacent level, from 3.9° (±2.7°) pre-op to 6.3° (±4.7°) (P=0.007). ROM remained unchanged, in the interlaminar-stabilizer patients, at both the index and adjacent levels. By 60-months, ROM in the fusion patients had returned to 3.9° (±2.6°). At 60-months, mean disc-space heights at the 1st adjacent level had decreased in both the fusion control & investigational groups. However, the loss of height was significantly greater in the fusion controls than in the investigational patients: 2.15±2.2mm (30.1%) versus 1.06±1.5mm (13.7%), respectively (P=0.007). The estimated difference between treatment cohorts in the mean reduction in disc height was 1.06mm (95%CI: 0.26 to 1.86). Analysis of covariance (ANCOVA) was used to statistically control for between-group baseline differences in disc height, age & patient height, the estimated difference in loss of disc space height between treatment groups was 0.92mm (95%CI: 0.01-1.09, p=0.046). Amongst the dynamic stabilization patients, fifty-five percent lost less than ten percent of their pre-operative, adjacent level disc-space height compared with thirty-two percent of fusion patients. Mean disc space heights decreased at the 2nd adjacent level, in both cohorts, by 1.0mm (±1.5mm) and 0.5mm (±0.8mm), respectively (P=0.03).
Conclusion
Based on accurately measured post-operative changes in disc-space height, the current study provides high-level in vivo evidence that lumbar spinal fusion is a risk factor for ASD. The increased degeneration may be associated with the temporary increase in adjacent level angular ROM, observed post-fusion in the fusion patients. The finding of less severe ASDegen at 2nd adjacent levels and in patients randomized to motion preservation surgery suggests that factors other than fusion also play a role in ASD.
