Abstract
Introduction Numerous in-vitro studies demonstrating increased stress at levels adjacent to a lumbar fusion have raised concerns of accelerated degeneration. However, the significance of this increased stress in the in-vivo setting remains unclear, especially with long-term follow-up. The objective of this study was to assess the level of degeneration on MRI in this same cohort of patients at a minimum of 20 years follow-up.
Methods Thirty-seven patients undergoing lower lumbar anterior lumbar interbody fusion with a minimum of 20 years follow-up were identified. Only patients with normal pre-operative discograms at the level adjacent to the fusion were considered in this study. MRI scans were performed and evaluated for any evidence of degeneration by an independent radiologist. Advanced degeneration was defined as either: (1) absence of T2 signal intensity in the disk, (2) disk herniation, or (3) spinal canal stenosis.
Results Advanced degeneration was identified in eight (22%) patients, with five (14%) being isolated to the adjacent level. Nineteen (51%) other patients had evidence of early degeneration in their lumbar spine. Overall, 10 (26%) patients had some evidence of degeneration isolated to the level adjacent to the disk whereas 17 (31%) patients had multilevel degeneration and six patients (16%) had degeneration in their lumbar spine but preservation of the adjacent level. There was no relationship between function and radiographic degeneration.
Conclusions Without a control group, it is difficult to make firm conclusions on whether the changes seen on MRI represent the natural history of spinal deterioration or represent accelerated degeneration. However, after 20 years, only a handful of patients developed advanced adjacent level degeneration. Furthermore, the majority of degenerative changes seen occurred over multiple levels or at levels not adjacent to the fusion, suggesting that changes seen may be more likely related to constitutional factors inherent within the individual as opposed to the increased biomechanical stresses at the adjacent levels.
The abstracts were prepared by Mr Jerzy Sikorski. Correspondence should be addressed to him at the Australian Orthopaedic Association, Ground Floor, William Bland Centre, 229 Macquarie Street, Sydney NSW 2000, Australia.
None of the authors have received any payment or consideration from any source for the conduct of this study.
