Accelerated segment degeneration (ASD) adjacent to a lumbar fusion (LF) has been reported in several papers (1,1,3). However, most of the evidence is derived from series that have not accounted for the natural history of degenerative changes developing at the unfused levels (4). Several experimental studies have suggested an important role for biomechanical changes as the origin or cause of ASD (4,5,6,7). Fusion, especially posterior instrumented, produces increased stress at the adjacent segment, which might be the cause of this syndrome; the stress would be affected by the length, location, and stiffness of the fusion mass (4,5,6,8,9,10). However, one should be cautious when considering the value of much in vitro data because the in vivo situation might be much more complex than is reproduced in vitro (11). Some investigators believe that degenerative changes appearing in the nonoperated segments after fusion may be predetermined by factors other than the presence of fusion (12,13). ASD could be nothing more than the normal degenerative process, largely determined by individual characteristics, rather than a consequence of biomechanical stress (14).

The great majority of studies analyzing ASD focus mainly on the motion segments immediately above and below the fusion. Little or no attention has been paid to the effects of lumbosacral fusion on nonadjacent mobile segments. Hence, the reported rate of ASD may include patients with true breakdown syndrome and isolated adjacent disc degeneration and patients with widespread degeneration.