Summary of Key Points
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Spondylosis is a naturally occurring degeneration of intervertebral discs that can result in neurologic compression.
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It is commonly treated by decompression at the site of narrowing followed by fusion, a procedure that can be complicated by degenerative changes at adjacent segments.
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Adjacent segment degeneration refers to radiographic evidence for degenerative changes, whereas adjacent segment disease refers to clinically significant degenerative changes.
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In the cervical spine, it is not clear whether or not adjacent segment changes reflect a natural progression of spondylosis or a consequence of fusion.
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In the lumbar spine, several risk factors have been shown to increase the risk of adjacent segment disease following fusion, including age and the degree of posterior decompression.
Spondylosis is a degeneration of intervertebral discs that can result in narrowing of the intervertebral foramen and neurologic compression. It is a naturally occurring process that most commonly arises in the cervical and lumbar spine. In the cervical spine, radiographic evidence of spondylosis is present in approximately 60% of asymptomatic persons over 40 years of age. By age 60, the prevalence is as high as 95% in men and 70% in women, respectively. In the lumbar spine, radiographic evidence of spondylosis is present in approximately 20% of individuals younger than 60 years of age and in approximately 57% of individuals older than age 60.
A common surgical strategy for spondylosis is decompression at the site of narrowing followed by fusion. However, one concern associated with this procedure is the development of degenerative changes adjacent to the site of the fused segment or segments. Adjacent segment degeneration refers to radiographic evidence for degeneration, whereas adjacent segment disease refers to cases where degeneration is clinically significant. A major question in the field is whether adjacent segment degeneration is a consequence of surgical fusion or whether it reflects the natural progression of spondylosis. This chapter considers both adjacent segment degeneration and disease for both the cervical and lumbar spines.
Cervical Spine
Biomechanical Evidence
In the 1960s, cervical spine fusion was introduced by Cloward, Bailey and Badgley, and Robinson and Smith. Today, anterior cervical discectomy and fusion (ACDF) is a common surgical treatment for symptomatic cervical spondylosis. It is suggested commonly that levels adjacent to a fused cervical segment are prone to develop accelerated degenerative changes, possibly due to forces transmitted to the adjacent levels following interbody fusion.
Biomechanical studies support the view that fusion results in enhanced loading to the adjacent segments. Eck and associates found that motion and intradiscal pressures were increased at adjacent levels in a cadaveric C5-6 anterior fusion model. Compared to intact specimens, flexion at C4-5 and C6-7 both increased, with greater increases in motion at the rostral level. Extension also increased at both levels adjacent to the fused level; however, motion was greater at the caudal level. Intradiscal pressures increased by 73% at C4-5 and by 45% at C6-7 compared to controls, indicating that fusion causes a transfer of loading to adjacent levels. In agreement with these findings, Park and colleagues showed that intradiscal pressures at C4-5 were increased in a cadaveric C5-7 anterior fusion model. In another cadaveric study, Prasarn and colleagues found that sagittal range of motion was increased in levels adjacent to a two-level ACDF (C5-7) compared to a one-level ACDF (C5-6). Thus, several cadaveric studies have shown increased motion and loading forces at levels adjacent to a fused segment (although, see Rao and colleagues ).
In addition to cadaveric studies, radiographic studies have also shed light on adjacent-segment kinematics. Cheng and coworkers used fluoroscopic imaging to compare patients with normal, degenerative, and fused (C5-6) cervical spines. Range of motion and estimated in vivo forces at levels adjacent to a C5-6 anterior fusion were both higher compared to normal and to degenerative cervical spines. Watanabe and associates studied cervical kinematics in patients who underwent ACDF. They observed increased flexion/extension range of motion at segments adjacent to the site of fusion, but they did not observe any significant differences in rotational range of motion at these segments. In a prospective, randomized study, Park and colleagues radiographically compared cervical kinematics in patients treated with ACDF and cervical total disc replacement (without fusion). Twelve months following surgery, they observed increased range of motion at the superior segment in patients who underwent ACDF, but not in patients who underwent disc replacement without fusion. Thus, both in vitro cadaveric studies and in vivo radiographic studies provide evidence of kinematic changes at levels adjacent to a fused segment.
Adjacent Segment Degeneration
Several authors have investigated adjacent segment degeneration (ASD) radiographically. Baba and colleagues retrospectively reviewed 133 patients who underwent anterior cervical fusion with an average follow-up of 8.5 years. The authors reported a 25% incidence of spinal stenosis and increased motion at the adjacent rostral level on dynamic radiographs. In another retrospective evaluation with an average 5-year follow-up of 121 patients who underwent anterior cervical fusion, Gore and Sepic reported a 25% incidence of progression of spondylosis and new spondylosis. In a radiographic review of 44 patients with a 4.5-year follow-up, Herkowitz and coworkers reported a 41% and 50% rate of adjacent-level degeneration in patients who underwent ACDF and posterior foraminotomy, respectively. In a prospective study with a mean follow-up of 12.5 years, Matsumoto and colleagues reported a higher incidence of degenerative changes at C4-5 (measured as decreased signal intensity) in patients who underwent ACDF (n = 64, 54.1%) compared to asymptomatic controls (n = 201, 25.1%). There was no correlation found in any of these studies between adjacent-level degeneration and clinical deterioration.
Adjacent Segment Disease
Several authors have attempted to define the incidence of adjacent segment disease, or clinically apparent adjacent degeneration. In 1968, Williams and colleagues retrospectively studied 60 patients who underwent ACDF with average follow-up of 4.5 years. They found that 17% of these patients required additional surgery for progressive spondylosis following fusion. Gore and Sepic reported in a larger series with an average follow-up of 5 years that 14% of patients required further surgery following ACDF. In 1993, Bohlman and colleagues reported a 9% incidence of the adjacent segment degeneration in 122 patients following ACDF, with average clinical and radiographic follow-up of 6 years. Nine of eleven (81%) of patients with adjacent segment degeneration required further surgery at the adjacent level. Hilibrand and associates performed a 10-year survivorship analysis of 409 anterior decompression and stabilization procedures. They reported a 2.9% annual incidence of adjacent-level disease and an overall prevalence of 14% (follow-up ranged from 2 to 21 years). The Kaplan-Meier survivorship analysis demonstrated a predicted prevalence of adjacent-level disease of 13.6% at 5 years and 25.6% at 10 years. The authors also concluded that the greatest risk of adjacent-level deterioration involved single-level fusions, particularly at the C5-6 and C6-7 levels. The authors could not determine from these results if degeneration was a result of the prior fusion or merely a manifestation of the natural progression of the spondylotic process. Song and colleagues retrospectively studied 87 patients who underwent single-level ACDF surgery with a minimum follow-up of 5 years (mean follow-up of 84.8 months). They found a greater incidence of degenerative changes at adjacent segments (16%) compared to nonadjacent segments (3%); however, they did not observe a significant difference in the incidence of clinically relevant disease at adjacent (2%) and nonadjacent segments (0.7%). These studies indicate that there is a 9% to 17% prevalence and an annual incidence of 1.5% to 4% of adjacent-level disease following ACDF.
The control arms for the Investigational Device Exemption trials for the various cervical artificial discs brought to market provide level I evidence and shed more light on the incidence of adjacent segment disease following one-level ACDF with allograft and plate. Mummaneni and colleagues and Murrey and colleagues reported a 3.2% and 1% incidence, respectively, of secondary surgeries for symptomatic adjacent segment degeneration at 2-year follow-up. Clearly, this refers to surgeries performed for adjacent segment disease and does not provide the absolute incidence. Presumably, there was a cohort of patients treated nonoperatively for adjacent-level symptoms.
Various authors have compared fusion and nonfusion procedures in order to further study adjacent-level disease. Lundsford and coworkers reported on 334 patients who underwent anterior discectomy, with and without fusion. They reported an annual prevalence of adjacent segment disease of 7% and an annual incidence of 2.5%. There was no difference in the development of adjacent-level disease between fusion and nonfusion procedures. In a review of 846 patients who underwent posterior foraminotomy without fusion, Henderson and colleagues reported an overall prevalence of adjacent segment disease of 9% and an annual incidence of about 3%. Maldonado and colleagues did not observe significant differences in the incidence of adjacent-level degeneration in patients who underwent ACDF (n = 105, 10.5%) compared to those who underwent cervical disc arthroplasty without fusion (n = 85, 8.8%). In a prospective, randomized study, Coric and coworkers also did not observe significant differences in the incidence of adjacent segment disease between patients who underwent ACDF (n = 33, 3%) and those who underwent cervical disc arthroplasty (without fusion) (n = 41, 4.9%). These reports are consistent with the view that fusion procedures do not increase the risk of adjacent segment disease relative to those who undergo arthroplasty. However, because of the low overall incidence of adjacent segment disease, larger studies may be needed to detect small differences in the incidence of adjacent segment disease following fusion and nonfusion procedures.
Prevention of Adjacent-Level Degeneration
Whether or not fusion causes adjacent-level degeneration remains a topic of debate. However, there are steps the surgeon can attend to in order to minimize iatrogenic injury to adjacent levels. Needle level localization during ventral cervical surgery has been studied by Nassr and colleagues. They retrospectively followed 87 patients who underwent one- or two-level ACDF, 15 of whom had incorrect needle placement during level localization. In these patients, there was a threefold increase in adjacent-level degeneration compared to patients who had correct needle localization. Given this compelling data, it is reasonable to instead place the needle into a vertebral body and avoid a potential disc injury. Surgeons should also avoid excessive subperiosteal dissection above or below the surgical levels. Typically, only 3 to 4 mm of the adjacent body will need to be exposed for plate placement. This will minimize the risk of injuring the adjacent level or compromising the integrity of the anterior longitudinal ligament and longus coli muscles.
The length of fusion may also be a contributing factor to the risk of developing adjacent segment disease. In a retrospective study, Komura and associates found a lower incidence of adjacent segment disease in patients who underwent fusion procedures four or more levels (“long group,” n = 50, 2%), compared to those who underwent fusion procedures with three or fewer segments (“short group,” n = 52, 11%). The authors suggested that the inclusion of C5-7 segments in the long-group fusions may have provided a protective effect against the development of adjacent segment disease.
Anterior plate placement is another factor that has been implicated in adjacent-level degeneration. Park and coworkers retrospectively reviewed 118 patients with solid anterior plated fusion. The authors demonstrated a statistically significant higher incidence of adjacent-level ossification when the end of cervical plate is < 5 mm from the adjacent disc space. Sixty-seven percent of rostral adjacent levels and 45% of adjacent caudal levels developed ossification disease when the plate was plate < 5 mm from the adjacent disc. To maintain an appropriate distance from the latter, the graft-vertebral body interface should be visible through the terminal screw holes of the plate when placing the screws. The rostral screws are placed in a superior trajectory and the caudal screws are placed in an inferior trajectory.
Lumbar Spine
Biomechanical Evidence
Similar to the biomechanical studies in the cervical spine, lumbar data also support the notion that fusion results in higher biomechanical loads and more motion at adjacent, unfused levels. In an early cadaveric study, Lee and colleagues demonstrated an increase in motion at unfused, adjacent levels following various forms of instrumented fusion. The authors also reported that loading of the cephalad adjacent facet joints increased more with posterior instrumentation compared to an anterior interbody fusion. In another cadaveric study, Ma and colleagues also observed increased strain at the cephalad adjacent segment in an L2-3 pedicle screw fusion model. Weinhoffer and coworkers demonstrated in a cadaveric study that intradiscal pressures increased during flexion at the level adjacent to a pedicle screw construct. They also reported that the rise in pressure occurred earlier in flexion above two-level constructs versus one-level constructs. Other authors have demonstrated biochemical degeneration of the lumbar intervertebral disc adjacent to fused segments in animal models.
Adjacent Segment Degeneration
A multitude of authors have reported the association of ASD and lumbar fusion, and the results are heterogenous. This represents the wide variety of study types, dissimilar end points (e.g., listhesis, loss of disc height, stenosis, and signal change), different radiographic measures (e.g., radiography, computerized tomography [CT], magnetic resonance imaging [MRI]), and various reporting methods. Nonetheless, the available studies do consistently report the association between lumbar fusion and ASD. However, one must also remember that this does not prove causality—that is, it may also reflect the natural history of spondylosis.
In 1987, Penta and colleagues reported a 32% incidence of adjacent-level degeneration following anterior lumbar interbody lumbar fusion and also noted that its evolution was independent of fusion achievement (versus pseudoarthrosis) and of length of fusion. These authors reported a 2.5% incidence of adjacent-level stenosis, which is in stark contrast to the study by Lehmann. Leong and associates also evaluated ASD following anterior lumbar interbody fusion but reported an incidence of 52%. In a prospective study of patients who underwent lumbar/lumbosacral instrumented fusion with a minimum follow-up of 5 years, Anandjiwala and colleagues observed radiographic evidence of adjacent segment degeneration in 14 of 68 patients (20.6%). They also identified preoperative adjacent-segment degeneration as a significant risk factor for the development of postoperative changes. Many other studies have reported a wide range (20% to 64%) of adjacent-level degeneration following posterior fusion.
Several authors have reported instability and listhesis (anteroposterior translation) at adjacent levels. Lehmann and colleagues evaluated long-term follow-up after posterior lumbar fusion. They reported a 45% incidence of adjacent-level instability. Luk and associates retrospectively reviewed a series of patients for 12.8 years following fusion for idiopathic scoliosis and reported asymptomatic hypermobility of the adjacent level. In 1997, Wimmer and coworkers reported a 10.8% incidence of asymptomatic adjacent-level listhesis following circumferential fusion. This was similar to the 9.7% incidence of instability noted by Chen and colleagues following posterior instrumented fusion, but less than the 30% to 35% rate of listhesis reported by Guigui and associates following posterior instrumented fusion.
Radiographically apparent spinal stenosis, a consequence of level degeneration, has been reported less commonly. Like the reported rates of disc degeneration and listhesis/instability, the incidence range of stenosis is also quite wide, 18% to 62%. This is likely due to the factors mentioned earlier.
Adjacent Segment Disease
The literature suggests that most patients who develop radiographically apparent adjacent-level degeneration following lumbar fusion do not have symptoms referable to it. Etebar and Cahill retrospectively reviewed 125 patients with a 44-month follow-up after instrumented posterior lumbar fusion for degenerative spondylolisthesis. They reported that 14% of patients required adjacent-level surgery. This is in contrast to another study that reported only a 3% incidence of symptomatic L5-S1 degeneration following L4-5 fusion at 7-year follow-up. Throckmorton and colleagues performed a retrospective review of 25 patients treated consecutively with a posterior lumbar fusion ending adjacent to a degenerative disc (N = 20) or a normal one (N = 5). Surprisingly, at a minimum 2-year follow-up, patients with normal adjacent discs scored more poorly on a standardized health status survey (Short Form-36), which suggests that radiographic degeneration alone is a poor indicator of future problems. In an important study, Ghiselli and associates retrospectively reviewed 215 patients following lumbar fusion and reported a 27.4% incidence of second surgery at adjacent levels (decompression N = 15; fusion N = 45). A Kaplan Meier analysis predicted that the rate of secondary surgery at adjacent levels for either decompression or fusion was 16% at 5 years and 36% at 10 years. In 2011, Sears and colleagues reported that further surgery for adjacent segment disease occurred with an incidence of 13% in a retrospective analysis of 912 patients who underwent posterior lumbar interbody fusions (with a mean follow-up of 63 months).
Prevention of Adjacent-Level Degeneration
Several risk factors for adjacent-level degeneration following lumbar fusion have been identified. The addition of instrumentation to fusion has consistently been associated with quicker appearance and higher rates of adjacent degeneration. Two separate studies demonstrated adjacent-level listhesis at 25 months and 27 months following posterior lumbar instrumented fusion. This is in large contrast to the studies of noninstrumented fusion by Schlegel and Lee that reported adjacent-level breakdown at 8 and 13 years postoperatively. The association of instrumentation and adjacent-level deterioration is likely multifactorial. Clearly, the instrumented segments are initially more rigid, particularly when an interbody fusion is added to the construct. This may accelerate the initial loading of the adjacent level and, henceforth, its degeneration. As mentioned in a previous section, the fusion itself is associated with increased loading of both the disc and the facet joints, and as such, it is possible that fusion really is a cause of accelerated degeneration at adjacent levels. Consistent with this view, Sears and associates identified the number of fused segments as a risk factor for additional surgery for adjacent segment disease in a retrospective analysis of 961 patients who underwent posterior lumbar interbody fusions. Additional risk factors for adjacent segment surgery included increasing age, adjacent-segment laminectomy at the initial surgery, and stopping a fusion at L5, rather than S1. In another large retrospective analysis (511 patients with a mean follow-up of 39.73 months), Bydon and colleagues also found that “floating fusions” (that did not include the S1 segment) were more likely to result in adjacent segment disease than instrumented fusions that included the sacrum.
A likely risk to the adjacent level is the index procedure itself. Exposure of the rostral facet with injury to the capsule or excessive denervation or stripping of the muscular insertions can predispose it to degeneration. Two studies provide support for this view. First, Miyagi and colleagues identified adjacent segment decompression as a risk factor for radiographically evident adjacent segment degeneration in a retrospective study of 23 patients who underwent posterior lumbar interbody fusion. Second, in a randomized study, Liu and associates assigned 120 patients undergoing L4-5 instrumented fusions to three groups that varied in the degree of decompression (facet joint resection, hemilaminectomy, and complete laminectomy, respectively). After 6 years, they observed adjacent segment disease in 17 of the 40 patients who underwent complete laminectomy (71%, 7 of whom required reoperation), but rarely observed adjacent segment disease in the two minimally decompressed groups (3 and 4 patients, respectively). Thus, adjacent segment decompression during lumbar fusion appears to be a risk factor for the development of both adjacent segment degeneration and disease. Also, the common use of pedicle screws in no way makes them innocuous to the adjacent level. It is mandatory that a proper starting point be chosen for the rostral screws to avoid violation of the facet joint.
Although there is a paucity of data to corroborate the notion that sagittal alignment is important in terms of adjacent-level degeneration, it is at least plausible to think that maintaining normal lordosis is ideal. Minimizing fusion segment length is also thought to be optimal in terms of maximizing normal kinematics at unfused lumbar levels. However, one must pay particular attention to long lumbar constructs that extend to L1 or L2. The thoracolumbar junction is biomechanically, and anatomically, rather unique. Ending a long lumbar fusion at L1 rather than crossing the junction with the fusion should be avoided if possible given the anticipated high risk of degeneration at the rostral end of the construct.

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