CME Review Article Free

Adjacent Segment Disease

Sohrab S. Virk, MD, MBA; Steven Niedermeier, BS; Elizabeth Yu, MD; Safdar N. Khan, MD

Abstract

Educational Objectives

As a result of reading this article, physicians should be able to:


Understand the forces that predispose adjacent cervical segments to degeneration.

Understand the challenges of radiographic evaluation in the diagnosis of cervical and lumbar adjacent segment disease.

Describe the changes in biomechanical forces applied to adjacent segments of lumbar vertebrae with fusion.

Know the risk factors for adjacent segment disease in spinal fusion.

 

Adjacent segment disease (ASD) is a broad term encompassing many complications of spinal fusion, including listhesis, instability, herniated nucleus pulposus, stenosis, hypertrophic facet arthritis, scoliosis, and vertebral compression fracture. The area of the cervical spine where most fusions occur (C3–C7) is adjacent to a highly mobile upper cervical region, and this contributes to the biomechanical stress put on the adjacent cervical segments postfusion. Studies have shown that after fusion surgery, there is increased load on adjacent segments. Definitive treatment of ASD is a topic of continuing research, but in general, treatment choices are dictated by patient age and degree of debilitation. Investigators have also studied the risk factors associated with spinal fusion that may predispose certain patients to ASD postfusion, and these data are invaluable for properly counseling patients considering spinal fusion surgery. Biomechanical studies have confirmed the added stress on adjacent segments in the cervical and lumbar spine. The diagnosis of cervical ASD is complicated given the imprecise correlation of radiographic and clinical findings. Although radiological and clinical diagnoses do not always correlate, radiographs and clinical examination dictate how a patient with prolonged pain is treated. Options for both cervical and lumbar spine ASD include fusion and/or decompression. Current studies are encouraging regarding the adoption of arthroplasty in spinal surgery, but more long-term data are required for full adoption of arthroplasty as the standard of care for prevention of ASD. [Orthopedics. 2014; 37(8):547–555.]

The authors are from the Department of Orthopaedics, The Ohio State University, Columbus, Ohio.

The material presented in any Keck School of Medicine of USC continuing education activity does not necessarily reflect the views and opinions of Orthopedics or Keck School of Medicine of USC. Neither Orthopedics nor Keck School of Medicine of USC nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

Correspondence should be addressed to: Safdar N. Khan, MD, Department of Orthopaedics, The Ohio State University, 725 Prior Hall, 376 W Tenth St, Columbus, OH 43210 ( safdar.khan@osumc.edu).

Received: May 21, 2013

Accepted: December 03, 2013

Spinal fusion has been studied as a means to treat pathology related to the spine for more than a century.1 Because the proportion of the American population older than 65 years will increase from 12.4% in 2000 to 19.6% in 2030,2 and due to the many surgical advancements in spinal surgery over the past few decades, the rate of fusion surgeries rose between 1993 and 20033 and between 1979 and 1990.4 Given the current environment, it is imperative that orthopedic surgeons understand the possible outcomes of fusion surgery.

One complication of spinal fusion is adjacent segment disease (ASD) following cervical, lumbar, or lumbosacral fusion. This is a broad term that encompasses symptoms such as listhesis, instability, herniated nucleus pulposus, stenosis, hypertrophic facet arthritis, scoliosis, and vertebral compression fracture.5 The cause of this degenerative process has been extensively studied in biomechanical studies using animal and cadaver models.6–9 Whether these degenerative changes also cause clinical, rather than solely radiological, changes has also been studied extensively.10–15

Treatment modalities for ASD are complicated by the increased risks associated with revision spinal surgeries and the evolving technology of spinal arthroplasty. Definitive management of ASD continues to be studied, and treatment priorities should be dictated by patient age and the degree of debilitation associated with ASD for each patient. Investigators have also studied the risk factors associated with spinal fusion that may predispose certain patients to ASD postfusion.14,16–25 These data are invaluable for properly counseling patients considering spinal fusion surgery.

Adjacent Segment Disease Associated With Cervical Spinal Fusion

Biomechanics

The motion of adjacent segments after cervical spinal fusion has been modeled in several studies in an attempt to understand the forces that predispose adjacent cervical segments to degeneration.6–9 The area of the cervical spine where most fusions occur (C3–C7) is adjacent to a highly mobile upper cervical region, and this contributes to the biomechanical stress put on the adjacent cervical segments postfusion. Studies have shown that after fusion surgery, there is increased load on adjacent segments. In a study by Eck et al,6 six cadaveric spine specimens were tested and stabilized at T1. Pressure increased in both C4–C5 and C6–C7. An image of this experimental apparatus is shown in Figure 1. A finite element model was used by Maiman et al7 to examine the effects of C4–C5 and C5–C6 fusions, and increased internal stress in adjacent segments was found. Researchers studying a multisegment cervical fusion found that stress on adjacent segments increased between single and double fusions.8 Lopez-Espina et al8 used a finite element model and facet-constraining methods to prevent increases in stress. Increases in stress up to 96% were found in the annulus, nucleus, and endplates postfusion. Canine models have also shown a change in proteoglycan population in intervertebral disks postfusion. Cole et al9 found that the proteoglycan population produced in both the nucleus pulposus and annulus fibrosus postfusion is similar to the proteoglycan population in immature tissue.

Photograph of the pressure transducer used to measure the biomechanical stress placed on adjacent segments after stabilizing at T1. (Reprinted with permission from Eck JC, Humphreys SC, Lim TH, et al. Biomechanical study on the effect of cervical spine fusion on adjacent level intradiscal pressure and segmental motion. Spine [Phila Pa 1976]. 2002; 27[22]:2431–2434.)

Figure 1:

Photograph of the pressure transducer used to measure the biomechanical stress placed on adjacent segments after stabilizing at T1. (Reprinted with permission from Eck JC, Humphreys SC, Lim TH, et al. Biomechanical study on the effect of cervical spine fusion on adjacent level intradiscal pressure and segmental motion. Spine [Phila Pa 1976]. 2002; 27[22]:2431–2434.)

Clinical and Radiographic Diagnosis

The diagnosis of cervical ASD is complicated given the imprecise correlation of radiographic and clinical findings. Evaluation is difficult because the normal degenerative process in patients is difficult to separate from the effects of the fusion surgery on adjacent segments. No validated classification system exists for cervical ASD.10 A study by Baba et al11 followed more than 100 patients for an average of 8.5 years and found an increase in tilting angle in the upper adjacent and lower adjacent segments, as well as newly diagnosed spinal stenosis in 25% of patients.11 Herkowitz et al26 prospectively studied 28 patients who had undergone cervical fusion and found that 41% of patients had adjacent level degeneration on radiographs at an average 4.5-year follow-up. Matsumoto et al12 investigated the use of magnetic resonance imaging (MRI) for ASD by comparing a group of 64 patients undergoing anterior cervical decompression and fusion with 201 asymptomatic volunteers. Disk degeneration at adjacent segments was significantly more likely in the fusion group compared with the control group, although disk degeneration at adjacent segments was not always related to clinical symptoms. Postoperative ASD is shown in Figure 2.

Adjacent segment disease in the cervical spine. Preoperative radiograph showing disk disease between levels C5–C7 (A). Five-year postoperative radiograph showing fusion of levels C4–C6 with cervical disk space narrowing at C6–C7 (arrow) (B). Five-year postoperative myelography showing intervertebral disk herniation at C6–C6 and complete block of the dural sack at C6–C7 (arrow) (C). Radiograph taken after reoperation for fusion of C6–C7 (D). (Reprinted with permission from Ishihara H, Kanamori M, Kawaguchi Y, et al. Adjacent segment disease after cervical nterbody fusion. Spine J. 2004; 4[6]:624–628.)

Figure 2:

Adjacent segment disease in the cervical spine. Preoperative radiograph showing disk disease between levels C5–C7 (A). Five-year postoperative radiograph showing fusion of levels C4–C6 with cervical disk space narrowing at C6–C7 (arrow) (B). Five-year postoperative myelography showing intervertebral disk herniation at C6–C6 and complete block of the dural sack at C6–C7 (arrow) (C). Radiograph taken after reoperation for fusion of C6–C7 (D). (Reprinted with permission from Ishihara H, Kanamori M, Kawaguchi Y, et al. Adjacent segment disease after cervical nterbody fusion. Spine J. 2004; 4[6]:624–628.)

Although the rate of radiographic signs of ASD is high, the rate of clinical symptoms of ASD is lower. Baba et al11 retrospectively studied 146 patients undergoing cervical fusion and found that 13.5% of patients had identifiable problems at a level other than the level fused. Lunsford et al13 reported a reoperation rate of 10% at a different segment after anterior cervical fusion at less than 3-year follow-up. Hilibrand et al14 followed 374 patients over a maximum of 21 years postoperatively and found that symptomatic ASD occurred at a rate of 2.9% over 10 years postoperatively and that 25.6% of patients had ASD within 10 years postoperatively. Yue et al15 studied 71 patients undergoing anterior cervical diskectomy and fusion over more than 5 years and found that 16.9% of patients needed revision surgery for symptomatic adjacent level disease, although 73.2% of patients had new-onset or worsening degeneration of disk spaces adjacent to the operated levels.15

Risk Factors

Adjacent segment disease only occurs in a certain portion of patients after spinal fusion. Various studies have investigated the risk factors for the development of ASD after cervical spinal fusion. Hilibrand et al14 analyzed risk factors that contributed to the progression of symptomatic ASD. Patients who had adjacent segments with neural element compression, surgery at C5–C6 and/or C6–C7 levels, or anterior cervical fusion surgery of more than 1 level were less likely to develop ASD. Williams et al16 studied the factors that contributed to positive and negative postoperative outcomes in 90 patients undergoing cervical diskectomy and interbody fusion over 2 to 9 years. Patients with apparently normal preoperative radiographs had worse outcomes than those with osteophyte formation, narrowing of the interspace, or both. Katsuura et al17 studied the effect of postoperative malalignment of the cervical spine in a prospective study over 9.8 years and found that 43% of patients with ASD had malalignment of the cervical spine. In patients who have an anterior cervical plate, the distance between the plate and adjacent segments may influence the amount of ossification at adjacent segments.18 Park et al18 found a positive association between plate-to-disk distance and the amount of ossification at adjacent segments.

Two recent systematic reviews specifically studied risk factors related to ASD postoperatively.10,19 Lawrence et al19 found 5 quality research studies and concluded that fusing segments adjacent to C5–C6 and/or C6–C7 increased the risk of ASD. Of note, the authors mentioned that even after performing a systematic review of more than 170 articles, the development of clinical adjacent segment pathology is difficult to differentiate from the natural history of spinal degeneration. A population-based study from Taiwan noted a low rate of reoperation (0.8%) for clinically significant ASD.20 Lee et al21 found that radiographic signs of ASD were more likely in patients who had degenerative indications for cervical spinal fusion.

Adjacent Segment Disease Associated With Lumbar Spine Fusion

Biomechanics

The fusion of lumbar vertebrae has been associated with changes in the biomechanical forces applied to adjacent segments.27 The area of adjacent segment biomechanical forces and motion has been studied since the 1980s.28,29 In 1984, Lee and Langrana28 put 16 cadaveric models under combined compression and bending loads to observe motion. They found increased stress on adjacent segments and increased loading on facet joints within unfused segments. Further evidence of facet joint strain postfusion was demonstrated by Ha et al30 in an experiment with in vitro canine spines. They found increased segmental mobility and changed contact patterns within the joint. Using a finite model, Chen et al31 also found increased forces in adjacent disks postfusion and noted larger stress increases at the upper adjacent disk rather than the lower disk.

Increased motion at adjacent segments has been postulated as a reason for ASD. Axelsson et al32 studied 6 patients undergoing radiographic analysis of segment motion before and after L4–L5 fusion surgery. Increased mobility occurred in adjacent segments for 2 of the 6 patients. In an in vivo model, Hayes et al33 specifically examined mobility and found increased translational motion in adjacent segments when L3–L4 was fused, and this motion correlated with lower back pain. Esses et al34 studied changes in motion with different fusion techniques in cadaveric models. Posterolateral fusions were found to have less motion in adjacent segments as compared with anterior fusions.

In both cadaveric and finite models, increased intradiskal pressure has been found within adjacent segments.35–37 Weinhoffer et al36 studied intradiskal pressure in adjacent segments during flexion in cadaveric models. Intradiskal pressure increased during flexion, and the more segments that were fused, the greater the intradiskal pressure. Similar results were found by Cunningham et al,38 who studied 11 cadaveric models and found that intradiskal pressure increased by as much as 45%.

Using an in vivo mouse model and a finite element model, Lotz et al39 studied both the changes in stress in adjacent segments and the biochemical changes within adjacent segments. The finite element model predicted an increase in hydrostatic stress in the middle regions of the annulus by nearly ten-fold. Numerous harmful responses occurred at the histological and cellular levels, including disorganization of the annulus fibrosus, an increase in apoptosis with associated loss of cellularity, and damaging changes in gene expression. In an animal model by Phillips et al,40 results included loss of chondrocytes and notochordal cells within the nucleus pulposus.

Clinical and Radiographic Diagnosis

Separating the progression of osteoarthritis in patients postfusion from lumbar ASD is difficult. In a study by Kumar et al,41 patients were followed postfusion with the Short Form 36 and Oswestry Disability Index, functional testing, and radiographs. Their results were compared with those from age- and sex-matched controls. Radiographic changes above the level of fusion were worse in those with fusion compared with those not fused. There was no statistically significant difference in clinical outcomes. Wai et al42 studied MRI results over 20 years for patients undergoing lumbar fusion surgery and found that the prevalence of degenerative changes in patients undergoing surgery was similar to age-matched controls. Hambly et al43 reported that radiographic changes occur in the transition zone cephalad to lumbosacral fusion, regardless of whether surgery occurred.

As with ASD in the cervical spine, the correlation between clinical, MRI, and radiographic signs of ASD is controversial. Interpretation of radiographic evidence is also complicated by the fact that asymptomatic patients have been found to have substantial abnormalities on MRI.44 Plain radiographs have been found to be of little help in the diagnosis of ASD. Frymoyer et al45 examined plain radiographs from 96 patients who had undergone fusion surgery. Results showed no correlation between radiographic findings and clinical symptoms. The progressive changes seen on radiographs of adjacent segments are illustrated in Figure 3.46 In the current authors’ experience treating ASD, severe degenerative changes cause symptoms of spinal stenosis. Figure 4 shows an area of neural foraminal narrowing at the L2–L3 level.

Radiographs showing progressive changes after lumbar spinal fusion preoperatively (A) and 2 years (B), 5 years (C), and 9 years (D) postoperatively. In this patient, definite signs of adjacent segment disease are present by 13 years after L4–L5 spinal fusion (E). However, it is unclear whether these radiographic changes signify clinical significance. (Reprinted with permission from Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thora-columbar fusion with pedicle screw instrumentation. Spine [Phila Pa 1976]. 2007; 32[20]:2253–2257.)

Figure 3:

Radiographs showing progressive changes after lumbar spinal fusion preoperatively (A) and 2 years (B), 5 years (C), and 9 years (D) postoperatively. In this patient, definite signs of adjacent segment disease are present by 13 years after L4–L5 spinal fusion (E). However, it is unclear whether these radiographic changes signify clinical significance. (Reprinted with permission from Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thora-columbar fusion with pedicle screw instrumentation. Spine [Phila Pa 1976]. 2007; 32[20]:2253–2257.)

Radiograph of a patient with a L3–L5 posterior spinal fusion with instrumentation who presented to clinic after months of severe back pain and radiating pain down bilateral legs (A). Computed tomography myelogram showing spinal stenosis at L2–L3 with bilateral facet hypertrophy (B). This patient eventually had her spinal instrumentation removed and underwent fusion of her L2–L3 segment with instrumentation.

Figure 4:

Radiograph of a patient with a L3–L5 posterior spinal fusion with instrumentation who presented to clinic after months of severe back pain and radiating pain down bilateral legs (A). Computed tomography myelogram showing spinal stenosis at L2–L3 with bilateral facet hypertrophy (B). This patient eventually had her spinal instrumentation removed and underwent fusion of her L2–L3 segment with instrumentation.

Many studies have examined the prevalence of clinical symptoms associated with ASD. In a long-term retrospective study by Ghiselli et al,47 215 patients were followed postfusion for an average of 6.7 years. The rate of reoperation at adjacent segments was 16.5% in the first 5 years and 36.1% at 10 years. Similar results were reported by Gillet48 in a retrospective study that found a reoperation rate of 20% over a range of 2 to 15 years of follow-up. Penta et al49 studied MRIs for 10 years after lumbar interbody fusion, and of the 81 patients studied, 32% had radiographically diagnosed ASD. In a large retrospective cohort study by Sears et al50 of 1000 consecutive posterior lumbar interbody fusion procedures with a mean follow-up of 63 months, the 10-year prevalence of further surgery for ASD was 22.2%. The annual incidence of surgery for ASD was 2.2%.

The rate of ASD after lumbar fusion varies widely between studies.5 In a review by Park et al5 of 22 studies, the reported range of ASD was 5.2% to 100% based on either radiographic or clinical diagnosis. The authors attributed this wide variation to the range of patient populations, differing clinical or radiographic definitions of ASD, and the retrospective nature of many of the studies.

Risk Factors

Several studies have examined the risk factors that put a portion of patients at risk for ASD. Aota et al22 reported that the factor most influential in postfusion instability was age. The study showed that 11 of 30 patients older than 55 years developed ASD postfusion, whereas only 3 of 25 patients younger than 55 years developed ASD postfusion. Similarly, a retrospective study by Etebar and Cahill23 found that ASD was higher in postmenopausal women. The link between menopause and worsening osteoarthritis is not entirely clear, but active research is ongoing into the mechanism by which a lack of estrogen influences osteoarthritis development and progression.24 In a retrospective review of 49 patients, Rahm and Hall25 found that increasing age, as well as inter-body fusion, was associated with a higher risk of ASD.

Investigators have studied whether the length of fusion in fusion surgery factors into the development of ASD. Penta et al49 examined MRIs and radiographs from 52 patients who had normal preoperative findings in adjacent levels.49 In this group of patients, the length of fusion did not factor into whether ASD occurred. Wimmer et al51 studied the effect of polysegmental fusions on anteroposterior translation in 120 patients with painful spondylolisthesis who were treated with combined anterior and posterior fusions. The study group was divided into a monosegmental fusion group (n=46) and a polysegmental fusion group (n=74). Polysegmental fusion was associated with a greater degree of anteroposterior translation.

Fusion involving the L4–L5 segment has been cited as a possible cause of disk degeneration at L5-S1. This was specifically studied by Ghiselli et al52 in a group of 32 patients over 7.3 years. Their investigation found a general progression of degenerative changes in the L5-S1 segments. However, the authors concluded that there was no need for routine fusion of L5-S1 in patients with isolated L4–L5 symptoms.

Another significant factor in determining ASD postfusion is the anatomical alignment of spinal segments preoperatively. Investigators have noted increased ASD in patients with a preoperative L1 and S1 axis distance greater than 35 mm.53 In a retrospective study, Kumar et al41 reported that patients with a normal C7 plumb line and sacral inclination had the lowest rate of ASD. In a study by Lazennec et al54 of 81 patients who had undergone fusion, there was a statistically significant relationship between postoperative pain and sacral tilt. Oda et al55 used a sheep model to determine the biomechanical changes in adjacent segments in kyphotic spines. Results showed that kyphotic posterolateral fusion significantly altered supra-adjacent segments by inducing more stiffness in the posterior ligamentous complex and increasing lamina strain under flexion-extension loading. There were significant degenerative changes in the supra-adjacent segments in these sheep. Lehmann et al56 found a correlation between preoperative segmental instability in the segment above fusion and lumbar spinal stenosis. The greater the translation instability, the more likely the adjacent segment would become unstable post-fusion. Biomechanical studies have also shown that once degeneration occurs at one segment, the risk of degeneration at other adjacent segments increases.57 Schlegel et al58 reported that segments that were 2 segments removed from fusion were just as likely to show degeneration as adjacent segments.

The alignment of fusion in the lumbar spine was investigated in a biomechanical cadaveric study by Akamaru et al.59 They reported that fusion in either hyper- or hypolordotic alignment of L4–L5 resulted in different loads on adjacent spinal segments. Hypolordotic alignment of L4–L5 resulted in the greatest amount of flexion-extension motion at L3–L4, whereas hyperlordotic alignment of L4–L5 resulted in the greatest amount of flexion-extension motion at L5-S1. In a study of patients undergoing 360° fusion with healthy adjacent segments preoperatively, it was found that maintaining the lordotic angle at approximately 20° postoperatively was associated with the prevention of ASD.60

Several studies have investigated ASD in the lumbar spine following different treatment decisions. In a prospective study of 111 patients with spondylolisthesis who were randomized to exercise, uninstrumented posterolateral fusion, or instrumented posterolateral fusion, accelerated adjacent segment degeneration was found in the patients that had fusion and laminectomy.61 Abdu et al62 studied 380 surgical candidates with degenerative spondylolisthesis who underwent 1 of 3 surgical interventions: posterior in situ fusion, posterolateral instrumented fusion with pedicle screws, or posterolateral instrumented fusion with pedicle screws plus interbody fusion (360°). At 3- and 4-year follow-up, there was no statistical difference in outcome criteria (ie, Short Form 36 bodily pain, physical function scales, and the modified Oswestry Disability Index) between the different operative techniques. Furthermore, in a randomized, controlled trial performed by Videbaek et al,63 patients who underwent anterior lumbar interbody fusion combined with posterolateral lumbar fusion or posterolateral lumbar fusion alone showed no increased risk of ASD. Therefore, it does not appear that a specific treatment technique accelerates the onset of increases the likelihood of developing ASD compared with any other.

Edwards et al64 investigated long adult fusions of the thoracolumbar spine to L5 and the resultant degenerative changes to S1. Thirty-four patients were followed for a mean of 5.6 years. Results showed that 61% of patients had resultant degenerative disk disease. Risk factors for degenerative changes were a positive sagittal balance, younger age at operation, and any signs of radiographic degeneration at L5-S1.

Added instrumentation during spinal fusion has been studied as a possible risk factor for ASD. Shono et al65 investigated whether fusion surgeries augmented with instrumentation such as a compression hook and a transpedicular screw fixation system increased motion in adjacent segments. The study was conducted with a calf lumbosacral spine model. As spinal instrumentation increased, higher segmental displacement occurred at the upper residual intact motion segment. Interestingly, different results were reported by Wiltse et al66 with the use of pedicle screws. They studied pedicle screws and their relationship to transition zone changes above or below the fused segment. No increase in ASD incidence was found with pedicle screw placement.

Ahn et al60 retrospectively studied 3188 patients who underwent thoracolumbar spinal fusion to find the rate of ASD, as well as risk factors. Results showed a failure rate of 6% at 10 years at adjacent segments. Risk factors noted were multiple level fusions, old age, degenerative disease prior to fusion, and male sex. A study by Lee et al21 investigated overall risk factors for revision surgery due to ASD. Of 1069 patients undergoing spinal fusion surgery, 2.62% required revision surgery. Postoperative facet degeneration was associated with revision surgery, and the incidence of ASD in proximal segments was found to be higher than that in more distal segments. Preexisting degeneration was found to be a significant risk factor for ASD requiring surgery.

The intraoperative decision of distracted disk height of the fused segment caused by cage or bone insertion has been studied as a risk factor for ASD. Kaito et al67 studied 84 patients with L4 spondylolisthesis who were treated with posterior lumbar interbody fusion. Patients who developed ASD were found to have higher L4–L5 disk space distraction.

Nassr et al68 investigated whether incorrect needle localization during anterior cervical diskectomy and fusion caused ASD. Of 87 patients undergoing anterior cervical diskectomy and fusion, 15 had incorrect needle localization. The group with incorrect needle localization was associated with a 3 times higher rate of ASD. The authors concluded that either needle trauma or unnecessary surgical dissection may have caused ASD during the study. A recent systematic review for risk factors for ASD after lumbar fusion showed that age older than 60 years was associated with an increased risk of ASD after spinal fusion.19 Similarly, if the patient had preexisting facet degeneration, degenerative disk disease, multilevel fusion, laminectomy performed adjacent to a segment, a construct stopped at L5, or excessive disk height distraction, then the risk of ASD may be higher.

Treatment

There is no gold standard treatment for ASD, but there are methods to treat its symptoms. Several studies have shown that treatment with decompression of neural elements with possible extension of fusion may relieve symptoms.31,69,70 Although there seems to be some pain relief with extension of fusion, these studies indicated that extension of fusion may result in higher rates of ASD in the newly created adjacent segments. These studies reported significant complication rates, and the number of treated patients was small. Arthroplasty has been promoted as a potential solution to ASD, but results from numerous studies indicate that more data are needed to ensure improved clinical outcomes.71–76 An example of a total disk arthroplasty device is shown in Figure 5.77 A recent Cochrane review showed that although there was a statistically significant improvement in outcome measures associated with total disk arthroplasty, it was not clear whether this difference was clinically significant.78 The authors of the review emphasized caution in adoption of the new technology.

The Activ L (B. Braun, Melsungen, Germany) total disk arthroplasty device designed for disk replacement in the spine. There are both superior and inferior endplates, and an ultra-high-molecular-weight polyethylene liner that sits between the plates. (Reprinted with permission from Grupp TM, Yue JJ, Garcia R Jr, et al. Biotribological evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro wear simulation. Eur Spine J. 2009; 18[1]:98–108.)

Figure 5:

The Activ L (B. Braun, Melsungen, Germany) total disk arthroplasty device designed for disk replacement in the spine. There are both superior and inferior endplates, and an ultra-high-molecular-weight polyethylene liner that sits between the plates. (Reprinted with permission from Grupp TM, Yue JJ, Garcia R Jr, et al. Biotribological evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro wear simulation. Eur Spine J. 2009; 18[1]:98–108.)

Conclusion

Adjacent segment disease is a complication related to spinal fusion. Its diagnosis is clouded by the fact that many patients have underlying degenerative changes that may mimic ASD. Biomechanical studies have confirmed the added stress on adjacent segments in the cervical and lumbar spine. Although radiological and clinical diagnoses do not always correlate, radiographs and clinical examination dictate how a patient with prolonged pain is treated. Options for both cervical and lumbar spine ASD include fusion and/or decompression. Although current studies are encouraging regarding the adoption of arthroplasty in spinal surgery, more long-term data are required for full adoption of arthroplasty as the standard of care for the prevention of ASD.

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  22. Aota Y, Kumano K, Hirabayashi S. Postfusion instability at the adjacent segments after rigid pedicle screw fixation for degenerative lumbar spinal disorders. J Spinal Disord. 1995; 8:464–473. doi:10.1097/00002517-199512000-00008 [CrossRef]
  23. Etebar S, Cahill DW. Risk factors for adjacent-segment failure following lumbar fixation with rigid instrumentation for degenerative instability. J Neurosurg. 1999; 90:163–169.
  24. Roman-Blas JA, Castaneda S, Largo R, Herrero-Beaumont G. Osteoarthritis associated with estrogen deficiency. Arthritis Res Ther. 2009; 11:241. doi:10.1186/ar2791 [CrossRef]
  25. Rahm MD, Hall BB. Adjacent-segment degeneration after lumbar fusion with instrumentation: a retrospective study. J Spinal Disord. 1996; 9:392–400. doi:10.1097/00002517-199610000-00005 [CrossRef]
  26. Herkowitz HN, Kurz LT, Overholt DP. Surgical management of cervical soft disc herniation: a comparison between the anterior and posterior approach. Spine (Phila Pa 1976). 1990; 15(10):1026–1030. doi:10.1097/00007632-199015100-00009 [CrossRef]
  27. Nagata H, Schendel MJ, Transfeldt EE, Lewis JL. The effects of immobilization of long segments of the spine on the adjacent and distal facet force and lumbosacral motion. Spine (Phila Pa 1976). 1993; 18:2471–2479. doi:10.1097/00007632-199312000-00017 [CrossRef]
  28. Lee CK, Langrana NA. Lumbosacral spinal fusion: a biomechanical study. Spine (Phila Pa 1976). 1984; 9:574–581. doi:10.1097/00007632-198409000-00007 [CrossRef]
  29. Quinnell RC, Stockdale HR. Some experimental observations of the influence of a single lumbar floating fusion on the remaining lumbar spine. Spine (Phila Pa 1976). 1981; 6:263–267. doi:10.1097/00007632-198105000-00008 [CrossRef]
  30. Ha KY, Schendel MJ, Lewis JL, Ogilvie JW. Effect of immobilization and configuration on lumbar adjacent-segment biomechanics. J Spinal Disord. 1993; 6(2):99–105. doi:10.1097/00002517-199304000-00002 [CrossRef]
  31. Chen WJ, Lai PL, Niu CC, Chen LH, Fu TS, Wong CB. Surgical treatment of adjacent instability after lumbar spine fusion. Spine (Phila Pa 1976). 2001; 26:E519–E524. doi:10.1097/00007632-200111150-00024 [CrossRef]
  32. Axelsson P, Johnsson R, Stromqvist B. The spondylolytic vertebra and its adjacent segment: mobility measured before and after posterolateral fusion. Spine (Phila Pa 1976). 1997; 22:414–417. doi:10.1097/00007632-199702150-00012 [CrossRef]
  33. Hayes MA, Tompkins SF, Herndon WA, Gruel CR, Kopta JA, Howard TC. Clinical and radiological evaluation of lumbosacral motion below fusion levels in idiopathic scoliosis. Spine (Phila Pa 1976). 1988; 13:1161–1167. doi:10.1097/00007632-198810000-00019 [CrossRef]
  34. Esses SI, Doherty BJ, Crawford MJ, Dreyzin V. Kinematic evaluation of lumbar fusion techniques. Spine (Phila Pa 1976). 1996; 21:676–684. doi:10.1097/00007632-199603150-00003 [CrossRef]
  35. Kim YE, Goel VK, Weinstein JN, Lim TH. Effect of disc degeneration at one level on the adjacent level in axial mode. Spine (Phila Pa 1976). 1991; 16:331–335. doi:10.1097/00007632-199103000-00013 [CrossRef]
  36. Weinhoffer SL, Guyer RD, Herbert M, Griffith SL. Intradiscal pressure measurements above an instrumented fusion: a cadaveric study. Spine (Phila Pa 1976). 1995; 20:526–531. doi:10.1097/00007632-199503010-00004 [CrossRef]
  37. Chen CS, Cheng CK, Liu CL. A biomechanical comparison of posterolateral fusion and posterior fusion in the lumbar spine. J Spinal Disord Tech. 2002; 15:53–63. doi:10.1097/00024720-200202000-00010 [CrossRef]
  38. Cunningham BW, Kotani Y, McNulty PS, Cappuccino A, McAfee PC. The effect of spinal destabilization and instrumentation on lumbar intradiscal pressure: an in vitro biomechanical analysis. Spine (Phila Pa 1976). 1997; 22:2655–2663. doi:10.1097/00007632-199711150-00014 [CrossRef]
  39. Lotz JC, Colliou OK, Chin JR, Duncan NA, Liebenberg E. Compression-induced degeneration of the intervertebral disc: an in vivo mouse model and finite-element study. Spine (Phila Pa 1976). 1998; 23:2493–2506. doi:10.1097/00007632-199812010-00004 [CrossRef]
  40. Phillips FM, Reuben J, Wetzel FT. Intervertebral disc degeneration adjacent to a lumbar fusion: an experimental rabbit model. J Bone Joint Surg Br. 2002; 84:289–294. doi:10.1302/0301-620X.84B2.11937 [CrossRef]
  41. Kumar MN, Baklanov A, Chopin D. Correlation between sagittal plane changes and adjacent segment degeneration following lumbar spine fusion. Eur Spine J. 2001; 10:314–319. doi:10.1007/s005860000239 [CrossRef]
  42. Wai EK, Santos ER, Morcom RA, Fraser RD. Magnetic resonance imaging 20 years after anterior lumbar interbody fusion. Spine (Phila Pa 1976). 2006; 31:1952–1956. doi:10.1097/01.brs.0000228849.37321.a8 [CrossRef]
  43. Hambly MF, Wiltse LL, Raghavan N, Schneiderman G, Koenig C. The transition zone above a lumbosacral fusion. Spine (Phila Pa 1976). 1998; 23:1785–1792. doi:10.1097/00007632-199808150-00012 [CrossRef]
  44. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg Am. 1990; 72:403–408.
  45. Frymoyer JW, Hanley EN Jr, Howe J, Kuhlmann D, Matteri RE. A comparison of radiographic findings in fusion and nonfusion patients ten or more years following lumbar disc surgery. Spine (Phila Pa 1976). 1979; 4(5):435–440. doi:10.1097/00007632-197909000-00008 [CrossRef]
  46. Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thoracolumbar fusion with pedicle screw instrumentation: a minimum 5-year follow-up. Spine (Phila Pa 1976). 2007; 32:2253–2257. doi:10.1097/BRS.0b013e31814b2d8e [CrossRef]
  47. Ghiselli G, Wang JC, Bhatia NN, Hsu WK, Dawson EG. Adjacent segment degeneration in the lumbar spine. J Bone Joint Surg Am. 2004; 86:1497–1503.
  48. Gillet P. The fate of the adjacent motion segments after lumbar fusion. J Spinal Disord Tech. 2003; 16:338–345. doi:10.1097/00024720-200308000-00005 [CrossRef]
  49. Penta M, Sandhu A, Fraser RD. Magnetic resonance imaging assessment of disc degeneration 10 years after anterior lumbar interbody fusion. Spine (Phila Pa 1976). 1995; 20:743–747. doi:10.1097/00007632-199503150-00018 [CrossRef]
  50. Sears WR, Sergides IG, Kazemi N, Smith M, White GJ, Osburg B. Incidence and prevalence of surgery at segments adjacent to a previous posterior lumbar arthrodesis. Spine J. 2011; 11:11–20. doi:10.1016/j.spinee.2010.09.026 [CrossRef]
  51. Wimmer C, Gluch H, Krismer M, Ogon M, Jesenko R. AP-translation in the proximal disc adjacent to lumbar spine fusion: a retrospective comparison of mono- and polysegmental fusion in 120 patients. Acta Orthop Scand. 1997; 68:269–272. doi:10.3109/17453679708996699 [CrossRef]
  52. Ghiselli G, Wang JC, Hsu WK, Dawson EG. L5-S1 segment survivorship and clinical outcome analysis after L4–L5 isolated fusion. Spine (Phila Pa 1976). 2003; 28:1275–1280. doi:10.1097/01.BRS.0000065566.24152.D3 [CrossRef]
  53. Kawakami M, Tamaki T, Ando M, Yamada H, Hashizume H, Yoshida M. Lumbar sagittal balance influences the clinical outcome after decompression and posterolateral spinal fusion for degenerative lumbar spondylolisthesis. Spine (Phila Pa 1976). 2002; 27:59–64. doi:10.1097/00007632-200201010-00014 [CrossRef]
  54. Lazennec JY, Ramare S, Arafati N, et al. Sagittal alignment in lumbosacral fusion: relations between radiological parameters and pain. Eur Spine J. 2000; 9:47–55. doi:10.1007/s005860050008 [CrossRef]
  55. Oda I, Cunningham BW, Buckley RA, et al. Does spinal kyphotic deformity influence the biomechanical characteristics of the adjacent motion segments? An in vivo animal model. Spine (Phila Pa 1976). 1999; 24:2139–2146. doi:10.1097/00007632-199910150-00014 [CrossRef]
  56. Lehmann TR, Spratt KF, Tozzi JE, et al. Long-term follow-up of lower lumbar fusion patients. Spine (Phila Pa 1976). 1987; 12:97–104. doi:10.1097/00007632-198703000-00004 [CrossRef]
  57. Ruberte LM, Natarajan RN, Andersson GB. Influence of single-level lumbar degenerative disc disease on the behavior of the adjacent segments: a finite element model study. J Biomech. 2009; 42:341–348. doi:10.1016/j.jbiomech.2008.11.024 [CrossRef]
  58. Schlegel JD, Smith JA, Schleusener RL. Lumbar motion segment pathology adjacent to thoracolumbar, lumbar, and lumbosacral fusions. Spine (Phila Pa 1976). 1996; 21:970–981. doi:10.1097/00007632-199604150-00013 [CrossRef]
  59. Akamaru T, Kawahara N, Tim Yoon S, et al. Adjacent segment motion after a simulated lumbar fusion in different sagittal alignments: a biomechanical analysis. Spine (Phila Pa 1976). 2003; 28:1560–1566. doi:10.1097/01.BRS.0000076820.44132.99 [CrossRef]
  60. Ahn DK, Park HS, Choi DJ, Kim KS, Yang SJ. Survival and prognostic analysis of adjacent segments after spinal fusion. Clin Orthop Surg. 2010; 2:140–147. doi:10.4055/cios.2010.2.3.140 [CrossRef]
  61. Ekman P, Moller H, Shalabi A, Yu YX, Hedlund R. A prospective randomised study on the long-term effect of lumbar fusion on adjacent disc degeneration. Eur Spine J. 2009; 18:1175–1186. doi:10.1007/s00586-009-0947-3 [CrossRef]
  62. Abdu WA, Lurie JD, Spratt KF, et al. Degenerative spondylolisthesis: does fusion method influence outcome? Four-year results of the spine patient outcomes research trial. Spine (Phila Pa 1976). 2009; 34:2351–2360. doi:10.1097/BRS.0b013e3181b8a829 [CrossRef]
  63. Videbaek TS, Egund N, Christensen FB, Grethe Jurik A, Bunger CE. Adjacent segment degeneration after lumbar spinal fusion: the impact of anterior column support: a randomized clinical trial with an eight- to thirteen-year magnetic resonance imaging follow-up. Spine (Phila Pa 1976). 2010; 35:1955–1964. doi:10.1097/BRS.0b013e3181e57269 [CrossRef]
  64. Edwards CC II, Bridwell KH, Patel A, et al. Thoracolumbar deformity arthrodesis to L5 in adults: the fate of the L5-S1 disc. Spine (Phila Pa 1976). 2003; 28:2122–2131. doi:10.1097/01.BRS.0000084266.37210.85 [CrossRef]
  65. Shono Y, Kaneda K, Abumi K, McAfee PC, Cunningham BW. Stability of posterior spinal instrumentation and its effects on adjacent motion segments in the lumbosacral spine. Spine (Phila Pa 1976). 1998; 23:1550–1558. doi:10.1097/00007632-199807150-00009 [CrossRef]
  66. Wiltse LL, Radecki SE, Biel HM, et al. Comparative study of the incidence and severity of degenerative change in the transition zones after instrumented versus noninstrumented fusions of the lumbar spine. J Spinal Disord. 1999; 12:27–33. doi:10.1097/00002517-199902000-00004 [CrossRef]
  67. Kaito T, Hosono N, Mukai Y, Makino T, Fuji T, Yonenobu K. Induction of early degeneration of the adjacent segment after posterior lumbar interbody fusion by excessive distraction of lumbar disc space. J Neurosurg Spine. 2010; 12:671–679. doi:10.3171/2009.12.SPINE08823 [CrossRef]
  68. Nassr A, Lee JY, Bashir RS, et al. Does incorrect level needle localization during anterior cervical discectomy and fusion lead to accelerated disc degeneration?Spine (Phila Pa 1976). 2009; 34:189–192. doi:10.1097/BRS.0b013e3181913872 [CrossRef]
  69. Phillips FM, Carlson GD, Bohlman HH, Hughes SS. Results of surgery for spinal stenosis adjacent to previous lumbar fusion. J Spinal Disord. 2000; 13:432–437. doi:10.1097/00002517-200010000-00011 [CrossRef]
  70. Whitecloud TS III, Davis JM, Olive PM. Operative treatment of the degenerated segment adjacent to a lumbar fusion. Spine (Phila Pa 1976). 1994; 19:531–536. doi:10.1097/00007632-199403000-00007 [CrossRef]
  71. Harrop JS, Youssef JA, Maltenfort M, et al. Lumbar adjacent segment degeneration and disease after arthrodesis and total disc arthroplasty. Spine (Phila Pa 1976). 2008; 33:1701–1707. doi:10.1097/BRS.0b013e31817bb956 [CrossRef]
  72. Wang JC, Arnold PM, Hermsmeyer JT, Norvell DC. Do lumbar motion preserving devices reduce the risk of adjacent segment pathology compared with fusion surgery? A systematic review. Spine (Phila Pa 1976). 2012; 37:S133–S143. doi:10.1097/BRS.0b013e31826cadf2 [CrossRef]
  73. Huang RC, Tropiano P, Marnay T, Girardi FP, Lim MR, Cammisa FP Jr, . Range of motion and adjacent level degeneration after lumbar total disc replacement. Spine J. 2006; 6:242–247. doi:10.1016/j.spinee.2005.04.013 [CrossRef]
  74. Park DK, Lin EL, Phillips FM. Index and adjacent level kinematics after cervical disc replacement and anterior fusion: in vivo quantitative radiographic analysis. Spine (Phila Pa 1976). 2011; 36:721–730. doi:10.1097/BRS.0b013e3181df10fc [CrossRef]
  75. Singh K, Phillips FM, Park DK, Pelton MA, An HS, Goldberg EJ. Factors affecting reoperations after anterior cervical discectomy and fusion within and outside of a Federal Drug Administration investigational device exemption cervical disc replacement trial. Spine J. 2012; 12:372–378. doi:10.1016/j.spinee.2012.02.005 [CrossRef]
  76. Jawahar A, Cavanaugh DA, Kerr EJ III, Birdsong EM, Nunley PD. Total disc arthroplasty does not affect the incidence of adjacent segment degeneration in cervical spine: results of 93 patients in three prospective randomized clinical trials. Spine J. 2010; 10:1043–1048. doi:10.1016/j.spinee.2010.08.014 [CrossRef]
  77. Grupp TM, Yue JJ, Garcia R Jr, et al. Biotribological evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro wear simulation. Eur Spine J. 2009; 18:98–108. doi:10.1007/s00586-008-0840-5 [CrossRef]
  78. Jacobs WC, van der Gaag NA, Kruyt MC, et al. Total disc replacement for chronic discogenic low back pain: a Cochrane review. Spine (Phila Pa 1976). 2013; 38:24–36. doi:10.1097/BRS.0b013e3182741b21 [CrossRef]

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10.3928/01477447-20140728-08

Educational Objectives

As a result of reading this article, physicians should be able to:


Understand the forces that predispose adjacent cervical segments to degeneration.

Understand the challenges of radiographic evaluation in the diagnosis of cervical and lumbar adjacent segment disease.

Describe the changes in biomechanical forces applied to adjacent segments of lumbar vertebrae with fusion.

Know the risk factors for adjacent segment disease in spinal fusion.

 

Adjacent segment disease (ASD) is a broad term encompassing many complications of spinal fusion, including listhesis, instability, herniated nucleus pulposus, stenosis, hypertrophic facet arthritis, scoliosis, and vertebral compression fracture. The area of the cervical spine where most fusions occur (C3–C7) is adjacent to a highly mobile upper cervical region, and this contributes to the biomechanical stress put on the adjacent cervical segments postfusion. Studies have shown that after fusion surgery, there is increased load on adjacent segments. Definitive treatment of ASD is a topic of continuing research, but in general, treatment choices are dictated by patient age and degree of debilitation. Investigators have also studied the risk factors associated with spinal fusion that may predispose certain patients to ASD postfusion, and these data are invaluable for properly counseling patients considering spinal fusion surgery. Biomechanical studies have confirmed the added stress on adjacent segments in the cervical and lumbar spine. The diagnosis of cervical ASD is complicated given the imprecise correlation of radiographic and clinical findings. Although radiological and clinical diagnoses do not always correlate, radiographs and clinical examination dictate how a patient with prolonged pain is treated. Options for both cervical and lumbar spine ASD include fusion and/or decompression. Current studies are encouraging regarding the adoption of arthroplasty in spinal surgery, but more long-term data are required for full adoption of arthroplasty as the standard of care for prevention of ASD. [Orthopedics. 2014; 37(8):547–555.]

The authors are from the Department of Orthopaedics, The Ohio State University, Columbus, Ohio.

The material presented in any Keck School of Medicine of USC continuing education activity does not necessarily reflect the views and opinions of Orthopedics or Keck School of Medicine of USC. Neither Orthopedics nor Keck School of Medicine of USC nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

Correspondence should be addressed to: Safdar N. Khan, MD, Department of Orthopaedics, The Ohio State University, 725 Prior Hall, 376 W Tenth St, Columbus, OH 43210 ( safdar.khan@osumc.edu).

Received: May 21, 2013

Accepted: December 03, 2013

Educational Objectives

As a result of reading this article, physicians should be able to:


Understand the forces that predispose adjacent cervical segments to degeneration.

Understand the challenges of radiographic evaluation in the diagnosis of cervical and lumbar adjacent segment disease.

Describe the changes in biomechanical forces applied to adjacent segments of lumbar vertebrae with fusion.

Know the risk factors for adjacent segment disease in spinal fusion.

 

Adjacent segment disease (ASD) is a broad term encompassing many complications of spinal fusion, including listhesis, instability, herniated nucleus pulposus, stenosis, hypertrophic facet arthritis, scoliosis, and vertebral compression fracture. The area of the cervical spine where most fusions occur (C3–C7) is adjacent to a highly mobile upper cervical region, and this contributes to the biomechanical stress put on the adjacent cervical segments postfusion. Studies have shown that after fusion surgery, there is increased load on adjacent segments. Definitive treatment of ASD is a topic of continuing research, but in general, treatment choices are dictated by patient age and degree of debilitation. Investigators have also studied the risk factors associated with spinal fusion that may predispose certain patients to ASD postfusion, and these data are invaluable for properly counseling patients considering spinal fusion surgery. Biomechanical studies have confirmed the added stress on adjacent segments in the cervical and lumbar spine. The diagnosis of cervical ASD is complicated given the imprecise correlation of radiographic and clinical findings. Although radiological and clinical diagnoses do not always correlate, radiographs and clinical examination dictate how a patient with prolonged pain is treated. Options for both cervical and lumbar spine ASD include fusion and/or decompression. Current studies are encouraging regarding the adoption of arthroplasty in spinal surgery, but more long-term data are required for full adoption of arthroplasty as the standard of care for prevention of ASD. [Orthopedics. 2014; 37(8):547–555.]

The authors are from the Department of Orthopaedics, The Ohio State University, Columbus, Ohio.

The material presented in any Keck School of Medicine of USC continuing education activity does not necessarily reflect the views and opinions of Orthopedics or Keck School of Medicine of USC. Neither Orthopedics nor Keck School of Medicine of USC nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

Correspondence should be addressed to: Safdar N. Khan, MD, Department of Orthopaedics, The Ohio State University, 725 Prior Hall, 376 W Tenth St, Columbus, OH 43210 ( safdar.khan@osumc.edu).

Received: May 21, 2013

Accepted: December 03, 2013

Spinal fusion has been studied as a means to treat pathology related to the spine for more than a century.1 Because the proportion of the American population older than 65 years will increase from 12.4% in 2000 to 19.6% in 2030,2 and due to the many surgical advancements in spinal surgery over the past few decades, the rate of fusion surgeries rose between 1993 and 20033 and between 1979 and 1990.4 Given the current environment, it is imperative that orthopedic surgeons understand the possible outcomes of fusion surgery.

One complication of spinal fusion is adjacent segment disease (ASD) following cervical, lumbar, or lumbosacral fusion. This is a broad term that encompasses symptoms such as listhesis, instability, herniated nucleus pulposus, stenosis, hypertrophic facet arthritis, scoliosis, and vertebral compression fracture.5 The cause of this degenerative process has been extensively studied in biomechanical studies using animal and cadaver models.6–9 Whether these degenerative changes also cause clinical, rather than solely radiological, changes has also been studied extensively.10–15

Treatment modalities for ASD are complicated by the increased risks associated with revision spinal surgeries and the evolving technology of spinal arthroplasty. Definitive management of ASD continues to be studied, and treatment priorities should be dictated by patient age and the degree of debilitation associated with ASD for each patient. Investigators have also studied the risk factors associated with spinal fusion that may predispose certain patients to ASD postfusion.14,16–25 These data are invaluable for properly counseling patients considering spinal fusion surgery.

Adjacent Segment Disease Associated With Cervical Spinal Fusion

Biomechanics

The motion of adjacent segments after cervical spinal fusion has been modeled in several studies in an attempt to understand the forces that predispose adjacent cervical segments to degeneration.6–9 The area of the cervical spine where most fusions occur (C3–C7) is adjacent to a highly mobile upper cervical region, and this contributes to the biomechanical stress put on the adjacent cervical segments postfusion. Studies have shown that after fusion surgery, there is increased load on adjacent segments. In a study by Eck et al,6 six cadaveric spine specimens were tested and stabilized at T1. Pressure increased in both C4–C5 and C6–C7. An image of this experimental apparatus is shown in Figure 1. A finite element model was used by Maiman et al7 to examine the effects of C4–C5 and C5–C6 fusions, and increased internal stress in adjacent segments was found. Researchers studying a multisegment cervical fusion found that stress on adjacent segments increased between single and double fusions.8 Lopez-Espina et al8 used a finite element model and facet-constraining methods to prevent increases in stress. Increases in stress up to 96% were found in the annulus, nucleus, and endplates postfusion. Canine models have also shown a change in proteoglycan population in intervertebral disks postfusion. Cole et al9 found that the proteoglycan population produced in both the nucleus pulposus and annulus fibrosus postfusion is similar to the proteoglycan population in immature tissue.

Photograph of the pressure transducer used to measure the biomechanical stress placed on adjacent segments after stabilizing at T1. (Reprinted with permission from Eck JC, Humphreys SC, Lim TH, et al. Biomechanical study on the effect of cervical spine fusion on adjacent level intradiscal pressure and segmental motion. Spine [Phila Pa 1976]. 2002; 27[22]:2431–2434.)

Figure 1:

Photograph of the pressure transducer used to measure the biomechanical stress placed on adjacent segments after stabilizing at T1. (Reprinted with permission from Eck JC, Humphreys SC, Lim TH, et al. Biomechanical study on the effect of cervical spine fusion on adjacent level intradiscal pressure and segmental motion. Spine [Phila Pa 1976]. 2002; 27[22]:2431–2434.)

Clinical and Radiographic Diagnosis

The diagnosis of cervical ASD is complicated given the imprecise correlation of radiographic and clinical findings. Evaluation is difficult because the normal degenerative process in patients is difficult to separate from the effects of the fusion surgery on adjacent segments. No validated classification system exists for cervical ASD.10 A study by Baba et al11 followed more than 100 patients for an average of 8.5 years and found an increase in tilting angle in the upper adjacent and lower adjacent segments, as well as newly diagnosed spinal stenosis in 25% of patients.11 Herkowitz et al26 prospectively studied 28 patients who had undergone cervical fusion and found that 41% of patients had adjacent level degeneration on radiographs at an average 4.5-year follow-up. Matsumoto et al12 investigated the use of magnetic resonance imaging (MRI) for ASD by comparing a group of 64 patients undergoing anterior cervical decompression and fusion with 201 asymptomatic volunteers. Disk degeneration at adjacent segments was significantly more likely in the fusion group compared with the control group, although disk degeneration at adjacent segments was not always related to clinical symptoms. Postoperative ASD is shown in Figure 2.

Adjacent segment disease in the cervical spine. Preoperative radiograph showing disk disease between levels C5–C7 (A). Five-year postoperative radiograph showing fusion of levels C4–C6 with cervical disk space narrowing at C6–C7 (arrow) (B). Five-year postoperative myelography showing intervertebral disk herniation at C6–C6 and complete block of the dural sack at C6–C7 (arrow) (C). Radiograph taken after reoperation for fusion of C6–C7 (D). (Reprinted with permission from Ishihara H, Kanamori M, Kawaguchi Y, et al. Adjacent segment disease after cervical nterbody fusion. Spine J. 2004; 4[6]:624–628.)

Figure 2:

Adjacent segment disease in the cervical spine. Preoperative radiograph showing disk disease between levels C5–C7 (A). Five-year postoperative radiograph showing fusion of levels C4–C6 with cervical disk space narrowing at C6–C7 (arrow) (B). Five-year postoperative myelography showing intervertebral disk herniation at C6–C6 and complete block of the dural sack at C6–C7 (arrow) (C). Radiograph taken after reoperation for fusion of C6–C7 (D). (Reprinted with permission from Ishihara H, Kanamori M, Kawaguchi Y, et al. Adjacent segment disease after cervical nterbody fusion. Spine J. 2004; 4[6]:624–628.)

Although the rate of radiographic signs of ASD is high, the rate of clinical symptoms of ASD is lower. Baba et al11 retrospectively studied 146 patients undergoing cervical fusion and found that 13.5% of patients had identifiable problems at a level other than the level fused. Lunsford et al13 reported a reoperation rate of 10% at a different segment after anterior cervical fusion at less than 3-year follow-up. Hilibrand et al14 followed 374 patients over a maximum of 21 years postoperatively and found that symptomatic ASD occurred at a rate of 2.9% over 10 years postoperatively and that 25.6% of patients had ASD within 10 years postoperatively. Yue et al15 studied 71 patients undergoing anterior cervical diskectomy and fusion over more than 5 years and found that 16.9% of patients needed revision surgery for symptomatic adjacent level disease, although 73.2% of patients had new-onset or worsening degeneration of disk spaces adjacent to the operated levels.15

Risk Factors

Adjacent segment disease only occurs in a certain portion of patients after spinal fusion. Various studies have investigated the risk factors for the development of ASD after cervical spinal fusion. Hilibrand et al14 analyzed risk factors that contributed to the progression of symptomatic ASD. Patients who had adjacent segments with neural element compression, surgery at C5–C6 and/or C6–C7 levels, or anterior cervical fusion surgery of more than 1 level were less likely to develop ASD. Williams et al16 studied the factors that contributed to positive and negative postoperative outcomes in 90 patients undergoing cervical diskectomy and interbody fusion over 2 to 9 years. Patients with apparently normal preoperative radiographs had worse outcomes than those with osteophyte formation, narrowing of the interspace, or both. Katsuura et al17 studied the effect of postoperative malalignment of the cervical spine in a prospective study over 9.8 years and found that 43% of patients with ASD had malalignment of the cervical spine. In patients who have an anterior cervical plate, the distance between the plate and adjacent segments may influence the amount of ossification at adjacent segments.18 Park et al18 found a positive association between plate-to-disk distance and the amount of ossification at adjacent segments.

Two recent systematic reviews specifically studied risk factors related to ASD postoperatively.10,19 Lawrence et al19 found 5 quality research studies and concluded that fusing segments adjacent to C5–C6 and/or C6–C7 increased the risk of ASD. Of note, the authors mentioned that even after performing a systematic review of more than 170 articles, the development of clinical adjacent segment pathology is difficult to differentiate from the natural history of spinal degeneration. A population-based study from Taiwan noted a low rate of reoperation (0.8%) for clinically significant ASD.20 Lee et al21 found that radiographic signs of ASD were more likely in patients who had degenerative indications for cervical spinal fusion.

Adjacent Segment Disease Associated With Lumbar Spine Fusion

Biomechanics

The fusion of lumbar vertebrae has been associated with changes in the biomechanical forces applied to adjacent segments.27 The area of adjacent segment biomechanical forces and motion has been studied since the 1980s.28,29 In 1984, Lee and Langrana28 put 16 cadaveric models under combined compression and bending loads to observe motion. They found increased stress on adjacent segments and increased loading on facet joints within unfused segments. Further evidence of facet joint strain postfusion was demonstrated by Ha et al30 in an experiment with in vitro canine spines. They found increased segmental mobility and changed contact patterns within the joint. Using a finite model, Chen et al31 also found increased forces in adjacent disks postfusion and noted larger stress increases at the upper adjacent disk rather than the lower disk.

Increased motion at adjacent segments has been postulated as a reason for ASD. Axelsson et al32 studied 6 patients undergoing radiographic analysis of segment motion before and after L4–L5 fusion surgery. Increased mobility occurred in adjacent segments for 2 of the 6 patients. In an in vivo model, Hayes et al33 specifically examined mobility and found increased translational motion in adjacent segments when L3–L4 was fused, and this motion correlated with lower back pain. Esses et al34 studied changes in motion with different fusion techniques in cadaveric models. Posterolateral fusions were found to have less motion in adjacent segments as compared with anterior fusions.

In both cadaveric and finite models, increased intradiskal pressure has been found within adjacent segments.35–37 Weinhoffer et al36 studied intradiskal pressure in adjacent segments during flexion in cadaveric models. Intradiskal pressure increased during flexion, and the more segments that were fused, the greater the intradiskal pressure. Similar results were found by Cunningham et al,38 who studied 11 cadaveric models and found that intradiskal pressure increased by as much as 45%.

Using an in vivo mouse model and a finite element model, Lotz et al39 studied both the changes in stress in adjacent segments and the biochemical changes within adjacent segments. The finite element model predicted an increase in hydrostatic stress in the middle regions of the annulus by nearly ten-fold. Numerous harmful responses occurred at the histological and cellular levels, including disorganization of the annulus fibrosus, an increase in apoptosis with associated loss of cellularity, and damaging changes in gene expression. In an animal model by Phillips et al,40 results included loss of chondrocytes and notochordal cells within the nucleus pulposus.

Clinical and Radiographic Diagnosis

Separating the progression of osteoarthritis in patients postfusion from lumbar ASD is difficult. In a study by Kumar et al,41 patients were followed postfusion with the Short Form 36 and Oswestry Disability Index, functional testing, and radiographs. Their results were compared with those from age- and sex-matched controls. Radiographic changes above the level of fusion were worse in those with fusion compared with those not fused. There was no statistically significant difference in clinical outcomes. Wai et al42 studied MRI results over 20 years for patients undergoing lumbar fusion surgery and found that the prevalence of degenerative changes in patients undergoing surgery was similar to age-matched controls. Hambly et al43 reported that radiographic changes occur in the transition zone cephalad to lumbosacral fusion, regardless of whether surgery occurred.

As with ASD in the cervical spine, the correlation between clinical, MRI, and radiographic signs of ASD is controversial. Interpretation of radiographic evidence is also complicated by the fact that asymptomatic patients have been found to have substantial abnormalities on MRI.44 Plain radiographs have been found to be of little help in the diagnosis of ASD. Frymoyer et al45 examined plain radiographs from 96 patients who had undergone fusion surgery. Results showed no correlation between radiographic findings and clinical symptoms. The progressive changes seen on radiographs of adjacent segments are illustrated in Figure 3.46 In the current authors’ experience treating ASD, severe degenerative changes cause symptoms of spinal stenosis. Figure 4 shows an area of neural foraminal narrowing at the L2–L3 level.

Radiographs showing progressive changes after lumbar spinal fusion preoperatively (A) and 2 years (B), 5 years (C), and 9 years (D) postoperatively. In this patient, definite signs of adjacent segment disease are present by 13 years after L4–L5 spinal fusion (E). However, it is unclear whether these radiographic changes signify clinical significance. (Reprinted with permission from Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thora-columbar fusion with pedicle screw instrumentation. Spine [Phila Pa 1976]. 2007; 32[20]:2253–2257.)

Figure 3:

Radiographs showing progressive changes after lumbar spinal fusion preoperatively (A) and 2 years (B), 5 years (C), and 9 years (D) postoperatively. In this patient, definite signs of adjacent segment disease are present by 13 years after L4–L5 spinal fusion (E). However, it is unclear whether these radiographic changes signify clinical significance. (Reprinted with permission from Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thora-columbar fusion with pedicle screw instrumentation. Spine [Phila Pa 1976]. 2007; 32[20]:2253–2257.)

Radiograph of a patient with a L3–L5 posterior spinal fusion with instrumentation who presented to clinic after months of severe back pain and radiating pain down bilateral legs (A). Computed tomography myelogram showing spinal stenosis at L2–L3 with bilateral facet hypertrophy (B). This patient eventually had her spinal instrumentation removed and underwent fusion of her L2–L3 segment with instrumentation.

Figure 4:

Radiograph of a patient with a L3–L5 posterior spinal fusion with instrumentation who presented to clinic after months of severe back pain and radiating pain down bilateral legs (A). Computed tomography myelogram showing spinal stenosis at L2–L3 with bilateral facet hypertrophy (B). This patient eventually had her spinal instrumentation removed and underwent fusion of her L2–L3 segment with instrumentation.

Many studies have examined the prevalence of clinical symptoms associated with ASD. In a long-term retrospective study by Ghiselli et al,47 215 patients were followed postfusion for an average of 6.7 years. The rate of reoperation at adjacent segments was 16.5% in the first 5 years and 36.1% at 10 years. Similar results were reported by Gillet48 in a retrospective study that found a reoperation rate of 20% over a range of 2 to 15 years of follow-up. Penta et al49 studied MRIs for 10 years after lumbar interbody fusion, and of the 81 patients studied, 32% had radiographically diagnosed ASD. In a large retrospective cohort study by Sears et al50 of 1000 consecutive posterior lumbar interbody fusion procedures with a mean follow-up of 63 months, the 10-year prevalence of further surgery for ASD was 22.2%. The annual incidence of surgery for ASD was 2.2%.

The rate of ASD after lumbar fusion varies widely between studies.5 In a review by Park et al5 of 22 studies, the reported range of ASD was 5.2% to 100% based on either radiographic or clinical diagnosis. The authors attributed this wide variation to the range of patient populations, differing clinical or radiographic definitions of ASD, and the retrospective nature of many of the studies.

Risk Factors

Several studies have examined the risk factors that put a portion of patients at risk for ASD. Aota et al22 reported that the factor most influential in postfusion instability was age. The study showed that 11 of 30 patients older than 55 years developed ASD postfusion, whereas only 3 of 25 patients younger than 55 years developed ASD postfusion. Similarly, a retrospective study by Etebar and Cahill23 found that ASD was higher in postmenopausal women. The link between menopause and worsening osteoarthritis is not entirely clear, but active research is ongoing into the mechanism by which a lack of estrogen influences osteoarthritis development and progression.24 In a retrospective review of 49 patients, Rahm and Hall25 found that increasing age, as well as inter-body fusion, was associated with a higher risk of ASD.

Investigators have studied whether the length of fusion in fusion surgery factors into the development of ASD. Penta et al49 examined MRIs and radiographs from 52 patients who had normal preoperative findings in adjacent levels.49 In this group of patients, the length of fusion did not factor into whether ASD occurred. Wimmer et al51 studied the effect of polysegmental fusions on anteroposterior translation in 120 patients with painful spondylolisthesis who were treated with combined anterior and posterior fusions. The study group was divided into a monosegmental fusion group (n=46) and a polysegmental fusion group (n=74). Polysegmental fusion was associated with a greater degree of anteroposterior translation.

Fusion involving the L4–L5 segment has been cited as a possible cause of disk degeneration at L5-S1. This was specifically studied by Ghiselli et al52 in a group of 32 patients over 7.3 years. Their investigation found a general progression of degenerative changes in the L5-S1 segments. However, the authors concluded that there was no need for routine fusion of L5-S1 in patients with isolated L4–L5 symptoms.

Another significant factor in determining ASD postfusion is the anatomical alignment of spinal segments preoperatively. Investigators have noted increased ASD in patients with a preoperative L1 and S1 axis distance greater than 35 mm.53 In a retrospective study, Kumar et al41 reported that patients with a normal C7 plumb line and sacral inclination had the lowest rate of ASD. In a study by Lazennec et al54 of 81 patients who had undergone fusion, there was a statistically significant relationship between postoperative pain and sacral tilt. Oda et al55 used a sheep model to determine the biomechanical changes in adjacent segments in kyphotic spines. Results showed that kyphotic posterolateral fusion significantly altered supra-adjacent segments by inducing more stiffness in the posterior ligamentous complex and increasing lamina strain under flexion-extension loading. There were significant degenerative changes in the supra-adjacent segments in these sheep. Lehmann et al56 found a correlation between preoperative segmental instability in the segment above fusion and lumbar spinal stenosis. The greater the translation instability, the more likely the adjacent segment would become unstable post-fusion. Biomechanical studies have also shown that once degeneration occurs at one segment, the risk of degeneration at other adjacent segments increases.57 Schlegel et al58 reported that segments that were 2 segments removed from fusion were just as likely to show degeneration as adjacent segments.

The alignment of fusion in the lumbar spine was investigated in a biomechanical cadaveric study by Akamaru et al.59 They reported that fusion in either hyper- or hypolordotic alignment of L4–L5 resulted in different loads on adjacent spinal segments. Hypolordotic alignment of L4–L5 resulted in the greatest amount of flexion-extension motion at L3–L4, whereas hyperlordotic alignment of L4–L5 resulted in the greatest amount of flexion-extension motion at L5-S1. In a study of patients undergoing 360° fusion with healthy adjacent segments preoperatively, it was found that maintaining the lordotic angle at approximately 20° postoperatively was associated with the prevention of ASD.60

Several studies have investigated ASD in the lumbar spine following different treatment decisions. In a prospective study of 111 patients with spondylolisthesis who were randomized to exercise, uninstrumented posterolateral fusion, or instrumented posterolateral fusion, accelerated adjacent segment degeneration was found in the patients that had fusion and laminectomy.61 Abdu et al62 studied 380 surgical candidates with degenerative spondylolisthesis who underwent 1 of 3 surgical interventions: posterior in situ fusion, posterolateral instrumented fusion with pedicle screws, or posterolateral instrumented fusion with pedicle screws plus interbody fusion (360°). At 3- and 4-year follow-up, there was no statistical difference in outcome criteria (ie, Short Form 36 bodily pain, physical function scales, and the modified Oswestry Disability Index) between the different operative techniques. Furthermore, in a randomized, controlled trial performed by Videbaek et al,63 patients who underwent anterior lumbar interbody fusion combined with posterolateral lumbar fusion or posterolateral lumbar fusion alone showed no increased risk of ASD. Therefore, it does not appear that a specific treatment technique accelerates the onset of increases the likelihood of developing ASD compared with any other.

Edwards et al64 investigated long adult fusions of the thoracolumbar spine to L5 and the resultant degenerative changes to S1. Thirty-four patients were followed for a mean of 5.6 years. Results showed that 61% of patients had resultant degenerative disk disease. Risk factors for degenerative changes were a positive sagittal balance, younger age at operation, and any signs of radiographic degeneration at L5-S1.

Added instrumentation during spinal fusion has been studied as a possible risk factor for ASD. Shono et al65 investigated whether fusion surgeries augmented with instrumentation such as a compression hook and a transpedicular screw fixation system increased motion in adjacent segments. The study was conducted with a calf lumbosacral spine model. As spinal instrumentation increased, higher segmental displacement occurred at the upper residual intact motion segment. Interestingly, different results were reported by Wiltse et al66 with the use of pedicle screws. They studied pedicle screws and their relationship to transition zone changes above or below the fused segment. No increase in ASD incidence was found with pedicle screw placement.

Ahn et al60 retrospectively studied 3188 patients who underwent thoracolumbar spinal fusion to find the rate of ASD, as well as risk factors. Results showed a failure rate of 6% at 10 years at adjacent segments. Risk factors noted were multiple level fusions, old age, degenerative disease prior to fusion, and male sex. A study by Lee et al21 investigated overall risk factors for revision surgery due to ASD. Of 1069 patients undergoing spinal fusion surgery, 2.62% required revision surgery. Postoperative facet degeneration was associated with revision surgery, and the incidence of ASD in proximal segments was found to be higher than that in more distal segments. Preexisting degeneration was found to be a significant risk factor for ASD requiring surgery.

The intraoperative decision of distracted disk height of the fused segment caused by cage or bone insertion has been studied as a risk factor for ASD. Kaito et al67 studied 84 patients with L4 spondylolisthesis who were treated with posterior lumbar interbody fusion. Patients who developed ASD were found to have higher L4–L5 disk space distraction.

Nassr et al68 investigated whether incorrect needle localization during anterior cervical diskectomy and fusion caused ASD. Of 87 patients undergoing anterior cervical diskectomy and fusion, 15 had incorrect needle localization. The group with incorrect needle localization was associated with a 3 times higher rate of ASD. The authors concluded that either needle trauma or unnecessary surgical dissection may have caused ASD during the study. A recent systematic review for risk factors for ASD after lumbar fusion showed that age older than 60 years was associated with an increased risk of ASD after spinal fusion.19 Similarly, if the patient had preexisting facet degeneration, degenerative disk disease, multilevel fusion, laminectomy performed adjacent to a segment, a construct stopped at L5, or excessive disk height distraction, then the risk of ASD may be higher.

Treatment

There is no gold standard treatment for ASD, but there are methods to treat its symptoms. Several studies have shown that treatment with decompression of neural elements with possible extension of fusion may relieve symptoms.31,69,70 Although there seems to be some pain relief with extension of fusion, these studies indicated that extension of fusion may result in higher rates of ASD in the newly created adjacent segments. These studies reported significant complication rates, and the number of treated patients was small. Arthroplasty has been promoted as a potential solution to ASD, but results from numerous studies indicate that more data are needed to ensure improved clinical outcomes.71–76 An example of a total disk arthroplasty device is shown in Figure 5.77 A recent Cochrane review showed that although there was a statistically significant improvement in outcome measures associated with total disk arthroplasty, it was not clear whether this difference was clinically significant.78 The authors of the review emphasized caution in adoption of the new technology.

The Activ L (B. Braun, Melsungen, Germany) total disk arthroplasty device designed for disk replacement in the spine. There are both superior and inferior endplates, and an ultra-high-molecular-weight polyethylene liner that sits between the plates. (Reprinted with permission from Grupp TM, Yue JJ, Garcia R Jr, et al. Biotribological evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro wear simulation. Eur Spine J. 2009; 18[1]:98–108.)

Figure 5:

The Activ L (B. Braun, Melsungen, Germany) total disk arthroplasty device designed for disk replacement in the spine. There are both superior and inferior endplates, and an ultra-high-molecular-weight polyethylene liner that sits between the plates. (Reprinted with permission from Grupp TM, Yue JJ, Garcia R Jr, et al. Biotribological evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro wear simulation. Eur Spine J. 2009; 18[1]:98–108.)

Conclusion

Adjacent segment disease is a complication related to spinal fusion. Its diagnosis is clouded by the fact that many patients have underlying degenerative changes that may mimic ASD. Biomechanical studies have confirmed the added stress on adjacent segments in the cervical and lumbar spine. Although radiological and clinical diagnoses do not always correlate, radiographs and clinical examination dictate how a patient with prolonged pain is treated. Options for both cervical and lumbar spine ASD include fusion and/or decompression. Although current studies are encouraging regarding the adoption of arthroplasty in spinal surgery, more long-term data are required for full adoption of arthroplasty as the standard of care for the prevention of ASD.

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Photograph of the pressure transducer used to measure the biomechanical stress placed on adjacent segments after stabilizing at T1. (Reprinted with permission from Eck JC, Humphreys SC, Lim TH, et al. Biomechanical study on the effect of cervical spine fusion on adjacent level intradiscal pressure and segmental motion. Spine [Phila Pa 1976]. 2002; 27[22]:2431–2434.)

Figure 1:

Photograph of the pressure transducer used to measure the biomechanical stress placed on adjacent segments after stabilizing at T1. (Reprinted with permission from Eck JC, Humphreys SC, Lim TH, et al. Biomechanical study on the effect of cervical spine fusion on adjacent level intradiscal pressure and segmental motion. Spine [Phila Pa 1976]. 2002; 27[22]:2431–2434.)

Adjacent segment disease in the cervical spine. Preoperative radiograph showing disk disease between levels C5–C7 (A). Five-year postoperative radiograph showing fusion of levels C4–C6 with cervical disk space narrowing at C6–C7 (arrow) (B). Five-year postoperative myelography showing intervertebral disk herniation at C6–C6 and complete block of the dural sack at C6–C7 (arrow) (C). Radiograph taken after reoperation for fusion of C6–C7 (D). (Reprinted with permission from Ishihara H, Kanamori M, Kawaguchi Y, et al. Adjacent segment disease after cervical nterbody fusion. Spine J. 2004; 4[6]:624–628.)

Figure 2:

Adjacent segment disease in the cervical spine. Preoperative radiograph showing disk disease between levels C5–C7 (A). Five-year postoperative radiograph showing fusion of levels C4–C6 with cervical disk space narrowing at C6–C7 (arrow) (B). Five-year postoperative myelography showing intervertebral disk herniation at C6–C6 and complete block of the dural sack at C6–C7 (arrow) (C). Radiograph taken after reoperation for fusion of C6–C7 (D). (Reprinted with permission from Ishihara H, Kanamori M, Kawaguchi Y, et al. Adjacent segment disease after cervical nterbody fusion. Spine J. 2004; 4[6]:624–628.)

Radiographs showing progressive changes after lumbar spinal fusion preoperatively (A) and 2 years (B), 5 years (C), and 9 years (D) postoperatively. In this patient, definite signs of adjacent segment disease are present by 13 years after L4–L5 spinal fusion (E). However, it is unclear whether these radiographic changes signify clinical significance. (Reprinted with permission from Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thora-columbar fusion with pedicle screw instrumentation. Spine [Phila Pa 1976]. 2007; 32[20]:2253–2257.)

Figure 3:

Radiographs showing progressive changes after lumbar spinal fusion preoperatively (A) and 2 years (B), 5 years (C), and 9 years (D) postoperatively. In this patient, definite signs of adjacent segment disease are present by 13 years after L4–L5 spinal fusion (E). However, it is unclear whether these radiographic changes signify clinical significance. (Reprinted with permission from Cheh G, Bridwell KH, Lenke LG, et al. Adjacent segment disease following lumbar/thora-columbar fusion with pedicle screw instrumentation. Spine [Phila Pa 1976]. 2007; 32[20]:2253–2257.)

Radiograph of a patient with a L3–L5 posterior spinal fusion with instrumentation who presented to clinic after months of severe back pain and radiating pain down bilateral legs (A). Computed tomography myelogram showing spinal stenosis at L2–L3 with bilateral facet hypertrophy (B). This patient eventually had her spinal instrumentation removed and underwent fusion of her L2–L3 segment with instrumentation.

Figure 4:

Radiograph of a patient with a L3–L5 posterior spinal fusion with instrumentation who presented to clinic after months of severe back pain and radiating pain down bilateral legs (A). Computed tomography myelogram showing spinal stenosis at L2–L3 with bilateral facet hypertrophy (B). This patient eventually had her spinal instrumentation removed and underwent fusion of her L2–L3 segment with instrumentation.

The Activ L (B. Braun, Melsungen, Germany) total disk arthroplasty device designed for disk replacement in the spine. There are both superior and inferior endplates, and an ultra-high-molecular-weight polyethylene liner that sits between the plates. (Reprinted with permission from Grupp TM, Yue JJ, Garcia R Jr, et al. Biotribological evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro wear simulation. Eur Spine J. 2009; 18[1]:98–108.)

Figure 5:

The Activ L (B. Braun, Melsungen, Germany) total disk arthroplasty device designed for disk replacement in the spine. There are both superior and inferior endplates, and an ultra-high-molecular-weight polyethylene liner that sits between the plates. (Reprinted with permission from Grupp TM, Yue JJ, Garcia R Jr, et al. Biotribological evaluation of artificial disc arthroplasty devices: influence of loading and kinematic patterns during in vitro wear simulation. Eur Spine J. 2009; 18[1]:98–108.)

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