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Adjacent segment degeneration and adjacent segment disease: the consequences of spinal fusion?
The Spine Journal 4 (2004) 190S–194S
Adjacent segment degeneration and adjacent segment disease: the consequences of spinal fusion? Alan S. Hilibrand, MDa,*, Matthew Robbins, BAb a
Department of Orthopaedic Surgery, Thomas Jefferson University and The Rothman Institute, 925 Chestnut Street, 5th Floor, Philadelphia, PA 19107, USA b Jefferson Medical College, 1015 Walnut Street, Philadelphia, PA 19107, USA
Abstract
Given the number of spinal fusions performed annually, concerns have mounted over the potential for adjacent segment degeneration (radiographic changes of degeneration at levels adjacent to a spinal fusion) and adjacent segment disease (development of new symptoms correlating with adjacent segment degeneration). This article reviews documented evidence on adjacent segment degeneration and disease as it relates to cervical and lumbar arthrodesis. There appears to be an incidence of adjacent segment degeneration and disease after arthrodesis that may be related to natural degeneration or the adjacent fusion. It remains to be seen whether restoration of motion with disc arthroplasty will alter the rate of adjacent segment degeneration or disease. 쑖 2004 Elsevier Inc. All rights reserved.
Keywords:
Adjacent segment; Degeneration; Cervical; Lumbar
Introduction The concept of spinal segment arthrodesis as a treatment for pathologic conditions of the human spinal column evolved almost 100 years ago. Spinal fusion was first described by Albee [1] for the treatment of Pott disease, and by Hibbs [2], who performed spinal fusion as a treatment for spinal deformity. Almost 50 years ago, cervical spine fusion was described by Bailey and Badgley, Robinson and Smith, and Cloward as a treatment for degenerative spondylotic conditions [3]. These early authors suggested that spinal fusion offered the surgeon an opportunity to remove the pathologic process (infection, arthritis or deformity), eliminate painful motion and allowed decompression of the neural elements with subsequent stabilization of the affected spine segments. Over the past 50 fifty years, spinal fusion has become a standard of care for numerous pathologic conditions of the human spine. For adolescents and adults with spinal deformity, thoracolumbar spinal fusion with instrumentation has
FDA device/drug status: not applicable. Nothing of value received from a commercial entity related to this research. * Corresponding author. The Rothman Institute, 925 Chestnut Street, 5th Floor, Philadelphia, PA 19107. Tel.: (267) 339-3620. E-mail address: [email protected] (A.S. Hilibrand) 1529-9430/04/$ – see front matter doi:10.1016/j.spinee.2004.07.007
쑖 2004 Elsevier Inc. All rights reserved.
demonstrated widespread success in arresting progression and correcting the scoliotic deformity. In the cervical spine, anterior cervical fusion in conjunction with decompression has been reported to provide greater than 90% likelihood of relief of radicular complaints and stabilization/improvement of myelopathic findings [4,5]. In the low back, lumbar decompression in conjunction with posterolateral fusion has been demonstrated in prospective randomized studies to be the superior form of surgical management for patients with degenerative spondylolisthesis [6]. The long-term consequences of spinal fusions have been thought to be of secondary importance given the high likelihood of success of these procedures in relieving the patient’s presenting complaints. However, as spinal fusions, especially those for idiopathic scoliosis, have been performed at younger ages, there has been increasing concerns regarding the long-term viability of the spinal motion segments adjacent to these fusions. These concerns have been amplified by the increasing rates of cervical and lumbar spine surgery in the United States over the past two decades [7]. In particular, as the indications for lumbar spinal fusions are stretched to include more patients with mechanical back pain with lower rates of clinical success, the concerns for the consequences of these procedures have increased. In this article the terms “adjacent segment degeneration” and “adjacent segment disease” will be used to define different types of postarthrodesis adjacent level pathology.
A.S. Hilibrand and M. Robbins / The Spine Journal 4 (2004) 190S–194S
The term “adjacent segment degeneration” will be used to describe radiographic changes seen at levels adjacent to a previous spinal fusion procedure that do not necessarily correlate with any clinical findings. On the other hand, the term “adjacent segment disease” will be used to refer to the development of new clinical symptoms that correspond to radiographic changes adjacent to the level of a previous spinal fusion. This article will consider the role spinal fusions may play in the development of adjacent segment degeneration and adjacent segment disease. These pathologies in the cervical spine and the lumbar spine will be considered separately, owing to the different biomechanical environments of cervical and lumbar spinal fusions. Cervical spine The anatomy of the cervical spine is unique in many ways, which may explain differences in the development of adjacent level problems in this portion of the spinal column as opposed to the lumbosacral region. Specifically, the region C3–C7 where most spinal fusion procedures are performed is bordered by a highly mobile upper cervical region, which accommodates approximately half of all cervical motion. The kinematics of the cervical spine have never been assessed in vitro in a model that includes the upper cervical region and therefore most closely approximates the in vivo potential for motion transfer to the upper cervical spine after cervical fusion procedures. The development of radiographic adjacent segment degeneration of the cervical spine has been studied. Baba et al. [8] assessed over 100 patients undergoing anterior cervical fusion for cervical myelopathy with an average of 8.5 years of follow-up. The authors observed that 25% of these patients subsequently developed new spinal canal stenosis above the previously fused segments. Similarly, Gore and Sepic [9] observed new spondylosis in 25% of 121 patients and progression of preexisting spondylosis in another 25% of patients who had previously undergone anterior cervical fusion with an average follow-up of 5 years. In neither of these studies, however, was there any correlation between the adjacent segment degeneration and the development of clinical symptoms referable to these radiographic changes. In a comparative radiographic study, Herkowitz et al. [10] studied 44 patients with 4.5 years of follow-up who had been randomized to anterior cervical discectomy and fusion or posterior foraminotomy without fusion for the treatment of cervical radiculopathy. Among the group undergoing anterior fusion, 41% developed adjacent segment degeneration. Surprisingly, however, 50% of the patients undergoing posterior foraminotomy without fusion had evidence of adjacent level degeneration. Once again, there was no correlation between the development of adjacent segment degeneration and the onset of new clinical symptoms referable to those radiographic changes. Clinical follow-up studies of patients undergoing anterior cervical discectomy and fusion have demonstrated that some
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patients undergoing anterior cervical fusion do appear to develop symptomatic adjacent segment disease. Bohlman et al. [4] reviewed 122 patients after anterior discectomy and fusion for radiculopathy with an average of 6 years of followup and found that 9% of these patients went on to develop adjacent segment disease requiring additional surgery. Similarly, Gore and Sepic [11] described 14% of the patients in their study requiring additional surgery for adjacent segment disease at an average follow-up of 5 years. In addition, Williams et al. [12] found that 17% of their 60 patients undergoing anterior cervical decompression and fusion developed adjacent segment disease requiring additional surgery with an average follow-up of 4.5 years. These three studies suggest that on average there is a prevalence of adjacent segment disease ranging from 9% to 17%. When the number of years of follow-up is divided into the overall prevalence, the annual incidence of adjacent segment disease requiring additional surgery appears to be between 1.5% and 4%. For the cervical spine, there are also data available for comparison of fusion and nonfusion procedures to determine whether the fusion itself might be causative in the development of adjacent segment disease. For example, Lunsford et al. [13] reported relatively short follow-up (less than 3 years) of 334 patients who underwent anterior cervical discectomy, many without fusion. They found that 22 of their patients developed adjacent segment disease for an overall prevalence of approximately 7% and an annual incidence of approximately 2.5%. Interestingly, they did not find any difference in the rate of adjacent segment disease between patients who underwent discectomy with fusion and those who underwent discectomy alone. In a very large series of patients undergoing posterior foraminotomy without fusion reported by Henderson et al. [14] with an average of 2.8 years of follow-up, the authors describe that 79 of their 846 patients developed adjacent segment disease requiring additional surgery. This represented an overall prevalence of 9% of their patients with an average annual incidence of approximately 3%. These clinical observations suggest that anterior decompression with fusion and posterior decompression without fusion may lead to similar rates of adjacent segment disease. In both instances there appears to be an average annual incidence of about 3% of patients requiring further surgery for adjacent segment disease. This does correlate with the radiographic findings of Herkowitz et al. [10] described earlier. In order to better understand the factors affecting the development of adjacent segment disease and the overall prevalence of this problem, one of us [15] reported the longterm follow-up of 409 anterior cervical decompression and stabilization procedures performed for radiculopathy and/ or myelopathy. All patients were assessed by chart review for the development of any new radicular or myelopathic symptoms that might be referable to adjacent level changes. Based on this information, a Kaplan-Meier survivorship
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A.S. Hilibrand and M. Robbins / The Spine Journal 4 (2004) 190S–194S
analysis was constructed to determine the likelihood of developing symptomatic adjacent segment changes, regardless of whether they ultimately required surgical intervention. Consistent with the reports of other authors, there was an overall prevalence of 14% of patients requiring additional surgery over a range of follow-up from 2 to 21 years with an annual incidence of approximately 3% of patients developing adjacent segment disease. However, the Kaplan-Meier survivorship analysis suggests that a much higher likelihood of the development of adjacent segment disease, reaching a predicted prevalence of 13.6% at 5 years and 25.6% at 10 years of follow-up. Risk factors for the development of adjacent segment disease were the existence of neural element compression at the adjacent levels at the time of the index procedure, as well as surgery performed adjacent to the C5–C6 and/or C6–C7 levels. Surprisingly, the authors found that anterior cervical fusions performed at more than one level had a significantly lower rate of adjacent segment disease than those performed at a single level (12% vs 18%, p⭐.001). The results of the study suggested that adjacent segment disease was indeed a common problem but may reflect the natural history of the underlying cervical spondylosis.
Lumbar spine The biomechanical environment of lumbar spinal fusion procedures is characterized by the presence of a rigid lever arm, represented by the sacrum and pelvis, adjacent to a series of increasingly mobile yet lordotic lower lumbar spinal motion segments. The lumbosacral junction is characterized by specific adaptations for greater stability, including an increased intrafacet distance and the presence of iliolumbar ligaments, which increase this level’s stability and render it better able to handle the increased stresses adjacent to the sacrum and pelvis. Proximal to the lumbosacral junction, the spinal motion segments from L2 through L5, although contained in a stable, lordotic region of the spinal column, are much more mobile, each accommodating a greater range of motion [16]. Biomechanical studies of lumbosacral fusions have demonstrated that with simulated spinal fusion procedures there are increased intradiscal pressures at the adjacent levels and that these increased intradiscal pressures increase with the number of levels fused [17]. It has also been shown that lumbosacral fusions increase the motion at the nonfused adjacent levels and that this transfer of motion appears to be greatest with the use of instrumentation [18]. Canine studies of lumbosacral fusions have demonstrated that the increased facet loads and adjacent level motions accelerate disc degeneration, characterized by chemical changes in the proteoglycans chains, with the production of shorter, less hydrophilic proteoglycan types [19]. Several authors have reviewed the radiographic and clinical follow-up of their patients after lumbar spinal fusion procedures to confirm this relationship between spinal
fusion and acceleration of adjacent segment changes, with conflicting results. In one of the longest follow-up studies in the spine literature, Lehmann et al. [20] reviewed 32 patients with more than 30 years of follow-up after lumbar fusion procedures. Although almost half developed instability at the segment above and a third became stenotic at the level above, these adjacent segment degenerative changes did not correlate with any clinical symptoms. Similarly, Luk et al. [21] had a 13-year follow-up of 22 patients who had undergone lumbosacral fusion. These authors also found hypermobility at the adjacent levels, especially with longer follow-up. However, these radiographic changes did not appear to correlate with the patient’s clinical symptoms. In a study attempting to compare the natural history of the lumbar segments in fused and nonfused patients, Penta et al. [22] obtained greater than 10-year follow-up of 52 patients who underwent anterior lumbar interbody fusion at the lumbosacral junction and compared the long-term follow-up of these patients with a similar group of patients treated without surgery. Interestingly, they found no difference in the rates of adjacent segment degeneration, with about a third of patients in both groups developing degenerative changes at the level above the spinal fusion. In addition, these authors found that increasing length of the fusion did not appear to increase the extent of degeneration at the adjacent levels. In contrast to these results are those of Rahm and Hall [23], who reported 5-year follow-up of 49 patients. In their study patients underwent posterior lumbar fusion with instrumentation and, in many cases, with posterior lumbar interbody fusion as well. They found that more than a third of their patients developed adjacent segment degeneration and found that those patients with adjacent segment degeneration did have worse clinical results. Furthermore, they found that the development of a pseudarthrosis within their cohort of patients appeared to be a protective factor against the development of adjacent segment degeneration. Similarly, Whitecloud et al. [24] also described an apparent biomechanical role in the development of adjacent segment degeneration. These authors reviewed 14 patients who had undergone a previous lumbar fusion and had adjacent segment disease requiring additional surgery. They found it much more difficult to obtain a solid fusion when performing surgery at the adjacent level, with a pseudarthrosis rate of 80% among individuals who underwent fusion without instrumentation. Recently, there have been a few studies published that have specifically looked at the development of adjacent segment disease after previous lumbar spinal fusion procedures. Etebar and Cahill [25] reviewed 125 patients who had undergone previous instrumented lumbar fusion with an average of 4.5 years of follow-up. The authors found that 14% of the patients developed symptomatic disease related to degeneration at adjacent levels for which surgical intervention was considered. On the other hand, Ghiselli et al. [26] studied the development of adjacent segment disease specifically at the L5–S1 level in a subset of 32 patients who had
A.S. Hilibrand and M. Robbins / The Spine Journal 4 (2004) 190S–194S
undergone L4–L5 posterolateral fusion for degenerative spondylolisthesis and spinal stenosis. At an average followup of 7.3 years, 31 of the 32 patients had not developed any symptomatic disease, although there was a trend for progressive disc degeneration at this level with increasing length of follow-up. One of us recently published a study looking at the impact of adjacent level disc degeneration on the outcome of posterior lumbar spinal fusion surgery [27]. The authors stratified a series of lumbar spinal fusion patients between those who were fused adjacent to a “degenerated disc” (dehydration and/or disc space collapse on magnetic resonance imaging) versus those fused adjacent to a “normal” disc. They compared the Short Form-36 (SF-36) clinical outcomes between the groups with degenerated and normal adjacent discs and found that the clinical outcomes were actually worse among the patients with normal adjacent discs. In addition, there was no difference between the two groups in the subsequent need for additional surgical procedures. The authors concluded that evidence of radiographic degeneration at adjacent levels did not appear to be sufficient cause for inclusion of those levels in the fusion construct. In an important study recently published, Ghiselli et al. [28] specifically look at adjacent segment disease of the lumbar spine. The authors review a series of 223 patients with an average of 6.7 years of follow-up for the development of new disease requiring additional surgery because of degenerative changes adjacent to thoracolumbar, lumbar and lumbosacral fusions. Based on a Kaplan-Meier survivorship analysis, the authors concluded that 37% of the patients in their cohort would be expected to require an additional surgical procedure for adjacent segment disease of the lumbar spine within 10 years of their index procedure. They found that the likelihood of adjacent segment disease requiring additional surgery was highest among patients undergoing a “floating lumbar fusion” (i.e., not including the thoracic or sacral regions) and lowest for those undergoing a thoracolumbar fusion.
Conclusions Several long-term follow-up studies of cervical and lumbar fusion procedures suggest that adjacent segment degeneration and adjacent segment disease are common. These pathologies appear to be most common above posterior lumbar fusions, below thoracolumbar scoliosis fusions and above or below anterior cervical fusions. Among lumbar fusion procedures, those performed between the thoracolumbar junction and the lumbosacral junction (so-called “floating fusions”) appear to be at greatest risk. Among cervical fusion procedures, those performed at a single level with advanced degenerative changes at the adjacent level appear to be at greatest risk. However, based on the present scientific literature, it is still unclear whether these radiographic and clinical findings are the result of the spinal fusion with the
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iatrogenic production of a rigid motion segment or whether these represent the progression of the natural history of the underlying degenerative disease.
References [1] Albee FH. Transplantation of a portion of the tibia into the spine for Pott’s disease. JAMA 1911;57:885. [2] Hibbs RA. An operation for progressive spinal deformities. NY Med J 1911;93:1013. [3] Yoon ST, Howard SA. Cervical Degnerative disc disease. In: Vaccaro AR, Betz RR, Zeidman SM, editors. Principles and practice of spine surgery. Philadelphia: Mosby, 2003:319–32. [4] Bohlman HH, Emery SE, Goodfellow DB, Jones PK. Robinson anterior cervical discectomy and arthrodesis for cervical radiculopathy. Long-term follow-up of one hundred and twenty-two patients. J Bone Joint Surg 1993;75A:1298–307. [5] Robinson RA, Smith GW. Anterolateral cervical disc removal and interbody fusion for cervical disc syndrome. Bull Johns Hopkins Hosp 1955;96:223–4. [6] Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis. A prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg Am 1991;73(6):802–8. [7] Davis H. Increasing rates of cervical and lumbar spine surgery in the United States, 1979–1990. Spine 1994;19(10):1117–24. [8] Baba H, Furusawa N, Imura S, Kawahara N, Tsuchiya H, Tomita K. Late radiographic findings after anterior cervical fusion for spondylotic myeloradiculopathy. Spine 1993;18(15):2167–73. [9] Gore DR, Sepic SB. Anterior cervical fusion for degenerated or protruded discs: a review of one hundred forty-Six patients. Spine 1984; 9(7):667–71. [10] Herkowitz HN, Kurz LT, Overholt DP. Surgical management of cervical soft disc herniation: a comparison between the anterior and posterior approach. Spine 1990;15(10):1026–30. [11] Gore DR, Sepic SB. Anterior cervical fusion for degenerated or protruded discs: a review of one hundred forty-six patients. Spine 1984; 9(7):667–71. [12] Williams JL, Allen MB, Harkess JW. Late results of cervical discectomy and interbody fusion: some factors influencing the results. J Bone Joint Surg 1968;50A:277–86. [13] Lunsford LD, Bissonette DJ, Jannetta PJ, Sheptak PE, Zorub DS. Anterior surgery for cervical disc disease, part 1: treatment of lateral cervical disc herniation in 253 cases. J Neurosurg 1980;53:1–11. [14] Henderson CM, Hennessy RG, Shuey HM, Shackelford EG. Posteriorlateral foraminotomy as an exclusive operative techinque for cervical radiculopathy: a review of 846 consecutively operated cases. Neurosurgery 1983;13(5):504–12. [15] Hilibrand AS, Carlson GD, Palumbo MA, Jones PK, Bohlman HH. Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg 1999; 81A(4):519–28. [16] White AA, Panjabi MM. Kinematics of the spine. In: White AA and Panjabi MM, editors. Clinical biomechanics of the spine. Philadelphia: Lippincott, 1990:107. [17] Weinhoffer SL, Guyer RD, Herbert M, Griffith SL. Intradiscal pressure measurements above an instrumented fusion. Spine 1995;20(5): 526–31. [18] Lee CK, Langrana NA. Lumbosacral spinal fusion: a biomechanical study. Spine 1984;9(6):574–81. [19] Bushell GR, Ghosh P, Taylor TF, Sutherland JM, Braund KG. The effect of spinal fusion on the collagen and proteoglycans of the canine intervertebral disc. J Surg Res 1978;25:61–9. [20] Lehmann TR, Spratt KF, Tozzi JE, et al. Long-term follow-up of lower lumbar fusion patients. Spine 1987;12(2):97–104.
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[21] Luk KD, Lee FB, Leong JC, Hsu LC. The effect on the lumbosacral spine of long spinal fusion for idiopathic scoliosis: a minimum 10-year follow-up. Spine 1987;12:996–1000. [22] Penta M, Sandhu A, Fraser RD. Magnetic resonance imaging assessment of disc degeneration 10 years after anterior lumbar interbody fusion. Spine 1995;20(6):743–7. [23] Rahm MD, Hall BB. Adjacent-segment degeneration after lumbar fusion with instrumentation: a retrospective study. J Spinal Dis 1996; 9(5):392–400. [24] Whitecloud TS, Davis JM, Olive PM. Operative treatment of the degenerated segment adjacent to a lumbar fusion [comment]. Spine 1994;19(5):531–6.
[25] Etebar S, Cahill DW. Risk factors for adjacent-segment failure following lumbar fixation with rigid instrumentation for degenerative instability. J Neurosurg 1999;90:163–9. [26] Ghiselli G, Wang JC, Wellington KH, Dawson EG. L5-S1 segment survivorship and clinical outcome analysis after L4-L5 isolated fusion. Spine 2003;28(12):1275–80. [27] Throckmorton TW, Hilibrand AS, Mencio GA, Hodge AL, Spengler DM. The impact of adjacent level disc degeneration on health status outcomes following lumbar fusion. Spine 2003;28(22):2546–50. [28] Ghiselli G, Wang JC, Bhatia NN, Wellington KH, Dawson EG. Adjacent segment degeneration in the lumbar spine. J Bone Joint Surg 2004;86:1497–503.
Adjacent segment degeneration and adjacent segment disease: the consequences of spinal fusion? Alan S. Hilibrand, MDa,*, Matthew Robbins, BAb a
Department of Orthopaedic Surgery, Thomas Jefferson University and The Rothman Institute, 925 Chestnut Street, 5th Floor, Philadelphia, PA 19107, USA b Jefferson Medical College, 1015 Walnut Street, Philadelphia, PA 19107, USA
Abstract
Given the number of spinal fusions performed annually, concerns have mounted over the potential for adjacent segment degeneration (radiographic changes of degeneration at levels adjacent to a spinal fusion) and adjacent segment disease (development of new symptoms correlating with adjacent segment degeneration). This article reviews documented evidence on adjacent segment degeneration and disease as it relates to cervical and lumbar arthrodesis. There appears to be an incidence of adjacent segment degeneration and disease after arthrodesis that may be related to natural degeneration or the adjacent fusion. It remains to be seen whether restoration of motion with disc arthroplasty will alter the rate of adjacent segment degeneration or disease. 쑖 2004 Elsevier Inc. All rights reserved.
Keywords:
Adjacent segment; Degeneration; Cervical; Lumbar
Introduction The concept of spinal segment arthrodesis as a treatment for pathologic conditions of the human spinal column evolved almost 100 years ago. Spinal fusion was first described by Albee [1] for the treatment of Pott disease, and by Hibbs [2], who performed spinal fusion as a treatment for spinal deformity. Almost 50 years ago, cervical spine fusion was described by Bailey and Badgley, Robinson and Smith, and Cloward as a treatment for degenerative spondylotic conditions [3]. These early authors suggested that spinal fusion offered the surgeon an opportunity to remove the pathologic process (infection, arthritis or deformity), eliminate painful motion and allowed decompression of the neural elements with subsequent stabilization of the affected spine segments. Over the past 50 fifty years, spinal fusion has become a standard of care for numerous pathologic conditions of the human spine. For adolescents and adults with spinal deformity, thoracolumbar spinal fusion with instrumentation has
FDA device/drug status: not applicable. Nothing of value received from a commercial entity related to this research. * Corresponding author. The Rothman Institute, 925 Chestnut Street, 5th Floor, Philadelphia, PA 19107. Tel.: (267) 339-3620. E-mail address: [email protected] (A.S. Hilibrand) 1529-9430/04/$ – see front matter doi:10.1016/j.spinee.2004.07.007
쑖 2004 Elsevier Inc. All rights reserved.
demonstrated widespread success in arresting progression and correcting the scoliotic deformity. In the cervical spine, anterior cervical fusion in conjunction with decompression has been reported to provide greater than 90% likelihood of relief of radicular complaints and stabilization/improvement of myelopathic findings [4,5]. In the low back, lumbar decompression in conjunction with posterolateral fusion has been demonstrated in prospective randomized studies to be the superior form of surgical management for patients with degenerative spondylolisthesis [6]. The long-term consequences of spinal fusions have been thought to be of secondary importance given the high likelihood of success of these procedures in relieving the patient’s presenting complaints. However, as spinal fusions, especially those for idiopathic scoliosis, have been performed at younger ages, there has been increasing concerns regarding the long-term viability of the spinal motion segments adjacent to these fusions. These concerns have been amplified by the increasing rates of cervical and lumbar spine surgery in the United States over the past two decades [7]. In particular, as the indications for lumbar spinal fusions are stretched to include more patients with mechanical back pain with lower rates of clinical success, the concerns for the consequences of these procedures have increased. In this article the terms “adjacent segment degeneration” and “adjacent segment disease” will be used to define different types of postarthrodesis adjacent level pathology.
A.S. Hilibrand and M. Robbins / The Spine Journal 4 (2004) 190S–194S
The term “adjacent segment degeneration” will be used to describe radiographic changes seen at levels adjacent to a previous spinal fusion procedure that do not necessarily correlate with any clinical findings. On the other hand, the term “adjacent segment disease” will be used to refer to the development of new clinical symptoms that correspond to radiographic changes adjacent to the level of a previous spinal fusion. This article will consider the role spinal fusions may play in the development of adjacent segment degeneration and adjacent segment disease. These pathologies in the cervical spine and the lumbar spine will be considered separately, owing to the different biomechanical environments of cervical and lumbar spinal fusions. Cervical spine The anatomy of the cervical spine is unique in many ways, which may explain differences in the development of adjacent level problems in this portion of the spinal column as opposed to the lumbosacral region. Specifically, the region C3–C7 where most spinal fusion procedures are performed is bordered by a highly mobile upper cervical region, which accommodates approximately half of all cervical motion. The kinematics of the cervical spine have never been assessed in vitro in a model that includes the upper cervical region and therefore most closely approximates the in vivo potential for motion transfer to the upper cervical spine after cervical fusion procedures. The development of radiographic adjacent segment degeneration of the cervical spine has been studied. Baba et al. [8] assessed over 100 patients undergoing anterior cervical fusion for cervical myelopathy with an average of 8.5 years of follow-up. The authors observed that 25% of these patients subsequently developed new spinal canal stenosis above the previously fused segments. Similarly, Gore and Sepic [9] observed new spondylosis in 25% of 121 patients and progression of preexisting spondylosis in another 25% of patients who had previously undergone anterior cervical fusion with an average follow-up of 5 years. In neither of these studies, however, was there any correlation between the adjacent segment degeneration and the development of clinical symptoms referable to these radiographic changes. In a comparative radiographic study, Herkowitz et al. [10] studied 44 patients with 4.5 years of follow-up who had been randomized to anterior cervical discectomy and fusion or posterior foraminotomy without fusion for the treatment of cervical radiculopathy. Among the group undergoing anterior fusion, 41% developed adjacent segment degeneration. Surprisingly, however, 50% of the patients undergoing posterior foraminotomy without fusion had evidence of adjacent level degeneration. Once again, there was no correlation between the development of adjacent segment degeneration and the onset of new clinical symptoms referable to those radiographic changes. Clinical follow-up studies of patients undergoing anterior cervical discectomy and fusion have demonstrated that some
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patients undergoing anterior cervical fusion do appear to develop symptomatic adjacent segment disease. Bohlman et al. [4] reviewed 122 patients after anterior discectomy and fusion for radiculopathy with an average of 6 years of followup and found that 9% of these patients went on to develop adjacent segment disease requiring additional surgery. Similarly, Gore and Sepic [11] described 14% of the patients in their study requiring additional surgery for adjacent segment disease at an average follow-up of 5 years. In addition, Williams et al. [12] found that 17% of their 60 patients undergoing anterior cervical decompression and fusion developed adjacent segment disease requiring additional surgery with an average follow-up of 4.5 years. These three studies suggest that on average there is a prevalence of adjacent segment disease ranging from 9% to 17%. When the number of years of follow-up is divided into the overall prevalence, the annual incidence of adjacent segment disease requiring additional surgery appears to be between 1.5% and 4%. For the cervical spine, there are also data available for comparison of fusion and nonfusion procedures to determine whether the fusion itself might be causative in the development of adjacent segment disease. For example, Lunsford et al. [13] reported relatively short follow-up (less than 3 years) of 334 patients who underwent anterior cervical discectomy, many without fusion. They found that 22 of their patients developed adjacent segment disease for an overall prevalence of approximately 7% and an annual incidence of approximately 2.5%. Interestingly, they did not find any difference in the rate of adjacent segment disease between patients who underwent discectomy with fusion and those who underwent discectomy alone. In a very large series of patients undergoing posterior foraminotomy without fusion reported by Henderson et al. [14] with an average of 2.8 years of follow-up, the authors describe that 79 of their 846 patients developed adjacent segment disease requiring additional surgery. This represented an overall prevalence of 9% of their patients with an average annual incidence of approximately 3%. These clinical observations suggest that anterior decompression with fusion and posterior decompression without fusion may lead to similar rates of adjacent segment disease. In both instances there appears to be an average annual incidence of about 3% of patients requiring further surgery for adjacent segment disease. This does correlate with the radiographic findings of Herkowitz et al. [10] described earlier. In order to better understand the factors affecting the development of adjacent segment disease and the overall prevalence of this problem, one of us [15] reported the longterm follow-up of 409 anterior cervical decompression and stabilization procedures performed for radiculopathy and/ or myelopathy. All patients were assessed by chart review for the development of any new radicular or myelopathic symptoms that might be referable to adjacent level changes. Based on this information, a Kaplan-Meier survivorship
192S
A.S. Hilibrand and M. Robbins / The Spine Journal 4 (2004) 190S–194S
analysis was constructed to determine the likelihood of developing symptomatic adjacent segment changes, regardless of whether they ultimately required surgical intervention. Consistent with the reports of other authors, there was an overall prevalence of 14% of patients requiring additional surgery over a range of follow-up from 2 to 21 years with an annual incidence of approximately 3% of patients developing adjacent segment disease. However, the Kaplan-Meier survivorship analysis suggests that a much higher likelihood of the development of adjacent segment disease, reaching a predicted prevalence of 13.6% at 5 years and 25.6% at 10 years of follow-up. Risk factors for the development of adjacent segment disease were the existence of neural element compression at the adjacent levels at the time of the index procedure, as well as surgery performed adjacent to the C5–C6 and/or C6–C7 levels. Surprisingly, the authors found that anterior cervical fusions performed at more than one level had a significantly lower rate of adjacent segment disease than those performed at a single level (12% vs 18%, p⭐.001). The results of the study suggested that adjacent segment disease was indeed a common problem but may reflect the natural history of the underlying cervical spondylosis.
Lumbar spine The biomechanical environment of lumbar spinal fusion procedures is characterized by the presence of a rigid lever arm, represented by the sacrum and pelvis, adjacent to a series of increasingly mobile yet lordotic lower lumbar spinal motion segments. The lumbosacral junction is characterized by specific adaptations for greater stability, including an increased intrafacet distance and the presence of iliolumbar ligaments, which increase this level’s stability and render it better able to handle the increased stresses adjacent to the sacrum and pelvis. Proximal to the lumbosacral junction, the spinal motion segments from L2 through L5, although contained in a stable, lordotic region of the spinal column, are much more mobile, each accommodating a greater range of motion [16]. Biomechanical studies of lumbosacral fusions have demonstrated that with simulated spinal fusion procedures there are increased intradiscal pressures at the adjacent levels and that these increased intradiscal pressures increase with the number of levels fused [17]. It has also been shown that lumbosacral fusions increase the motion at the nonfused adjacent levels and that this transfer of motion appears to be greatest with the use of instrumentation [18]. Canine studies of lumbosacral fusions have demonstrated that the increased facet loads and adjacent level motions accelerate disc degeneration, characterized by chemical changes in the proteoglycans chains, with the production of shorter, less hydrophilic proteoglycan types [19]. Several authors have reviewed the radiographic and clinical follow-up of their patients after lumbar spinal fusion procedures to confirm this relationship between spinal
fusion and acceleration of adjacent segment changes, with conflicting results. In one of the longest follow-up studies in the spine literature, Lehmann et al. [20] reviewed 32 patients with more than 30 years of follow-up after lumbar fusion procedures. Although almost half developed instability at the segment above and a third became stenotic at the level above, these adjacent segment degenerative changes did not correlate with any clinical symptoms. Similarly, Luk et al. [21] had a 13-year follow-up of 22 patients who had undergone lumbosacral fusion. These authors also found hypermobility at the adjacent levels, especially with longer follow-up. However, these radiographic changes did not appear to correlate with the patient’s clinical symptoms. In a study attempting to compare the natural history of the lumbar segments in fused and nonfused patients, Penta et al. [22] obtained greater than 10-year follow-up of 52 patients who underwent anterior lumbar interbody fusion at the lumbosacral junction and compared the long-term follow-up of these patients with a similar group of patients treated without surgery. Interestingly, they found no difference in the rates of adjacent segment degeneration, with about a third of patients in both groups developing degenerative changes at the level above the spinal fusion. In addition, these authors found that increasing length of the fusion did not appear to increase the extent of degeneration at the adjacent levels. In contrast to these results are those of Rahm and Hall [23], who reported 5-year follow-up of 49 patients. In their study patients underwent posterior lumbar fusion with instrumentation and, in many cases, with posterior lumbar interbody fusion as well. They found that more than a third of their patients developed adjacent segment degeneration and found that those patients with adjacent segment degeneration did have worse clinical results. Furthermore, they found that the development of a pseudarthrosis within their cohort of patients appeared to be a protective factor against the development of adjacent segment degeneration. Similarly, Whitecloud et al. [24] also described an apparent biomechanical role in the development of adjacent segment degeneration. These authors reviewed 14 patients who had undergone a previous lumbar fusion and had adjacent segment disease requiring additional surgery. They found it much more difficult to obtain a solid fusion when performing surgery at the adjacent level, with a pseudarthrosis rate of 80% among individuals who underwent fusion without instrumentation. Recently, there have been a few studies published that have specifically looked at the development of adjacent segment disease after previous lumbar spinal fusion procedures. Etebar and Cahill [25] reviewed 125 patients who had undergone previous instrumented lumbar fusion with an average of 4.5 years of follow-up. The authors found that 14% of the patients developed symptomatic disease related to degeneration at adjacent levels for which surgical intervention was considered. On the other hand, Ghiselli et al. [26] studied the development of adjacent segment disease specifically at the L5–S1 level in a subset of 32 patients who had
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undergone L4–L5 posterolateral fusion for degenerative spondylolisthesis and spinal stenosis. At an average followup of 7.3 years, 31 of the 32 patients had not developed any symptomatic disease, although there was a trend for progressive disc degeneration at this level with increasing length of follow-up. One of us recently published a study looking at the impact of adjacent level disc degeneration on the outcome of posterior lumbar spinal fusion surgery [27]. The authors stratified a series of lumbar spinal fusion patients between those who were fused adjacent to a “degenerated disc” (dehydration and/or disc space collapse on magnetic resonance imaging) versus those fused adjacent to a “normal” disc. They compared the Short Form-36 (SF-36) clinical outcomes between the groups with degenerated and normal adjacent discs and found that the clinical outcomes were actually worse among the patients with normal adjacent discs. In addition, there was no difference between the two groups in the subsequent need for additional surgical procedures. The authors concluded that evidence of radiographic degeneration at adjacent levels did not appear to be sufficient cause for inclusion of those levels in the fusion construct. In an important study recently published, Ghiselli et al. [28] specifically look at adjacent segment disease of the lumbar spine. The authors review a series of 223 patients with an average of 6.7 years of follow-up for the development of new disease requiring additional surgery because of degenerative changes adjacent to thoracolumbar, lumbar and lumbosacral fusions. Based on a Kaplan-Meier survivorship analysis, the authors concluded that 37% of the patients in their cohort would be expected to require an additional surgical procedure for adjacent segment disease of the lumbar spine within 10 years of their index procedure. They found that the likelihood of adjacent segment disease requiring additional surgery was highest among patients undergoing a “floating lumbar fusion” (i.e., not including the thoracic or sacral regions) and lowest for those undergoing a thoracolumbar fusion.
Conclusions Several long-term follow-up studies of cervical and lumbar fusion procedures suggest that adjacent segment degeneration and adjacent segment disease are common. These pathologies appear to be most common above posterior lumbar fusions, below thoracolumbar scoliosis fusions and above or below anterior cervical fusions. Among lumbar fusion procedures, those performed between the thoracolumbar junction and the lumbosacral junction (so-called “floating fusions”) appear to be at greatest risk. Among cervical fusion procedures, those performed at a single level with advanced degenerative changes at the adjacent level appear to be at greatest risk. However, based on the present scientific literature, it is still unclear whether these radiographic and clinical findings are the result of the spinal fusion with the
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iatrogenic production of a rigid motion segment or whether these represent the progression of the natural history of the underlying degenerative disease.
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