Increasing prevalence and better understanding of the principles of spinal deformity correction, coupled with advances in technology, have led to a substantial increase in complex reconstructive surgeries for adult spine deformity.1–6 Complications associated with long-segment thoracolumbar (TL) fusions are well recognized in both pediatric and adult populations.7–12 Although first-line treatment for adult deformity should generally be nonoperative, a subset of patients may ultimately warrant consideration of operative treatment.2,3,13
Previous reports have documented medical and perioperative complications that may be associated with adult deformity surgery.14–18 In addition, there remains a widely held belief that creation of rigid segments in the spine can lead to increased stress on and premature degeneration of the motion segments adjacent to an arthrodesis, which can manifest as proximal or distal junctional pathology.7,13,19–23 This belief is supported by in vitro evidence of increased stress and intradiscal pressure at segments adjacent to a lumbar spinal fusion.13,22,24,25 Distal adjacent segment degeneration, implant failure, and pseudarthrosis can be a source of pain, sagittal malalignment, and poor cosmesis, and may create increased mechanical stress on adjacent segments, eventually resulting in adjacent segment pathology (ASP).7,20,21,24,26–28
After spinal fusion, the radiographical presence of disc deterioration adjacent to the terminal fusion level is referred to as adjacent segment degeneration. This is often differentiated from adjacent segment disease, which is the development of clinically symptomatic junctional degeneration. Adjacent segment disease may lead to additional surgery and thus impact negatively on functional outcome, as opposed to adjacent segment degeneration, which is purely a radiographical finding that may remain asymptomatic.29 Although there has been a tendency to distinguish between adjacent segment degeneration and adjacent segment disease, it might be that these 2 entities reflect different stages of development of ASP. It is possible that adjacent segment degeneration may be a harbinger of subsequent adjacent segment disease. Whether all patients with adjacent segment degeneration progress over time to develop adjacent segment disease is unknown. There is a lack of consistency regarding the terminology used to describe these entities. As stated in the introduction of this focus issue, the term ASP is proposed as an umbrella term to refer to the breadth of clinical and/or radiographical changes at adjacent motion segments that developed subsequent to a previous spinal intervention. Under this umbrella, radiographical ASP (RASP) and clinical ASP (CASP) are then used to categorize radiographical features (e.g., degenerative changes on magnetic resonance imaging and clinical manifestations) (e.g., new radiculopathy), respectively.
The purpose of this systematic review was to examine the following key questions regarding distal ASP: (1) What is the frequency of distal ASP after long TL fusions? (2) What are the main risk factors associated with the development of distal ASP? (3) Is the frequency of and risk factors for distal ASP the same or different in surgery performed in adolescent and adult populations? (4) What surgical approach is best for management of distal ASP (anterior lumbar interbody fusion, transforaminal lumbar interbody fusion, posterolateral fusion alone)? (5) Is extension to the sacrum or pelvis needed for treatment of distal ASP? and (6) What are the complications of distal ASP revision surgery?
MATERIALS AND METHODS
We conducted a systematic search in Medline and the Cochrane Collaboration Library for literature published between January 1983 and March 15, 2012. The search results were limited to human studies published in the English language. Reference lists of key articles were also systematically checked to identify additional eligible articles. We included studies evaluating adult and adolescent patients who had long TL spinal surgery for the treatment of spinal deformity (Table 1). All studies evaluating risk factors for distal CASP and RASP in a TL population were included. We were interested in the following prognostic categories: patient factors such as age, sex, increased body mass index, smoking status; surgical factors such as length of fusion, number of levels fused, anterior versus posterior approach; and radiographical factors such as pre- and postoperative thoracic and lumbar curves, lordosis, disc degeneration, and sagittal and coronal balances. Exclusion criteria included patients with neuromuscular scoliosis, and studies that reported outcomes such as range of motion, kinematic measures, disc height, lordosis/angle changes at adjacent levels rather than CASP or RASP, studies that included less than 10 patients, and animal, cadaver, and biomechanical studies. Full texts of potential articles meeting the inclusion criteria were reviewed by 2 independent investigators (J.R.D., C.G.E.) to obtain the final collection of included studies (Figure 1). The definition of CASP varied among studies, with some including symptoms with or without revision surgery, and others including only revision surgery. Likewise, RASP had varying definitions (Table 2).
From the included articles, the following data were extracted: study design and study purpose, patient demographics, inclusion and exclusion criteria, follow-up duration and the percentage of follow-up for each treatment group, risk factors analyzed, applied definitions of CASP and RASP, and risk of and potential risk factors for CASP and RASP.
Study Quality and Overall Strength of Body of Literature
Level of evidence ratings were assigned to each article independently by 2 reviewers (J.R.D., C.G.E.) using criteria set by the Journal of Bone and Joint Surgery, American Volume30 for prognostic studies and modified to delineate criteria associated with methodological quality as described elsewhere31 (see Electronic Supplemental Material, Supplemental Digital Content 1, available at http://links.lww.com/BRS/A699 for individual study ratings). The overall body of evidence with respect to each clinical question was determined based on precepts outlined by the Grades of Recommendation Assessment, Development, and Evaluation working group32 and recommendations made by the Agency for Healthcare Research and Quality.33 Risk of bias was evaluated during the individual study evaluation as described earlier. This system, which derives strength of evidence grade for each outcome or clinical question of “high,” “moderate,” “low,” or “insufficient,” is described in further detail in the methods article for this focus issue (refer to methods article). The supplemental digital material (Supplemental Digital Content 1, available at http://links.lww.com/BRS/A699) contains the details of how we arrived at the strength of evidence for each key question.
Where the data were available, we reported the cumulative incidence or prevalence of CASP. The cumulative incidence (%) of CASP was defined as the proportion of patients who had been CASP free at the time of the index fusion, had subsequent development of new CASP at final follow-up, and had CASP from which one cannot recover (e.g., when CASP is defined as symptoms requiring reoperation). Prevalence was defined in 1 of 2 ways: (1) as the proportion of patients who had been CASP free at the time of the index fusion, had subsequent development of new CASP at final follow-up, and had CASP from which one can recover before the follow-up evaluation (e.g., when CASP was defined as pain); (2) as the proportion of patients with RASP at follow-up from among all patients in the study, some of whom had RASP at the time of the index procedure. For risk factor analysis, we report effect sizes from multivariate analysis (i.e., adjusted effect size estimates) and/or of significance based on adjustment for confounders when provided by the authors. In studies that did not use multivariate analysis, crude risk ratios (RRs) and 95% confidence intervals (CIs) were calculated to provide an estimate of effect size. All calculations were performed using Stata 9.0. (StataCorp LP, College Station, TX).34 RRs, prevalence ratios or hazard ratios whose confidence interval includes the value of 1 are not statistically significant. Values above 1 suggest increased risk and values below 1 suggest decreased risk for the factor.
Consensus statements were made through a modified Delphi approach by applying the Grades of Recommendation Assessment, Development, and Evaluation/Agency for Healthcare Research and Quality criteria that imparts a deliberate separation between the strength of the evidence (i.e., high, moderate, low, or insufficient) from the strength of the recommendation. When appropriate, recommendations or statements “for” or “against” were given “strong” or “weak” designations based on the quality of the evidence, the balance of benefits/harms, and values and patient preferences. In some instances, costs may have been considered. A more thorough description of this process can be found in the focus issue methods article (refer to methods article).
We identified 7 studies from our search strategy that met the inclusion criteria (Figure 1). Our initial search produced 20 possible studies for review for key questions 1 and 2, 7 possible studies for key question 3, and 52 possible studies for key questions 4 to 6. After abstract review, we excluded 7 studies for key questions 1 and 2, 5 studies for key question 3, and 47 studies for key questions 4 to 6, the majority of which did not include long fusion to L4 or L5 or were studies of effectiveness and did not evaluate risk factors for ASP. Among the 13 full-text articles subsequently reviewed for key questions 1 and 2, 6 were excluded after review because the procedures were not long fusions to L4 or L5 (n = 6). Between the 2 full-text articles subsequently reviewed for key question 3, both studies were excluded after review due to no report on distal CASP or RASP (n = 1) or the procedure was not long fusion to L4 or L5 (n = 1). Among the 5 full-text articles subsequently reviewed for key questions 4 to 6, all 5 studies were excluded because 4 did not report on revision surgery and 1 was not long fusion to L4 or L5. A list of excluded articles can be obtained in the electronic supplemental material (see Supplemental Digital Content 1, available at http://links.lww.com/BRS/A699). We finally included 7 retrospective cohort studies that reported on the risk of distal CASP/RASP and risk factors (key questions 1–2) for developing CASP and/or RASP after long TL fusions35–41 (Table 2). No studies addressing key questions 4 to 6 were identified.
CASP and RASP were defined differently among studies. For CASP, 1 study defined it as revision surgery,35 3 studies defined it as lumbosacral pain or discomfort combined with radiographical confirmation,38–40 and 1 defined it as the presence of clinical symptoms caused by herniated disc, spinal stenosis, or junctional kyphosis.36 For RASP, 4 used a modification of the Weiner classification36,38,39,41; 1 used the presence and progression of L5–S1 spondylolisthesis by more than 2 mm and/or progressive loss of L5–S1 disc height by more than 2 mm;35 1 used the University of California Los Angeles disc degeneration score;40 and 1 used the presence of at least 2 of the following: more than 5° loss of lordosis across a disc space, progressive disc space narrowing more than 2 mm, sclerosis of endplates/facets with osteophyte formation, or subluxation more than 2 mm37 (Table 2).
Frequency of CASP and RASP
The frequency of CASP varied among studies, ranging from 9% to 46% after long TL fusions. Five studies with a follow-up between 2 and 6 years had a mean prevalence of CASP of 17.7%.35–39 Two studies with a 9-year follow-up had a mean prevalence of CASP of 19.8%.40,41 The frequency of revision surgeries due to CASP also varied among studies, ranging from 2% to 23%. The 5 studies with a 2 to 6 year follow-up reported a reoperation incidence of 15.6%, whereas 2 studies with a 9-year follow-up reported a reoperation incidence of 14.4% (Figure 2). The prevalence of RASP ranged from 14% to 69% after long TL fusions. The studies with a follow-up between 2 and 6 years had a mean RASP incidence of 44.7%, whereas the 2 studies with a 9-year follow-up had a mean RASP incidence of 65.5% (Figure 2). Figure 3 demonstrates a clinical case complicated by development of distal CASP after long TL fusion for adult idiopathic deformity.
Risk Factors for CASP
Two studies identified risk factors for development of CASP.35,36 Cho et al36 examined the role of preoperative disc degeneration and preoperative sagittal imbalance with regard to CASP development (Table 3). Patients with preoperative sagittal imbalance (C7–S1 plumb >50 mm) were found to be almost 5 times more likely to develop CASP after surgery than patients with good preoperative sagittal balance (C7–S1 plumb <50 mm) (36.4% vs. 7.7%, respectively; RR, 4.70; 95% CI, 0.61–36.3; P = 0.142). However, the retrospective nature of the study, small number of patients, nonsignificant P value, and the wide confidence interval should be considered when interpreting the results. Brown et al35 also compared mean radiographical factors between those with and without revision surgery (Table 4). They identified an association between higher postoperative fractional curve angle and the need for revision surgery, but did not find an association between preoperative positive sagittal imbalance and increased risk of CASP.
Risk Factors for RASP
Five studies examined risk factors for development of RASP.35,36,38,39,41 Risk factors were classified into 3 main categories: patient factors, surgical factors, and radiographical factors (Tables 5 and 6).
Two articles reporting on the same patient population at 2 different follow-up periods evaluated age and smoking status as potential patient-risk factors. Edwards et al39 after a 5.6-year follow-up, determined a statistically significant difference in age of patients who developed RASP versus those who did not develop RASP (40.8 vs. 48.0 yr, respectively; P = 0.03), suggesting that younger patients are at greater risk of degeneration. Kuhns et al41 reported on the same population after a 9-year follow-up and continued to find that younger patients were at greater risk for developing RASP than older patients (44.3 vs. 48.1 yr), although this was not statistically significant (P = 0.25). Edwards et al39 determined no significant difference with respect to smoking status and development of RASP (P = 0.76).
Edwards et al.39 and Kuhns et al41 also examined surgical risk factors for RASP. After a 9-year follow-up, Kuhns et al41 determined that patients who underwent longer fusions (T1–T7–L5) were 2.5 times more likely to develop RASP than patients who received shorter fusions (T8–T12–L5) (72% vs. 28%, respectively; P = 0.02). However, there was no significant difference (P = 0.17) in development of RASP based on shorter versus longer fusion in the study by Edwards etal.39 Although both the studies reported that patients who underwent a circumferential approach were more likely to develop RASP than patients who underwent a posterior approach alone, the difference was significant only in the study by Kuhns et al.41 Edwards et al39 also examined whether a deep-seated L5 was associated with RASP and determined no significant association (P = 0.40).
Multiple radiographical factors were identified as affecting the risk of developing RASP. Two studies reported that a preoperative disc degeneration of Grade 1 (mild degeneration) put the patient at a 2.5 to 3 times greater risk of developing moderate to advanced RASP (Grade 2 or 3) than patients with a preoperative disc degeneration Grade 0 (healthy-–no degeneration). Cho et al36 reported that 33% of Grade 0 patients and 85% of Grade 1 patients went on to develop moderate to advanced RASP (P = 0.136), whereas Edwards et al39 similarly determined that 27% of Grade 0 and 80% of Grade 1 patients went on to develop RASP (P = 0.007).
Four studies identified preoperative sagittal imbalance as a risk factor for developing moderate to advanced RASP after long TL fusions.35,36,39,41 Although all 4 studies reported a greater risk for developing RASP in patients with preoperative sagittal imbalance, only Edwards et al39 and Brown et al35 found this difference to be statistically significant (Tables 5 and 6). Cho et al36 and Kuhns et al41 reported a greater risk for developing RASP in patients with preoperative sagittal imbalance; however their findings were not statistically significant (73% vs. 62%; P = 0.679; and +3.2 vs. +1.3; P = 0.31, respectively).
Brown et al35 reported a statistically significant difference between postoperative L5–S1 disc space height between patients who developed RASP compared with those who did not (8.5 vs. 11 mm, respectively; P < 0.05), suggesting that narrowing of the L5–S1 disc space could present a greater risk for development of RASP.
To summarize, although younger age at TL fusion was reported to be associated with increased risk of RASP, the significance was lost at long-term follow-up. Preoperative disc degeneration was associated with higher chances of developing RASP in 2 studies; however, only 1 of them reported the difference to be significant. Preoperative sagittal imbalance was uniformly found to be associated with increased risk of developing RASP in 4 studies; only 2 of them found the difference to be significant. Only 1 postoperative parameter (postoperative L5–S1 disc space narrowing) was associated with increased risk of RASP.
Adult Versus Adolescent Populations
No studies meeting inclusion criteria were identified that reported on the frequency or risk factors of distal CASP that met our inclusion criteria.
Surgical Approach (TLIF Vs. ALIF)
No studies meeting inclusion criteria were identified that compared the effectiveness and safety of transforaminal lumbar interbody fusion versus anterior lumbar interbody fusion in the treatment of distal ASP after long TL fusion.
Treatment of Distal CASP
No studies meeting inclusion criteria were identified that reported on the treatment of distal CASP and whether to extend the fusion to the sacrum or pelvis.
Complications of Distal CASP Revision Surgery
No studies were identified that reported on the complications of distal CASP revision surgery that met our inclusion criteria.
The overall strength of evidence evaluating the frequency of distal clinical or RASP after long TL fusions is “low”; that is, we have low confidence in the absolute estimate and further research may change the estimate (Table 7). The overall strength of evidence evaluating risk factors for the development of CASP is “low” (low confidence in effect size) to “insufficient” (the evidence does not permit a conclusion). There was no evidence found to address key questions 3 to 6 (Table 7).
There have been a number of studies that have documented the occurrence of ASP after lumbar fusion.20,21,42 Most of these studies have focused on 2-level lumbar fusions and did not address the impact of long TL fusions, which are often performed for correction of spinal deformity. Adult spinal deformity often involves the lumbar spine and fusions that extend into the lower lumbar (L4 or L5) or sacral spine.2,4,13,17 Long fusions terminating in the distal lumbar spine can have resulting ASP and failure to maintain sagittal balance, likely due at least in part to subsequent L5–S1 disc degeneration and associated loss of disc space lordosis.36,38,39 Various studies have recommended extending long fusions, which would otherwise stop at L4–L5, to the sacrum to try to avoid this potential complication, but this remains controversial.22,38,39,43,44 Fusion to the L5 offers the theoretical benefits of preserved lumbosacral motion, smaller surgery, and a decreased likelihood of pseudarthrosis.43 On the contrary, the literature is also replete with poor results with use of S1 screws without distal augmentation, with fusion rates as low as 22%.45–48
The purpose of this systematic review was to determine the incidence and risk factors leading to distal ASP after performance of long TL instrumentation in adults and adolescents, and to compare the outcome of various approaches for management of distal ASP and associated complications. We initially sought studies that had reports of distal CASP/RASP after TL fusions for deformity in adults and adolescents. Finding no such study in the pediatric population, this systematic review is predominantly restricted to adults.
This review suggests that development of distal ASP after long TL fusion is not uncommon. CASP developed in 17.7% and 19.9% of patients after 2 to 6 years and 9-year mean follow-up, respectively. Reoperation due to CASP was reported in 15.6% of the patients after 2 to 6 years and 14.4% of patients after 9 years. RASP was more frequent, occurring in approximate 1 half of the patients.
The criteria for defining CASP and RASP were variable across different studies, which might account for differences in the reported incidences. For example, in the study by Brown et al,35 their definition of CASP required revision surgery, which likely underestimated the incidence of CASP because there may be patients who might be symptomatic but may not undergo revision surgery.35–41 Differences in definition for RASP between studies also likely impacted the reported incidences and comparisons across studies. Surprisingly, there was a decreased incidence of CASP in the study reporting 9 years of follow-up as compared with the study with 2 to 6 years of follow-up, although there was an increase in incidence of RASP, which exemplifies the complexity of patient-related factors and differences in the criteria used in different studies.35–41
There has been an increasing recognition of the importance of sagittal balance and clinical symptoms in adults with spinal deformity.1,3,4 Interestingly, patients with preoperative sagittal imbalance were 5 times more likely to develop CASP after long TL fusions.36 Patients with positive sagittal imbalance often have pain and disability, and it is possible that the increased risk of developing CASP in this population might partially reflect symptoms related to persistent positive sagittal balance rather than symptoms related to ASP. Studies that defined CASP based mainly on clinical factors and need of revision surgery may be most susceptible to this potential overlap of symptoms. However, in the study by Cho et al,36 most of the patients who had preoperative sagittal imbalance and developed CASP had restoration of their sagittal balance after surgery, suggesting that CASP can develop regardless of surgical correction of sagittal imbalance and may relate to preoperative sagittal imbalance. Apart from preoperative sagittal imbalance, unfavorable postoperative sagittal balance has been advocated as a risk factor for accelerated adjacent segment disease in in vitro studies.49,50 Whether coronal imbalance at the caudal level impacts the development of distal adjacent disease remains unclear due to a lack of literature relevant to this issue.
The presence of preoperative disc degeneration at the adjacent level has been suggested to increase the risk of subsequent ASP, which has been the basis for using magnetic resonance imaging and discography to decide whether to extend the fusion to the sacrum.43 However, magnetic resonance imaging assessment of hydration is more difficult for oblique discs and although discography has been suggested to reflect degeneration, the use of discography has been strongly debated, especially considering its potential to accelerate degeneration of normal healthy discs and its false positivity.51,52 Two studies in the present review demonstrated 2.5 to 3 times increased risk of RASP after long TL fusion in mild disc degeneration preoperatively as compared with patients with a healthy disc.36,39 However, in 1 of the 2 studies, there was no association between preoperative disc degeneration and symptomatic ASP (CASP). 36 Thus, although long fusions may lead to increased incidence of RASP in patients with mild preoperative disc degeneration, the clinical significance of this remains unclear. Hence, extension of fusion to the sacrum based on the presence of mild disc degeneration without presence of other predisposing factors for ASP is controversial.
There was an association between the development of CASP and higher postoperative fractional curve in the study by Brown et al.35 Considering the fact that presence of a lumbosacral fractional curve makes balancing the spine very difficult without extension to sacrum and that with an oblique takeoff, often the foramen is narrow on the concave side, the increased chances of CASP as reported by Brown et al35 in patients with higher postoperative fractional curve might be secondarily attributed to poor deformity correction or foraminal stenosis in the fractional curve, both of which can be clinically symptomatic.4,5,43 Interestingly, the diagnosis of CASP in their study was made on clinical criteria, rather than the need for revision surgery.
This review determined that patients who underwent a circumferential approach and received longer fusions (T1–T7–L5) were 2 to 2.5 times more likely to develop RASP than patients who underwent a posterior approach and shorter fusions, respectively. Although there is robust biomechanical evidence to support this, the clinical evidence is unclear, with studies documenting no risk versus increased risk of ASP after lumbar fusion, which precludes definitive conclusions.7,22,39,53–55 The clinical impact of this might be to consider extension of fusion to S1 if performing multilevel fusion or circumferential fusion at L4–L5 to prevent ASP at L5–S1. However, there is no strong clinical evidence to support or refute this approach.
Strengths of this study include the systematic approach to searching for and evaluating relevant studies to answer well-defined clinical questions. Combined with use of specified inclusion/exclusion criteria defined a priori, this approach enhances the validity of this report and facilitates identification of specific gaps in understanding the incidence, risk factors, and management of ASP after long TL instrumentation for spinal deformity.
The results of this review have several limitations. Although we were able to perform a thorough literature review, our conclusions are compromised somewhat due to the lack of studies addressing some of our key questions (key questions 4–6). This underscores the need for further studies to address these issues. Also, the included studies were all retrospective and are prone to the inherent limitations of retrospective design. The rate of ASP seen in this review is subject to bias secondary to variable follow-up times and varies according to the definition applied in different studies.35–41 Also, only 1 study identified the presence of preoperative sagittal imbalance as a risk factor for development of CASP.36 Although the differences between risk of developing CASP in patients with or without preoperative sagittal imbalance was striking in the study of Cho et al,36 the wide confidence interval in the study possibly indicates that the stability of the estimate may be questionable and is likely at least in part due to small sample size and it also being under powered to find a difference beyond chance precluding results from reaching statistical significance. The assessment of ASP in this review is restricted to disc degeneration and excludes other modes of distal junctional failure including pseudarthrosis at the most caudal fused level and implant failure with screw loosening/breakage/rod fracture at the caudal end of fixation, which might underestimate the overall risk of the distal construct failure and complications.27 Although there is typically no well-formed disc below S1 and thus essentially no chance of ASP, extension of fusions to the sacrum does not necessarily equate with improved outcomes and decreased complications, because the literature is replete with studies addressing poor outcome after TL fusion that include the sacrum.26,45–48 This should be considered when interpreting rates of distal ASP after long TL fusions.
Low-quality evidence suggests a cumulative rate of 18% to 20% for CASP and 45% to 65% for RASP after long TL fusion for spinal deformity during 9-year follow-up. Low-quality evidence suggests an association between preoperative sagittal imbalance and distal ASP with higher risk of distal ASP in patients with sagittal imbalance. Low-quality evidence suggests increased risk of CASP in patients with higher postoperative fractional curve and increased risk of RASP in younger patients and those with preoperative disc degeneration, longer fusions, circumferential procedures, and postoperative L5–S1 disc space narrowing.
- The risk of developing new symptoms secondary to distal ASP after long TL fusion for deformity is approximately 18% to 20% during a period of 9 years of follow-up, and most of these patients will require revision surgery.Strength of Statement: Weak
- The risk of developing distal ASP may be higher in those with preoperative sagittal imbalance, preoperative disc degeneration, longer fusions, circumferential procedures, and postoperative L5-S1 disc space narrowing.Strength of Statement: Weak
- Distal CASP developed in 17.7% at 2- to 6-year follow-up and 19.8% at 9-year follow-up, whereas reoperation due to CASP was reported in 15.6% at 2 to 6 years and 14.4% at 9 years.
- Distal RASP occurred in approximately one half of the patients (44.7%–65.5%).
- Preoperative sagittal imbalance and greater postoperative fractional curve are suggested as risk factors for development of distal CASP.
- There is increased risk of distal RASP in younger patients and in those with presence of preoperative disc degeneration, longer TL fusions, circumferential procedures, and postoperative narrowing of the L5–S1 disc space.
The authors thank Ms. Nancy Holmes, RN, for her administrative assistance. The authors M.K.K. and J.S.S. contributed toward data interpretation, manuscript preparation, and manuscript revision; C.I.S. and L.G.L. study design, data interpretation, manuscript preparation, and manuscript revision; J.R.D.: study design, data analysis and interpretation, manuscript preparation, and manuscript revision; and C.G.E.: data analysis and interpretation, manuscript preparation, and manuscript revision.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.spinejournal.com).
1. Ames CP, Smith JS, Scheer JK, et al. Impact of spinopelvic alignment on decision making in deformity surgery in adults. J Neurosurg Spine 2012;16:547–64.
2. Bridwell KH, Glassman S, Horton W, et al. Does treatment (nonoperative and operative) improve the two-year quality of life in patients with adult symptomatic lumbar scoliosis: a prospective multicenter evidence-based medicine study. Spine 2009;34:2171–8.
3. Glassman SD, Bridwell K, Dimar JR, et al. The impact of positive sagittal balance in adult spinal deformity. Spine 2005;30:2024–9.
4. Schwab F, Lafage V, Patel A, et al. Sagittal plane considerations and the pelvis in the adult patient. Spine 2009;34:1828–33.
5. Schwab F, Ungar B, Blondel B, et al. Scoliosis Research Society–Schwab Adult Spinal Deformity Classification: a validation study. Spine 2012;37:1077–82.
6. Schwab F, Dubey A, Gamez L, et al. Adult scoliosis: prevalence, SF-36, and nutritional parameters in an elderly volunteer population. Spine 2005;30:1082–5.
7. 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 2007;32:2253–7.
8. Cho KJ, Suk SI, Park SR, et al. Risk factors of sagittal decompensation after long posterior instrumentation and fusion for degenerative lumbar scoliosis. Spine 2010;35:1595–601.
9. Cho KJ, Suk SI, Park SR, et al. Complications in posterior fusion and instrumentation for degenerative lumbar scoliosis. Spine 2007;32:2232–7.
10. Cho SK, Bridwell KH, Lenke LG, et al. Major complications in revision adult deformity surgery: risk factors and clinical outcomes with 2- to 7-year follow-up. Spine 2012;37:489–500.
11. Lowe TG, Lenke L, Betz R, et al. Distal junctional kyphosis of adolescent idiopathic thoracic curves following anterior or posterior instrumented fusion: incidence, risk factors, and prevention. Spine 2006;31:299–302.
12. Rinella A, Bridwell K, Kim Y, et al. Late complications of adult idiopathic scoliosis primary fusions to L4 and above: the effect of age and distal fusion level. Spine 2004;29:318–25.
13. Crawford CH III, Carreon LY. Long fusions to the sacrum in elderly patients with spinal deformity [Published online ahead of print April 27, 2012]. Eur Spine J.
14. Hamilton DK, Smith JS, Sansur CA, et al. Rates of new neurological deficit associated with spine surgery based on 108,419 procedures: a report of the scoliosis research society morbidity and mortality committee. Spine 2011;36:1218–28.
15. Sansur CA, Smith JS, Coe JD, et al. Scoliosis research society morbidity and mortality of adult scoliosis surgery. Spine 2011;36:E593–7.
16. Smith JS, Sansur CA, Donaldson WF III, et al. Short-term morbidity and mortality associated with correction of thoracolumbar fixed sagittal plane deformity: a report from the Scoliosis Research Society Morbidity and Mortality Committee. Spine 2011;36:958–64.
17. Smith JS, Shaffrey CI, Glassman SD, et al. Risk-benefit assessment of surgery for adult scoliosis: an analysis based on patient age. Spine 2011;36:817–24.
18. Smith JS, Shaffrey CI, Sansur CA, et al. Rates of infection after spine surgery based on 108,419 procedures: a report from the Scoliosis Research Society Morbidity and Mortality Committee. Spine 2011;36:556–63.
19. Huang RC, Meredith DS, Kepler CK, et al. Salvage of lumbar pseudarthrosis with customized large-diameter pedicle screws: report of two cases. Spine 2011;36:E1489–92.
20. Park P, Garton HJ, Gala VC, et al. Adjacent segment disease after lumbar or lumbosacral fusion: review of the literature. Spine 2004;29:1938–44.
21. Sears WR, Sergides IG, Kazemi N, et al. Incidence and prevalence of surgery at segments adjacent to a previous posterior lumbar arthrodesis. Spine J 2011;11:11–20.
22. Sudo H, Oda I, Abumi K, et al. Biomechanical study on the effect of five different lumbar reconstruction techniques on adjacent-level intradiscal pressure and lamina strain. J Neurosurg Spine 2006;5:150–5.
23. Glattes RC, Bridwell KH, Lenke LG, et al. Proximal junctional kyphosis in adult spinal deformity following long instrumented posterior spinal fusion: incidence, outcomes, and risk factor analysis. Spine 2005;30:1643–9.
24. Durrani A, Jain V, Desai R, et al. Could junctional problems at the end of a long construct be addressed by providing a graduated reduction in stiffness? A biomechanical investigation. Spine 2012;37:E16–22.
25. Rohlmann A, Neller S, Bergmann G, et al. Effect of an internal fixator and a bone graft on intersegmental spinal motion and intradiscal pressure in the adjacent regions. Eur Spine J 2001;10:301–8.
26. Kim YJ, Bridwell KH, Lenke LG, et al. Pseudarthrosis in long adult spinal deformity instrumentation and fusion to the sacrum: prevalence and risk factor analysis of 144 cases. Spine 2006;31:2329–36.
27. Kwon BK, Elgafy H, Keynan O, et al. Progressive junctional kyphosis at the caudal end of lumbar instrumented fusion: etiology, predictors, and treatment. Spine 2006;31:1943–51.
28. Lowe T, Berven SH, Schwab FJ, et al. The SRS classification for adult spinal deformity: building on the King/Moe and Lenke classification systems. Spine 2006;31:S119–25.
29. Harrop JS, Youssef JA, Maltenfort M, et al. Lumbar adjacent segment degeneration and disease after arthrodesis and total disc arthroplasty. Spine 2008;33:1701–7.
30. Wright JG, Swiontkowski MF, Heckman JD. Introducing levels of evidence to the journal. J Bone Joint Surg Am 2003;85-A:1–3.
31. Norvell DC, Dettori JR, Fehlings MG, et al. Methodology for the systematic reviews on an evidence based approach for the management of chronic LBP. Spine 2011;36:S10–8.
32. Atkins D, Best D, Briss PA, et al. Grading quality of evidence and strength of recommendations. BMJ 2004;328:1490.
33. West S, King V, Carey TS, et al. Systems to Rate the Strength of Scientific Evidence. Evidence Report/Technology Assessment No. 47. Prepared by the Research Triangle Institute-University of North Carolina Evidence-based Practice Center, Contract No. 290-97-0011. Rockville, MD: Agency for Healthcare Research and Quality; 2002.
34. StataCorp. Stata Statistical Software: Release 9. College Station, TX: StataCorp LP; 2005.
35. Brown KM, Ludwig SC, Gelb DE. Radiographic predictors of outcome after long fusion to L5 in adult scoliosis. J Spinal Disorders Techs 2004;17:358–66.
36. Cho KJ, Suk SI, Park SR, et al. Arthrodesis to L5 versus S1 in long instrumentation and fusion for degenerative lumbar scoliosis. Eur Spine J 2009;18:531–7.
37. Eck KR, Bridwell KH, Ungacta FF, et al. Complications and results of long adult deformity fusions down to L4, L5, and the sacrum. Spine 2001;26:E182–92.
38. Edwards CC II, Bridwell KH, Patel A, et al. Long adult deformity fusions to L5 and the sacrum. A matched cohort analysis. Spine 2004;29:1996–2005.
39. Edwards CC II, Bridwell KH, Patel A, et al. Thoracolumbar deformity arthrodesis to L5 in adults: the fate of the L5-S1 disc. Spine 2003;28:2122–31.
40. Harding IJ, Charosky S, Vialle R, et al. Lumbar disc degeneration below a long arthrodesis (performed for scoliosis in adults) to L4 or L5. Eur Spine J 2008;17:250–4.
41. Kuhns CA, Bridwell KH, Lenke LG, et al. Thoracolumbar deformity arthrodesis stopping at L5: fate of the L5-S1 disc, minimum 5-year follow-up. Spine 2007;32:2771–6.
42. Lund T, Oxland TR. Adjacent level disk disease—is it really a fusion disease? Orthop Clin North Am 2011;42:529–41
43. Bridwell KH, Edwards CC II, Lenke LG. The pros and cons to saving the L5-S1 motion segment in a long scoliosis fusion construct. Spine 2003;28:S234–42.
44. Horton WC, Holt RT, Muldowny DS. Controversy. Fusion of L5-S1 in adult scoliosis. Spine 1996;21:2520–2.
45. Bernhardt M, Swartz DE, Clothiaux PL, et al. Posterolateral lumbar and lumbosacral fusion with and without pedicle screw internal fixation. Clin Orthop Relat Res 1992; 284:109–15.
46. Horowitch A, Peek RD, Thomas JC, Jr, et al. The Wiltse pedicle screw fixation system. Early clinical results. Spine 1989;14:461–7.
47. Molinari RW, Bridwell KH, Lenke LG, et al. Complications in the surgical treatment of pediatric high-grade, isthmic dysplastic spondylolisthesis. A comparison of three surgical approaches. Spine 1999;24:1701–11.
48. Rechtine GR, Sutterlin CE, Wood GW, et al. The efficacy of pedicle screw/plate fixation on lumbar/lumbosacral autogenous bone graft fusion in adult patients with degenerative spondylolisthesis. J Spinal Disorders 1996;9:382–91.
49. 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 2003;28:1560–6.
50. Umehara S, Zindrick MR, Patwardhan AG, et al. The biomechanical effect of postoperative hypolordosis in instrumented lumbar fusion on instrumented and adjacent spinal segments. Spine 2000;25:1617–24.
51. Carragee EJ, Barcohana B, Alamin T, et al. Prospective controlled study of the development of lower back pain in previously asymptomatic subjects undergoing experimental discography. Spine 2004;29:1112–7.
52. Carragee EJ, Don AS, Hurwitz EL, et al. 2009 ISSLS Prize Winner: Does discography cause accelerated progression of degeneration changes in the lumbar disc: a ten-year matched cohort study. Spine 2009;34:2338–45.
53. Rahm MD, Hall BB. Adjacent-segment degeneration after lumbar fusion with instrumentation: a retrospective study. J Spinal Disorders 1996;9:392–400.
54. Esses SI, Doherty BJ, Crawford MJ, et al. Kinematic evaluation of lumbar fusion techniques. Spine 1996;21:676–84.
55. Shono Y, Kaneda K, Abumi K, et al. Stability of posterior spinal instrumentation and its effects on adjacent motion segments in the lumbosacral spine. Spine 1998;23:1550–8.