seminar adolescent idiopathic scoliosis · adolescent idiopathic scoliosis (ais) ... ﬂ uorescent...

Seminar

www.thelancet.com Vol 371 May 3, 2008 1527

Adolescent idiopathic scoliosisStuart L Weinstein, Lori A Dolan, Jack C Y Cheng, Aina Danielsson, Jose A Morcuende

Adolescent idiopathic scoliosis (AIS) aff ects 1–3% of children in the at-risk population of those aged 10–16 years. The aetiopathogensis of this disorder remains unknown, with misinformation about its natural history. Non-surgical treatments are aimed to reduce the number of operations by preventing curve progression. Although bracing and physiotherapy are common treatments in much of the world, their eff ectiveness has never been rigorously assessed. Technological advances have much improved the ability of surgeons to safely correct the deformity while maintaining sagittal and coronal balance. However, we do not have long-term results of these changing surgical treatments. Much has yet to be learned about the general health, quality of life, and self-image of both treated and untreated patients with AIS.

IntroductionAdolescent idiopathic scoliosis (AIS) is a structural, lateral, rotated curvature of the spine that arises in otherwise healthy children at or around puberty. The diagnosis is one of exclusion, and is made only when other causes of scoliosis, such as vertebral malformation, neuromuscular disorder, and syndromic disorders, have been ruled out. Patients are generally screened with Adams’ forward bend test and a scoliometer, although a defi nitive diagnosis cannot be made without measuring the Cobb angle on a standing coronal radiograph (fi gure 1). When defi ned as a Cobb angle of at least 10°, epidemiological studies estimate that 1–3% of the at-risk population (children aged 10–16 years) will have some degree of spinal curvature, although most curves will need no intervention.1,2 In this Seminar we discuss present notions about aetiopathogenesis, natural history, non-operative treatment, and surgery.

AetiopathogenesisDespite much clinical, epidemiological, and basic science research, the aetiopathogenesis of AIS remains unknown.3,4 AIS is often seen in multiple members of one family, which strongly suggests that it has a genetic component. A meta-analysis of studies of twins showed concordance for AIS in 73% of monozygotic twins and 36% of dizygotic twins.2 Several studies that assessed large pedigrees showed diff erent methods of inheritance, such as autosomal dominance, maternal factors, multiple gene inheritance, multifactorial inheritance, and X-linked dominance.3,5 However, Axenovich and colleagues6 analysed pedigrees of 101 families (778 individuals) and undertook a complex segregation analysis. They noted that genetic control of severe forms of AIS could be attributed to an autosomal dominant, major gene diallele model with incomplete sex-dependent penetrance of the genotypes. Moreover, four genome-wide screens of AIS have been reported.

Overall, results from these studies are disappointing since no one locus has been identifi ed.7–11 This absence can be explained by phenotypic or genotypic heterogeneity, incomplete penetrance, and variable expressivity. Multiple genes could be implicated in the disorder and a phenocopy could also arise in some families. Precise

measurement of the degree of curvature in each aff ected individual and identifi cation of any scoliosis in the family are of paramount importance for future genetic studies.

Several investigators have reported candidate-gene analyses of connective tissue genes. Results of these studies have excluded genes for fi brillin 1 (FBN1) and 2 (FBN2); collagen type I (COLα1) and II (COLα2); elastin (ELN); aggrecan (ACAN); and heparan sulfotransferases (HS3ST3A1 and HS3ST3B1) as causes of AIS.8,12–14 Inoue and colleagues15 studied polymorphisms in the genes for vitamin D receptor (MED4), oestrogen receptor (ESR1), and CYP17A1 in relation to curve progression. The results suggested that XbaJ site polymorphism in ESR1 was associated with curve progression.15,16 However, Tang and colleagues17 did not show an association between ESR1 and AIS.

On the basis of the hypothesis that AIS is related to an abnormality in melatonin metabolism, Morcuende and colleagues18 investigated several known receptors, such as hMel1A, hMel1B, and ROR-α, but reported no evidence of mutations in the coding regions of these genes.

Gao and colleagues19 discovered a potentially functional polymorphism in CHD7 that is over-transmitted to affected offspring and predicts disruption of a caudal-type (Cdx) transcription-factor binding site. They suggest that this gene is associated with the susceptibility of AIS and propose an overlap of causes between the rare, early onset CHARGE

Lancet 2008; 371: 1527–37

Department of Orthopaedic Surgery and Rehabilitation, University of Iowa, Iowa City, Iowa, IA, USA (S L Weinstein MD, L A Dolan PhD, J A Morcuende MD); Department of Orthopaedics and Traumatology, Chinese University of Hong Kong, Hong Kong SAR, China (J C Y Cheng MD); and Department of Orthopaedics, Sahlgrenska University Hospital, Göteborg University, Gothenburg, Sweden (A Danielsson MD)

Correspondence to:Dr Stuart L Weinstein, Department of Orthopaedic Surgery and Rehabilitation, University of Iowa, Hospitals and Clinics, 200 Hawkins Drive, Iowa City, Iowa, IA 52242, [email protected]

Search strategy and selection criteria

We searched the Cochrane Library and Medline from 1996 to 2006 for relevant literature and entered the following search terms: “adolescent idiopathic scoliosis”, “late onset scoliosis”, “scoliosis” AND “bracing” or “orthotic treatment”, “natural history”, “aetiology”, “pathogenesis”, “operative treatment”, “spinal fusion”, “surgical stapling”, “surgical stapler” or “thoracoscopy” or “video-assisted thoracic surgery” or “pedicle screw”. We mainly selected literature from the past 10 years, but did not exclude commonly referenced and highly regarded older studies. We also searched the reference lists of articles identifi ed by this search strategy and selected those we judged relevant. Pertinent review articles and book chapters were also included.

Seminar

1528 www.thelancet.com Vol 371 May 3, 2008

syndrome (coloboma of the eye; heart defects; atresia of the choanae; retardation of growth and development, or both; genital and urinary abnormalities, or both; and ear abnormalities and deafness) and AIS.19

Szappanos and colleagues20 reported a family with multiple familial occurrences of AIS coupled with the same anomaly of the karyotype [inv(10)(p11q26)]. However, analysis of restriction fragment length polymorphism showed no abnormality. Bashiardes and colleagues21 investigated another family in whom a pericentric inversion of chromosome 8 seemed to cosegregate with AIS in three generations. They used fl uorescent in-situ hybridisation and established that the p-arm break did not interrupt any known gene, but the q-arm break took place between exons 10 and 11 of the syntrophin, gamma-1 (SNTG1) gene. Mutational analysis of SNTG1 exons revealed a 6-bp deletion in exon 10, but this deletion did not consistently cosegregate with the disease in this family.21

What is the role of melatonin in the development of AIS? Several investigators have shown that pinealectomy in chickens, rats, and hamsters leads to scoliosis, and have attributed this eff ect to decreased melatonin production. However, other reports have failed to show this development of scoliosis.22–26 Additionally, patients with AIS do not have an inability to form melatonin, or impaired sleep or immune function. Moreover, several diseases associated with an abnormal melatonin rhythm do not have an obvious eff ect on the development of scoliosis. Thus scoliosis is unlikely to result from a simple absence of melatonin; rather, it might be the result of melatonin’s eff ect on other unknown growth mechanisms.3

Abnormalities in the structure and function of platelets have been noted in patients with AIS. Evidence suggests that raised concentrations of calmodulin result in altered skeletal muscle activity and subsequent progressive curvatures.27 Burwell4 formulated an integrative platelet-skeletal hypothesis whereby a small curve loads

intervertebral discs and vertebral body growth plates creating mechanical microinsults, vascular damage, and platelet activation with changes in calmodulin, leading to the release of growth factors that aff ect the compromised vertebral endplate. The end result of this postulated chain of events is a relative anterior spinal overgrowth and curve progression. However, the key questions of how and why the initial small curve develops have not been answered.

Several MRI studies have renewed interest in abnormal neuroanatomy associated with AIS. Chiari type-I malformations and spinal cord syrinx have been noted in cases of AIS; and in younger patients, drainage of the syrinx leads to resolution of the deformity.28–31 Additionally, the relation between impaired autonomous nervous system function and aetiopathogenesis of AIS has received some attention. Sympathectomy of intercostal nerves in growing rabbits results in hypervascularity of the soft tissues, increased rib growth on the side of the operation, and thoracic scoliosis convex to the opposite side.32,33

The hypothesis that an abnormality of the paravertebral muscles contributes to the development of AIS has been discussed for many years. Several have been recorded, including decreased number of type-II fi bres (fast-twitched), fi bre splitting, tubular bodies, myofi lament disarray consistent with myopathy, and generalised membrane defect (namely, impaired calcium pump). However, no defi nitive conclusion can be reached about these abnormalities, though they are likely to be secondary to the deformity itself.

Progressive AIS is attributed to relative anterior spinal overgrowth during the adolescent growth spurt. MRI studies of vertebral thoracic morphometry show that longitudinal growth of the vertebral bodies in patients with AIS is disproportionate and faster than age-matched and sex-matched controls, and takes place mainly by endochondral ossifi cation. By contrast, the circumfer-ential growth by membranous ossifi cation is slower in both the vertebral bodies and pedicles.34–38 However, the mechanisms of this growth asymmetry are not well understood.

Natural historyThe natural history of scoliosis varies with the aetiopathogenesis and curve pattern. Early long-term studies of so-called idiopathic scoliosis presented a grim prognosis, perpetuating the common misperception that all types of idiopathic scoliosis inevitably lead to disability from back pain and cardiopulmonary compromise.39–42 Shortcomings of these earlier studies were (1) the inclusion of patients with other causes of scoliosis or of early onset idiopathic scoliosis; and (2) failure to assess the outcomes related to the location of the curvature. Patients with AIS and their families are often unneces-sarily upset by the long-term picture painted by these early studies. Although the natural history of scoliosis

BA

Figure 1: Screening and diagnosis of scoliosis by scoliometer and radiography(A) Measurement of trunk rotation with a scoliometer with patient in forward bend position; and (B) posterior-anterior standing fi lm of a 13-year-old boy, Risser 2, presenting with a Cobb angle of 30°.

Seminar


clearly varies according to the aetiopathogenesis and curve pattern,43–48 screening and treatment policy for AIS has been formed on the basis of this misinformation.

Treatment of any disorder is an attempt to alter its natural history; therefore, long-term studies of both the natural history and treatment outcomes are necessary. Treatment should be proven to prevent the negative outcomes of natural history without introducing iatrogenic complications. The outcomes of untreated AIS through adulthood have been studied in Britain,43 Italy,44 Sweden,47 and the USA.45,49–52 The most frequently noted long-term sequelae of untreated AIS are curve progression, back pain, cardiopulmonary problems, and psychosocial concerns. Although present in most untreated patients, the severity of these sequelae and their eff ect on overall health and function is very variable.

The size of the curve tends to increase over the entire lifetime, but the degree of progression over a lifetime and the time-at-risk varies with many factors. Clinicians and patients need to be aware of the risk of curve progression as they make treatment decisions. Factors predicting curve progression include maturity (age at diagnosis, menarchal status, and the amount of skeletal growth remaining), curve size, and position of the curve apex. Many investigators agree that curves with a thoracic apex have the highest prevalence of progression, ranging from 58%53 to 100%.54 The more skeletally and sexually immature the patient is, the greater the probability of curve progression.44,49,54–56 Likewise, the larger the curve at presentation, the higher the likelihood of progression both before54 and after maturity.49 Table 1 summarises the risk of progression that results from the combined eff ects of maturity and curve size.56 Progression equations have also been developed to quantify the risk of progression. Peterson and Nachemson57 include Risser sign, level of apex, presence of trunk imbalance, and chronological age; the equation developed by Lonstein and Carlson55 includes the Cobb angle, Risser sign, and chronological age. These methods could be helpful to clinicians and patients who want to base their treatment decisions on the risk of progression.

The goal of non-operative treatment during adolescence is to prevent curve progression; the goal of surgical treatment is curve correction and maintenance. However, the only negative outcome of AIS strongly and consistently associated with curve size is pulmonary function. Besides the degree of lateral curvature, other factors such as high degrees of thoracic lordosis and vertebral rotation and decreased respiratory muscle strength aff ect pulmonary function.58–60 Unlike early onset (age 0–8 years) idiopathic scoliosis,41,43,46,47,61 in which substantial loss of vital capacity and forced expiratory volume in 1 s could cause pulmonary hypertension, right heart failure, and death, these problems rarely arise in AIS. Large curves (greater than 50°) with a thoracic apex have been associated with reduced vital capacity and

more frequent shortness of breath, but rarely, severe cardiopulmonary com promise.44,48,52,62

Most adults have back pain in some form during their lifetime. About 50% of adults have an episode of low back pain in any particular year and 15% report frequent back pain or pain lasting for more than 2 weeks in a year.63 Ascani and others44 reported the frequency of pain in adults with AIS (61%) to be similar to that of the general population, whereas another report52 showed that chronic pain was more frequent and of greater intensity and duration in scoliotics than in the general population. However, both groups of investigators agreed that back pain does not seem to cause excessive disability and, overall, patients work and undertake everyday activities similarly to their peers.44,52 Over a lifetime, most patients with AIS, as well as the general population, will develop clinically important radiographic osteoarthritic changes.52 However, history of backache seems to be unrelated to the presence or absence of osteoarthritis or curve severity. Back tenderness on palpation has not been related to the curve type or severity of osteoarthritis on radiography except for areas of lateral listhesis in lumbar and thoracolumbar curves. These curves, especially those with lateral listheses at the caudal end, tend to cause a higher frequency of back pain than do other curve patterns.44,48

Untreated AIS, and its possible sequelae such as back pain and pulmonary limitations, aff ects overall function and self-esteem. In this respect, publications are sparse and research is confl icting. Some studies show that patients perceive themselves to be less healthy and restricted in physical and social activities. Ascani and colleagues44 reported “real psychological disturbances” in 19% of their sample, 94% of whom had curves greater than 40°. Other studies have noted no signifi cant diff erence between people with AIS and controls in their ability to undertake activities or in quality of life.64 With respect to psychosocial aspects of AIS and presence of clinical depression, scoliosis patients fare as well as age-matched and sex-matched controls.65 However older, untreated AIS patients are much less satisfi ed than are controls with their body image, and appearance in clothes and swimsuits. About a third of patients believe that their curvature has restricted their life in some way, such as diffi culty in purchasing clothes, reduced physical ability, and self-consciousness.52,65

10–12 years 13–15 years 16 years

<19° 25% 10% 0%

20–29° 60% 40% 10%

30–39° 90% 70% 30%

>40° 100% 90% 70%

*Data reproduced from reference 56 with permission of authors.

Table 1: Percentage of curve progression: magnitude of curve at initial detection vs age*

Seminar


As they age, most patients with untreated AIS can have back pain and cosmetic concerns. Patients with untreated AIS can function well as young adults, become employed, get married, have children, and become active older adults. Unfortunately, patients can develop substantial deformity, and the cosmetic aspect of this disorder cannot be disregarded. Treatment recommendations—watchful waiting, physiotherapy, bracing, and surgery—should be made on an individual basis, and the patient and family should be well informed about the natural history of the disease.

Non-operative treatmentAlthough AIS is diagnosed and treated worldwide, treatment approaches vary internationally. In patients who still have growth remaining, watchful waiting (observation), followed by bracing if the curve progresses to greater than 25°, is the general course of care in North America.1,2 Physical therapy (outpatient and inpatient rehabilitation) has been recommended as the fi rst line of treatment for small curves and those with a low risk of progression by various, mostly European, clinicians.66,67 No defi nite evidence has shown that physical therapy or bracing reduces the risk of curve progression, corrects the existing deformity, or decreases the need for surgery. Patients should be aware of the absence of evidence for these treatments, and be provided with the opportunity to decide for themselves which treatment, if any, they believe will best fi t with their own personal assessment of risk, side-eff ects, and benefi ts.

The popularity of physical therapy for AIS has waxed and waned over time, but it continues to be favoured in France, Germany, and Spain. The aim of physiotherapy is to prevent aggravation of the deformity in mild scoliosis (ie, curves less than 25°) and to enhance the eff ect of a brace and counteract its side-eff ects in moderate scoliosis (ie, curves between 25° and 45°). These aims are met, theoretically, by a combination of prescribed and monitored sports activities and kinesitherapy to increase coordination, spinal proprioception, and movement control.68

The expectation of treatment with bracing is to prevent progression of the curve until the patient reaches skeletal maturity, at which time the risk of curve progression (and hence the risk of surgery) greatly diminishes. Over the years, the medical community has arrived at two diff erent conclusions. On the one hand, some believe that the weight of evidence favours a positive eff ect of bracing on the natural history of AIS. On the other hand, the US Preventive Services Task Force,69 its Canadian counter-part,70 and many individual practitioners worldwide believe that evidence to support bracing is poor or inconclusive. In fact, the eff ectiveness of bracing is being tested in two randomised trials in North America and the Netherlands.71,72

Blount fi rst used the Milwaukee brace (originally a postoperative orthotic) in 1958.73 Thoracolumbosacral orthoses (TLSO) were then developed, which improved on the Milwaukee brace by removal of the cervical component; use of lighter materials; and customisation to improve comfort, cosmesis, and compliance.74 Some braces have been developed for use only part-time or at night-time,75,76 whereas most others are worn for 18 or more hours per day.

Modifi cations to the typical rigid TLSO include the Cheneau bracing programme and the SpineCor dynamic brace (SpineCorporation, Chesterfi eld, UK). The Cheneau brace77,78 delivers a higher degree of initial correction through the use of a hypercorrected mould and pads to provide derotational forces throughout the trunk than did the original braces. Novel to this brace is the addition of expansion room to allow for active correction by respiratory movements.79 The SpineCor and TrIAC (Boston Brace International, Avon, MA, USA) are non-rigid braces for AIS treatment. Straps are placed to coincide with a specifi c correcting movement for each kind of curve, producing a progressive positional change, dynamic curve correction, and more appropriate muscle balance.80,81 Neither of these braces have been widely tested, but the inclusion of dynamic forces in addition to the traditional three-point control shows a more sophisticated understanding of the growing spine.

The nature of the dose–response relation between brace wear and outcome is not well established, most probably because of previous inability to accurately and reliably measure time that a brace is worn. On the basis solely of review of records and other subjective indicators of compliance, in a meta-analysis Rowe and colleagues82 reported that a 23-h per day protocol was more successful than 16-h or night-time protocols. Mechanical devices—mainly measuring temperature, pressure, and proximity sensors—to measure brace

Total sample size Surgical rate (%)

Wilmington84 brace 147 31%

Wilmington94 brace 79 11%

Providence75 brace 102 18%

Boston86 brace 212 13%

TLSO89 brace 54 26%

Boston vs Charleston95 brace 319 22%

TLSO96 brace 24 13%

Boston or Charleston97 brace 120 43%


Charleston99 brace 95 18%

Rosenberger100 brace 71 31%

Charleston93 brace 42 7%



TLSO=thoracolumbosacral orthosis.

Table 2: Surgery rates after TLSO treatment

Seminar


wear are now available. These devices create the opportunity to critically assess the relation between brace dose (ie, wear time) and curve response. Investigators used objective measures to show compliance to be much lower than that reported by the patient. However, a positive correlation between the time that a brace is worn and outcome is partly evident. In Rahman and colleagues’ study,83 34 patients had temperature monitors mounted in their braces for the duration of treatment. Of those patients who were highly compliant, 11% had progressive curves compared with 56% of those patients who were less compliant.

Many investigators have examined radiographic outcomes of TLSOs for AIS over the past half-century. Many regard a progression of greater than 5° to suggest a true change in curvature status, and often use this radiographic benchmark as their defi nition of treatment failure. This outcome has been used in many case series reports,84–88 although a few studies used improved designs such as case–control comparison89–91 and one prospective cohort study92 has been reported. The only prospective trial92 showed a lower rate of curve progression in the group with braces as compared with the non-treated group. Although the most rigorous so far, this study was non-randomised, non-blinded, with baseline diff erences between the groups not statistically adjusted for, and the results have not been replicated.

Another defi nition of brace treatment failure is the number of surgical procedures required despite treatment. The results of studies tracking surgical rates vary widely, most probably caused by diff erent sample characteristics. Table 2 gives an overview of the studies of patients who meet present indications for bracing treatment with the rate of surgery despite bracing. The surgical rate ranges from 7%93 to 43%.97

SurgeryThe primary objectives of surgical treatment with instrumentation are to (1) arrest progression, (2) achieve maximum permanent correction of the deformity in three dimensions, (3) improve appearance by balancing the trunk, and (4) keep short-term and long-term complications to a minimum. The generally agreed indication for surgery in adolescents is a primary curve greater than a Cobb angle of 45°. In adults, the surgical indications are pain related to the curvature that is unresponsive to non-operative management, curve progression that has exacerbated symptoms, and functional capabilities.103 Although adolescent patients can choose to delay surgery until they are adults, adults often have less fl exible curves that than seen in children, which could need anterior and posterior (staged or sequential) procedures. Additionally, the rate of complications in adults is much higher for the same procedures than it is in the adolescent population. Complications in adults are pseudarthrosis, proximal and distal junctional kyphosis, and extended recovery.104

Improved preoperative assessments supplemented by intraoperative neurophysiological monitoring and blood salvage techniques have made modern scoliosis surgery safer than previously. Enhancement of solid bony fusion over the surgical instrumentation can now be achieved through autogenous bone graft, allograft, demineralised bone matrix, or the latest biological bone substitutes.

Posterior instrumentation remains the mainstay of treatment for most idiopathic curves. From the fi rst generation of Harrington instrumentation introduced in the 1960s105 to modern third-generation instrumentation evolved from the Cotrel-Dubousset system in the 1980s,106 much progress has been achieved by improved multi-

A B C D

Figure 2: Radiographs of a teenager with progressive AIS treated by posterior instrumentation by hybrid (rods, hooks, and screws)(A) Preoperative standing posterior-anterior (PA); (B) preoperative standing lateral; (C) postoperative standing PA; and (D) postoperative standing lateral.

Seminar


planar (coronal, sagittal, and transverse plane) correction, stable fi xation, reduced levels of fusion, and avoidance of postoperative immobilisation with a cast or brace. Such progress has been possible through combinations of wires, hooks, and lumbar pedicle screw constructs over contoured rods, and interconnecting systems applied over several purchase sites posteriorly (the lamina, pedicle, transverse processes, and spinous processes)107,108

(fi gure 2).The extended use of many segmental pedicle screws in

the thoracic spine, originally pioneered by Suk,109 allows even better three-column mechanical fi xation, multiplanar corrections, such as the rib prominence reduction, and saving of fusion levels compared with standard hook-wire constructs110–112 (fi gure 3). The disadvantages of thoracic pedicle screws are a steep learning curve, increased cost, safety concerns, and diffi culties associated with accurately placing pedicle screws within dysplastic pedicles.113–115At present time, no conclusive evidence exists about improved radiographic outcomes in patients with AIS correlate with enhanced function, self-image, or health.104

Anterior instrumentation has been used mainly for isolated thoracolumbar and lumbar curves. Evolving from the early Dwyer cable to the vertebral screw system,116 Zeilke ventral derotation spondylodesis, screw-single rod system,117 and other similar systems have been used satisfactorily with good correction of the frontal and transverse plane, restoration of truncal balance,118,119 and reduction of fusion levels. The main disadvantages are the kyphosing tendency of these systems, higher rates of implant breakage, pseudarthrosis, and the necessity of postoperative cast or brace protection.120,121 The latest dual-rod, multiple vertebral

screw system provides good rigid fi xation, improved correction in the sagittal plane, and minimum need for postoperative protection.122,123

Anterior instrumentation has been extended to thoracic scoliosis to achieve improved sagittal plane correction and reduced number of fused levels, and to prevent crankshafting (continued anterior spinal growth in the face of a posterior fusion) in the immature patient (fi gure 4).124–126 The disadvantages of anterior open thoracotomy approach are the rate of implant breakage, pseudarthrosis, the surgical scar, and the unfavourable eff ect on lung function.124,127 Video-assisted thoracoscopic anterior instrumentation has been used to reduce the surgical scar. Such surgery, however, entails a very steep learning curve, risk of encroaching on adjacent vital structures, and problems related to anaesthesia in one lung.128–132 Hence, whether this method is useful cannot be addressed without clearly documented advantages over the latest posterior instrumentation with thoracic pedicle screws.133

A novel way to modulate the growth of the anterior vertebral epiphyses through thoracoscopic stapling of the convex apical vertebrae for scoliosis in skeletally immature patients is under investigation after promising preliminary work in animals (fi gure 5).134,135 The theoretical advantages are preservation of growth, and motion and function of the spine caused by non-fusion. However, apart from very limited experience, the need to refi ne the staple design, and other essential improvements, the most important questions relate to indications. So, who is the ideal candidate? In the absence of objective measures to reliably predict curve progression, one might be unnecessarily treating patients with curves that will never progress.

A B C D

Figure 3: Radiographs of a teenager with progressive right thoracic adolescent idiopathic scoliosis treated by posterior segmental pedicle screws(A) Preoperative standing lateral; (B) preoperative standing posterior-anterior (PA); (C) postoperative standing lateral; and (D) postoperative standing PA. Reproduced with permission of Dr Peter Newton, San Diego, CA, USA.

Seminar


Treatment outcome versus natural historyTypically, three types of treatment outcomes are reported: (1) radiographical (coronal and sagittal radiographic measurements); (2) clinical (complications, pulmonary function and symptoms, mobility, muscle strength, back function); and (3) self-reported outcomes (general health and health concerns specifi c to scoliosis and its treatment).

Several workers have reported that curve size or curve correction do not correlate with quality of life. Moreover several retrospective long-term studies have established that patients treated surgically or with a brace have nearly the same quality of life, both mentally and physically, after treatment as do healthy controls or national norms. However, this evidence is not conclusive.

Some retrospective investigations have shown that AIS causes disturbances in body image and in other indicators of mental health and adjustment.136–141 Each investigation used diff erent instruments to measure psychological indices and adherence. Despite these shortcomings, bracing clearly causes some psychological stress to the patient, at least at the initiation of treatment and possibly in the long term. Tones and colleagues142 reported a systematic review of publications about health-related quality of life and psychosocial issues in AIS. They concluded that adolescents can have poorer psychosocial functioning, body image, and health-related quality of life than have their peers, but that adults generally do not have psychological distress. However, adults are at risk of disability and concerns about body image. Stress as a result of treatment needs to be considered in the decision-to-treat equation, and the benefi ts of watchful waiting, bracing, or surgery should outweigh the risk of adverse psychological sequelae.

A long-term study from Sweden143,144 corroborates studies of the natural history of back pain and function. Danielsson and Nachemson,143,144 compared patients who

previously wore a brace and those who had undergone surgery each with a set of age-matched controls. They reported little evidence that either patient group was greatly impaired relative to their peers when the 36-item short form health survey and Oswestry low back pain disability questionnaire was used. The mean curve size in both groups was greater than 30°. Another follow-up report of more than 20 years145 showed no diff erence in quality of life, including back pain and function, between AIS patients who had undergone surgery and those who remained untreated, as inferred from several instruments, such as the Oswestry, Roland-Morris, and the EuroQol-5D. This fi nding is in contrast with that of Mayo and colleagues’ survey.65 Their sample consisted of patients who were untreated, had a brace, or had undergone surgery. The frequency of back pain did not diff er by Cobb angle, and these workers concluded that

A B C D

Figure 4: Radiographs of a teenager with progressive right thoracic adolescent idiopathic scoliosis treated by anterior spinal instrumentation(A) Preoperative standing lateral; (B) preoperative standing posterior-anterior (PA); (C) postoperative standing PA; and (D) postoperative standing lateral. Reproduced with permission of Dr Peter Newton, San Diego, CA, USA.

A B C

Figure 5: Radiographs of a skeletally immature 10 year old whose right thoracic curve progressed from 35° to 42° despite bracing (A) Preoperative but after bracing standing posterior-anterior (PA); (B) 3 years’ postoperative standing PA, Cobb angle 28°; and (C) 3 years’ postoperative standing lateral. He was treated with vertebral body stapling T6-L1. Reproduced with permission of Lippincott Williams & Wilkins from reference 134.

Seminar


the deformity could induce back pain and that surgery did not induce additional back pain beyond that caused by scoliosis itself. However, on the basis of their answers in the Oswestry questionnaire, people with severe curves or those who had been surgically treated felt restricted in their ability to manage pain, lift, and socialise. Dickson and colleagues103 compared outcomes of symptomatic, untreated patients who were off ered arthrodesis and fusion as adults with those who had arthrodesis and fusion. At an average of 5 years after surgery, 35% had substantial or severe pain compared with 70% of the patients who declined surgery and 7% of a non-scoliotic control group. They concluded that operative intervention, although associated with improvements in quality of life, self-image, pain, and disability, did not alleviate all symptoms or restore function to that of non-scoliotic individuals.

ConclusionAlthough many controversies and unanswered questions surround AIS, the most diffi cult one is the absence of information about its aetiopathogenesis. We do not know if AIS is one entity or a manifestation of several causes. We are uncertain of all the factors that lead to progression and secondary manifestations of spinal deformity. The identifi cation of aetiopathogenetic factors will enable improved prediction of progression and could aid in the development of more specifi c treatments.

Because of this absence of fundamental information, all treatment eff orts are aimed at prevention or correction of the primary manifestation of the disorder—ie, spinal deformity. Although bracing has been regarded as the standard of care for patients at a high risk of progression (curves between 25° and 40° in skeletally immature patients), it has never been subjected to rigorous assessment of either its effi cacy or eff ectiveness. Both the North American and Netherlands’ clinical trials are addressing quality of life and other psychosocial issues in individuals with AIS. If these studies show undue stress resulting from observation alone or brace treatment, this stress should be considered in the decision-to-treat equation.

With respect to surgical management, although technology has greatly increased the safety with which we can correct spinal deformity and preserve spinal balance, long-term results of these changing methods of management are absent. Surgery can reduce deformity and prevent further progression; thereby decreasing the risk of future cardiopulmonary compromise, but its role in the prevention of other negative long-term eff ects of scoliosis is not clear.Confl ict of interest statementWe declare that we have no confl ict of interest.

References1 Parent S, Newton PO, Wenger DR. Adolescent idiopathic scoliosis:

etiology, anatomy, natural history, and bracing. Instr Course Lect 2005; 54: 529–36.

2 Kesling KL, Reinker KA. Scoliosis in twins. A meta-analysis of the literature and report of six cases. Spine 1997; 22: 2009–14; discussion 2015.

3 Lowe TG, Edgar M, Margulies JY, et al. Etiology of idiopathic scoliosis: current trends in research. J Bone Joint Surg 2000; 82-A: 1157–68.

4 Burwell RG. Aetiology of idiopathic scoliosis: current concepts. Pediatr Rehabil 2003; 6: 137–70.

5 Hadley MN. Spine update: genetics of familial idiopathic scoliosis. Spine 2000; 25: 2416–18.

6 Axenovich TI, Zaidman AM, Zorkoltseva IV, Tregubova IL, Borodin PM. Segregation analysis of idiopathic scoliosis: demonstration of a major gene eff ect. Am J Med Genet 1999; 86: 389–94.

7 Wise CA, Barnes R, Gillum J, Herring JA, Bowcock AM, Lovett M. Localization of susceptibility to familial idiopathic scoliosis. Spine 2000; 25: 2372–80.

8 Salehi LB, Mangino M, De Serio S, et al. Assignment of a locus for autosomal dominant idiopathic scoliosis (IS) to human chromosome 17p11. Hum Genet 2002; 111: 401–04.

9 Miller NH, Justice CM, Marosy B, Zhang J, Wilson AF. Familial idiopathic scoliosis: evidence of autosomal susceptibility loci. Paper presented at the 38th Annual meeting of the Scoliosis Research Society Sept 10–13, 2003; Quebec, Canada.

10 Justice CM, Miller NH, Marosy B, Zhang J, Wilson AF. Familial idiopathic scoliosis: evidence of an X-linked susceptibility locus. Spine 2003; 28: 589–94.

11 Chan V, Fong GC, Luk KD, et al. A genetic locus for adolescent idiopathic scoliosis linked to chromosome 19p13.3. Am J Hum Genet 2002; 71: 401–06.

12 Carr AJ, Ogilvie DJ, Wordsworth BP, Priestly LM, Smith R, Sykes B. Segregation of structural collagen genes in adolescent idiopathic scoliosis. Clin Orthop Rel Res 1992; 274: 305–10.

13 Miller NH, Mims B, Child A, Milwicz DM, Sponseller PD, Blanton SH. Genetic analysis of structural elastic fi ber and collagen genes in familial adolescent idiopathic scoliosis. J Orthop Res 1996; 14: 994–99.

14 Merola AA, Mathur S, Igobou S, et al. Polymorphism of the Aggrecan gene as a marker for adolescent idiopathic scoliosis. Paper presented at the Scoliosis Research Society meeting 2003, Sept 10–13; Quebec, Canada.

15 Inoue M, Minami S, Nakata Y, et al. Prediction of curve progression in idiopathic scoliosis from gene polymorphic analysis. Stud Health Technol Inform 2002; 91: 90–96.

16 Wu J, Qiu Y, Zhang L, Sun Q, Qiu X, He Y. Association of estrogen receptor gene polymorphisms with susceptibility to adolescent idiopathic scoliosis. Spine 2006; 31: 1131–36.

17 Tang NL, Yeung HY, Lee KM, et al. A relook into the association of the estrogen receptor [alpha] gene (PvuII, XbaI) and adolescent idiopathic scoliosis: a study of 540 Chinese cases. Spine 2006; 31: 2463–68.

18 Morcuende JA, Minhas R, Dolan L, et al. Allelic variants of human melatonin 1A receptor in patients with familial adolescent idiopathic scoliosis. Spine 2003; 28: 2025–28.

19 Gao X, Gordon D, Zhang D, et al. CHD7 gene polymorphisms are associated with susceptibility to idiopathic scoliosis. Am J Hum Genet 2007; 80: 957–65.

20 Szappanos L, Balogh E, Szeszak F, Olah E, Nagy Z, Szepesi K. Idiopathic scoliosis: new surgical methods or search for the reasons. Acta Chir Hung 1997; 36: 343–45.

21 Bashiardes S, Veile R, Allen M, et al. SNTG1, the gene encoding gamma1-syntrophin: a candidate gene for idiopathic scoliosis. Hum Genet 2004; 115: 81–89.

22 Poon AM, Cheung KM, Lu DS, Leong JC. Changes in melatonin receptors in relation to the development of scoliosis in pinealectomized chickens. Spine 2006; 31: 2043–47.

23 Bagnall KM, Beuerlein M, Johnson P, Wilson J, Raso VJ, Moreau M. Pineal transplantation after pinealectomy in young chickens has no eff ect on the development of scoliosis. Spine 2001; 26: 1022–27.

24 Beuerlein M, Wilson J, Moreau M, et al. The critical stage of pinealectomy surgery after which scoliosis is produced in young chickens. Spine 2001; 26: 237–40.

Seminar


25 Cheung KM, Lu DS, Poon AM, Wang T, Luk KD, Leong JC. Eff ect of melatonin suppression on scoliosis development in chickens by either constant light or surgical pinealectomy. Spine 2003; 28: 1941–44.

26 O’Kelly C, Wang X, Raso J, et al. The production of scoliosis after pinealectomy in young chickens, rats, and hamsters. Spine 1999; 24: 35–43.

27 Lowe T, Lawellin D, Smith D, et al. Platelet calmodulin levels in adolescent idiopathic scoliosis: do the levels correlate with curve progression and severity? Spine 2002; 27: 768–75.

28 Benli IT, Uzumcugil O, Aydin E, Ates B, Gurses L, Hekimoglu B. Magnetic resonance imaging abnormalities of neural axis in Lenke type 1 idiopathic scoliosis. Spine 2006; 31: 1828–33.

29 Maiocco B, Deeney VF, Coulon R, Parks PF Jr. Adolescent idiopathic scoliosis and the presence of spinal cord abnormalities: preoperative magnetic resonance imaging analysis. Spine 1997; 22: 2537–41.

30 Emery E, Redondo A, Rey A. Syringomyelia and Arnold Chiari in scoliosis initially classifi ed as idiopathic: experience with 25 patients. Eur Spine J 1997; 6: 158–62.

31 Inoue M, Minami S, Nakata Y, et al. Preoperative MRI analysis of patients with idiopathic scoliosis: a prospective study. Spine 2005; 30: 108–14.

32 Agadir M, Sevastik B, Sevastik JA, Svensson L. Eff ects of intercostal nerve resection on the longitudinal rib growth in the growing rabbit. J Orthop Res 1989; 7: 690–95.

33 Sevastik JA. Right convex thoracic female adolescent scoliosis in the light of the thoracospinal concept. Stud Health Technol Inform 2006; 123: 552–58.

34 Chu WC, Lam WW, Chan YL, et al. Relative shortening and functional tethering of spinal cord in adolescent idiopathic scoliosis: study with multiplanar reformat magnetic resonance imaging and somatosensory evoked potential. Spine 2006; 31: E19–25.

35 Guo X, Chau WW, Chan YL, Cheng JC. Relative anterior spinal overgrowth in adolescent idiopathic scoliosis: results of disproportionate endochondral-membranous bone growth. J Bone Joint Surg 2003; 85-B: 1026–31.

36 Rajwani T, Bagnall KM, Lambert R, et al. Using magnetic resonance imaging to characterize pedicle asymmetry in both normal patients and patients with adolescent idiopathic scoliosis. Spine 2004; 29: E145–52.

37 Huynh AM, Aubin CE, Rajwani T, Bagnall K, Villemure I. Pedicle growth asymmetry as a cause of adolescent idiopathic scoliosis: a biomechanical study. Eur Spine J 2007; 16: 523–29.

38 Villemure I, Aubin CE, Dansereau J, Labelle H. Biomechanical simulations of the spine deformation process in adolescent idiopathic scoliosis from diff erent pathogenesis hypotheses. Eur Spine J 2004; 13: 83–90.

39 Fowles JV, Drummond DS, L’Ecuyer S, Roy L, Kassab MT. Untreated scoliosis in the adult. Clin Orthop Relat Res 1978; 134: 212–17.

40 Kolind-Sorensen V. A follow-up study of patients with idiopathic scoliosis. Acta Orthop Scand 1973; 44: 98–102.

41 Nachemson A. A long term follow-up study of non-treated scoliosis. Acta Orthop Scand 1968; 39: 466–76.

42 Nilsonne U, Lundgren KD. Long-term prognosis in idiopathic scoliosis. Acta Orthop Scand 1968; 39: 456–65.

43 Branthwaite MA. Cardiorespiratory consequences of unfused idiopathic scoliosis patients. Br J Dis Chest 1986; 80: 360–69.

44 Ascani E, Bartolozzi P, Logroscino CA, et al. Natural history of untreated idiopathic scoliosis after skeletal maturity. Symposium on epidemiology, natural history and non-operative treatment of idiopathic scoliosis. Spine 1986; 11: 784–89.

45 Dickson JH, Mirkovic S, Noble PC, Nalty T. Results of operative treatment of idiopathic scoliosis in adults. J Bone Joint Surg 1995; 77-A: 513–23.

46 Edgar MA, Mehta MH. Long-term follow-up of fused and unfused idiopathic scoliosis. J Bone Joint Surg 1988; 70-B: 712–16.

47 Pehrsson K, Bake B, Larsson S, Nachemson A. Lung function in adult idiopathic scoliosis: a 20 year follow up. Thorax 1991; 46: 474–78.

48 Weinstein SL, Zavala DC, Ponseti IV. Idiopathic scoliosis: long-term follow-up and prognosis in untreated patients. J Bone Joint Surg 1981; 63-A: 702–12.

49 Weinstein SL, Ponseti IV. Curve progression in idiopathic scoliosis. J Bone Joint Surg 1983; 65-A: 447–55.

50 Collis DK, Ponseti IV. Long-term follow-up of patients with idiopathic scoliosis not treated surgically. J Bone Joint Surg 1969; 51-A: 425–45.

51 Ponseti IV, Friedman B. Prognosis in idiopathic scoliosis. J Bone Joint Surg 1950; 52-A: 131–44.

52 Weinstein SL, Dolan LA, Spratt KF, Peterson KK, Spoonamore MJ, Ponseti IV. Health and function of patients with untreated idiopathic scoliosis: a 50-year natural history study. JAMA 2003; 289: 559–67.

53 Picault C, deMauroy JC, Mouilleseaux B, Diana G. Natural history of idiopathic scoliosis in girls and boys. Spine 1981; 11: 777–78.

54 Bunnell WP. The natural history of idiopathic scoliosis before skeletal maturity. Spine 1986; 11: 773.

55 Lonstein JE, Carlson JM. The prediction of curve progression in untreated idiopathic scoliosis during growth. J Bone Joint Surg 1984; 66-A: 1061–71.

56 Nachemson AL, Lonstein JE, Weinstein SL. Report of the prevalence and natural history committee of the Scoliosis Research Society. Denver: Scoliosis Research Society, 1982.

57 Peterson LE, Nachemson AL. Prediction of progression of the curve in girls who have adolescent idiopathic scoliosis of moderate severity. Logistic regression analysis based on data from The Brace Study of the Scoliosis Research Society. J Bone Joint Surg 1995; 77-A: 823–27.

58 Kafer ER. Respiratory and cardiovascular functions in scoliosis. Bull Eur de Physiopathol Respir 1977; 13: 299–321.

59 Kearon C, Viviani GR, Kirkley A, Killian KJ. Factors determining pulmonary function in adolescent idiopathic thoracic scoliosis. Am Rev Respir Dis 1993; 148: 288–94.

60 Lin MC, Liaw MY, Chen WJ, Cheng PT, Wong AM, Chiou WK. Pulmonary function and spinal characteristics: their relationships in persons with idiopathic and postpoliomyelitic scoliosis. Arch Phys Med Rehabil 2001; 82: 335–41.

61 Dickson RA. Early-onset idiopathic scoliosis. In: Weinstein SL, ed. The pediatric spine. New York: Raven Press, 1994: 421–29.

62 Pehrsson K, Danielsson A, Nachemson A. Pulmonary function in adolescent idiopathic scoliosis: a 25 ear follow up after surgery or start of brace treatment. Thorax 2001; 56: 388–93.

63 Deyo RA, Mirza SK, Martin BI. Back pain prevalence and visit rates: estimates from US national surveys, 2002. Spine 2006; 31: 2724–27.

64 Danielsson AJ, Wiklund I, Pehrsson K, Nachemson AL. Health-related quality of life in patients with adolescent idiopathic scoliosis: a matched follow-up at least 20 years after treatment with brace or surgery. Eur Spine J 2001; 10: 278–88.

65 Mayo NE, Goldberg MS, Poitras B, Scott S, Hanley J. The Ste-Justine Adolescent Idiopathic Scoliosis Cohort Study. Part III: back pain. Spine 1994; 19: 1573–81.

66 Negrini S, Aulisa L, Ferraro C, et al. Italian guidelines on rehabilitation treatment of adolescents with scoliosis or other spinal deformities. Eura Medicophys 2005; 41: 183–201.

67 Weiss HR, Negrini S, Rigo M, et al. Indications for conservative management of scoliosis (guidelines). Scoliosis 2006; 1: 5.

68 Negrini A, Verzini N, Parzini S, Negini A, Negrini S. Role of physical exercise in the treatment of mild adolescent idiopathic adolescent scoliosis. Review of the literature. Eura Medicophys 2001; 37: 181–90.

69 US Preventive Services Task Force. Screening for idiopathic scoliosis in adolescents: recommendation statement. Rockville, MD: Agency for Healthcare Research and Quality 2004. http://www.ahrq.gov/clinic/3rduspstf/scoliosis/scoliors.htm (accessed June, 2007).

70 Goldbloom RB. Screening for idiopathic adolescent scoliosis. In: Canadian Task Force on the Periodic Health Examination, ed. Canadian guide to clinical preventive health care. Ottawa: Health Canada, 1994; 346–54.

71 Weinstein SL, Dolan LA. BrAIST: the bracing in adolescent idiopathic scoliosis trial. Place of publication?: US National Institutes of Health, 2007. http://www.clinicaltrials.gov/ct/show/NCT00448448?order=4 (accessed June, 2007).

72 de Koning HJ. Eff ectiveness of bracing patients with adolescent idiopathic scoliosis. Nederlands Trial Register, 2007. http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=563 (accessed June, 2007).

Seminar


73 Blount WP. Principles of treatment of scoliosis and round back with the Milwaukee brace. Isr J Med Sci 1973; 9: 745–54.

74 Gavin TM, Bunch WH, Patwardhan AG, Meade KP, Shurr DG. Orthotic treatment for spinal disorders. In: Weinstein SL, ed. The pediatric spine: principles and practice. 2nd edn. New York: Lippincott Williams & Wilkins, 2001.

75 D’Amato CR, Griggs S, McCoy B. Nighttime bracing with the Providence brace in adolescent girls with idiopathic scoliosis. Spine 2001; 26: 2006–12.

76 Price CT, Scott DS, Reed FE, Jr., Riddick MF. Nighttime bracing for adolescent idiopathic scoliosis with the Charleston bending brace. Preliminary report. Spine 1990; 15: 1294–99.

77 Rigo M, Negrini S, Weiss H, Grivas T, Maruyama T, Kotwicki T. SOSORT consensus paper on brace action: TLSO biomechanics of correction (investigating the rationale for force vector selection). Scoliosis 2006; 1: 11.

78 Weiss HR, Weiss G, Schaar HJ. Conservative management in patients with scoliosis: does it reduce the incidence of surgery? Stud Health Technol Inform 2002; 91: 342–47.

79 Weiss HR. Rehabilitation of adolescent patients with scoliosis—what do we know. A review of the literature. Pediatr Rehabil 2003; 6: 183–94.

80 Veldhuizen AG, Cheung J, Bulthuis GJ, Nijenbanning G. A new orthotic device in the non-operative treatment of idiopathic scoliosis. Med Eng Phys 2002; 24: 209–18.

81 Coillard C, Leroux MA, Zabjek KF, Rivard CH. SpineCor—a non-rigid brace for the treatment of idiopathic scoliosis: post-treatment results. Eur Spine J 2003; 12: 141–48.

82 Rowe DE, Bernstein SM, Riddick MF, Adler F, Emans JB, Gardner-Bonneau D. A meta-analysis of the effi cacy of non-operative treatments for idiopathic scoliosis. J Bone Joint Surg 1997; 79-A: 664–74.

83 Rahman T, Bowen JR, Takemitsu M, Scott C. The association between brace compliance and outcome for patients with idiopathic scoliosis. J Pediatr Orthop 2005; 25:420–22.

84 Allington NJ, Bowen JR. Adolescent idiopathic scoliosis: treatment with the Wilmington brace. A comparison of full-time and part-time use. J Bone Joint Surg 1996; 78-A: 1056–62.

85 Bassett GS, Bunnell WP. Infl uence of the Wilmington brace on spinal decompensation in adolescent idiopathic scoliosis. Clin Orthop Rel Res 1987; 223: 164–69.

86 Emans J, Kaelin A, Bancel P, Hall JE. The Boston bracing system for idiopathic scoliosis. Follow-up results in 295 patients. Spine 1986; 11: 792–801.

87 Olafsson Y, Saraste H, Soderlund V, Hoff sten M. Boston brace in the treatment of idiopathic scoliosis. J Pediatr Orthop 1995; 15: 524–27.

88 Piazza MR, Bassett GS. Curve progression after treatment with the Wilmington brace for idiopathic scoliosis. J Pediatr Orthop 1990; 10: 39–43.

89 Fernandez-Feliberti R, Flynn J, Ramirez N, Trautmann M, Alegria M. Eff ectiveness of TLSO bracing in the conservative treatment of idiopathic scoliosis. J Pediatr Orthop 1995; 15: 176–81.

90 Goldberg CJ, Moore DP, Fogarty EE, Dowling FE. Adolescent idiopathic scoliosis: the eff ect of brace treatment on the incidence of surgery. Spine 2001; 26: 42–47.

91 Miller JA, Nachemson AL, Schultz AB. Eff ectiveness of braces in mild idiopathic scoliosis. Spine 1984; 9: 632–35.

92 Nachemson AL, Peterson LE. Eff ectiveness of treatment with a brace in girls who have adolescent idiopathic scoliosis. A prospective, controlled study based on data from the Brace Study of the Scoliosis Research Society. J Bone Joint Surg 1995; 77-A: 815–22.

93 Trivedi JM, Thomson JD. Results of Charleston bracing in skeletally immature patients with idiopathic scoliosis. J Pediatr Orthop 2001; 21: 277–80.

94 Bassett G, Bunnell W, MacEwen G. Treatment of idiopathic scoliosis with the Wilmington brace. Results in patients with a twenty to thirty-nine degree curve. J Bone Joint Surg 1986; 68-A: 602–05.

95 Katz DE, Richards BS, Browne RH, Herring JA. A comparison between the Boston brace and the Charleston bending brace in adolescent idiopathic scoliosis. Spine 1997; 22: 1302–12.

96 Korovessis P, Kyrkos C, Piperos G, Soucacos PN. Eff ects of thoracolumbosacral orthosis on spinal deformities, trunk asymmetry, and frontal lower rib cage in adolescent idiopathic scoliosis. Spine 2000; 25: 2064–71.

97 Little DG, Song KM, Katz D, Herring JA. Relationship of peak height velocity to other maturity indicators in idiopathic scoliosis in girls. J Bone Joint Surg 2000; 82-A: 685–93.

98 O’Neill PJ, Karol LA, Shindle MK, et al. Decreased orthotic eff ectiveness in overweight patients with adolescent idiopathic scoliosis. J Bone Joint Surg 2005; 87-A: 1069–74.

99 Price CT, Scott DS, Reed FR Jr, Sproul JT, Riddick MF. Nighttime bracing for adolescent idiopathic scoliosis with the Charleston Bending Brace: long-term follow-up. J Pediatr Orthop 1997; 17: 703–07.

100 Spoonamore MJ, Dolan LA, Weinstein SL. Use of the Rosenberger brace in the treatment of progressive adolescent idiopathic scoliosis. Spine 2004; 29: 1458–64.

101 Vijvermans V, Fabry G, Nijs J. Factors determining the fi nal outcome of treatment of idiopathic scoliosis with the Boston brace: a longitudinal study. J Pediatr Orthop Br 2004; 13: 143–49.

102 Wiley JW, Thomson JD, Mitchell TM, Smith BG, Banta JV. Eff ectiveness of the Boston brace in treatment of large curves in adolescent idiopathic scoliosis. Spine 2000; 25: 2326–32.

103 Dickson JH, Mirkovic S, Noble PC, Nalty T, Erwin WD. Results of operative treatment of idiopathic scoliosis in adults. J Bone Joint Surg 1995; 77-A: 513–23.

104 Bridwell KH, Anderson PA, Boden SD, Vaccaro AR, Wang JC. What’s new in spine surgery. J Bone Joint Surg 2007; 89: 1654–63.

105 Harrington PR. Treatment of scoliosis: correction and internal fi xation by spine instrumentation. June 1962. J Bone Joint Surg 2002; 84-A: 316.

106 Cotrel Y, Dubousset J, Guillaumat M. New universal instrumentation in spinal surgery. Clin Orthopaed Rel Res 1988; 227: 10–23.

107 Richards BS, Herring JA, Johnston CE, Birch JG, Roach JW. Treatment of adolescent idiopathic scoliosis using Texas Scottish Rite Hospital instrumentation. Spine 1994; 19: 1598–605.

108 Burton DC, Sama AA, Asher MA, et al. The treatment of large (>70 degrees) thoracic idiopathic scoliosis curves with posterior instrumentation and arthrodesis: when is anterior release indicated? Spine 2005; 30: 1979–84.

109 Suk SI, Kim WJ, Lee SM, Kim JH, Chung ER. Thoracic pedicle screw fi xation in spinal deformities: are they really safe? Spine 2001; 26: 2049–57.

110 Suk SI, Lee SM, Chung ER, Kim JH, Kim SS. Selective thoracic fusion with segmental pedicle screw fi xation in the treatment of thoracic idiopathic scoliosis: more than 5-year follow-up. Spine 2005; 30: 1602–09.

111 Lenke LG. Debate: Resolved, a 55 degrees right thoracic adolescent idiopathic scoliotic curve should be treated by posterior spinal fusion and segmental instrumentation using thoracic pedicle screws. Pro: Thoracic pedicle screws should be used to treat a 55 degrees right thoracic adolescent idiopathic scoliosis. J Pediatr Orthop 2004; 24: 329–34.

112 Kim YJ, Lenke LG, Kim J, et al. Comparative analysis of pedicle screw versus hybrid instrumentation in posterior spinal fusion of adolescent idiopathic scoliosis. Spine 2006; 31: 291–98.

113 Belmont PJ Jr, Klemme WR, Dhawan A, Polly DW Jr. In vivo accuracy of thoracic pedicle screws. Spine 2001; 26: 2340–46.

114 Parent S, Labelle H, Skalli W, de Guise J. Thoracic pedicle morphometry in vertebrae from scoliotic spines. Spine 2004; 29: 239–48.

115 Kim YJ, Lenke LG, Bridwell KH, Cho YS, Riew KD. Free hand pedicle screw placement in the thoracic spine: is it safe? Spine 2004; 29: 333–42.

116 Dwyer AF, Schafer MF. Anterior approach to scoliosis. Results of treatment in fi fty-one cases. J Bone Joint Surg 1974; 56-B: 218–24.

117 Moe JH, Purcell GA, Bradford DS. Zielke instrumentation (VDS) for the correction of spinal curvature. Analysis of results in 66 patients. Clin Orthop Rel Res 1983; 180: 133–53.

118 Turi M, Johnston CEd, Richards BS. Anterior correction of idiopathic scoliosis using TSRH instrumentation. Spine 1993; 18: 417–22.

119 Muschik MT, Kimmich H, Demmel T. Comparison of anterior and posterior double-rod instrumentation for thoracic idiopathic scoliosis: results of 141 patients. Eur Spine J 2006; 15: 1128–38.

120 Hammerberg KW, Rodts MF, DeWald RL. Zielke instrumentation. Orthopedics 1988; 11: 1365–71.

Seminar


121 Coe JD, Arlet V, Donaldson W, et al. Complications in spinal fusion for adolescent idiopathic scoliosis in the new millennium. A report of the Scoliosis Research Society Morbidity and Mortality Committee. Spine 2006; 31: 345–49.

122 Kaneda K, Shono Y, Satoh S, Abumi K. New anterior instrumentation for the management of thoracolumbar and lumbar scoliosis. Application of the Kaneda two-rod system. Spine 1996; 21: 1250–61; discussion 1261–62.

123 Bullmann V, Halm HF, Niemeyer T, Hackenberg L, Liljenqvist U. Dual-rod correction and instrumentation of idiopathic scoliosis with the Halm-Zielke instrumentation. Spine 2003; 28: 1306–13.

124 Betz RR, Harms J, Clements DH 3rd, et al. Comparison of anterior and posterior instrumentation for correction of adolescent thoracic idiopathic scoliosis. Spine 1999; 24: 225–39.

125 Lowe TG, Betz R, Lenke L, et al. Anterior single-rod instrumentation of the thoracic and lumbar spine: saving levels. Spine 2003; 28: S208–16.

126 Lenke LG. Anterior endoscopic discectomy and fusion for adolescent idiopathic scoliosis. Spine 2003; 28 (15 suppl): S36–43.

127 Graham EJ, Lenke LG, Lowe TG, et al. Prospective pulmonary function evaluation following open thoracotomy for anterior spinal fusion in adolescent idiopathic scoliosis. Spine 2000; 25: 2319–25.

128 Early SD, Newton PO, White KK, Wenger DR, Mubarak SJ. The feasibility of anterior thoracoscopic spine surgery in children under 30 kilograms. Spine 2002; 27: 2368–73.

129 Lenke LG, Newton PO, Marks MC, et al. Prospective pulmonary function comparison of open versus endoscopic anterior fusion combined with posterior fusion in adolescent idiopathic scoliosis. Spine 2004; 29: 2055–60.

130 Sucato DJ, Kassab F, Dempsey M. Analysis of screw placement relative to the aorta and spinal canal following anterior instrumentation for thoracic idiopathic scoliosis. Spine 2004; 29: 554–59; discussion 559.

131 Al-Sayyad MJ, Crawford AH, Wolf RK. Video-assisted thoracoscopic surgery: the Cincinnati experience. Clin Orthop Relat Res 2005; 434: 61–70.

132 Lonner BS, Kondrachov D, Siddiqi F, Hayes V, Scharf C. Thoracoscopic spinal fusion compared with posterior spinal fusion for the treatment of thoracic adolescent idiopathic scoliosis. J Bone Joint Surg 2006; 88-A: 1022–34.

133 Kuklo TR, Lenke LG, O’Brien MF, Lehman RA Jr, Polly DW Jr, Schroeder TM. Accuracy and effi cacy of thoracic pedicle screws in curves more than 90 degrees. Spine 2005; 30: 222–26.

134 Betz RR, D’Andrea LP, Mulcahey MJ, Chafetz RS. Vertebral body stapling procedure for the treatment of scoliosis in the growing child. Clin Orthop Relat Res 2005; 434: 55–60.

135 Braun JT, Hoff man M, Akyuz E, Ogilvie JW, Brodke DS, Bachus KN. Mechanical modulation of vertebral growth in the fusionless treatment of progressive scoliosis in an experimental model. Spine 2006; 31: 1314–20.

136 Bjure J, Nachemson A. Non-treated scoliosis. Clin Orthop Rel Res 1973; 93: 44–52.

137 Clayson D, Luz-Alterman S, Cataletto MM, Levine DB. Long-term psychological sequelae of surgically versus nonsurgically treated scoliosis. Spine 1987; 12: 983–86.

138 Fallstrom K, Cochran T, Nachemson A. Long-term eff ects on personality development in patients with adolescent idiopathic scoliosis. Infl uence of type of treatment. Spine 1986; 11: 756–58.

139 Kahanovitz N, Weiser S. The psychological impact of idiopathic scoliosis on the adolescent female. A preliminary multi-center study. Spine 1989; 14: 483–85.

140 Olafsson Y, Saraste H, Ahlgren RM. Does bracing aff ect self-image? A prospective study on 54 patients with adolescent idiopathic scoliosis. Eur Spine J 1999; 8: 402–05.

141 Schatzinger LH, Brower EM, Nash CL Jr. The patient with scoliosis. Spinal fusion: emotional stress and adjustment. Am J Nurs 1979; 79: 1608–12.

142 Tones M, Moss N, Polly DW. A review of quality of life and psychosocial issues in scoliosis. Spine 2006; 31: 3027–38.

143 Danielsson AJ, Nachemson AL. Back pain and function 22 years after brace treatment for adolescent idiopathic scoliosis: a case-control study-part I. Spine 2003; 28: 2078–85.

144 Danielsson AJ, Nachemson AL. Back pain and function 23 years after fusion for adolescent idiopathic scoliosis: a case-control study-part II. Spine 2003; 28: E373–83.

145 Grimard G, Lacroix G, Mayo NE, Vandal S, Labelle H, Poitras B. Long-term evaluation of the quality of life of subjects with adolescent idiopathic scoliosis. Seattle: Scoliosis Research Society Annual Meeting, 2002: 112 (abstr 60).

seminar adolescent idiopathic scoliosis · adolescent idiopathic scoliosis (ais) ... ﬂ uorescent...

Documents