There are numerous patient satisfaction questionnaires by none specific for an Independent Medical Examination (IME). The aim of this study was to develop and evaluate a questionnaire suitable for an IME.

The questionnaire (IMESQ) consisted of five process domains (“Interpersonal manner”, “Communication”, “Technical ability”, “Information exchange”, “Time allocation”) and an outcome domain (“Satisfaction”), each with a five-scale Likert response. An 11-point numerical satisfaction scale (NSS) and a 3-point scale question on the “willing to undergo another examination with the doctor if required” were alternative measures of validation. The questionnaire was tested against numerous independent variables.

Statistical analysis included Spearman correlation ((r_S) between the items in the questionnaire and the total score with the NSS, and “willing to undergo another examination with the doctor if required” with point-biserial correlation (r_pb). Internal consistent reliability was tested using split-half correlation coefficient (r_SB) and Cronbach's alpha coefficient (α). The construct was subjected to Factor Analysis.

The results from 53 respondents were analysed. There was moderate to strong inter-item correlation (r_s range 0.57 to 0.83, median 0.67, p < 0.01) and good correlation with the NSS (r_s = 0.79, p < 0.01) and dichotomous question (r_pb = 0.45, p < 0.01). Five respondents were “neither satisfied or dissatisfied” (Item 6) and 12 recorded “maybe” to further examination. The split-half correlation was strong (r_SB= 0.76, p < 0.01). There was good internal consistency reliability (α = 0.92). “Interpersonal manner” (ψ = 4.3) was the only item to have an eigenvalue greater than one, accounting to 72% of the variance across the scale. Eigenvector analysis confirmed the questionnaire was unidimentional.

The IMESQ is a brief questionnaire to assess satisfaction with an IME. It is validated and has good internal consistency reliability. The five process domains can identify areas of suboptimal performance: useful for a 360° audit.

Introduction Chicken studies implicate pinealectomy within a week of hatching as a cause of scoliosis. The nature of the scoliosis has been demonstrated to be similar to that of human idiopathic scoliosis. Scoliosis was not induced following pinealectomy in Rhesus monkeys (primate model). No human studies have been reported. The aim of this study is to determine if idiopathic scoliosis is associated with treatment for pineal lesions (presumably resulting in pinealectomy) in a human paediatric population.

Methods A medical records search was performed in five Australian States for pineal lesions. Identified patients underwent clinical or radiological evaluation for scoliosis. Pathology varied from germ cell tumour, germinoma, pineoblastoma, teratoma to a pineal cyst and an epidermoid cyst. Treatment ranged from biopsy/ extirpation to radiotherapy/chemotherapy.

Results Of 48 identified patients, thirteen are deceased. No scoliosis was present in the last imaging of the deceased. The mean age at presentation was 9.7 years (range 1–18 years). Ten are female. Two males have idiopathic scoliosis (4.2%). One has a 12° right upper thoracic curve (with 32° kyphosis) and the other has a 60° right thoracolumbar curve, requiring a two-stage arthrodesis

Discussion Although the incidence of idiopathic scoliosis in this cohort is greater than expected from Caucasian population studies (2–3%), it is not typical idiopathic-type, which has a female preponderance of larger deformities. New-born chicken studies demonstrate an incidence of between 50 and 100% scoliosis in the three months following pinealectomy. Chickens of both sexes are involved. Fundamental differences exist between chicken and human/primate models including the age at pinealectomy and the anatomical site of the pineal gland. Chickens have a naturally lordotic thoracic spinal curvature whilst humans/primates have a naturally kyphotic thoracic spine. Adolescents with idiopathic scoliosis have either thoracic hypokyphosis or a thoracic lordosis. Contrary to current beliefs, no causal link can be established between pineal lesions and the development of idiopathic scoliosis in a paediatric population.

Introduction Delayed puberty and delayed skeletal maturation have been implicated as risk factors for the progression of idiopathic scoliosis. Genetic defects (Turner syndrome) and hypothalamic- pituitary disorders are known causes of delayed puberty. Although it is recognized that the incidence of idiopathic scoliosis is elevated in Turner syndrome, human studies regarding the incidence/severity of scoliosis in children with suprasellar, hypothalamic region and pituitary tumours/ disorders is deficient.

Methods A medical records search in five Australian states for suprasellar, hypothalamic region and pituitary tumours/disorders was performed. Identified patients underwent clinical or radiological evaluation for scoliosis. Pathology varied from suprasellar-hypothalamic region tumours, pan-hypopituitarism, pituitary tumours and growth hormone deficiency as well as a craniopharyngioma, arachnoid cyst, retinoblastoma and encephalocele.

Results Of 23 identified patients, ten are female. Mean age at presentation was 8.4 years. Three have right thoracic scoliosis with a Cobb angle less than 20 degrees. Two are males; one with pituitary hormone deficiency and the other with Cushing’s disease treated with radiotherapy. The only female is on a growth hormone treatment program for idiopathic growth hormone deficiency.

Discussion The only female with scoliosis was 12 years old. Delayed puberty could not be linked to either male with scoliosis. Although the incidence of idiopathic scoliosis in this cohort is greater than expected from Caucasian population studies (2–3%), the male preponderance is unusual. No relationship between delayed skeletal maturation and idiopathic scoliosis could be established.

Introduction and Aims: SHOX haploinsufficiency presents with Turner syndrome dysmorphic skeletal features – micrognathia (60%), cubitus valgus (47%), high-arched palate (25%) and Madelung deformity (7%). Idiopathic scoliosis is also present in 11% of Turner syndrome. This clinical observation and radiological study explores the possibility of SHOX haploinsufficiency expression in the scoliotic spine in Turner syndrome.

Method: Turner syndrome presents a mesomelic short stature, thought to result from growth plate dysmorphism, presumably from SHOX gene haploinsufficiency. Forty-five Turner syndrome subjects on the Australian Growth Hormone program were clinically examined for the presence of idiopathic scoliosis. Of another 88 Turner syndrome subjects similarly examined, 46 had received growth hormone and 42 had never received growth hormone. Kosowicz (1959) and Preger (1968) noted irregular vertebral endplates of scoliotic spines in Turner syndrome subjects. This may imply dysmorphic vertebral growth plates. A spinal MRI and plain imaging study of idiopathic scoliosis with/without Turner syndrome was undertaken to examine for vertebral growth plate abnormalities.

Results: This study again demonstrates plain radiographic presence of irregular vertebral endplates of scoliotic spines in Turner syndrome. Spine MR imaging in Turner syndrome failed to clearly demonstrate the growth plates but demonstrated wedge-shaped distal vertebrae in the curve. Similar MR findings were noted in another 20 subjects with various causes of scoliosis. Wedged-shaped intervertebral discs were also noted, but are thought to be secondary changes. Of 87 Turner syndrome subjects from growth hormone programs, 18 (21%) were found to have idiopathic scoliosis. Thirteen of another 46 (28%) subjects who had never received growth hormone were also noted to have idiopathic scoliosis, indicating a combined incidence of 23%. These results contrast with Lippe (1991) and Kim (2001), who noted an incidence of 11% of 163 and 12% of 43 idiopathic scoliosis in Turner syndrome from retrospective observation. However, the incidence of scoliosis (41%) from the radiographic studies of Kosowicz (4/22) and Preger (19/34) is much greater than even the incidence noted clinically from this study.

Conclusion: SHOX haploinsufficiency expression is not yet described in Turner syndrome scoliotic spines, although it has been described in the distal radius (Munns, 2001) in Madelung deformity. The incidence of idiopathic scoliosis in Turner syndrome appears to be much larger than previously recognised, signalling a probable dysmorphic vertebral growth plate cause.

Introduction Patients who have undergone total joint arthroplasty have demonstrated elevated postoperative levels of the component metal ions (cobalt, chrome, titanium) in blood and urine. The metal ion release is due to wear particles produced by fretting and corrosion of the metal surfaces and interfaces. Postoperative levels may be many-fold greater than preoperative and normal population levels. The postoperative levels depend on a number of factors including component metals, implant design, and fixation.

Fretting corrosion of spinal implants has been previously demonstrated. Elevated metal ion levels in tissue fluids might be expected, however there are significant differences in stress on the spinal implant when compared with a mobile joint bearing. The aim of this study is to determine whether component metal ions can be measured in the blood and urine of patients who have previously undergone surgery with spinal instrumentation.

Methods Patients who had undergone surgery which included spinal instrumentation were recruited to the study. All had stainless steel implants. These cohorts were subdivided into two groups: those who had retained implants and those who had spinal implants which had been removed. A cohort of volunteers who had no metal implants served as controls. All subjects provide blood for serum nickel and serum chromium assays and (random) urine for measurement of chromium and creatinine. Serum chromium and nickel and urinary chromium/creatinine ratio were compared between groups. Non-parametric statistical analysis was used to test differences (MWU) and correlations (Spearman). A p-value less than 0.05 was considered significant.

Results The study group consisted of 44 patients who had undergone surgery 5–25 years previously. The implants had been removed in 12 patients. The mean number of spinal levels at operation was 10 (range 3–18) and the mean number of couplings was 10 (range 2–18). The average age at follow-up was 36 years (range18–75).

There was no difference in levels of serum nickel and blood chromium between controls and study cohorts. A significant difference between the controls and study groups was noted with the mean urinary chromium/ creatinine ratio being in the order of 100 times greater in the implant group. The mean level in the implant-retained group was1.6 times greater than in patients in whom the implants had been removed. The random urinary chromium/creatinine ratios correlated with the length of the instrumentation and the number of couplings in the spinal instrumentation.

Conclusions A raised level of chromium excretion in patients with spinal implants suggests that metal ions are released from the implants by electrolytic and fretting-corrosion. Removal of the implant reduces the excretion levels but not to base-line levels. The blood levels of both metal ions tested were no different from controls suggesting that the kidney was able to adequately handle the release of chromium from the implant without a build-up of chromium in the blood.

Introduction: Following a systematic review of the literature, de Kleuver¹ concluded that there was insufficient data to assess the performance of total disc replacement. In the absence of controlled trials, the relative merits and efficacy of artificial disc replacement as a treatment option for degenerative disc disease was unproven. Observational studies reported a moderate success rate (50-81%), but a relatively high complication rate (3%–50%). In particular, 4% of the operated levels fused spontaneously or after revision surgery.

Methods: Using the research methodology of the above study, all subsequent published studies of artificial lumbar disc replacement were identified and reviewed by meta-analysis. In the two years (2002–2003) since the above study, a further nine case series and three controlled studies have been reported. The three randomised controlled trials compared disc replacement with spinal fusion. Seven prospective studies (include the randomised controlled studies) had defined indications, exclusions and outcome measures.

Results: A total of 623 disc replacements were performed in 510 patients. The outcomes were classified as “good” or “excellent”, ranged from 70–93% (mean=83%). Complications were observed in up to 35% (mean=3%) of patients. Eight patients subsequently underwent spinal arthrodesis at the level of the disc replacement. Two patients were reported to have heterotopicossification.

The outcomes for the 2002–2003 publications were better (MWp=0.02) than for the de Kleuver study. Fewer patients had disc replacement at more than one level (FEp< 0.01). The number of patients undergoing secondary surgery (FEp< 0.01) and arthrodesis (FEp=0.04) was less and the incidence of prosthetic subsidence or migration was lower (FEp=0.28). This overall improvement in recent studies highlights the importance of patient selection and the use of a disc replacement of appropriate size.

Following disc replacement, there was a significant improvement in outcome measures at six-week follow-up. This improvement was maintained at two years. While disc replacement reported significantly less pain and disability in the early period following surgery compared with the fusion, the difference was not significant by six months.

Discussion: In the short to medium term, disc replacement is as effective as spinal fusion in the treatment of degenerative disc disease in critically selected patients. Although the number of complications has been reduced, some serious complications were reported.² A satisfactory salvage procedure for failed disc replacement is yet to be found. The long-term biological effects of disc replacement are unknown. Late failure of disc replacement is predictable in a substantial number of patients. Long-term studies of ten or more years are necessary to adequately define the place of disc replacement in the treatment of lumbar disc disorders. Because the numbers of disc replacement patients is likely to be small, protocols and outcome measures should be standardised and data centrally recorded.

Introduction: Retrospective reports of adverse events following growth hormone administration to short-statured children indicate that the incidence of scoliosis is elevated, largely due to the higher incidence of scoliosis in Turner/other syndromes within the group. The aims of this study are to analyse risk factors for scoliosis in these children.

Methods: Data on 184 of 267 (65%) current and recent Australian children from the Australian OZGROW program was collected in 2001/2002 (from three Australian States). This included medical records (including past history of known scoliosis), growth charts, timing of growth hormone and oestrogen administration and the presence and severity of scoliosis from clinical examination. Growth hormone dosage was controlled by Australian Health Department guidelines. Standard oestrogen dosage was similar for all pubertal girls. The cohort was noted to comprise many varying syndromes, some of whom were pituitary hormone deficient. Potential risk factors for the development of scoliosis were statistically analysed.

Results: Of 45 subjects with Turner Syndrome, 13 (30%) have idiopathic scoliosis and 2 have a hemi-vertebra. Of the other 139 subjects, 15 have scoliosis but 11 have syndromes which would normally be associated with scoliosis. Therefore, the incidence of idiopathic scoliosis in the remaining 128 subjects is 3.1% (4/128), which is within the normal population range. All 4 have mild scoliosis < 20 degrees. For the 139 subjects with idiopathic short stature or a specific syndrome, the age of commencement and total amount of growth hormone and/or oestrogen did not affect the degree of scoliosis.

Discussion: Having Turner Syndrome was the only variable identified as a risk factor for having scoliosis (p< .001). The incidence of scoliosis in growth hormone treated Turner Syndrome subjects is much larger than previously reported (11–12%)^1,2. To the authors’ knowledge, this is the first report derived from non-retrospective data on the incidence of scoliosis in a growth hormone–treated Turner Syndrome population. This stimulated the next study looking at the incidence of scoliosis in growth hormone-treated and non-growth hormone-treated subjects with Turner Syndrome.

Introduction: Following an Australian study on the incidence of scoliosis in a population of short-statured children treated with human growth hormone (conducted during 2001–2002), it was determined that the only risk factor for the presence of idiopathic scoliosis was having Turner/another syndrome. The 30% incidence in Turner syndrome was noted to be much higher than previously reported (11–12%). The aim of this study is to determine the incidence of scoliosis in a group of growth hormone-treated and non-treated Turner Syndrome subjects who attended the International Turner Syndrome Society meeting in Sydney, Australia in July 2003 and to correlate the results with the Australian 2001–2002 results.

Methods: 88 subjects were clinically examined for the presence and severity of idiopathic scoliosis. Their ages ranged from 11 to 60 years. All subjects provided information regarding previous growth hormone and/or oestrogen administration. Anthropometric data including sitting and standing height and arm span was also collated on this cohort.

Results: 13 of 46 (28.3%) subjects who had no growth hormone treatment were found to have scoliosis. Five of 42 (12%) subjects who were growth hormone treated were found to have scoliosis. 12 curves were thoracic, five were thoracolumbar and one was lumbar. The 13 subjects with scoliosis and no growth hormone treatment had curves between10 and 20° Cobb angle. Three growth hormone-treated subjects had curves of 10°, one had a curve of 30° and the last subject had already undergone scoliosis surgery. Combining the results of this study with the three Australian States study from 2001–2002, 18 of 87 (21%) growth hormone-treated Turner syndrome subjects have idiopathic scoliosis. 13 of 46 (28%) non-growth hormone-treated Turner syndrome subjects also have idiopathic scoliosis. Of the total 133 subjects in this cohort, 31 (23%) have idiopathic scoliosis.

Discussion: The incidence of idiopathic scoliosis in Turner syndrome appears to have been understated in previous studies. Data from this study would indicate that treating children who have Turner syndrome with adjuvant human growth hormone does not appear to result in a greater incidence or severity of idiopathic scoliosis. In this relatively small study, two of five children who had previous growth hormone treatment developed larger curves, one requiring corrective scoliosis surgery.

Introduction: The reduction of severe spondylolisthesis remains controversial and is not without risk. The reduction should aim, primarily, to restore the lumbosacral angle.

Aim: To review the principle author’s experience with reduction of severe lumbosacral spondylolisthesis with emphasis on the restoration of the lumbosacral alignment.

Methods: Thirty patients have undergone reductions of severe lumbosacral spondylolistheses. All were treated by two-staged operations with variation. The anterior operations involved subtotal disc clearances with leverage to distract the discs and restore the lumbosacral angulation. Posteriorly, ala-transverse fusions and L5 laminectomies were performed. More recently pedicle screws were used. Initially hyperextension traction was employed between operations, but this was subsequently abandoned.

Results: Significant reductions (p< 0.01) of displacements were achieved at each stage but significant improvements in slip-angles only occurred with the initial operations. Loss of sagittal and angular corrections were noted at the one-year follow-up. Loss of angular corrections were significantly less with internal fixation (p=0.03). The final alignments were significantly improved when compared with the initial positions.

Conclusions: Satisfactory restoration of the lumbosacral alignment was achieved in severe spondylolisthesis by staged anterior and posterior procedures. Leverage to restore lumbosacral angulation during the anterior procedure facilitated reduction. Post-operative loss of correction was limited by pedicle screw fixation.

Introduction: Progression of lumbosacral spondylolisthesis during adolescence is not uncommon, but it is rare in adults. Structural changes in adolescent spondylolisthesis have been reported as possibly predictive and contributory to progression.

Aim: To review the structural changes that occur with and possibly contribute to slip progression in lumbosacral spondylolisthesis.

Methods: The radiographs of 42 patients with lumbosacral spondylolisthesis who had been followed for a mean period of six years were reviewed. The following radiological parameters were determined from the initial and latest radiographs:

Percentage slip

Results: Strong correlations (p< 0.01) existed between all radiological parameters at the time of the initial examination and at follow-up. Changes in percentage slip over time correlated with changes in all radiological parameters (p< 0.01). Slip progression correlated with increased slip angle (p< 0.01), increased trapezoid index (p< 0.05), and increased lordosis (p< 0.01) but not with age (p=0.16), adolescence (p=0.10), gender or with spondylolysis. The risk of slip progression was greatest for adolescents with an initial slip of 30% or more (p=0.13, Odds Ratio=5.7).

Conclusions: Slip progression in lumbosacral spondylolisthesis was associated with corresponding proportional structural changes in the sacrum and the L5 vertebral body, possibly related to growth and remodelling. The tendency to progress was greatest in adolescents with slips of greater than 30%. This relationship was sufficiently strong to consider prophylactic fusion.

The association between spondylolisthesis and scoliosis was studied in 84 patients who presented during a 30-year period with symptomatic spondylolisthesis. The incidence of scoliosis was 42 per cent, the majority of cases being lumbar or thoracolumbar curves of less than 15 degrees. The incidence was highest in the group of patients with spondylolisthesis at L4--5 where all except one had scoliosis. Scoliosis was present in 47 per cent of patients with dysplastic spondylolisthesis at the lumbosacral junction; in this group, the incidence of scoliosis was greater where the displacement exceeded 25 per cent. The lowest incidence (25 per cent) was found in the group with isthmic spondylolisthesis at the lumbosacral junction. There appeared to be no relationship between excessive lumbar lordosis or tightness of the hamstrings and scoliosis.