Can clinical pilates decrease pain and improve function in people complaining of non-specific chronic low back pain? A pilot study.
It is estimated that at least 70% of adults suffer from low back pain (LBP) at some point in their lifetime (Andersson 1999). Low back pain can be divided into two subsets (specific or nonspecific) with specific LBP being defined as symptoms caused by a particular pathophysiological mechanism (e.g. fracture, tumour, osteoporosis); non-specific LBP is defined as symptoms without a clear or named cause (Koes et al 2006). Non-specific LBP is thought to constitute approximately 90% of all LBP cases (Koes et al 2006). Most episodes of LBP resolve either spontaneously or with treatment; however, an estimated 15% of people develop chronic LBP and continue to have persistent pain one year after the initial episode (Atkinson 2004). Chronic LBP is defined by New Zealand's Accident Compensation Corporation (ACC) as persistent LBP symptoms with or without disability for a period greater than three months (Kendall et al 1997).
There is some indication that non-specific chronic LBP provokes changes in the central nervous system that include neuronal hyperactivity, changes in membrane excitability and expression of new genes that may perpetuate the perception of pain in the absence of ongoing tissue damage (Deyo and Weinstein 2001). These changes alter the neuromuscular control of the trunk (i.e. dynamic stability), and so become a contributing factor to the chronic nature of the problem (Henry et al 2006).
Exercise therapy, the most commonly recommended treatment for chronic LBP, is supported by several systematic reviews that report improvements in function and pain for this intervention (van Tulder et al 2006; Hayden et al 2005a; Hayden et al 2005; van Tulder et al 2000). However, at the time of this pilot study there were no guidelines on which approach to exercise was most useful. For example there were no recommendations for what type of exercise should be employed, the number of repetitions, sets of exercises or the frequency with which these exercises should be performed.
One type of exercise reported to be effective in decreasing pain and improving function is segmental stabilisation exercises (SSE) or trunk strengthening (Ferreira et al 2006; Rackwitz, et al 2006; Slade and Keating 2006). SSE initially focus on contracting the deep muscles of the spine to stabilise the spinal column, progress to refining the ability to contract these deep muscles in varying postures and positions, and eventually stabilising the spine in functional activities (Hodges 2003; Stevans and Hall 1998).
Clinical Pilates is a theory-based exercise regime, founded on the rationale of improving segmental stability and functional movement, using some of the traditional exercises and equipment created by Joseph Pilates in the 1920s (La Touche et al 2008). Clinical Pilates has been adapted from the traditional Pilates form by physiotherapists throughout the world and is becoming a widely used approach in the treatment of musculoskeletal disorders (La Touche et al 2008). Clinical Pilates is described as exercise based on the Pilates method adapted for rehabilitation purposes (La Touche et al 2008). That is, the exercises contain some elements of traditional Pilates exercise with the physiotherapist prescribing exercises based on clinically relevant findings and research, therefore providing a rationale for the intervention rather than merely performing a series of exercises for well-being purposes (Rydeard et al 2006). The focus of Clinical Pilates is to integrate dynamic stabilisation exercises with pathology management, using a progression from closed chain activities which encourage proprioceptive activity to open chain activities in functional positions to stimulate both the local and global mechanisms to integrate normal efficient function (Rydeard et al 2006). Clinical Pilates may use the traditional Pilates equipment such as a Clinical Pilates reformer, which is a carriage on a roller with detachable springs for variable resistance (See Figure 1). The symmetrical nature of the Clinical Pilates exercises and equipment is suggested to be an appropriate rehabilitative and therapeutic agent for patients with muscular imbalances (Blum 2002).
Pilates exercises activate transversus abdominis (TrA) and obliquus internus abdominis (OI) muscles (Endleman and Critchley 2008), as well as muscles involved in dynamic stability of the spine (Hodges 2003; Henry et al 2006). Treatment for chronic LBP using Clinical Pilates exercises have shown a reduction in pain and an improvement in function (Gladwell et al 2006; Rydeard et al 2006) compared to no treatment, though there appears to be no significant difference when compared to other forms of exercises (Curnow et al 2009; Donzelli et al 2006). Recent randomised trials in other countries have investigated the effects of Clinical Pilates and chronic LBP with results suggesting function may be improved and pain reduced following the intervention (Donzelli et al 2006; Gladwell et al 2006; Rydeard et al 2006). Through retraining core stabilisers, Clinical Pilates exercises may contribute to improvement in movement patterns and this is thought to decrease pain and dysfunction (Segal et al 2004).
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At the time of planning this pilot study in early 2006, there was little published research about the effects of Clinical Pilates for chronic LBP although some has been reported since then and is summarised above. The aims of this pilot study were to: (a) investigate the outcomes of a six week, physiotherapist prescribed and supervised, Clinical Pilates intervention in a sample of New Zealanders complaining of non-specific chronic low back pain; (b) measure the longer term outcomes (six and 26 weeks after treatment completion) and (c) explore the feasibility of the intervention and study procedures to underpin the planning of a clinical trial if indicated by the pilot data.
Ethical approval for the pilot study was obtained from the Central Regional Health and Disability Ethics Committee, New Zealand. The sample size for this before and after study was estimated using a paired t-test. We needed to recruit sufficient participants that a paired t-test (comparing baseline and post treatment ODI scores in our treated participants) would give a statistically significant result if the mean change in ODI score was greater than the change that could be expected in adults with CLBP over time without intervention. We used ODI data from untreated adult controls in previous chronic LBP research, specifically a mean difference in ODI between zero and six months of 2.7 (Resnik and Dobrykowski 2005) and a within subject standard deviation of 5.3 (Davidson and Keating 2002). Based on these data it was estimated that a minimum of 12 participants were needed to allow for change in symptoms that might be expected with time without any intervention.
Participants and recruitment
Fifteen adults with chronic LBP living in the Hawke's Bay region were recruited from July 2006 to June 2007. Potential participants were offered information about the research through study packs distributed to local doctors' clinics, orthopaedic specialists and physiotherapy clinics. Potential participants expressed interest in the research by returning the reply slip within the study pack to the researcher by pre-paid envelope. The researcher met 20 potential participants who were screened for eligibility (See Table 1 for inclusion and exclusion criteria). Fifteen were eligible for inclusion and gave written informed consent to participate.
Each participant completed a full physiotherapy assessment to investigate deficits in range of movement, muscular strength and/or endurance, flexibility, core stability and muscle balance (See Table 2). The findings from the assessment provided the basis for the individualised Clinical Pilates exercise intervention and home exercise programme. Range of movement deficiencies were addressed within the intervention with exercises targeting specific joint movements. Patients with muscular strength deficits were prescribed strengthening exercises of eight to 12 repetitions in three sets with the resistance increased as appropriate. Endurance deficits were addressed with exercises performed with 25 repetitions in three sets. Stability exercises mimicked functional activities and consisted of greater than 20 repetitions; the emphasis was on the quality of the activity.
For all types of exercise, the initial spring resistance was set at a level that participants could complete the exercises correctly, maintaining correct positioning, and starting to fatigue at the end of the set. Spring resistance was progressed for each type of exercise as appropriate. Spring resistance was increased for strengthening and endurance exercises. Progressing stability exercises used a decrease in spring resistance to increase the work of the participant to maintain correct positioning.
The intervention lasted six weeks, with all participants completing a one hour fully supervised one-on-one session, twice per week at a local physiotherapy clinic using a Pilates reformer (See Figure 1). Each session was supervised by a Clinical Pilates trained physiotherapist. All exercises during the intervention period were performed pain free and modified to meet the requirements of the individual and progressed in accordance with the participants' abilities.
The first three sessions also included instruction on Clinical Pilates floor exercises to be completed as a home exercise programme taking 30 minutes, three times per week. Examples of exercises to improve strength, endurance and stability are provided in Table 3. Written and illustrated descriptions of the home exercises were provided to each participant. At the end of the intervention period, all participants were given a new home exercise programme and asked to continue these exercises for the next 26 weeks. All assessments and exercise programmes were completed by the primary researcher (LT).
[TABLE 3 OMITTED]
All measures were administered pre intervention (baseline, T0), at completion of the intervention (week six, T6), then at six weeks post completion (T12) and 26 weeks post completion (T32).
Primary outcome and primary endpoint:
The Oswestry Disability Index (ODI) was used to assess the limitation of various daily living activities. The ODI is reported to have good construct validity, showing consistency when compared against other outcomes measures assessing function for LBP (Vianin 2008).
The ODI is reported to have sound psychometric properties (Vianin 2008) and a decrease in ODI score represents a positive improvement in functional status. The minimal important difference indicating clinically meaningful change in ODI score is ten points or more (Davidson and Keating 2002). The primary comparison of interest was the difference in ODI score between baseline (T0) and completion of the intervention (T6).
The visual analogue pain scale (VAS) is considered a reliable and valid measure of pain for research purposes (Nielsen et al 2005; Grotle et al 2004); the minimal important difference representing clinically meaningful change is 20mm for LBP (Ostelo and de Vet 2005).
The Short Form-36 health survey version 2 (SF-36v2) is a generic measure of health status (Ferrer et al 2006). Sub-domains within the SF-36v2 were analysed separately which included physical functioning, role of physical, bodily pain, general health, vitality, social functioning, role of emotion and mental health. The SF-36v2 also gives summary scores for a physical health component and a mental health component. Test-retest reliability coefficients are greater than 0.75 for all sub-domains except social functioning (Brazier et al 1992) and construct validity for all components of the SF-36 is also good with correlations greater than 0.65 when compared to pain, function, well-being, disability and patient satisfaction scales (Ferrer et al 2006). When interpreting the normative-based data a score of 50 implies average health and functioning; less than 50 implies below average and greater than 50 implies above average health and functioning (Qualitymetric 2005).
A four item questionnaire about understanding of and adherence to home exercises and advice was given to each participant to complete at the end of the six week intervention and at the two subsequent follow ups. Participants completed a five point (1 to 5) Likert scale to indicate their understanding of how often they were asked to do their exercises, whether they understood how to do the exercises and how often they completed the exercises. The Likert scale was then converted into a percentage (score/5 x 100 e.g. 3/5=60%). The questionnaire was developed by the researcher (LT) for use in this study and has not been validated.
Data were expressed as means with standard deviations (SD). All data were tested for normality using the Kolmogorov-Smirnov statistic. Where normally distributed, the paired t-test was used to investigate difference between baseline (T0) and the primary endpoint (T6). Data that were not normally distributed were analysed using a Wilcoxon Signed Ranks test. Secondary analysis of differences between (T6) and other post completion data (T12, T36) was done using a repeated measures analysis of variance (ANOVA) to determine if there was a statistically significant change in outcome over time. Analysis was carried out using the statistical package SPSS version 14 (IBM); and the SF-36v2 used the QualityMetric (2005) software which converted the SF-36v2 results into sub-domain scores. Statistical significance was set at [alpha]<0.05.
Of the 100 information packs distributed, 20 participants contacted the researcher and these 20 were screened; 15 met the inclusion criteria and were recruited. Five were not eligible for inclusion due to spondylolisthesis, inflammatory disease and recurrent rather than chronic LBP (one person each) or they were receiving current treatment from either a physiotherapist or osteopath for their chronic LBP (two people). There were no withdrawals during the intervention and no reports of adverse reactions. One participant was lost to follow up between T12 and T32 due to leaving the region. This participant's data were included in the primary analysis (paired t-test) but not in secondary analysis (ANOVA) of post completion results. Participant characteristics are presented in Table 4. The sample population consisted of a near one to one ratio of men and women, with the mean age of men slightly older than the women.
Primary outcome at primary endpoint (T6)
There was a statistically significant reduction in ODI score after the supervised intervention ceased, representing a clinically meaningful improvement in function (Table 5).
Secondary outcomes at primary endpoint (T6)
There was a statistically significant improvement in the functional components of the SF-36v2 physical functioning, role physical sub-domains and the physical health component summary at the end of the intervention (T6) (Table 5). Statistically significant differences in VAS score were found when comparing baseline (T0) to the end of the intervention (T6) with similar results from the bodily pain sub-domain of the SF36v2 (Table 5). Other statistically significant differences between baseline (T0) and the end of the intervention (T6) were found in the SF-36v2 sub-domains of general health, vitality and mental health (Table 5).
Secondary analyses--comparison of outcome at T6, T12 and T32
Analysis of variance between the post completion (T6) and follow up time points (T12, T32) found no statistically significant differences in function, pain and general health over time (Table 6).
Participants self-reported home exercise adherence is presented in Table 7. It can be seen that self-reported adherence appeared to decrease over the 26 weeks after treatment completed, although an understanding of the exercises was sustained over the same period.
To our knowledge this is the first study in New Zealand to assess the outcomes of physiotherapist prescribed and supervised Clinical Pilates exercise intervention for non-specific chronic LBP. The findings from this pilot study indicated that this intervention improved function and decreased pain levels, and these improvements were maintained for up to 26 weeks after supervised treatment was completed. Furthermore Clinical Pilates appeared to improve overall general health and have some positive influence on mental health and vitality.
The findings of this case series are congruent with a systematic review (with meta analysis) of trials of exercise therapy for chronic LBP, which found exercise was effective to improve function and reduce pain (Hayden et al 2005b). Recent systematic reviews of segmental stability exercises (SSE) found that this type of exercise is more effective than general practitioner (GP) management and equally as effective as physiotherapy treatment excluding SSE (Ferreira et al 2006; Rackwitz et al 2006; Slade and Keating 2006). As segmental stabilisation or dynamic stability is the rationale that underpins Clinical Pilates there was an assumption that similar effects would be seen with the Clinical Pilates intervention used in this research; the findings of this pilot study suggested this assumption is worthy of further testing in the form of a randomised clinical trial.
The mean ODI score in the study sample was 22.4 at the initial assessment (T0) which suggested moderate disability due to LBP (Resnik and Dobrykowski 2005). This score reduced to levels suggestive of minimal disability at all follow up points (T6, T12, T32) and was reduced by enough points (ten or more) to suggest clinically meaningful difference (Davidson and Keating 2002).
Although not published at the time this study was planned, subsequently published randomised controlled trials of Clinical Pilates for chronic LBP with baseline levels of function suggestive of minimal disability also found significant improvements as assessed by ODI and Roland Morris Disability Questionnaire (RDQ) (Donzelli et al 2006; Rydeard et al 2006). In the present study we used the ODI as it is one of the most common instruments for assessing functional disability and is reported as a valid and reliable condition-specific assessment measure (Vianin 2008). However, this measure may not be responsive enough to determine change in individuals with slight functional limitations. Results from the SF-36v2 physical sub-domains reinforced the functional improvements of the participants following the Clinical Pilates intervention.
Pain levels, assessed by the VAS and bodily pain sub-domain of the SF-36v2, were found to be significantly reduced at the completion of the intervention and remained lower at all follow up points. However, the difference was not of sufficient magnitude to suggest clinical importance with the mean differences of T6, T12 and T32 being less than the reported 20mm required (Ostelo & de Vet, 2005).
No systematic reviews of exercise therapy for chronic LBP have selected generic health status as an outcome of interest. Only one previous Clinical Pilates trial has measured generic health status and reported a statistically significance difference in general health at the end of a six week intervention using the Short Form-12 health survey (SF-12) (Gladwell et al 2006). The results from the current pilot study indicate statistically significant differences in general health, vitality and mental health status following the intervention (T6) which were maintained at both follow up points (T12, T32). While an association between improved generic health status and Clinical Pilates exercises in people with chronic LBP has yet to be determined, evidence from this pilot study provides some encouragement for further investigation into the possibility of such a relationship.
Logically, adherence to a home exercise programme will enhance the likelihood of a therapeutic effect by ensuring a sufficient dose of the therapeutic intervention. Adherence rates were comparable with other trials investigating exercise and chronic LBP (Frost et al 1998; Kolt and McEvoy 2003) but lower than that reported in a Clinical Pilates trial (Gladwell et al 2006). While the adherence to the home exercise programme decreased over time, the self reported knowledge of how to do the exercises and the frequency at which these exercises were to be completed remained high (>90%). However, it is important to note that self reporting measures are likely to overestimate adherence (Kolt and McEvoy 2003). Reinforcing home exercises with written and illustrated material is thought to improve adherence (Kolt and McEvoy 2003) and higher levels of exercise are associated with greater improvements in pain and function (Hayden et al 2005).
With regard to representativeness of the study sample, the majority of the participants identified as New Zealand Europeans with two New Zealand Maori participating (13%). This did not reflect the Hawke's Bay population which is approximately 24% Maori (Statistics New Zealand 2006). However, ongoing LBP claims with ACC for the Hawke's Bay region (June 2005 to July 2006) comprised 77% New Zealand Europeans and 10% Maori (Accident Compensation Corporation 2006). Thus, this study was reasonably representative of the local population of people with chronic LBP who have ACC claims. Using the World Health Organisation (WHO) guidelines, the mean BMI for New Zealand Europeans were categorised as overweight whilst the Maori participants were classified as healthy (Ministry of Health New Zealand, 2007).
While the results of this study are promising enough to suggest Clinical Pilates exercises may have a beneficial effect on functional activity levels, pain and general health status several limitations were noted. With a small sample size and multiple statistical testing there was the danger of family wise error, that is, the finding of positive statistical tests that are due to chance (Type I error). The small sample size may have been the cause for the wide confidence intervals. The obvious lack of a control group for comparison could not discount improvements in outcomes due to the Hawthorne effect, nor was observer bias controlled for with the primary researcher conducting the assessments and intervention. A non-validated questionnaire was used to gather self-reported information about home exercise adherence; it was possible this overestimated adherence although it was thought important to get some indication of participants understanding about how to perform the exercises, their understanding of how often they were to perform the exercises and whether they completed the prescribed exercises in order to inform further development of the intervention protocol in any future study.
While the findings of this research add to the growing pool of data indicating positive outcomes when using Clinical Pilates exercises for people with chronic non-specific LBP further research in the form of randomised trials are required to conclusively show that Clinical Pilates is an effective exercise intervention within the New Zealand population of non-specific chronic LBP. Previous trials have not found an association between mental health status and Clinical Pilates exercises therefore more research is justified to investigate the potential effects of Clinical Pilates.
One of the research objectives was to establish the feasibility of a clinical trial. The data support further investigation into the effects of Clinical Pilates exercises and non-specific chronic LBP. Based on data from this pilot study, a power calculation using a paired t-test with a mean difference (SD) 10.6 (8.2) between ODI measures at T32 and T0 at 80% power, estimates a minimum of 32 participants (i.e. n=16 control group, n=16 intervention group). With power at 90% the minimum number increases to 42 subjects (Lenth 2006). The viability of completing future clinical trials is supported by the low attrition rate during the intervention phase, good completion rates by participants and reasonable self-reported adherence.
The ideal research design would be a randomised trial of physiotherapist prescribed and supervised Clinical Pilates exercise compared with either usual care and/or usual physiotherapy treatment. The intervention protocol should be similar to the pilot study i.e. one hour twice weekly sessions for six weeks with a home exercise programme, with the individualised Clinical Pilates regimes based on an initial assessment and progressed as appropriate.
Outcome measures should include condition specific functioning, generic health status, pain, work disability and qualitative data with regards to patient satisfaction as suggested by Bombardier (2000) and a measure of exercise adherence. Recommended outcomes measures would be the ODI, the SF36, using the bodily pain subsection of the SF-36 as a measure of pain. Questions regarding work absenteeism and days that work activities were reduced due to LBP, an open-ended question regarding the overall satisfaction of the intervention and a valid and reliable exercise adherence questionnaire should also be included. Cost analysis of the Clinical Pilates intervention should also be assessed and compared to either usual care and/or physiotherapy treatment. These outcome measures would be assessed initially and followed up at three, six months, 12 months and 24 months to determine the short, medium and longer term effects of this intervention.
The findings of this pilot study add to the growing pool of research indicating beneficial outcomes when using physiotherapy prescribed and supervised Clinical Pilates exercise for people with chronic LBP. The results of this research, in conjunction with previous investigations, support the need for further rigorous research to understand the potential effects of Clinical Pilates on outcomes such as pain, function, general health, vitality and mental health with a clear description of the exercise parameters. The procedures and intervention tested in this pilot, and the data, could be used to assist in the planning of and power calculation for a randomised trial to establish if Clinical Pilates is an effective intervention for non-specific chronic LBP.
Research completed as a part of Masters in Health Science (Rehabilitation), University of Otago, New Zealand. Sarah Dean's position is supported by the National Institute of Health Research, UK.
ADDRESS FOR CORRESPONDENCE
Lee-Anne Taylor, Health and Sport Sciences, Eastern Institute of Technology, New Zealand. Email: firstname.lastname@example.org
Accident Compensation Corporation website (2006): ACC Injury Statistics 2006 (First Edition). http://www.acc.co.nz/about-acc/acc-injurystatistics-2006/SS_WIM2_062683 Retrieved 17 September 2007
Andersson G (1999): Epidemiological features of chronic low back pain. Lancet, 354: 581-585.
Atkinson J (2004): Chronic back pain: searching for causes and cures. Journal of Rheumatology 31(12): 2323-2325.
Blum C (2002): Chiropractic and Pilates therapy for the treatment of adult scoliosis. Journal of Manipulative and Physiological Therapeutics 25(3): E3.
Bombardier C (2000): Outcome assessments in the evaluation of treatment of spinal disorders. Summary and general recommendations. Spine 25(24): 3100-3103.
Brazier J, Harper R, Jones N, O'Cathain A, Thomas K, Usherwood T, et al (1992): Validating the SF-36 health survey questionnaire: new outcome measure for primary care. British Medical Journal 305(6846): 160-164.
Curnow D, Cobbin D, Wyndham J and Choy B (2009): Altered motor control, posture and the Pilates method of exercise prescription. Journal of Bodywork and Movement Therapies 13: 104-111
Davidson M and Keating J (2002): A comparison of five low back disability questionnaires: reliability and responsiveness. Physical Therapy 82(1): 8-24.
Deyo R and Weinstein J (2001): Low back pain. New England Journal of Medicine 344(5): 363-370.
Donzelli S, Di Domenica F, Cova A, Galletti R and Giunta, N (2006): Two different techniques in the rehabilitation treatment of low back pain; a randomised controlled trial. Europa Medicophysica 42(3): 205-210.
Endleman I and Critchley D (2008): Transversus abdominis and obliquus internus activity during Pilates exercises: Measurement with ultrasound scanning. Archives of Physical Medical Rehabilitation 89: 2205-2212
Ferreira P, Ferreira M, Maher C, Herbert R and Refshauge K (2006): Specific stabilisation exercise for spinal and pelvic pain: a systematic review. Australian Journal of Physiotherapy 52(2): 79-88.
Ferrer M, Pellise F, Escudero O, Alvarez L, Pont A, Alonso J, et al (2006): Validation of a Minimum Outcome Core Set in the Evaluation of Patients With Back Pain. Spine 31(12): 1372-1379.
Frost H, Lamb S, Klaber Moffett J, Fairbank J and Moser J (1998): A fitness programme for patients with chronic low back pain: 2-year followup of a randomised controlled trial. Pain 75(2-3): 273-279.
Gladwell V, Head S, Haggar M and Beneke R (2006): Does a program of Pilates improve chronic non-specific low back pain? Journal of Sport Rehabilitation 15: 338-350.
Grotle M, Brox J and V0llestad N (2004): Concurrent comparison of responsiveness in pain and functional status measurements used for patients with low back pain. Spine 29(21): E492-501.
Hartigan C, Rainville J, Sobel J and Hipona M (2000): Long-term exercise adherence after intensive rehabilitation for chronic low back pain. Medicine and Science in Sports and Exercise 32(3): 551-557
Hayden J, van Tulder M, Malmivaara A and Koes B (2005a): Exercise therapy for treatment of non-specific low back pain. Cochrane Database systematic reviews, July 20(3): CD000335.
Hayden J, van Tulder M, Malmivaara A and Koes, B (2005b): Meta-analysis: exercise therapy for nonspecific low back pain. Annals of Internal Medicine 142(9): 765-775.
Hayden J, van Tulder M and Tomlinson G (2005): Systematic review: Strategies for using exercise therapy to improve outcomes in chronic low back pain. Annals of Internal Medicine 142(9): 776-785.
Herrington L and Davies R (2005): The influence of Pilates training on the ability to contract the transversus abdominis muscle in asymptomatic individuals. Journal of bodywork and movement therapies 9(1): 52-57.
Henry S, Hitt J, Jones S and Bunn J (2006): Decreased limits of stability in response to postural perturbations in subjects with low back pain. Clinical Biomechanics (Bristol, Avon) 21(9): 881-892.
Hodges P (2003): Core stability exercise in chronic low back pain. Orthopaedic Clinical North America 34(2): 245-254.
Kendall N, Linton S and Main C (1997): Guide to Assessing Psycho-social yellow flags in acute low back pain: Risk factors for long-term disability and work loss (October, 2004 ed.). Wellington, New Zealand: Accident Compensation Corporation and the New Zealand Guidelines Group.
Koes B, van Tulder M and Thomas S (2006): Diagnosis and treatment of low back pain. British Medical Journal 332(7555): 1430-1434.
Kolt G and McEvoy J (2003): Adherence to rehabilitation in patients with low back pain. Manual Therapy 8(2): 110-116.
La Touche R, Escalante K and Linares M (2008): Treating non-specific chronic low back pain through the Pilates method. Journal of Bodywork and Movement Therapy 12(4): 364-370.
Lenth RV (2006): Java Applets for Power and Sample Size [Computer software]. http://www.stat.uiowa.edu/~rlenth/Power. Retrieved 13 September 2007
Ministry of Health New Zealand (2007): Food and nutrition guidelines for healthyadults. http://www.moh.govt.nz/moh.nsf/ ae8bff4c2724ed6f4c256669006aed56/e7c395b7c7046650cc256d73007 df607?OpenDocument Retrieved 5 July 2007
Nielsen C, Price D, Vassend O, Stubhaug A and Harris J (2005): Characterizing individual differences in heat-pain sensitivity. Pain 119(1-3): 65-74.
Ostelo R and de Vet H (2005): Clinically important outcomes in low back pain. Best Practice and Research: Clinical Rheumatology 19(4): 593-607. QualityMetric Incorporated (2005): SF-36 generic health questionnaire. (Computer software).,
Rackwitz B, de Bie R, Limm H, von Garnier K, Ewert T and Stucki G (2006): Segmental stabilizing exercises and low back pain. What is the evidence? A systematic review of randomized controlled trials. Clinical Rehabilitation 20(7): 553-567.
Resnik L and Dobrykowski E (2005): Outcomes measurement for patients with low back pain. Orthopaedic Nursing 24(1): 14-24.
Rydeard R, Leger A and Smith D (2006): Pilates-based therapeutic exercise: effect on subjects with nonspecific chronic low back pain and functional disability: a randomized controlled trial. Journal of Orthopaedic Sports Physical Therapy 36(7): 472-484.
Segal N, Hein J and Basford J (2004): The effects of Pilates training on flexibility and body composition: an observational study. Archives of Physical Medical Rehabilitation 85(12): 1977-1981.
Slade S and Keating J (2006): Trunk-strengthening exercises for chronic low back pain: a systematic review. Journal of Manipulative and Physiological Therapeutics 29(2): 163-173.
Statistics New Zealand (2006): 2006 Census of populations and dwellings. http://www.stats.govt.nz/NR/rdonlyres/19D6A4B9-7D98-4AF9-970D5BBD139794CA/ 0/RegionalSummaryTablesRegionalCouncil.xls Retrieved 5 July 2007
Stevans J and Hall K (1998): Motor skill acquisition strategies for rehabilitation of low back pain. Journal of Orthopaedic Sports Physical Therapy 28(3): 165-167.
van Tulder M, Koes B and Malmivaara A (2006): Outcome of non-invasive treatment modalities on back pain; an evidence-based review. European Spine Journal 15: S64-S81.
van Tulder M, Malmivaara A, Esmail R and Koes B (2000): Exercise therapy for low back pain: a systematic review within the framework of the Cochrane collaboration back review group. Spine 25(21): 2784-2796.
Vianin M (2008): Psychometric properties and clinical usefulness of the Oswestry Disability Index. Journal of Chiropractic Medicine 7:161-163.
Lee-Anne Taylor, MHealSc (Rehabilitation), BPhty, BSc
Programme Coordinator Recreation and Sport, Eastern Institute of Technology, Hawke's Bay, New Zealand
E Jean C Hay-Smith, PhD, MSc, DipPhys
Senior Lecturer in Rehabilitation, Rehabilitation Teaching and Research Unit, Wellington School of Medicine and Health Sciences, University of Otago, Wellington, New Zealand
Sarah Dean, PhD, C.Psychol, MSc, MCSP, Grad Dip Phys, BSc Joint Hons
Senior Lecturer in Health Services Research, Peninsula College of Medicine and Dentistry, University of Exeter, UK
Table 1: physiotherapy assessment Subjective questions Objective examination Body chart of pain areas Postural observations (sitting, standing, single leg standing, squat, single leg squat, gait) History of Chronic LBP AROM Lumbar/Thoracic spine (fingertip to floor cm), Hip (goniometer) (Hartigan et al 2000) Present symptoms TrA using biofeedback cuff (crook lying, +/- leg lifts) (Herrington and Davies 2005) Aggravating/easing factors Thomas test (Hartigan et al 2000) 24 hour behaviour SLR and Slump tests (Hartigan et al 2000) Past medical history Resisted muscle tests as indicated (Oxford scale) (Rydeard et al 2006) General health Functional tasks (sit to stand, lifting floor to waist, floor to shoulder height, waist to shoulder) achieved/not achieved; weight in kg if appropriate (Hartigan et al 2000) LBP--Low back pain, AROM--Active range of movement, TrA--Transversus abdominis, SLR--Straight leg raise. Table 2: Inclusion and exclusion criteria Inclusion Exclusion Chronic LBP >3 months Constant or persistent severe pain due to nerve root irritation, with or Aged 18-65 years old without neurology symptoms Able to travel independently Other forms of spinal injury (e.g. Declared fit by their spondylolisthesis) primary health practitioner Pregnancy Any other illnesses that would prevent the ability to perform an exercise regime e.g. Rheumatoid arthritis Unable to walk without a walking aid Major surgery within the past year Received treatment for chronic LBP within past 3 months or already involved in regular or frequent sporting activities at least twice a week for the past 3 months LBP--Low back pain Table 4: Demographic data of participants (n=15) Characteristic Sex number (%) Females 8 (53) Males 7 (47) Age in years mean (SD) 39.8 (10.9) Females 37.8 (11.2) Males 42.1 (10.8) Ethnicity number (%) NZ European 12 (80) Maori 2 (13) Irish 1 (7) BMI mean (SD) 26.9 (4.3) NZ European 27.8 (3.9) Maori 22.8 (5.9) Duration of chronic LBP in years mean (SD) 9.0 (12.0) Men 13.5 (16.0) Women 5.2 (5.4) SD--Standard deviation Table 5: paired t-tests (unless otherwise stated), T0 versus T6 (n=15) Mean (SD) Mean (SD) T0 T6 ODI 22.4(14.0) 10.9 (9.8) VAS 3.6 (2.1) 1.7 (1.6) SF-36v2 Physical Health component Physical Functioning 45.0 (10.4) 50.7 (6.7) Role Physical 42.3 (9.4) 48.9 (11.1) Bodily Pain 39.5 (8.2) 47.9 (8.0) General Health 44.3 (11.4) 50.2 (10.7) Physical Health component summary 42.2 (9.2) 48.8 (9.4) Mental Health component Vitality 44.6 (9.4) 50.2 (9.3) Social Functioning 45.6 (9.3) 49.6 (7.0) Role Emotion 46.0 (11.6) 50.4 (6.0) Mental Health 45.7 (9.9) 51.7 (5.7) Mental Health component summary 46.8 (10.2) 51.1 (4.8) Mean 95 Confidence difference Interval ODI 11.5 -7.5 to -15.4 VAS 1.9 -0.5 to -2.7 SF-36v2 Physical Health component Physical Functioning 5.7 -8.6 to -2.9 Role Physical 6.6 -11.1 to -2.0 Bodily Pain 8.4 -12.0 to -4.9 General Health 5.9 -9.4 to -2.4 Physical Health component summary 6.6 -9.6 to -3.7 Mental Health component Vitality 5.6 -9.8 to -1.5 Social Functioning 4.4 -10.0 to 1.4 Role Emotion 5.1 -11.7 to 1.4 Mental Health 6.2 -11.2 to -1.2 Mental Health component summary 4.7 -9.9 to 0.5 t-value p-value ODI 6.21 0.00002 * VAS 2.58 0.022 * SF-36v2 Physical Health component Physical Functioning 4.30 0.001 * Role Physical 3.06 0.008 * Bodily Pain 5.13 0.0002 * General Health 3.58 0.003 * Physical Health component summary 3.80 0.0003 * Mental Health component Vitality z=-2.29 0.022 * (a) Social Functioning 1.63 0.125 Role Emotion 1.70 0.111 Mental Health 2.65 0.019 * Mental Health component summary 1.66 0.07 * Significant at a = 0.05 (a) Wilcoxon Signed Ranks test Table 6: Mean scores post completion (T6, T12, T32) (n=14) Post completion Variable T6 mean (SD) T12 mean (SD) ODI 11.3 (10.1) 12.3 (11.7) VAS 1.7 (1.7) 2.6 (2.4) SF-36v2 Physical Health component Physical Functioning 50.9 (6.9) 49.8 (7.7) Role Physical 48.5 (11.4) 50.7 (8.2) Bodily Pain 47.6 (8.2) 46.4 (8.1) General Health 49.8 (11.0) 50.3 (11.0) Physical Health component summary 48.5 (9.6) 48.5 (7.6) Mental Health component Vitality 50.1 (9.6) 50.5 (11.5) Social Functioning 49.4 (7.3) 49.0 (9.7) Role Emotion 50.9 (6.0) 51.4 (9.1) Mental Health 51.8 (5.9) 51.6 (8.5) Mental Health component summary 51.4 (4.9) 51.6 (10.0) Variable T32 mean (SD) P-value (1) ODI 12.4 (13.5) 0.839 VAS 1.8 (1.9) 0.163 SF-36v2 Physical Health component Physical Functioning 51.3 (6.3) 0.211 Role Physical 50.6 (11.0) 0.188 Bodily Pain 46.9 (9.3) 0.874 General Health 51.6 (11.2) 0.637 Physical Health component summary 50.6 (8.5) 0.196 Mental Health component Vitality 50.0 (12.0) 0.985 Social Functioning 49.5 (8.7) 0.985 Role Emotion 49.8 (7.1) 0.582 Mental Health 48.2 (11.4) 0.091 Mental Health component summary 48.8 (10.5) 0.317 (1) From repeated measures ANOVA SD--Standard deviation Table 7: summary of percentage adherence to home exercises (n=15) How often they How often they Did they were to perform did their home know how to their home exercises complete their exercises home exercises Mean (SD) Mean (SD) Mean (SD) T6 100.0 (0.0) 84.0 (18.8) 92.0 (12.7) T12 100.0 (0.0) 76.7 (23.8) 96.0 (11.2) T32 ** 100.0 (0.0) 72.9 (26.7) 91.4 (12.9) SD--Standard deviation ** n=14
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|Title Annotation:||RESEARCH REPORT|
|Author:||Taylor, Lee-Anne; Hay-Smith, E.Jean C.; Dean, Sarah|
|Publication:||New Zealand Journal of Physiotherapy|
|Date:||Mar 1, 2011|
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