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A growing body of literature associates musculoskeletal disorders with cortical reorganisation. One condition in which reorganisation is established and treatments that 'train the brain' are being widely used is chronic back pain. Recent evidence suggests that treatments that involve tactile training are more effective if they incorporate multisensory mechanisms, most obviously vision. With regard to back pain however, we must first determine if tactile function is enhanced by incorporating other modalities. A series of three cross-over experiments were conducted in healthy pain-free subjects to determine whether tactile acuity is enhanced when participants can see the skin of their back during testing. An initial randomised cross-over experiment suggested tactile acuity was significantly enhanced when participants could see their backs (t(25) = similar to 4.226, p < 0.001, r = 0.65). However, a second replication experiment was not corroborative. Both the second (F(3,66) = 1.00, p = 0.398) and third (t(9) = 0.969, p = 0.358) experiments suggested that seeing the back did not significantly affect tactile acuity, confirming that our initial results were likely due to chance. The principle that visual feedback improves tactile acuity at the hand does not apply to the back. These results strongly suggest that attempts to enhance tactile training by incorporating vision will not offer the benefit to treatment of back pain that has been observed for treatment of hand pain. Refereed/Peer-reviewed

Introduction Pain education is a complex intervention developed to help clinicians manage low back pain. Although complex interventions are usually evaluated by their effects on outcomes, such as pain or disability, most do not directly target these outcomes; instead, they target intermediate factors that are presumed to be associated with the outcomes. The mechanisms underlying treatment effects, or the effect of an intervention on an intermediate factor and its subsequent effect on outcome, are rarely investigated in clinical trials. This leaves a gap in the evidence for understanding how treatments exert their effects on outcomes. Mediation analysis provides a method for identifying and quantifying the mechanisms that underlie interventions. Aim To determine whether the effect of pain education on pain and disability is mediated by changes in self-efficacy, catastrophisation and back pain beliefs. Design Causal mediation analysis of the PREVENT randomised controlled trial. Participants and setting Two hundred and two participants with acute low back pain from primary care clinics in the Sydney metropolitan area. Intervention Participants will be randomised to receive either ‘pain education' (intervention group) or ‘sham education' (control group). Measurements All outcome measures (including patient characteristics), primary outcome measures (pain and disability), and putative mediating variables (self-efficacy, catastrophisation and back pain beliefs) will be measured prior to randomisation. Putative mediators and primary outcome measures will be measured 1 week after the intervention, and primary outcome measures will be measured 3 months after the onset of low back pain. Analysis Causal mediation analysis under the potential outcomes framework will be used to test single and multiple mediator models. A sensitivity analysis will be conducted to evaluate the robustness of the estimated mediation effects on the influence of violating sequential ignorability – a critical assumption for causal inference. Discussion and significance Mediation analysis of clinical trials can estimate how much the total effect of the treatment on the outcome is carried through an indirect path. Using mediation analysis to understand these mechanisms can generate evidence that can be used to tailor treatments and optimise treatment effects. In this study, the causal mediation effects of a pain education intervention for acute non-specific low back pain will be estimated. This knowledge is critical for further development and refinement of interventions for conditions such as low back pain.

© 2016 Australian Physiotherapy Association Introduction Low back pain is the leading worldwide cause of disability, and results in significant personal hardship. Most available treatments, when tested in high-quality randomised, controlled trials, achieve only modest improvements in pain, at best. Recently, treatments that target central nervous system function have been developed and tested in small studies. Combining treatments that target central nervous system function with traditional treatments directed towards functioning of the back is a promising approach that has yet to be tested in adequately powered, prospectively registered, clinical trials. The RESOLVE trial will be the first high-quality assessment of two treatment programs that combine central nervous system-directed and traditional interventions in order to improve chronic low back pain. Aim To compare the effectiveness of two treatment programs that combine central nervous system-directed and traditional interventions at reducing pain intensity at 18 weeks post randomisation in a randomised clinical trial of people with chronic low back pain. Design Two-group, randomised, clinical trial with blinding of participants and assessors. Participants and setting Two hundred and seventy-five participants with chronic low back pain that has persisted longer than 3 months and no specific spinal pathology will be recruited from the community and primary care in Sydney, Australia. Interventions Both of the interventions contain treatments that target central nervous system function combined with treatments directed towards functioning of the back. Adherence to the intervention will be monitored using an individual treatment diary and adverse events recorded through passive capture. Participants are informed prior to providing informed consent that some of the treatments are not active. Blinding is maintained by not disclosing any further information. Complete disclosure of the contents of the intervention has been made with the UNSW HREC (HC15357) and an embargoed project registration has been made on the Open Science Framework to meet the Declaration of Helsinki requirement for transparent reporting of trial methods a priori. Intervention A Participants randomised to Intervention A will receive a 12-session treatment program delivered as 60-minute sessions, scheduled approximately weekly, over a period of 12 to 18 weeks. All treatment sessions are one-on-one. The program includes a home treatment component of 30 minutes, five times per week. The intervention comprises discussion of the participant's low back pain experience, graded sensory training, graded motor imagery training and graded, precision-focused and feedback-enriched, functional movement training. Treatment progression is determined by participant proficiency, with mandatory advancement at set time points with respect to a standard protocol. Intervention B Participants randomised to Intervention B will receive a 12-session treatment program of the same duration and structure as Intervention A. The intervention comprises discussion of the participant's low back pain experience, transcranial direct current stimulation to the motor and pre-frontal cortices, cranial electrical stimulation, and low-intensity laser therapy and pulsed electromagnetic energy to the area of greatest pain. Treatment is delivered according to published recommendations and progressed with respect to a standard protocol. Measurements The primary outcome is pain intensity at 18 weeks post randomisation. Secondary outcomes will include disability, depression, pain catastrophising, kinesiophobia, beliefs about back pain, pain self-efficacy, quality of life, healthcare resource use, and treatment credibility. Assessment will occur at baseline and at 18, 26 and 52 weeks after randomisation. Treatment credibility will be assessed at baseline and 2 weeks after randomisation only. Analysis A statistician blinded to group status will analyse the data by intention-to-treat using linear mixed models with random intercepts. Linear contrasts will be constructed to compare the adjusted mean change (continuous variables) in outcome from baseline to each time point between intervention A and intervention B. This will provide effect estimates and 95% confidence intervals for any difference between the interventions. Significance Preliminary data suggest that combining treatments that target central nervous system function with traditional interventions is a promising approach to chronic low back pain treatment. In the context of modest effects on pain intensity from most available treatments, this approach may lead to improved clinical outcomes for people with chronic low back pain. The trial will determine which, if either, of two treatment programs that combine central nervous system-directed and traditional interventions is more effective at reducing pain intensity in a chronic low back pain cohort. Central nervous system-directed interventions constitute a completely new treatment paradigm for chronic low back pain management. The results have the potential to be far reaching and change current physiotherapy management of chronic low back pain in Australia and internationally.

The objective of this chapter is to present a state-of-the-art overview on the question whether motor control changes are a cause and/or an effect of low back pain (LBP). It is based on a discussion among all the authors of this volume and a review of the literature. We have attempted to avoid overlap with the preceding chapters as much as possible, but have found it necessary in some places to repeat arguments made there or refer to data reported there.The question at hand has obvious implications for the feasibility of motor control training as an approach to primary and/or secondary prevention of LBP. However, it should be kept in mind that even when, for example, poor motor control can cause LBP, this does not necessarily imply that motor control training is an effective, let alone the most effective, approach to primary prevention.The first section of this chapter reviews observations on motor behaviour in individuals with LBP. In the second section, we discuss the evidence that motor control changes can be a primary cause of LBP. In the third section, we discuss evidence that LBP causes changes in motor control. Subsequently, we address the question whether these changes are adaptive, i.e. help the individual to deal with LBP-related impairments, or maladaptive, i.e. contribute to the transition to chronic pain and/or recurrence of pain. The final section summarizes the main conclusions and presents implications for clinical research and practice.

There is increasing evidence that chronic pain problems are characterised by alterations in brain structure and function. Chronic back pain is no exception. There is a growing sentiment, with accompanying theory, that these brain changes contribute to chronic back pain, although empirical support is lacking. This paper reviews the structural and functional changes of the brain that have been observed in people with chronic back pain. We cast light on the clinical implications of these changes and the possibilities for new treatments but we also advise caution against concluding their efficacy in the absence of solid evidence to this effect. National Health & Medical Research Council of Australia.

Studies of lumbar intradiscal pressure (IDP) in standing and upright sitting have mostly reported higher pressures in sitting. It was assumed clinically that flexion of the lumbar spine in sitting relative to standing, caused higher IDP, disc degeneration or rupture, and low back pain. IDP indicates axial compressive load upon a non-degenerate disc, but provides little or no indication of shear, axial rotation or bending. This review is presented in two main parts. First, in vivo IDP data in standing and upright sitting for non-degenerate discs are comprehensively reviewed. As methodology, results and interpretations varied between IDP studies, in vivo studies measuring spinal shrinkage and spinal internal-fixator loads to infer axial compressive load to the discs are also reviewed. When data are considered together, it is clear that IDP is often similar in standing and sitting. Secondly, clinical assumptions related to IDP in sitting are considered in light of basic and epidemiologic studies. Current studies indicate that IDP in sitting is unlikely to pose a threat to non-degenerate discs, and sitting is no worse than standing for disc degeneration or low back pain incidence. If sitting is a greater threat for development of low back pain than standing, the mechanism is unlikely to be raised IDP.