Associate Professor James McAuley

PUBLICATIONS

Measuring two-point discrimination threshold with a caliper.

Cashin AG, McAuley JH

Persistent Pain After Wrist or Hand Fracture: Development and Validation of a Prognostic Model.

Cashin AG, Traeger AC, Hübscher M, Moseley GL, di Pietro F, Parkitny L, McAuley JH

To develop and validate a prognostic model from a comprehensive range of candidate prognostic factors that can identify patients who are at risk of developing persistent pain following wrist or hand fracture. We developed and externally validated a prognostic model to predict persistent pain 4 months after a wrist or hand fracture. Future studies are needed to assess whether the accuracy of this model can be improved by updating and validating it in local settings.

Correspondence: Living systematic reviews.

Bagg MK, McAuley JH

Comparing interventions with network meta-analysis.

Bagg MK, Salanti G, McAuley JH

Recent data from radiofrequency denervation trials further emphasise that treating nociception is not the same as treating pain.

Bagg MK, McAuley JH, Moseley GL, Wand BM

Comment: A Comparison of the Efficacy and Tolerability of the Treatments for Sciatica: A Network Meta-Analysis.

Bagg MK, McAuley JH

What does the grey matter decrease in the medial prefrontal cortex reflect in people with chronic pain?

Kang D, McAuley JH, Kassem MS, Gatt JM, Gustin SM

Alterations in the grey matter volume of several brain regions have been reported in people with chronic pain. The most consistent observation is a decrease in grey matter volume in the medial prefrontal cortex. These findings are important as the medial prefrontal cortex plays a critical role in emotional and cognitive processing in chronic pain. Although a logical cause of grey matter volume decrease may be neurodegeneration, this is not supported by the current evidence. Therefore, the purpose of this review was to evaluate the existing literature to unravel what the decrease in medial prefrontal cortex grey matter volume in people with chronic pain may represent on a biochemical and cellular level. Our model proposes new mechanisms in chronic pain pathophysiology responsible for mPFC grey matter loss as alternatives to neurodegeneration.

Reassurance for patients with non-specific conditions - a user's guide.

Traeger AC, O'Hagan ET, Cashin A, McAuley JH

Targeted reassurance, including enhanced, prognosis-specific education, could optimize reassurance and possibly prevent disabling symptoms.

Reassurance for patients with non-specific conditions - a user's guide.

Traeger AC, O'Hagan ET, Cashin A, McAuley JH

Targeted reassurance, including enhanced, prognosis-specific education, could optimize reassurance and possibly prevent disabling symptoms.

An embedded randomised controlled trial of a Teaser Campaign to optimise recruitment in primary care.

Lee H, Hübscher M, Moseley GL, Kamper SJ, Traeger AC, Skinner IW, Williams CM, McAuley JH

A Teaser Campaign using a series of branded promotional postcards did not improve clinic engagement for a randomised controlled trial in primary care.

What you wear does not affect the credibility of your treatment: A blinded randomized controlled study.

Traeger AC, Skinner IW, Hübscher M, Henschke N, Moseley GL, McAuley JH

Professional appearance is easily modifiable, and might alter the effects of a clinical encounter. We aimed to determine whether professional attire influences a patient's perception of treatment credibility. In a trial setting, whether or not a clinician is formally dressed has no effect on perceptions of treatment credibility in patients with acute low back pain.

A randomized, placebo-controlled trial of patient education for acute low back pain (PREVENT Trial): statistical analysis plan.

Traeger AC, Skinner IW, Hübscher M, Lee H, Moseley GL, Nicholas MK, Henschke N, Refshauge KM, Blyth FM, Main CJ, Hush JM, Pearce G, Lo S, McAuley JH

Making public the pre-specified statistical analysis plan for the PREVENT trial minimizes the potential for bias in the analysis of trial data, and in the interpretation and reporting of trial results.

How does pain lead to disability? A systematic review and meta-analysis of mediation studies in people with back and neck pain.

Lee H, Hübscher M, Moseley GL, Kamper SJ, Traeger AC, Mansell G, McAuley JH

Disability is an important outcome from a clinical and public health perspective. However, it is unclear how disability develops in people with low back pain or neck pain. More specifically, the mechanisms by which pain leads to disability are not well understood. Mediation analysis is a way of investigating these mechanisms by examining the extent to which an intermediate variable explains the effect of an exposure on an outcome. This systematic review and meta-analysis aimed to identify and examine the extent to which putative mediators explain the effect of pain on disability in people with low back pain or neck pain. Five electronic databases were searched. We found 12 studies (N = 2961) that examined how pain leads to disability with mediation analysis. Standardized regression coefficients (β) of the indirect and total paths were pooled. We found evidence to show that self-efficacy (β = 0.23, 95% confidence interval [CI] = 0.10 to 0.34), psychological distress (β = 0.10, 95% CI = 0.01 to 0.18), and fear (β = 0.08, 95% CI = 0.01 to 0.14) mediated the relationship between pain and disability, but catastrophizing did not (β = 0.07, 95% CI = -0.06 to 0.19). The methodological quality of these studies was low, and we highlight potential areas for development. Nonetheless, the results suggest that there are significant mediating effects of self-efficacy, psychological distress, and fear, which underpins the direct targeting of these constructs in treatment.

Effect of Primary Care-Based Education on Reassurance in Patients With Acute Low Back Pain: Systematic Review and Meta-analysis.

Traeger AC, Hübscher M, Henschke N, Moseley GL, Lee H, McAuley JH

To determine whether patient education in primary care increases reassurance in patients with acute or subacute low back pain (LBP). There is moderate- to high-quality evidence that patient education in primary care can provide long-term reassurance for patients with acute or subacute LBP.

Understanding how pain education causes changes in pain and disability: protocol for a causal mediation analysis of the PREVENT trial.

Lee H, Moseley GL, Hübscher M, Kamper SJ, Traeger AC, Skinner IW, McAuley JH

Development and validation of a screening tool to predict the risk of chronic low back pain in patients presenting with acute low back pain: a study protocol.

Traeger A, Henschke N, Hübscher M, Williams CM, Kamper SJ, Maher CG, Moseley GL, McAuley JH

Tweeting back: predicting new cases of back pain with mass social media data.

Lee H, McAuley JH, Hübscher M, Allen HG, Kamper SJ, Moseley GL

These findings give directions for future research that could use social media for innovative public health interventions.

Emotional distress drives health services overuse in patients with acute low back pain: a longitudinal observational study.

Traeger AC, Hübscher M, Henschke N, Williams CM, Maher CG, Moseley GL, Lee H, McAuley JH

Emotional distress in the acute stage of low back pain increased subsequent consultation rates. Interventions that target emotional distress during the initial consultation are likely to reduce costly and potentially inappropriate future healthcare use for patients with non-specific low back pain.

Does changing pain-related knowledge reduce pain and improve function through changes in catastrophizing?

Lee H, McAuley JH, Hübscher M, Kamper SJ, Traeger AC, Moseley GL

Evidence from randomized controlled studies shows that reconceptualizing pain improves patients' knowledge of pain biology, reduces catastrophizing thoughts, and improves pain and function. However, causal relationships between these variables remain untested. It is hypothesized that reductions in catastrophizing could mediate the relationship between improvements in pain knowledge and improvements in pain and function. To test this causal mechanism, we conducted longitudinal mediation analyses on a cohort of 799 patients who were exposed to a pain education intervention. Patients provided responses to the neurophysiology of pain questionnaire, catastrophic thoughts about pain scale, visual analogue pain scale, and the patient specific functional scale, at baseline, 1-month, 6-month, and 12-month follow-up. With adjustment for potential confounding variables, an improvement in pain biology knowledge was significantly associated with a reduction in pain intensity (total effect = -2.20, 95% confidence interval [CI] = -2.96 to -1.44). However, this effect was not mediated by a reduction in catastrophizing (indirect effect = -0.16, 95% CI = -0.36 to 0.02). This might be due to a weak, nonsignificant relationship between changes in catastrophizing and pain intensity (path b = 0.19, 95% CI = -0.03 to 0.41). Similar trends were found in models with function as the outcome. Our findings indicate that change in catastrophizing did not mediate the effect of pain knowledge acquisition on change in pain or function. The strength of this conclusion is moderated, however, if patient-clinician relational factors are conceptualized as a consequence of catastrophizing, rather than a cause.