PainSci summary of Littlewood 2013?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible. ★★★☆☆3-star ratings are for typical studies with no more (or less) than the usual common problems. Ratings are a highly subjective opinion, and subject to revision at any time. If you think this paper has been incorrectly rated, please let me know.
Explanations for pain based on “peripherally driven nociceptive mechanisms secondary to structural abnormality, or failed healing, appear inadequate” — at least in the context of rotator cuff tendinopathy (and probably much else). Instead, Littlewood et al. propose that the symptoms of tendinopathy can occur without any actual or impending tissue damage: the CNS may react to relative overuse of a de-conditioned tendon with fearful avoidance of movement, a vicious cycle of painfsrul inhibition of function. The supporting evidence for this hypothesis is circumstantial but substantial.
original abstract†Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
Tendinopathy is a term used to describe a painful tendon disorder but despite being a well-recognised clinical presentation, a definitive understanding of the pathoaetiology of rotator cuff tendinopathy remains elusive. Current explanatory models, which relate to peripherally driven nocioceptive mechanisms secondary to structural abnormality, or failed healing, appear inadequate on their own in the context of current literature. In light of these limitations this paper presents an extension to current models that incorporates the integral role of the central nervous system in the pain experience. The role of the central nervous system (CNS) is described and justified along with a potential rationale to explain the favourable response to loaded therapeutic exercises demonstrated by previous studies. This additional consideration has the potential to offer a useful way to explain pain to patients, for clinicians to prescribe appropriate therapeutic management strategies and for researchers to advance knowledge in relation to this clinically challenging problem.
- “Adhesive capsulitis: An age related symptom of metabolic syndrome and chronic low-grade inflammation?,” Max Pietrzak, Medical Hypotheses, 2016.
These two articles on PainScience.com cite Littlewood 2013 as a source:
- PS Your Back Is Not Out of Alignment — Debunking the obsession with alignment, posture, and other biomechanical bogeymen as major causes of pain
- PS Frozen Shoulder Guide — An extremely detailed & readable guide to one of the strangest of all common musculoskeletal problems, for both patients and pros
This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights:
- A Bayesian model-averaged meta-analysis of the power pose effect with informed and default priors: the case of felt power. Gronau 2017 Comprehensive Results in Social Psychology.
- The neck and headaches. Bogduk 2014 Neurol Clin.
- Agreement of self-reported items and clinically assessed nerve root involvement (or sciatica) in a primary care setting. Konstantinou 2012 Eur Spine J.
- Effect of NSAIDs on Recovery From Acute Skeletal Muscle Injury: A Systematic Review and Meta-analysis. Morelli 2017 Am J Sports Med.
- Association of Spinal Manipulative Therapy With Clinical Benefit and Harm for Acute Low Back Pain: Systematic Review and Meta-analysis. Paige 2017 JAMA.