Purposes of the study and background. An increasing number of clinical studies involving a range of chronic pain conditions report widespread mechanical pressure pain hypersensitivity, which is commonly interpreted as resulting from central sensitization (CS). Secondary hyperalgesia (increased pinprick sensitivity surrounding the site of injury) is considered to be a manifestation of central sensitization. However, it has not been rigorously tested whether central sensitization induced by peripheral nociceptive input, involves widespread mechanical pressure pain hypersensitivity. The aim of this study was to assess whether high frequency electrical stimulation (HFS), which induces a robust secondary hyperalgesia, also induces a widespread decrease of pain pressure thresholds (PPTs). Summary of the methods and results. We measured PPTs bilaterally on the temples (temporalis muscles), on the legs (tibialis anterior muscles) and on the ventral forearm (flexor carpi radialis muscles) before, 20 min after, and 45 min after applying HFS on the ventral forearm of sixteen healthy young volunteers. To evaluate the presence of secondary hyperalgesia, mechanical pin-prick sensitivity was assessed on the skin surrounding the site where HFS was applied and also on the contralateral arm. HFS induced a significant increase in mechanical pinprick sensitivity on the HFS-treated arm. However, HFS did not decrease PPTs either in the area of increased pinprick sensitivity nor at more distant sites. Conclusion. The present study provides no evidence for the hypothesis that central sensitization, induced after intense activation of skin nociceptors, involves a widespread decrease of PPTs. No conflicts of interest. Sources of Funding: This study was funded by the Université Catholique de Louvain

Introduction. Pain is an expected and appropriate experience following traumatic musculoskeletal injury. By contrast, chronic pain and disability are unhelpful yet common sequelae of trauma-related injuries. Presently, the mechanisms that underlie the transition from acute to chronic disabling post-traumatic pain are not fully understood. The aim of this study is to identify prognostic factors for risk of developing chronic pain and disability following acute musculoskeletal trauma. Methods. A prospective observational study will recruit two temporally staggered cohorts (n=250 each cohort; 10 cases per candidate predictor) of consecutive acute musculoskeletal trauma patients aged ≥16 years, who are emergency admissions into a Major Trauma Centre in the United Kingdom, with an episode inception defined as the traumatic event. The first cohort will identify prognostic factors to develop a screening tool to predict development of chronic and disabling pain, and the second will allow evaluation of the predictive performance of the tool (validation). The outcome being predicted is an individual's absolute risk of poor outcome measured at 6-months follow-up using the Chronic Pain Grade Scale (poor outcome ≥Grade II). Candidate predictors encompass the four primary mechanisms of pain: nociceptive (e.g. injury characteristics), neuropathic (e.g. painDETECT), inflammatory (biomarkers), and central hypersensitivity (e.g. quantitative sensory testing). Concurrently, patient-reported outcome measures will assess general health and psychosocial factors. Risk of poor outcome will be calculated using multiple variable regression analysis. Conclusion. A prognostic screening tool for post-trauma pain will inform precision rehabilitation, targeting interventions to individual patients to improve clinical and cost effectiveness. Conflicts of interest: None. Sources of funding: NIHR Surgical Reconstruction and Microbiology Research Centre

Aims

The aim of this study was to determine if positive Waddell signs were related to patients’ demographics or to perception of their quality of life.

Objectives

In order to elucidate the influence of sympathetic nerves on lumbar radiculopathy, we investigated whether sympathectomy attenuated pain behaviour and altered the electrical properties of the dorsal root ganglion (DRG) neurons in a rat model of lumbar root constriction.

The purpose of this study was to evaluate whether concerns about the release of metal ions in metal-on-metal total hip replacements (THR) should be extended to patients with metal-bearing total disc replacements (TDR).

Cobalt and chromium levels in whole blood and serum were measured in ten patients with a single-level TDR after a mean follow-up of 34.5 months (13 to 61) using inductively-coupled plasma mass spectrometry. These metal ion levels were compared with pre-operative control levels in 81 patients and with metal ion levels 12 months after metal-on-metal THR (n = 21) and resurfacing hip replacement (n = 36). Flexion-extension radiographs were used to verify movement of the TDR.

Cobalt levels in whole blood and serum were significantly lower in the TDR group than in either the THR (p = 0.007) or the resurfacing group (p < 0.001). Both chromium levels were also significantly lower after TDR versus hip resurfacing (p < 0.001), whereas compared with THR this difference was only significant for serum levels (p = 0.008). All metal ion levels in the THR and resurfacing groups were significantly higher than in the control group (p < 0.001). In the TDR group only cobalt in whole blood appeared to be significantly higher (p < 0.001). The median range of movement of the TDR was 15.5° (10° to 22°).

These results suggest that there is minimal cause for concern about high metal ion concentrations after TDR, as the levels appear to be only moderately elevated. However, spinal surgeons using a metal-on-metal TDR should still be aware of concerns expressed in the hip replacement literature about toxicity from elevated metal ion levels, and inform their patients appropriately.

We describe three patients with pre-ganglionic (avulsion) injuries of the brachial plexus which caused a partial Brown-Séquard syndrome.