European journal of pain : EJP
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Intramuscular injection of Nerve Growth Factor (NGF) may influence the responsiveness of active chemo-sensitive channels affecting muscle pain sensitivity. This double-blinded crossover study in healthy humans assessed contraction-evoked pain responses and pain sensitivity during acute ischaemia in the tibialis anterior (TA) muscle before and 24 hr after five distributed NGF injections (1 µg, 4 cm interval) compared with control injections (isotonic-saline). ⋯ Acidification of the muscle environment may affect muscle nociceptors and pain by different mechanisms, including activation of ASIC3 and TRPV1. In this study, pain evoked following ischaemic contractions was increased in the Nerve Growth Factor (NGF)-sensitized muscle compared with non-ischaemic contractions and in the non-sensitized muscle. These findings illustrate that responses of peripheral afferents under ischaemic conditions are altered by a pre-sensitized muscle. This highlights the role of growth factors, including NGF, in peripheral muscle sensitization with clinical implications for ischaemic myalgia.
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This study describes a low-cost and time-efficient clinical sensory test (CST) battery and evaluates its concurrent validity as a screening tool to detect somatosensory dysfunction as determined using quantitative sensory testing (QST). ⋯ Quantitative sensory testing, albeit considered the gold standard to evaluate somatosensory dysfunction, requires expensive equipment, specialized examiner training and substantial time commitment which challenges its use in a clinical setting. Our study describes a CST as a low-cost and time-efficient alternative. Some of the CST tools (cold, warm, mechanical detection thresholds; pressure pain thresholds) significantly correlated with the respective QST parameters, suggesting that they may be useful in a clinical setting to detect sensory dysfunction.
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Efficacy of pain modulation is assessed as the difference in pain sensitivity during a painful conditioning, compared to before (conditioning pain modulation, CPM). Attention can be assessed with the Stroop task, in which participants report the number of words on a screen; either congruent or incongruent with the value of the words. Attention away from painful stimuli during CPM enhances the CPM effect. However, it is unknown if attention influences CPM effects when the two are done in sequence. ⋯ Pain sensitivity is reduced after an attention task in healthy men. The delayed effects from attention only have minor effects on Conditioned Pain Modulation (CPM), and results support that attention-driven analgesia works independently of CPM. Results indicate that individual strategies for pain inhibition exist and that an overlap between the mechanisms of CPM and selective attention is limited. Moreover, painful phasic stimuli may increase the number of healthy volunteers with negative CPM effects.
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The posterior insula and the medial parietal operculum (PIMO) are part of the pain network. Pain can be induced by direct stimulation of the PIMO, but the clinical consequence of lesions in this brain area is not well known. ⋯ Most of the data concerning the functional role of the PIMO come from stereoelectroencephalography in presurgical evaluation of epilepsy, or from functional imaging (PET or fMRI). There is, however, very few data on the consequences of the lesion of the PIMO. Here, we report the first case of a transient widespread pain syndrome associated to a single, small and reversible inflammatory lesion of the PIMO. Thus, this case highlights the key role of the PIMO in spatial perception of pain.
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Delayed onset muscle soreness (DOMS) is characterized by mechanical hyperalgesia after lengthening contractions (LC). It is relatively common and causes disturbance for many people who require continuous exercise, yet its molecular and peripheral neural mechanisms are poorly understood. ⋯ Here, we show that not only C- but also Aδ-fibre nociceptors in the muscle are involved in mechanical hypersensitivity after lengthening contractions, and that acid-sensing ion channel (ASIC)-3 expressed in the thin-fibre nociceptors is responsible for the mechanical hypersensitivity. ASIC3 might be a novel pharmacological target for pain after exercise.