Articles: hyperalgesia.
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This investigation aimed to quantify and compare sensory responses to hypertonic saline-induced pain in the tendoachilles and the common extensor tendon of the elbow. Healthy subjects (n=14; seven males) received in randomised order, injections of sterile saline (0.5ml, 5.8% hypertonic or 0.9% isotonic saline) at each tendon bilaterally at two sessions separated by one week. Mechanical sensitivity (pressure pain threshold), muscle pain intensity (visual analogue scale; VAS area-under-curve, pain duration, peak pain) and pain distribution were assessed pre, immediately after and post saline injection. ⋯ Significant maximal force attenuation occurred immediately after hypertonic saline injections in both tendons (P<0.001) compared with control injections. The greater induced deep tissue pain and hyperalgesia demonstrated at tendoachilles compared with the common extensor tendon may relate to anatomical differences such as higher nociceptor density or increased vascular perfusion at the injection site. This translational tendon pain model may contribute to the further understanding of pain mechanisms in tendinopathic conditions.
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Painful heat reveals hyperexcitability of the temporal pole in interictal and ictal migraine States.
During migraine attacks, alterations in sensation accompanying headache may manifest as allodynia and enhanced sensitivity to light, sound, and odors. Our objective was to identify physiological changes in cortical regions in migraine patients using painful heat and functional magnetic resonance imaging (fMRI) and the structural basis for such changes using diffusion tensor imaging (DTI). In 11 interictal patients, painful heat threshold + 1°C was applied unilaterally to the forehead during fMRI scanning. ⋯ In 8 patients, fMRI activation in TP with painful heat was exacerbated during migraine, suggesting that repeated migraines may sensitize TP. This article investigates a nonclassical role of TP in migraineurs. Observed temporal lobe abnormalities may provide a basis for many of the perceptual changes in migraineurs and may serve as a potential interictal biomarker for drug efficacy.
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Comparative Study
Intraepidermal nerve fiber loss corresponds to the development of taxol-induced hyperalgesia and can be prevented by treatment with minocycline.
Loss of intraepidermal nerve fibers (IENFs) has been speculated to play a critical role in the development of various neuropathies. In this study, the density of IENFs were studied over time during the induction of Taxol (Bristol-Myers Squibb, NY, USA)-induced chemoneuropathy and compared with the changes in IENFs in animals co-treated with Taxol plus the protective agent minocycline. Rats were injected (intraperitoneally) with 2mg/kg of Taxol every other day for four injections (day 1, 3, 5, and 7). ⋯ Animals receiving minocycline plus Taxol showed no hyperalgesia or loss of IENFs. This study confirms, for the first time, that a loss of IENFs occurs as a neuropathy develops, and further shows a protection against both IENF loss and hyperalgesia with minocycline treatment. The progression of Taxol-induced mechanical hypersensitivity coincides with loss of intraepidermal nerve fibers, and the hyperalgesia and nerve fiber loss were prevented with minocycline treatment.
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Given the complex relationships between fibromyalgia and major depressive disorder (MDD), it has been suggested that fibromyalgia is a "masked" MDD. In experimental settings, fibromyalgia is associated with lowered pain thresholds (hyperalgesia) and deficient pain inhibition. Similarly, it has been recently proposed that the proneness of patients with MDD to develop chronic pain results from a deficit in pain inhibition. This cross-sectional study measured experimentally induced pain perception and inhibition in patients with MDD and patients with fibromyalgia. ⋯ Our results suggest that (1) fibromyalgia and MDD are both associated with signs of hyperalgesia, (2) hyperalgesia is more pronounced in fibromyalgia, and (3) the deficit of pain inhibition is specific to fibromyalgia. As such, these results suggest that there is an overlap between fibromyalgia and MDD, but that fibromyalgia can be distinguished from MDD in terms of DNIC efficacy.
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Am. J. Physiol. Renal Physiol. · Feb 2011
EphrinB2 induces pelvic-urethra reflex potentiation via Src kinase-dependent tyrosine phosphorylation of NR2B.
Recently, the role of EphB receptor (EphBR) tyrosine kinase and their ephrinB ligands in pain-related neural plasticity at the spinal cord level have been identified. To test whether Src-family tyrosine kinase-dependent glutamatergic N-methyl-d-aspartate receptor NR2B subunit phosphorylation underlies lumbosacral spinal EphBR activation to mediate pelvic-urethra reflex potentiation, we recorded external urethra sphincter electromyogram reflex activity and analyzed protein expression in the lumbosacral (L(6)-S(2)) dorsal horn in response to intrathecal ephrinB2 injections. ⋯ Pretreatment with PP2 (50 μM, 10 μl it), an Src-family kinase antagonist, reversed the reflex potentiation, as well as Src kinase and NR2B phosphorylation. Together, these results suggest the ephrinB2-dependent EphBR activation, which subsequently provokes Src kinase-mediated N-methyl-d-aspartate receptor NR2B phosphorylation in the lumbosacral dorsal horn, is crucial for the induction of spinal reflex potentiation contributing to the development of visceral pain and/or hyperalgesia in the pelvic area.