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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the underlying cause of pathophysiological mechanisms triggering multiple chemical sensitivity (MCS) remains disputed.Recently, alterations in the central nervous system, for example,central sensitization, similar to various chronic pain disorders, have been suggested. Capsaicin is used in experimental pain models to provoke peripheral and central sensitization. In patients with symptoms elicited by odorous chemicals capsaicin-induced secondary hyperalgesia and temporal summation were assessed as markers for abnormal central nociceptive processing together with neurogenic inflammation (flare). ⋯ this is the first study to show facilitated pain processing in MCS and EC patients with the most abnormal responses in MCS.
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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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Although spinal cord stimulation (SCS) is an established treatment for chronic neuropathic pain, pain relief is still not successful in a large group of patients. We suggest that the success of SCS may be related to the timing of SCS during the development of chronic neuropathic pain. We therefore compared the effect of SCS applied after 24h of neuropathic pain (early SCS) and after 16days of neuropathic pain (late SCS). ⋯ In more than half of these animals, pre-stimulation withdrawal thresholds were reached only the next day. Early SCS resulted in an increased number of responders to SCS and furthermore an increased duration of the effect of SCS as compared to late SCS. Early SCS treatment of neuropathic rats is more effective as compared to the late SCS treatment.