Articles: hyperalgesia.
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Controlled Clinical Trial
Capsaicin or menthol sensitization induces quantitative but no qualitative changes to thermal and mechanical pain thresholds.
To analyze whether sensitization procedures employed in experimental human pain models introduce additional components to pain measurements resulting in a different kind of pain or whether they are limited to quantitative changes resulting in the same pain at higher intensity. ⋯ The main effect of sensitization by capsaicin or menthol application is a quantitative decrease in thermal and mechanical pain threshold with the methodologic benefit of decreasing the incidence of censored data. A qualitative change in pain thresholds by sensitization is not supported by the present statistical analysis at level of primary hyperalgesia.
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B vitamins can effectively attenuate inflammatory and neuropathic pain in experimental animals, while their efficacy in treating clinical pain syndromes remains unclear. To understand possible mechanisms underlying B vitamin-induced analgesia and provide further evidence that may support the clinical utility of B vitamins in chronic pain treatment, this study investigated effects of thiamine (B1) on the excitability and Na currents of dorsal root ganglion (DRG) neurons that have been altered by nerve injury. ⋯ Thiamine can reduce hyperexcitability and lessen alterations of Na currents in injured DRG neurons, in addition to suppressing thermal hyperalgesia.
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Increasing evidence suggests that chronic stress plays an important role in the pathophysiology of several functional gastrointestinal disorders. We investigated whether cannabinoid receptor 1 (CB1) and vanilloid receptor 1 (TRPV1; transient receptor potential vanilloid 1) are involved in stress-induced visceral hyperalgesia. ⋯ These results suggest that the endocannabinoid (CB1) and TRP (TRPV1) pathways may play a potentially important role in stress-induced visceral hyperalgesia.
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Area-specific representation of mechanical nociceptive stimuli within SI cortex of squirrel monkeys.
While functional imaging studies in humans have consistently reported activation of primary somatosensory cortex (SI) with painful stimuli, the specific roles of subdivisions of areas 3a, 3b, and 1 within SI during pain perception are largely unknown, particularly in the representation of mechanical evoked pain. In this study, we investigated how modality, location, and intensity of nociceptive stimuli are represented within SI by using high-spatial resolution optical imaging of intrinsic signals in Pentothal-anesthetized squirrel monkeys. Perceptually comparable mechanical nociceptive and innocuous tactile stimuli were delivered by indenting the glabrous skin of the distal finger pads with 0.2 and 2mm diameter probes, respectively. ⋯ However, with innocuous tactile stimulation, mainly areas 3b and 1 exhibited response modulation with different levels of stimulation. In summary, mechanical nociceptive inputs are area-specific and topographically represented within SI. We propose that all areas of SI are implicated in encoding the features of mechanical nociception, where areas 3a and 3b are distinctively involved in coding nociceptive and pressure sensation components of stimulation.
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The aim of the study was to evaluate whether or not there exists nociceptive and non-nociceptive hypersensitivity at latent myofascial trigger points (MTrPs). ⋯ These results confirm the existence of nociceptive hypersensitivity at latent MTrPs and provide the first evidence that there exists non-nociceptive hypersensitivity (allodynia) at latent MTrPs. Finally, the occurrence of referred muscle pain is associated with higher pain sensitivity at latent MTrPs.