Scandinavian journal of pain
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Background and aims Preclinical data suggest that the chemokine receptor 2 (CCR2) is involved in the pathophysiology of neuropathic pain through modulation of neuronal excitability, synaptic transmission and activation of spinal cord microglia. CCR2-antagonists have shown to be effective in preclinical models of neuropathic pain. The aim of this study was to evaluate the analgesic efficacy, safety and tolerability of a novel CCR2-antagonist, AZD2423, in patients with painful diabetic neuropathy (PDN). ⋯ The NPSI data suggested possible effects on certain sensory components of pain. There were no major safety or tolerability concerns. Implications Treatment with a CCR2-antagonist does not have a clinically important analgesic effect in an overall PDN population.
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Background Peripheral and central sensitisation is prominent in knee osteoarthritis (KOA) and could be important for the reduced efficacy in some cases after as well surgery as pharmacological interventions. Although sensitisation is important in KOA it is not known to what degree it contributes to the overall clinical pain problem. The aim was therefore to investigate how much a combination of quantitative pain measures assessing various pain mechanisms (local and spreading hyperalgesia, temporal and spatial summation, descending inhibition) could predict peak pain intensity in patients with KOA. ⋯ The lack of other correlations between the methods used in assessing pain mechanisms in this study highlights the importance of applying different tests and different pain modalities when assessing the sensitised pain system as different methods add complementary information. Implications Clinical pain intensity can be explained by influences of different central pain mechanisms in KOA. This has implications for pain management in KOA where treatment addressing central pain components may be more important than previously acknowledged.
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Aabstract Background and purpose Women exhibit higher prevalence of most painful disorders. Several explanations have been proposed for this discrepancy, one being that endogenous pain modulatory pathways, which affect incoming nociceptive signals, act differently in men and women. A less efficient pain inhibitory system has been proposed as a contributing factor to explain why women exhibit higher prevalence of most painful disorders. ⋯ Conclusions and implications The present findings indicate that painful contact heat inhibits electrically induced muscle pain and that inhibition was not different between men and women, when women were tested in the interval 12-14 days after their last menstruation. Some inhibition of muscle pain was seen during non-painful conditioning, indicating that nonspecific inhibitory effects were triggered. Also the nonspecific inhibitory effects were similar in men and women.
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Background Neuropathic pain remains a significant challenge with unsatisfactory therapeutic options. Its pathogenesis may involve the neuropathic triad of neuronal, glial and immune cells. Communication between these cells is possibly perpetuated by mitogen-activated protein kinase (MAPK)-signaling. ⋯ Conclusions/implications EGFR-inhibition resulted in dramatic relief of neuropathic pain. A plausible biological explanation involves the interruption of MAPK-signaling. The role of EGFR-inhibition as a target for the treatment of neuropathic pain appears promising and warrants investigation.
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Background and purpose The UV-B model is an established pain model of different types of hyperalgesia in animal and human pain research. Beside the skin region of the sunburn in human volunteers pinprick hyperalgesia has been described in a large zone of non-inflamed skin adjacent to the sunburn. However, there are opposing results on the existence of pinprick hyperalgesia and most notably a controversial discussion is still on-going whether this mechanical hyperalgesia in the undamaged tissue adjacent to and at some distance from the site of inflammation is of peripheral or central origin. ⋯ Furthermore, these findings are in line with other pain models demonstrating comparable central hypersensitivity around the site of injury. Implications As for other pain models this finding provides further evidence that the UV-B model offers secondary mechanical hyperalgesia in addition to its known primary hyperalgesia. Consequently, this is a further validation for the utilisation of the UV-B model in human pain research.