Scandinavian journal of pain
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Background There are a number of false myths about buprenorphine based on unconfirmed animal data, even from isolated animal organs, and early clinical research. These myths came into textbooks on pharmacology and pain about 30 years ago and have been difficult to eradicate. Animal models of pain and pain relief are notoriously unreliable as predictors of human clinical effects. ⋯ Implications Buprenorphine is a well studied and often misunderstood analgesic opioid drug. The evidence base predicts that it will be an increasingly important alternative for treatment of chronic pain conditions caused by cancer and non-cancer diseases. It will continue to be an attractive alternative to methadone for opioid abuse rehabilitation.
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Background and aims Peripheral neuropathic pain (PNeP) is a chronic and disabling condition for which no predictors of response to treatment have yet been identified. Clinical studies show that while many patients with PNeP respond positively to treatment with the capsaicin 8% patch, others do not. This study used quantitative sensory testing (QST) to determine whether any patient characteristics can predict response to treatment with the capsaicin 8% patch. ⋯ Conclusions This study suggests that differences can be identified in the sensory profiles of patients with PNeP who respond to the capsaicin 8% patch and those who do not, specifically pressure pain threshold and degree of allodynia. Notably, both responders and non-responders experienced meaningful reductions in the size of the painful area following treatment. Implications The findings warrant further investigation in a larger number of patients and in prospective trials.
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Background Transient receptor potential ankyrin 1 (TRPA1) is a non-selective cation channel permeable to calcium that is expressed on pain-mediating primary afferent nerve fibers. Here we review recent experimental evidence supporting the hypothesis that activation of the TRPA1 channel by reactive compounds generated in diabetes mellitus, such as 4-hydroxynonenal and methylglyoxal, exerts an important role in the pathophysiology of peripheral diabetic neuropathy (PDN). The hypothesis includes development of the early diabetic pain hypersensitivity and the later loss of cutaneous nerve endings of pain fibers and their dysfunction, which are hallmarks of peripheral diabetic neuropathy (PDN). ⋯ Conclusions Together the in vitro and in vivo results indicate that reactive compounds generated in diabetes exert, through action on the TRPA1 channel, an important role in the pathophysiology of PDN. Sustained activation of the TRPA1 channel is a plausible mechanism that contributes to the early diabetic pain hypersensitivity and the later loss of cutaneous pain fiber endings and their dysfunction with prolonged diabetes. Implications Blocking the TRPA1 channel with a selective antagonist provides a promising disease-modifying treatment for PDN, with only minor, if any, side-effects.