Scandinavian journal of pain
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Background Mechanistic, translational, human experimental pain assessment technologies (pain bio markers) can be used for: (1) profiling the responsiveness of various pain mechanisms and pathways in healthy volunteers and pain patients, and (2) profiling the effect of new or existing analgesic drugs or pain management procedures. Translational models, which may link mechanisms in animals to humans, are important to understand pain mechanisms involved in pain patients and as tools for drug development. This is urgently needed as many drugs which are effective in animal models fail to be efficient in patients as neither the mechanisms involved in patients nor the drugs' mechanistic actions are known. ⋯ Mechanism-based pain bio markers can help to qualify the development programmes and at the same time help qualifying them by pain profiling (phenotyping) and recognising the right patients for specific trials. The success rate from preclinical data to clinical outcome may be further facilitated by using specific translational pain bio-markers. As human pain bio markers are getting more and more advanced it could be expected that FDA and EMA in the future will pay more attention to such mechanism-related measures in the approval phase as proof-of-action.
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Objective No single drug is broadly efficacious in the long-term treatment of fibromyalgia syndrome (FMS). Spironolactone is known to ameliorate mood and tension headache or migraine in women with premenstrual syndrome or clinical signs of hyperandrogenism. In a case series of women with treatment resistant FMS spironolactone was therefore added to their medication, and they were observed for at least 12 months. ⋯ The high rate of non-responsive patients underlines that FMS may represent several subgroups. Pain relief and improvement of associated FHS-symptoms and positive effects on additional diseases or dysfunctions give reasons for marked and sustained improvement in the quality of life. Well-controlled, double-blind, and randomised trials are necessary to confirm our potentially very important observations.
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Background and aims We have previously reported that sinomenine, an alkaloid isolated from the root of the plant Sinomenium acutum, had antinociceptive effect in rodent models of acute inflammatory or neuropathic pain. As a traditional medicine, sinomenine is used in China to treat rheumatoid arthritis (RA). Methods In the present study, we evaluated the potential antinociceptive effect of sinomenine in a mouse model of RA, collagen type II antibody (CII Ab) induced arthritis (CAIA) after acute and chronic administration. ⋯ Conclusions We have shown that sinomenine is effective in alleviating localized and spread hypersensitivities in CAIA mice both during acute inflammation and in post-inflammatory phase. Further, repeated sinomenine administration has elevated the baseline mechanical threshold without producing tolerance. Implications Sinomenine may be clinically useful to treat chronic pain in RA, including wide-spread pain which appears to be a difficult clinical problem despite the improvement in the acute treatment of RA by disease modifying agents.
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Background and purpose 'Central sensitization' (CS) may play a major role in maintaining several chronic pain conditions. CS has been proposed to play a significant role in a range of musculoskeletal pain conditions, such as trapezius myalgia, fibromyalgia, temporomandibular disorders, and low back pain. Whether CS varies over time within an individual is not known. ⋯ The study indicates that 'central sensitization' does not explain intra-individual variations in clinical pain. Implications This study raises the question of the role of 'central sensitization' in clinical musculoskeletal pain disorders. Furthermore, a precise definition of the 'central sensitization' concept is called for.
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Background It is unknown why an acute pain condition under various circumstances can transition into a chronic pain condition. There has been a shift towards neuroinflammation and hence glial cell activations specifically in the dorsal root ganglion and spinal cord as a mechanism possibly driving the transition to chronic pain. This has led to a focus on non-neuronal cells in the peripheral and central nervous system. ⋯ Implications Communication between glia and neurons is proposed to be a critical component of neuroinflammatory changes that may lead to chronic pain. Sensory ganglia neurons are surrounded by satellite glial cells but how communication between the cells contributes to altered pain sensitivity is still unknown. Better understanding may lead to new possibilities for (1) preventing development of chronic pain and (2) better pain management.