European journal of pain : EJP
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Primary hyperalgesia to mechanical and thermal stimuli are major clinical symptoms of inflammatory pain and can be induced experimentally by ultraviolet-B (UV-B) irradiation in humans. We set-up a pig model in order to have more options for pharmacological intervention on primary hyperalgesia. Pig skin was irradiated with a dose one- to threefold higher than the minimum erythema dose (MED) and investigated for mechanical and heat responsiveness 24 and 48 h post UV-B treatment. ⋯ No significant differences of mechanically or thermally induced hypersensitivity were seen between 24 and 48 h after irradiation. We conclude that UV-B induced mechanical and heat sensitization of primary afferent nociceptors can be assessed in pig skin, providing a new human-like model of primary hyperalgesia. Sensitization of primarily mechano-insensitive (silent) nociceptors, which are underlying the flare response in humans, most probably contributes to the observation presented here.
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A position of scapula depression will maintain the upper trapezius muscle region in a lengthened position, causing excessive strain. This strain could lead to peripheral nociceptive nerves sensitization in the affected area, changing the pressure pain threshold (PPT). Thus, people with a faulty alignment of scapular depression may have lower PPT levels in the upper trapezius region when compared to subjects with normal vertical scapular position. ⋯ An electronic pressure algometer was used to measure the PPT on the upper trapezius muscle region. The results showed a significant difference between groups, with the DS group (19.0+/-9.0 N/cm(2)) demonstrated lower mean PPT values when compared to NS group (26.1+/-9.6 N/cm(2)) (p<0.01). Our results showed that healthy young subjects with depressed scapula position had significant lower upper trapezius PPT values when compared to subjects with normal scapula position.
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Randomized Controlled Trial Multicenter Study
Pregabalin for relief of neuropathic pain associated with diabetic neuropathy: a randomized, double-blind study.
Seven published, randomized, placebo-controlled clinical trials with pregabalin have shown robust efficacy for relief of neuropathic pain from DPN and PHN. An investigation of the efficacy and safety of twice daily pregabalin enrolled 395 adults with painful DPN for > or = 1 year in a 12-week, double-blind, placebo-controlled trial. Patients were randomized to placebo, 150, 300, or 600 mg/day pregabalin (n = 96, 99, 99, and 101). ⋯ Pregabalin 600 mg/day was significantly superior to placebo in improving pain-related sleep-interference scores (p = 0.003), PGIC (p = 0.021), and CGIC (p = 0.009). (Neither pregabalin 150 nor 300 mg/day separated from placebo on these measures, largely because of an atypically large placebo response in one country representing 42% of patients.) All pregabalin dosages were superior to placebo in improving EQ-5D utility scores (all p > or = 0.0263 vs placebo). Pregabalin was well tolerated at all dosages; adverse events were generally mild to moderate. Number needed to harm (discontinuation because of adverse events) was 10.3 for pregabalin 600 mg/day.
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The cost of low back pain (LBP) to employers is high, with an estimated pound 9090 million lost in the United Kingdom in 1998. Economic analysis of LBP has focused on work absence among the employed. There is little research characterising individuals who report reduced duties or who are not in employment because of LBP. ⋯ These findings indicate that the economic impact of LBP may be higher than previously estimated when data on reduced duties is combined with work absence. The additional impact of unemployment due to LBP should also be included in future assessments of the impact of LBP on the workforce.
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Guanethidine displaces noradrenaline from sympathetic varicosities, and blocks sympathetic noradrenergic neurotransmission by inhibiting the release of noradrenaline from depleted neural stores. The aim of this study was to determine whether depletion of noradrenaline with guanethidine would oppose thermal hyperalgesia and/or electrically-evoked pain in mildly-burnt skin. Guanethidine was transferred by iontophoresis into a small patch of skin on the forearm of 35 healthy human subjects. ⋯ These findings indicate that ongoing sympathetic neural discharge does not normally influence thermal hyperalgesia in inflamed skin, because depleting noradrenergic stores had no effect. However, electrically-evoked release of noradrenaline may increase nociceptive sensations. Further clarification of this human pain model could provide insights into the mechanism of adrenergic hyperalgesia in certain neuropathic pain syndromes.