Pain
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Randomized Controlled Trial Clinical Trial
Ketamine, an NMDA receptor antagonist, suppresses spatial and temporal properties of burn-induced secondary hyperalgesia in man: a double-blind, cross-over comparison with morphine and placebo.
Effects of morphine and ketamine (NMDA receptor antagonist) on temporally summated pain ('wind-up-like pain') and spatial aspects of secondary hyperalgesia were investigated in 12 healthy volunteers. Hyperalgesia was produced by a local 1 degree burn injury covering 12.5 cm2 on the medial surface of the calf. Primary hyperalgesia was determined by measuring heat pain detection threshold (HPDT) within the site of injury. ⋯ Morphine did not significantly change the size of the area of secondary hyperalgesia and did not affect 'wind-up-like pain'. Ketamine or morphine did not change thermal detection thresholds. We conclude that spatial and temporal mechanisms, underlying secondary hyperalgesia, are mediated by glutamatergic transmission via NMDA receptors.
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Clinical Trial Controlled Clinical Trial
The relationship of phantom limb pain to other phantom limb phenomena in upper extremity amputees.
In thirty-two unilateral upper extremity amputees with and without phantom limb pain, various phantom limb phenomena were investigated. In general, the incidence of non-painful phantom limb sensations was higher in patients with phantom limb pain than in pain-free amputees. Kinesthetic and kinetic phantom limb sensations were reported more frequently than exteroceptive cutaneous sensations. ⋯ Patients more frequently assigned sensory than affective pain qualities to their phantom limb pain, whereas no differences between pain qualities were observed for stump pain. No support was found for a relationship between the presence of telescoping (i.e., shrinkage of the phantom limb) and phantom limb pain. These findings point to central as well as to peripheral factors contributing to phantom limb pain.
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This manuscript describes the development and initial validation of a self-report questionnaire designed to assess an individual's readiness to adopt a self-management approach to their chronic pain condition. Theory and preliminary empirical work informed the development of a pool of items that were administered to a sample of individuals reporting chronic pain. ⋯ Each of the four factors, precontemplation, contemplation, action, and maintenance, was found to be internally consistent and stable over time. There was also substantial support for each factor's discriminant and criterion-related validity.
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Wallerian degeneration is required for both neuropathic pain and sympathetic sprouting into the DRG.
Chronic loose constriction of the sciatic nerve produces mechanoallodynia and thermal hyperalgesia in rats and mice, and the behaviour develops during the time in which the nerve distal to the ligature site is undergoing Wallerian degeneration. There is a sympathetic component to the pain generated by this and other rodent models of neuropathic pain, yet the site at which this sympathetic-sensory coupling remains unknown. It has been shown that following sciatic nerve transection or spinal nerve lesion, sympathetic axons invade the dorsal root ganglion (DRG) where they sometimes form pericellular baskets around mostly large diameter DRG neurons--a possible anatomical substrate for sympathetically maintained pain (SMP). ⋯ We found that both indices of neuropathic pain were significantly attenuated in Wld mice compared to wild-type mice, with the wild-type mice increasing in sensitivity to both thermal and mechanical stimulation in the first week post-operative (PO), while Wld mice showed marked hypoalgesia following CCI. Histological examination of the DRG showed that sympathetic sprouting into the DRG was also markedly delayed in Wld mice compared to wild-type mice: 1 week following injury, sympathetic fibres had invaded the ipsilateral DRG of wild-type mice, while sprouting in ipsilateral DRG of Wld mice was only slightly increased at 3 weeks PO. These results show that Wallerian degeneration is tightly linked to the development of both pain and sympathetic sprouting following CCI, and we speculate on the possible role of NGF as a mediator of both phenomena.
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Clinical Trial Controlled Clinical Trial
The clinical significance of behavioral treatment for chronic low back pain: an evaluation of effectiveness.
The clinical effectiveness of behavioral treatment for chronic low back pain (CLBP) was evaluated using an empirical strategy to quantify individual patient change. Patients with CLBP (n = 17) presenting to an outpatient pain clinic were evaluated at baseline and six months posttreatment on variables of pain, disability and distress. Similar patients receiving usual medical care (n = 17) were evaluated on the same outcome measures and time line for purposes of descriptive comparison. ⋯ Forty-seven percent of patients receiving behavioral treatment evidenced clinically significant improvement in at least one of the dimensions of pain, disability and depression associated with CLBP. However, clinically significant improvement across all three measures was rare. These findings are discussed in terms of the viability of behavioral treatment for CLBP, the need to enhance the degree of clinically significant outcome associated with behavioral treatments, and the value of empirical evaluation of clinically significant improvement following treatment interventions.