Pain
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Clinical Trial
The expression of pain in infants and toddlers: developmental changes in facial action.
Age-related changes in the facial expression of pain during the first 18 months of life have important implications for our understanding of pain and pain assessment. We examined facial reactions video recorded during routine immunization injections in 75 infants stratified into 2-, 4-, 6-, 12-, and 18-month age groups. Two facial coding systems differing in the amount of detail extracted were applied to the records. ⋯ Temperament was not related to the degree of pain expressed. Systematic variations in parental soothing behaviour indicated accommodation to the age of the child. Reasons for the differing patterns of facial activity are examined, with attention paid to the development of inhibitory mechanisms and the role of negative emotions such as anger and anxiety.
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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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The present study found in lightly anesthetized rats that the radiant heat-evoked tail flick (TF) reflex was markedly inhibited by a unilateral electrical stimulation (a 20 ms train of 0.2 ms, 100 Hz, 30-100 microA pulses) of the ventrolateral orbital cortex (VLO), with the tail flick latency (TFL) being increased. The mean threshold of VLO stimulation for producing inhibition of the TF reflex was 39.2 +/- 8.7 microA (n = 26), and this inhibitory effect increased following increasing stimulation intensity from 40 to 70 microA. The inhibition developed and remained during the stimulation and disappeared rapidly after termination of the stimulation. ⋯ The difference was significant between the TFL changes produced by VLO stimulation before and after PAG lesion (P < 0.01). The results suggest that the antinociception elicited by VLO stimulation is mediated by PAG, leading to activation of the brainstem descending inhibitory system which depresses the nociceptive transmission at the spinal level. The role played by VLO in pain modulation was discussed in association with the proposed endogenous analgesic system consisting of spinal cord-Sm-VLO-PAG-spinal cord.
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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.