Pain
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Comparative Study
Prostaglandin E2 in the midbrain periaqueductal gray produces hyperalgesia and activates pain-modulating circuitry in the rostral ventromedial medulla.
Recent years have seen significant advances in our understanding of the peripheral and spinal mechanisms through which prostaglandins contribute to nociceptive sensitization. By contrast, the possibility of a supraspinal contribution of these compounds to facilitated pain states has received relatively little attention. One possible mechanism through which prostaglandins could act supraspinally to facilitate nociception would be by recruitment of descending facilitation from brainstem pain-modulating systems. ⋯ Microinjection of PGE(2) (50 fg in 200 nl) into the PAG produced a significant decrease in paw withdrawal latency. The PGE(2) microinjection activated on-cells, RVM neurons thought to facilitate nociception, and suppressed the firing of off-cells, RVM neurons believed to have an inhibitory effect on nociception. These data demonstrate a prostaglandin-sensitive descending facilitation from the PAG, and suggest that this is mediated by on- and off-cells in the RVM.
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Comparative Study
Site 1 sodium channel blockers prolong the duration of sciatic nerve blockade from tricyclic antidepressants.
Many recent reports in the literature address the local anesthetics efficacy of tricyclic antidepressants (TCAs). Here we investigated whether nerve block from TCAs is prolonged by site 1 sodium channel blockers such as tetrodotoxin and saxitoxin, which are known to prolong block from conventional local anesthetics. Tetrodotoxin and saxitoxin greatly prolonged block from TCAs. ⋯ Systemic (subcutaneous) delivery of tetrodotoxin or amitriptyline did not result in prolongation of block from the other class of drug injected at the sciatic nerve. In TCA-containing formulations, motor blockade was consistently longer than thermal nociceptive block; motor blockade was also prolonged by tetrodotoxin and saxitoxin. In summary site 1 sodium channel blockers prolong the duration of TCAs via a locally mediated mechanism.
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The main aim of this study was to explore the occurrence and changes of neck pain in pain-free preadolescents. The evaluation was performed at 1- and 4-year follow-ups. Of the pain-free preadolescents, 366 (71.9%) completed structured pain questionnaires at 1 and 4 years. ⋯ This study strengthens the results of the previous cross-sectional studies that occurrence of neck pain increases with age, and that neck pain becomes more common among girls than boys in adolescence. Among preadolescents who were originally pain-free, there was only a small proportion who reported frequent neck pain at both 1 and 4 years. It also showed that the frequency of neck pain reflects the intensity of pain fairly well.