The journal of pain : official journal of the American Pain Society
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In a Norwegian prospective population-based cohort study, we examined whether the number of chronic musculoskeletal pain sites changed over an 11-year period, and if the number of pain sites at follow-up was associated with health-related and lifestyle factors at baseline. The study included data on 78,973 adults participating in the Nord-Trøndelag Health Study (HUNT) in 1995 to 1997 (HUNT2) and 2006 to 2008 (HUNT3). On the basis of 3 categories of baseline pain sites, associations between baseline health-related, lifestyle, and demographic factors and number of pain sites at follow-up were analyzed with linear regression models adjusted for age, sex, marital status, physical activity, education, and other chronic diseases. ⋯ The within-subject analyses showed largely similar associations for the health-related factors, whereas associations of lifestyle factors were attenuated. The mean number of pain sites remained unchanged between the 2 surveys. Overall, our study revealed prospective associations between several factors and pain sites 11 years later, regardless of the number of pain sites at baseline.
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Stimulation-evoked antinociception (SEA) from the anterior pretectal nucleus (APtN) activates mechanisms that descend to the spinal cord through the dorsolateral funiculus, but the encephalic route followed by the descending pathways from the APtN is not completely known. This study evaluated the changes in the SEA from the APtN in the Wistar rat tail-flick test after lidocaine-induced neural block or N-methyl-d-aspartate-induced neurotoxic lesion of the deep mesencephalic nucleus (DpMe), tegmental pedunculopontine nucleus (PPTg), or lateral paragigantocellular nucleus (LPGi). ⋯ Antinociception did not occur when APtN stimulation was carried out 5 minutes after lidocaine or 6 days after N-methyl-d-aspartate injections into the contralateral DpMe and the ipsilateral LPGi, or into the contralateral PPTg and the ipsilateral LPGi. We conclude that the SEA from the APtN activates 2 descending pain inhibitory pathways, one relaying in the ipsilateral LPGi and another relaying sequentially in the contralateral DpMe and PPTg.