The journal of pain : official journal of the American Pain Society
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The nonmedical use of prescription opioids (POs), and related harmful consequences, has increased in many populations in recent years in North America. Existing survey data are typically limited to descriptive prevalence statistics, and fail to examine important determinants or circumstances (including motives) of nonmedical PO use. We advocate that such analytical queries should become integral elements in future surveys. Developing the needed survey items, however, requires conceptual thoughtfulness and rigor, especially given POs' potential for both therapeutic (eg, analgesic) effects and abuse. These considerations are concretely relevant for possible "self-medicating" nonmedical usage of POs as well as with regards to varying definitions of "pain." Furthermore, we support the harmonization of survey items on nonmedical PO use to allow for cross-national comparisons, yet also call for cross-cultural examinations into the determinants of the currently vastly discrepant medical and nonmedical PO use rates across Western countries. ⋯ We support Zacny and Lichtor's call for systematic examination of motives presented by individuals engaging in nonmedical prescription opioid use. Such motives could relate to factors instrinsic or extrinsic to the user, yet their understanding is crucial for the devising of evidence-based interventions.
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Characterization of a model of chronic orofacial hyperalgesia in the rat: contribution of NA(V) 1.8.
The purpose of this study was to develop and characterize a model of orofacial inflammatory hyperalgesia. Injection of complete Freund's adjuvant (CFA) into the upper lip/whisker pad of the rat produced significant and long-lasting thermal (> or =14 days) and mechanical (> or =28 days) hyperalgesia in the area of CFA injection. Both indomethacin and morphine, given systemically, significantly attenuated thermal hyperalgesia; the effect of morphine was shown to be opioid receptor-mediated. We also examined the contribution of the tetrodotoxin-resistant voltage-gated sodium channel Na(v)1.8 in CFA-produced orofacial mechanical hypersensitivity. Na(v)1.8 mRNA was increased > or =2.5-fold in trigeminal ganglion neurons 1 and 2 weeks after CFA treatment, and Na(v)1.8 protein was increased in the infraorbital nerve over a similar time course. The changes observed were time-dependent and had returned to baseline when examined 2 months after inflammation; there were no changes in Na(v)1.9 mRNA in trigeminal ganglion neurons after CFA treatment. In support of this, Na(v)1.8 antisense oligodeoxynucleotide treatment significantly attenuated CFA-produced mechanical hypersensitivity. These results document development of a model of inflammatory orofacial hyperalgesia, which, consistent with other reports, indicate a contribution of tetrodotoxin-resistant, voltage-gated sodium channel Na(v)1.8. ⋯ Orofacial hypersensitivity develops postoperatively as a routine course of orofacial surgery, and mechanical allodynia is characteristic of temporomandibular joint disorder. The results described in this report are novel with respect to the duration of orofacial hypersensitivity produced and suggest that pharmacological targeting of the voltage-gated sodium channel Na(v)1.8 may be useful in managing hypersensitivity.