Pain
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Long-term opioid therapy for non-cancer pain has increased. Caution is advised in prescribing for persons with substance use disorders, but little is known about actual health plan practices. This paper reports trends and characteristics of long-term opioid use in persons with non-cancer pain and a substance abuse history. ⋯ Among persons with an opioid disorder, KPNC rates increased from 44.1% to 51.1%, and GH rates increased from 15.7% to 52.4%. Long-term opioid users with a prior substance abuse diagnosis received higher dosage levels, were more likely to use Schedule II and long-acting opioids, and were more often frequent users of sedative-hypnotic medications in addition to their opioid use. Since these patients are viewed as higher risk, the increased use of long-term opioid therapy suggests the importance of improved understanding of the benefits and risks of opioid therapy among persons with a history of substance abuse, and the need for more careful screening for substance abuse history than is the usual practice.
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Substance P (SP) signaling facilitates nociceptive sensitization in various inflammatory and chronic pain models and we postulated that SP signaling might also contribute to the development of post-incisional hyperalgesia. These studies used mice with a deletion of the pre-protachykinin A gene (ppt-A(-/-)) which codes for SP to determine the role of SP signaling in post-incisional pain and in the increased cytokine and nerve growth factor (NGF) expression observed in the incised skin. SP deficient ppt-A(-/-) mice displayed reduced mechanical allodynia and heat hyperalgesia compared to the wild-type (wt) mice at all post-incision time points, despite similar baseline values (p<0.001). ⋯ Hind paw injection of IL-6 and NGF dose dependently produced less mechanical allodynia in the ppt-A(-/-) compared to wt mice. Additionally, SP produced mechanical allodynia in a dose-dependent fashion in wt mice. Therefore, SP supports nociceptive sensitization after hind paw incision and potentially participates directly in modulating the intensity of inflammatory response in peri-incisional tissue.
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The effect of Spinal Cord Stimulation (SCS) in chronic neuropathic pain is inversely related to the severity of mechanical allodynia and the underlying mechanisms are poorly understood. To understand these mechanisms further we aimed to develop a model of SCS in a neuropathic mouse. Further, the CatWalk analysis, which is claimed to be an improved test for mechanical allodynia and therapeutic intervention, was used to analyze the effect of SCS on mechanical allodynia. ⋯ In conclusion, we developed a model of SCS in a chronic neuropathic pain C57BL/6 mouse. The CatWalk gait analysis does not result in the detection of behavioral changes to SCS in mice with chronic neuropathic pain and control animals. This model allows future molecular-genetic studies on the mechanisms of SCS in chronic neuropathic pain.