The journal of pain : official journal of the American Pain Society
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There is substantial evidence supporting the notion that the primary somatosensory (S1) cortex is an important structure involved in the perceptional component of pain. However, investigations have mainly focused on other pain-related formations, and few reports have been provided to investigate the synaptic plasticity in the S1 cortex in response to persistent pain. In the present study, we report that bee venom (BV) injection triggered an imbalance between excitatory and inhibitory synaptic transmission in the S1 cortex in rats. ⋯ Perspective: Increased synaptic plasticity was detected in S1 after peripheral nociception, with enhanced excitatory and decreased inhibitory synaptic transmissions. Increased GluR1, and decreased GABAAα1 and GluR2 membrane trafficking were detected. Therefore, the disrupted excitatory/inhibitory balance in transmissions is involved in nociception processing, and S1 can be a potential antinociceptive site.
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Policies that address opioid dose limits may help to decrease high-risk opioid prescribing. We evaluated 3 sequential and progressive decreases in high-dose (HD) opioid limits implemented by Massachusetts Medicaid over 15 years. The study population included members ages 18 to 64 years with ≥1 claim for a schedule II opioid between January 2002 and March 2017. ⋯ The natural log of the AD_MED decreased among members after implementation of 3 sequential and progressive HD prior authorization limits, as did the percentage of members exceeding each of the HD limits. PERSPECTIVE: This study demonstrates the longitudinal impact of a prior authorization policy-based HD limit in a Medicaid population. This study contributes to options for policymakers and other Medicaid programs as a potential strategy to assist in addressing the opioid epidemic.
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Review Meta Analysis
Reward for pain. Hyperalgesia and allodynia induced by operant conditioning: systematic review and meta-analysis.
Learning processes have been discussed in the context of pain chronicity for decades. Particularly, operant conditioning has been used to experimentally induce and modulate pain in healthy humans. In this systematic review and meta-analysis, research findings on pain facilitation (hyperalgesic effect) and pain elicitation (allodynic effect) are evaluated. ⋯ PERSPECTIVE: Operant conditioning can be a mechanism of pain chronicity. All experimental studies investigating this hypothesis have been identified and summarized. It has been demonstrated that allodynic and hyperalgesic effects can be induced by operant conditioning.
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Native Americans (NAs) have a higher prevalence of chronic pain than any other U. S. racial/ethnic group; however, little is known about the mechanisms for this pain disparity. This study used quantitative sensory testing to assess pain experience in healthy, pain-free adults (n = 137 NAs (87 female), n = 145 non-Hispanic whites (NHW; 68 female)) after painful electric, heat, cold, ischemic, and pressure stimuli. ⋯ This could place NAs at risk for future chronic pain and could ultimately lead to a vicious cycle that maintains pain (eg, pain → anxiety/catastrophizing → pain). PERSPECTIVE: NAs experienced heightened sensory, anxiety, and catastrophizing reactions in response to multiple pain stimuli. Given the potential for anxiety and catastrophic thoughts to amplify pain, this characteristic may place them at risk for pain disorders and could lead to a vicious cycle that maintains pain.