Pain
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This case report presents data regarding endogenous opioid analgesia in a healthy female subject prior to developing chronic pain, and again 4 and 13 months following onset of chronic daily back pain. At each assessment period, the subject underwent identical protocols involving two sessions one week apart with randomized double-blind crossover administration of saline placebo and naloxone, an opioid antagonist. Each session included a 5-min anger recall interview, followed by finger pressure and ischemic acute pain tasks. ⋯ The mean magnitude of this opioid blockade effect for the finger pressure task exceeded the 99% confidence interval for the healthy control population based on a previous study using a similar opioid blockade protocol [4]. At 13-month follow-up, naloxone produced a mean 45% decrease in acute pain ratings compared to placebo, arguing against presence of endogenous opioid analgesia. Although results must be interpreted cautiously, findings are consistent with the hypothesis that chronic pain may initially be associated with upregulation of endogenous opioid analgesic systems which then may become dysfunctional over time.
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Activity-dependent slowing of conduction velocity (ADS) differs between classes of human nociceptors. These differences likely reflect particular expression and use-dependent slow inactivation of axonal ion channels and other mechanisms governing axonal excitability. In this study, we compared ADS of porcine and human cutaneous C-fibers. ⋯ We conclude that mechano-insensitive C-fiber nociceptors can be differentiated by their characteristic pattern of ADS which are alike in pig and human. Notably, cold nociceptors with a distinct ADS pattern were first detected in pig. Our results therefore suggest that the pig is a suitable model to study nociceptor class-specific changes of ADS.
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The relationship between persistent pain and self-directed, non-reactive awareness of present-moment experience (i.e., mindfulness) was explored in one of the dominant psychological theories of chronic pain - the fear-avoidance model[53]. A heterogeneous sample of 104 chronic pain outpatients at a multidisciplinary pain clinic in Australia completed psychometrically sound self-report measures of major variables in this model: Pain intensity, negative affect, pain catastrophizing, pain-related fear, pain hypervigilance, and functional disability. Two measures of mindfulness were also used, the Mindful Attention Awareness Scale [4] and the Five-Factor Mindfulness Questionnaire [1]. ⋯ Hierarchical multiple regression analysis showed that mindfulness uniquely predicts pain catastrophizing when other variables are controlled, and moderates the relationship between pain intensity and pain catastrophizing. This is the first clear evidence substantiating the strong link between mindfulness and pain catastrophizing, and suggests mindfulness might be added to the fear-avoidance model. Implications for the clinical use of mindfulness in screening and intervention are discussed.
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Although a large body of evidence has shown that peripheral nerve injury usually induces neuropathic pain, there are also clinical studies demonstrating that injury of the sural nerve, which almost only innervates skin, fails to do so. The underlying mechanism, however, is largely unknown. In the present work, we found that the transection of either the gastrocnemius-soleus (GS) nerve innervating skeletal muscle or tibial nerve supplying both muscle and skin, but not of the sural nerve produced a lasting mechanical allodynia and thermal hyperalgesia in adult rats. ⋯ Spinal application of low dose BDNF (10pg/ml) enabled HFS of the sural nerve to produce homotopic L-LTP. Finally, we found that injury of the GS nerve but not that of the sural nerve up-regulated BDNF in DRG neurons, and that the up-regulation of BDNF occurred not only in injured neurons but also in many uninjured ones. Therefore, the sural nerve injury failing to produce neuropathic pain may be due to the nerve containing insufficient BDNF under both physiological and pathological conditions.
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Randomized Controlled Trial Clinical Trial
Neuronal correlates in the modulation of placebo analgesia in experimentally-induced esophageal pain: a 3T-fMRI study.
Visceral pain/discomfort is the cardinal complaints and treatment targets for functional gastrointestinal disorders (FGID). However, effective treatment for such pain is limited and often associated with high placebo effects. The mechanisms of placebo effects in visceral pain are unclear. ⋯ PAS cannot predict the placebo effect in visceral pain. In conclusion, pronounced placebo analgesia was coupled with prominent changes of brain activity in visceral pain matrix, which are thus likely involved in high placebo efficacy during the treatment of visceral pain in FGID. VLPFC activation during the anticipation of placebo analgesia suggests top-down control in the modulation of pain experience.