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 mechanisms of chronic pain in irritable bowel syndrome (IBS) have been widely investigated but remain unclear. The present study investigated the relation between visceral hypersensitivity, cutaneous thermal sensitivity, and central pain mechanisms. Rectal sensitivity was assessed with a barostat, and forearm and calf sensitivity with a contact thermode. ⋯ Furthermore, covariance analyses indicated that psychological factors accounted for group differences in visceral hypersensitivity and pain inhibition deficits. In conclusion, this study confirms the relation between altered pain inhibition processes and widespread hypersensitivity in IBS. The present results also suggests that psychological symptoms and altered pain processing in IBS patients may reflect at least in part, common underlying mechanisms.
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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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Pain is a major symptom in 70% of patients with advanced cancer. We analyzed data of 251 cancer patients (142 men and 109 women aged 29-89 years, Karnofsky status 10-90, 65.7+/-13.9) for association of a reduced-function haplotype in the GTP cyclohydrolase 1 (GCH1) gene with cancer pain therapy. ⋯ Thus, reduced GCH1 upregulation, here conferred by non-coding and non-splice site GCH1 variants known to lead to decreased tetrahydrobiopterin expression, delays the need for opioid therapy in cancer. This suggests the future possibility of using partial GCH1 blockade or BH4 inhibition as a prophylactic to prevent or delay the development of cancer pain.