Pain
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Multicenter Study
Pain-related catastrophizing and perceived social responses: Inter-relationships in the context of chronic pain.
Pain-related coping, particularly catastrophizing, plays a significant role in shaping pain responses. One way catastrophizing is hypothesized to amplify pain and disability is via its effect on patients' social environments (e.g., communal coping model), though empirical support is limited. The present study tested whether the association between catastrophizing and deleterious pain-related outcomes was mediated by patients' perceptions of significant others' responses to their pain in a sample of 1356 pain patients. ⋯ In sum, perceived social responses were found to play a small role in mediating the relationship between catastrophizing and pain-related outcomes, and these mediational effects may be strongest in particular patient subgroups. The present data suggest that interpersonal mechanisms may not constitute a primary route by which catastrophizing exerts its maladaptive effects on pain responses. The study and further understanding of what principal factors mediate catastrophizing's deleterious effects on pain will be important in illuminating the biopsychosocial model of pain.
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This study used positron emission tomography (PET) and [11C]diprenorphine to compare the in vivo distribution abnormalities of brain opioid receptors (OR) in patients with peripheral (n=7) and central post-stroke pain (CPSP, n=8), matched for intensity and duration. Compared with age- and sex-matched controls, peripheral neuropathic pain (NP) patients showed bilateral and symmetrical OR binding decrease, while in CPSP binding decrease predominated in the hemisphere contralateral to pain. In CPSP patients, interhemispheric comparison demonstrated a significant decrease in opioid binding in posterior midbrain, medial thalamus and the insular, temporal and prefrontal cortices contralateral to the painful side. ⋯ While bilateral binding decrease in both NP groups may reflect endogenous opioid release secondary to chronic pain, the more important and lateralised decrease specific to CPSP suggests opioid receptor loss or inactivation in receptor-bearing neurons. Opioid binding decrease was much more extensive than brain anatomical lesions, and was not co-localised with them; metabolic depression (diaschisis) and/or degeneration of OR neurons-bearing secondary to central lesions appears therefore as a likely mechanism. Central and peripheral forms of NP may differ in distribution of brain opioid system changes and this in turn might underlie their different sensitivity to opiates.
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The analgesic effects of local administration of opioid agonists into peripheral tissues in alleviating pain have been well documented in both clinical and preclinical studies, although few studies have examined their effects in neuropathic pain. In this study, we investigated the anti-allodynic effects of peripherally acting delta opioid receptor (DOR) agonists in a rat model of neuropathic pain. Peripheral nerve injury (PNI) produced a time-dependent decrease in mechanical withdrawal thresholds that was attenuated by local administration into the hind paw of either morphine or the DOR agonist deltorphin II. ⋯ Results obtained from immunohistochemical studies confirmed up-regulation in small and large DRG neurons in neuropathic compared to sham animals. Additionally, there was an increase in DOR protein within the ipsilateral sciatic nerve of neuropathic animals compared to sham and contralateral neuropathic conditions indicating the occurrence of receptor trafficking to the site of injury. Taken together, our findings suggest that functional peripheral DORs are present in sensory neurons following PNI and validate the development of selective DOR agonists for alleviating neuropathic pain.