Pain
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Randomized Controlled Trial
Nocebo hyperalgesia induced by social observational learning.
Nocebo effects can be acquired by verbal suggestion, but it is unknown whether they can be induced through observational learning and whether they are influenced by factors known to influence pain perception, such as pain anxiety or pain catastrophizing. Eighty-five female students (aged 22.5 ± 4.4 years) were randomly assigned to one of three conditions. Participants in the control condition (CC) received information that an ointment had no effect on pain perception. ⋯ The nocebo response correlated with pain catastrophizing but not with pain anxiety or somatosensory amplification. A nocebo response to pressure pain was induced by observational learning but not by verbal suggestion. This finding highlights the importance of investigating the influence of observational learning on nocebo hyperalgesia.
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Oxytocin (OT) and arginine vasopressin (AVP) are 2 neuropeptides that display well-known effects on the reproductive system. Although still controversial, oxytocin and vasopressin were demonstrated to exert potent effects on the nociceptive system when administered directly in various central nervous structures. On the other hand, little is known about their peripheral (hormonal) actions on nociception and pain responses. ⋯ Stress-induced analgesia was transiently lost after i.v. administration of OTR antagonist. Together, the present work provides straightforward evidence that blood levels of OT and AVP modulate nociception, windup plasticity and pain responses. The final target structures explaining these effects remains to be identified but are likely to be C-type nociceptors.
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Few studies have examined abuse of prescription opioids among individuals with chronic pain under buprenorphine/naloxone (Bup/Nx) maintenance. The current 7-week inpatient study assessed oral oxycodone self-administration by patients with chronic pain who had a history of opioid abuse. Participants (n=25) were transitioned from their preadmission prescribed opioid to Bup/Nx. ⋯ However, factors associated with oxycodone preference were lower Bup/Nx maintenance dose, more withdrawal symptoms and more pain. These data suggest that Bup/Nx was effective in reducing pain and supplemental oxycodone use. Importantly, adequate management of pain and withdrawal symptoms by Bup/Nx may reduce oxycodone preference in this population.
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Review Meta Analysis
Evidence for working memory deficits in chronic pain: a systematic review and meta-analysis.
People with chronic pain commonly report impaired cognitive function. However, to date, there has been no systematic evaluation of the body of literature concerning cognitive impairment and pain. Nor have modern meta-analytical methods been used to verify and clarify the extent to which cognition may be impaired. ⋯ High heterogeneity within the field was found with the inclusion of 24 papers using 21 different working memory tests encompassing 9 different working memory constructs and 9 different chronic pain populations. Notwithstanding high heterogeneity, pooled results from behavioural outcomes reflected a consistent, significant moderate effect in favour of better performance by healthy controls and, with the exception of one study, pooled results from physiological outcomes reflected no evidence for an effect. Future research would benefit from the use of clearly defined constructs of working memory, as well as standardised methods of testing.
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Inflammatory processes in the sensory ganglia contribute to many forms of chronic pain. We previously showed that local inflammation of the lumbar sensory ganglia rapidly leads to prolonged mechanical pain behaviors and high levels of spontaneous bursting activity in myelinated cells. Abnormal spontaneous activity of sensory neurons occurs early in many preclinical pain models and initiates many other pathological changes, but its molecular basis is not well understood. ⋯ In vivo knockdown of NaV1.6 locally in the lumbar DRG at the time of DRG inflammation completely blocked development of pain behaviors and abnormal spontaneous activity, while having only minor effects on unmyelinated C cells. Current research on isoform-specific sodium channel blockers for chronic pain is largely focused on NaV1.8 because it is present primarily in unmyelinated C fiber nociceptors, or on NaV1.7 because lack of this channel causes congenital indifference to pain. However, the results suggest that NaV1.6 may be a useful therapeutic target for chronic pain and that some pain conditions may be mediated primarily by myelinated A fiber sensory neurons.