European journal of pain : EJP
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Recent developments within CBT have emphasized acceptance rather than control of pain and distress in treatments aimed at improving functioning and life quality, but there is still a lack of reliable and valid instruments to assess relevant processes in such interventions. The Psychological Inflexibility in Pain Scale (PIPS) was developed to assess target variables in exposure and acceptance oriented treatments. A preliminary validation study resulted in a two-factor solution with subscales for avoidance and cognitive fusion related to pain, showing satisfactory psychometric properties. ⋯ Notably, hierarchical regression analyses illustrated that PIPS explained more variance than TSK in pain, disability, life satisfaction and depression. Furthermore, PIPS was found to mediate the relationship between e.g. pain and disability, suggesting the usefulness of PIPS as a process measure in treatments of people with chronic pain. Thus, it is argued that this 12-item version of PIPS may be used to explore the importance of psychological in/flexibility in chronic pain and to analyse processes of change in exposure based interventions, as well as for clinicians in tailoring interventions for patients with chronic debilitating pain.
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In animals, decades of research have shown that serotonin (5-HT) is involved in endogenous pain inhibition systems, which are deficient in chronic pain disorders such as fibromyalgia (FM). In humans, there is preliminary evidence showing that 5-HT is involved in the FM pathophysiology. In the current endophenotyping study, we sought to investigate, for the first time in humans, the relationships between the serotonin transporter promoter region (5-HTTLPR) polymorphism and experimentally-induced pain perception/inhibition in healthy controls (HC) and FM patients. ⋯ Our results further confirm that FM is associated with thermal hyperalgesia and deficient DNIC. However, we found no evidence showing that the 5-HTTLPR polymorphism influences pain perception and DNIC. Potential reasons for this negative result will be discussed. Further endophenotyping studies of 5-HT-related gene polymorphisms are required to ascertain the potential relationships between 5-HT and human pain perception/inhibition.
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Withdrawal from analgesic and addictive substances such as opioids or ethanol is associated with increased sensitivity to sensory stimulation in animal models. Here, we investigated perception of innocuous and noxious thermal or electric stimuli applied to the left hand or sternum in 30 male patients undergoing withdrawal from alcohol, 30 male abstained alcoholics and matched controls. The alcohol withdrawal scale and the Banger score were obtained to estimate the severity of withdrawal. ⋯ No differences were found between patients of the abstained group and control subjects for any pain parameter. In conclusion, we demonstrate withdrawal-induced hyperalgesia upon thermal stimulation in patients. Since the influence of affective symptoms on pain perception during withdrawal is remarkable, we assume that peripheral and central mechanisms might account for this finding, which should be assessed in detail in future studies.
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Tricyclic antidepressants (TCAs) are among the first line treatments clinically recommended against neuropathic pain. However, the mechanism by which they alleviate pain is still unclear. Pharmacological and genetic approaches evidenced a critical role of delta-opioid receptors (DORs) in the therapeutic action of chronic TCA treatment. ⋯ Moreover, morphine induced an acute analgesia in control and in neuropathic wild-type mice, but was without effect in MOR-deficient mice. While MORs are crucial for morphine action, they are not critical for nortriptyline action. Our results highlight the functional difference between DORs and MORs in mechanisms of pain relief.
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Painful diabetic neuropathy may be due to impairments in descending modulation of nociceptive transmission at the spinal cord. In the present study, streptozotocin diabetic rats (STZ rats) with neuropathic symptoms (mechanical hypersensitivity) were used to perform a time-course evaluation of neuronal activity at the spinal dorsal horn and at the periaqueductal grey matter (PAG), a major brainstem area of pain modulation. The expression of Fos protein, a marker of nociceptive activation, progressively increased at the spinal dorsal horn at 4 and 10 weeks. ⋯ The present study shows that diabetic neuropathy is accompanied by a progressive increase of the spontaneous neuronal activity at the spinal cord. Changes in descending modulation of nociceptive transmission from the PAG are likely to occur during diabetic neuropathy, probably with exacerbation of facilitatory actions. The effects of gabapentin in reversing the behavioural signs of diabetic neuropathy and neuronal hyperactivity in the spinal cord and PAG reinforce the central causes of diabetic neuropathy and point to the central targets of the drug.