Pain
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The important role of operant learning in the development and maintenance of chronic pain is widely recognized. A specific type of reinforcement based on the reduction of painful stimulation when a person's perception changes in the desired direction has been termed intrinsic reinforcement of pain. In the present study, the role of intrinsic operant learning in chronic pain was tested in fibromyalgia (FM) patients with and without comorbid irritable bowel syndrome (IBS) compared with healthy persons. ⋯ Whereas healthy persons learned perceptual changes according the experimental protocol, both patient groups failed to show normal operant perceptual learning: FM patients without IBS demonstrated sensitization learning comparable to that in healthy persons, but unexpectedly these patients learned even more pronounced sensitization in the habituation learning condition, contradicting the experimental protocol; FM patients with IBS demonstrated neither learning of enhanced sensitization nor enhanced habituation; no signs of differential operant learning were observable. Thus, operant perceptual learning was impaired in FM patients; whether learning of both enhanced perceptual sensitization and habituation was impaired depended on the presence of comorbid IBS and could not be explained by other clinical characteristics of the patients such as pain threshold, duration of pain, depressive symptoms, or anxiety. While healthy participants learned sensitization and habituation according to an operant task, FM patients without IBS showed enhanced sensitization and FM with IBS no learning.
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Glycine inhibitory dysfunction provides a useful experimental model for studying the mechanism of dynamic mechanical allodynia, a widespread and intractable symptom of neuropathic pain. In this model, allodynia expression relies on N-methyl-d-aspartate receptors (NMDARs), and it has been shown that astrocytes can regulate their activation through the release of the NMDAR coagonist d-serine. Recent studies also suggest that astrocytes potentially contribute to neuropathic pain. ⋯ These results suggest the following scenario: removal of glycine inhibition makes tactile stimuli able to activate astrocytes; activated astrocytes may provide d-serine to enable NMDAR activation and thus allodynia. Such a contribution of astrocytes to pathological pain fuels the emerging concept that astrocytes are critical players in pain signaling. Glycine disinhibition makes tactile stimuli able to activate astrocytes, which may provide d-serine to enable NMDA receptor activation and thus allodynia.
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This study compared individuals with fibromyalgia (FM) and individuals with chronic low back pain (CLBP) on repetition-induced summation of activity-related pain (RISP). Fear of movement, pain catastrophizing and depression were examined as potential mediators of group differences. The sample consisted of 50 women with FM and 50 women with CLBP who were matched on age, pain severity and pain duration. ⋯ Discussion addresses the processes by which individuals with FM might have increased RISP responses. The findings of this study point to possible neurophysiological mechanisms that could help explain the high levels of pain-related disability seen in individuals with FM. Patients with fibromyalgia showed greater activity-related summation of pain than patients with chronic low back pain.
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Insomnia is a common problem for people with chronic pain. Cortical GABAergic neurons are part of the neurobiological substrate that underlies homeostatic sleep regulation. In the present study, we confirmed that sciatic nerve ligation caused thermal hyperalgesia and tactile allodynia in mice. ⋯ These findings provide novel evidence that sciatic nerve ligation decreases extracellular-released GABA in the cingulate cortex of mice. These phenomena may, at least in part, explain the insomnia in patients with neuropathic pain. Neuropathic pain-like stimuli suppress the GABAergic transmission with increased GABA (γ-aminobutyric acid) transporters located on activated astrocytes in the cingulate cortex related to sleep disturbance.