Articles: hyperalgesia.
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Curr Pain Headache Rep · Dec 2009
ReviewMechanisms by which sleep disturbance contributes to osteoarthritis pain: a conceptual model.
Sleep disturbance is prevalent in aging and painful rheumatologic populations, but it has largely been a neglected dimension of the routine clinical care of arthritis patients. Pain associated with osteoarthritis (OA) is a leading cause of disability worldwide, and factors that contribute to pain in OA are poorly understood. Sleep disturbance is not only a consequence of pain, it is also likely to play an integral role in pain expression. ⋯ This article reviews the extant literature on sleep disturbance and hyperalgesia in patients with OA. We propose a conceptual working model describing pathways by which sleep disturbance interacts directly with central pain processing mechanisms and inflammatory processes, and indirectly with mood and physical functioning to augment clinical OA pain. The clinical and research implications of the model are discussed.
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Curr Pain Headache Rep · Dec 2009
ReviewEnhanced pain perception in rheumatoid arthritis: novel considerations.
Enhanced pain perception is common among patients with rheumatoid arthritis (RA). Given the putative role of proinflammatory cytokines in the development of hyperalgesia, a greater understanding of factors that facilitate increased cytokine expression in RA stands to increase understanding of the sources of enhanced pain perception. Patients with RA have significantly greater stress-induced proinflammatory cytokine release. ⋯ Parasympathetic insufficiency has also been demonstrated, which may enhance pain perception indirectly through disinhibited cytokine expression. Several psychological variables have also been demonstrated to affect pain perception in patients with RA. Identification of factors that contribute to enhanced pain perception in RA may aid in the development of novel analgesic strategies that, in turn, may decrease disease activity and improve general clinical outcomes.
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Most of our knowledge about chronic musculoskeletal pain is based on cutaneous pain models. To test the hypothesis that animals develop chronic muscular hyperalgesia following intramuscular acidic saline injections, primary hyperalgesia within the gastrocnemius muscle was analyzed compared to secondary cutaneous hyperalgesia in the hind paw that develops following intramuscular acid saline injection. Two acidic saline (pH 4) injections were administrated into the gastrocnemius of female CF-1 mice. The results indicate that mice developed a robust hypersensitivity bilaterally in primary (gastrocnemius muscle) secondary (cutaneous hind paw) sites that lasted up to 2 weeks. In addition, primary hyperalgesia correlated well with levels of Fos expression. Fos expression patterns in the spinal cord were different for primary secondary site stimulation. Hind-paw palpation stimulated ipsilateral Fos expression in the superficial spinal laminae at L4/L5 levels, bilaterally in deep laminae at L2-L5 spinal levels. In contrast, gastrocnemius compression stimulated widespread Fos expression in all regions of the ipsilateral dorsal horn within L2-L6 spinal segments. These findings indicate that acidic saline injection induces primary hyperalgesia in muscle that the patterns of Fos expression in response to primary vs secondary stimulation are strikingly different. ⋯ This study assesses primary site muscular pain, which is the main complaint of people with musculoskeletal conditions, and identifies spinal patterns activated by noxious mechanical stimuli to the gastrocnemius. This study demonstrates approaches to test nociception arising from muscle aids in our understanding of spinal processing of primary secondary site hyperalgesia.
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Several studies reported a decreased pain sensitivity in patients with depression, but the underlying neurobiological mechanisms of this phenomenon are unclear. While there is extensive evidence that the serotoninergic system plays a key role in pain modulation, especially in pain inhibitory mechanisms via descending pathways, as well as in the pathophysiology of depression, no study so far has examined its potential relevance in mediating the alteration of pain processing. The present study addresses the question of whether indices of serotoninergic dysfunction, as investigated by a neuroendrocine challenge paradigm, are related to pain sensitivity. ⋯ No such group differences were found with regard to somatosensory thresholds, measures of pain complaints and mood. Subgrouping on the basis of prolactin responsiveness did not reveal significant differences in any parameter. In summary, a decreased pain sensitivity was demonstrated in patients characterized by a reduced neuroendocrine responsiveness to clomipramine, suggesting an involvement of serotoninergic dysfunction underlying altered pain perception in depression.