Articles: hyperalgesia.
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Chronic stressful events induce biochemical, physiological and psychological changes, resulting in stress-related neuropsychiatric disorders, such as anxiety or depression. Using repeated social defeat as a stressful event model, we show that this preclinical paradigm induces a transient increase in the expression of the genes encoding the pro-inflammatory molecules iNOS and COX-2. We provide the first demonstration that chronic stress affects spinal plasticity through a mechanism involving local neuroinflammation. ⋯ The present study highlights the adverse effects of chronic stress on spinal neuroinflammation triggering sensory hypersensitivity. Exploration of this phenomenon points out the divergence between pain sensitivity and anxiety-induced hyperalgesia, which is in agreement with clinical observations. Altogether, these data open up new perspectives for clinical research devoted to the evaluation and treatment of pain in anxio-depressive patients.
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To review mechanisms that might contribute to sensory disturbances and sympathetically-maintained pain in complex regional pain syndrome (CRPS). ⋯ Sympathetic neural activity might contribute to pain and sensory disturbances in CRPS by feeding into nociceptive circuits at the site of injury or elsewhere in the CRPS-affected limb, within the dorsal horn, or via thalamo-cortical projections.
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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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This study aimed at investigating in details the spatial characteristics of muscular hyperalgesia after development of delayed onset muscle soreness (DOMS) in the trapezius muscle. High density pressure pain mapping consisting of 36 pain pressure threshold (PPT) recording points were assessed over the trapezius muscle from 20 subjects. PPT were recorded before, immediately after and 24h after eccentric exercise/rest for the exercise group (N=10) and the control group (N=10). ⋯ The hyperalgesia was also mostly developed in the muscle belly sites (P<0.001), further enhancing its position as the most sensitive part of the muscle. The present results showed the topographical distribution of pressure pain sensitivity over the trapezius muscle and also that hyperalgesia developed in a heterogeneous manner over the trapezius muscle in response to eccentric exercise underlining sensory partitioning of the muscle. The technique of high density pressure pain topographical mappings can be helpful in characterizing muscle hyperalgesia and its heterogeneity.
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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.