Articles: hyperalgesia.
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Annals of neurology · Feb 2008
Editorial CommentA touch of increased pain: cutaneous allodynia in migraine.
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Guanethidine displaces noradrenaline from sympathetic varicosities, and blocks sympathetic noradrenergic neurotransmission by inhibiting the release of noradrenaline from depleted neural stores. The aim of this study was to determine whether depletion of noradrenaline with guanethidine would oppose thermal hyperalgesia and/or electrically-evoked pain in mildly-burnt skin. Guanethidine was transferred by iontophoresis into a small patch of skin on the forearm of 35 healthy human subjects. ⋯ These findings indicate that ongoing sympathetic neural discharge does not normally influence thermal hyperalgesia in inflamed skin, because depleting noradrenergic stores had no effect. However, electrically-evoked release of noradrenaline may increase nociceptive sensations. Further clarification of this human pain model could provide insights into the mechanism of adrenergic hyperalgesia in certain neuropathic pain syndromes.
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The aim of the study was to investigate if an abnormal brain response to pain exists in patients with myofascial pain syndrome (MPS) when stimulated in a hypersensitive myofascial trigger point (MTP). Event-related functional magnetic resonance imaging was used to characterize the brain response to pain evoked from an MTP. Activation patterns from patients were compared with those evoked from an equivalent site in healthy controls with stimulus intensity matched and pain intensity matched stimuli. ⋯ At matched pain intensity, enhanced activity was found in the same somatosensory areas but not in limbic areas. Our results show that the hyperalgesic state observed in MPS patients was associated with abnormal hyperactivity in regions processing stimulus intensity and negative affect. We speculate that suppressed hippocampal activity might reflect stress-related changes in relation to chronic pain as an effective physical and emotional stressor.
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To investigate allodynia in patients with different primary headaches. ⋯ Allodynia is not specific to migraine but is frequent in all headache patients: acute allodynia was reported in half those interviewed and in over a third of patients in each headache category; interictal allodynia was reported by nearly 25%.
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Brain Behav. Immun. · Feb 2008
IL-1 beta signaling is required for mechanical allodynia induced by nerve injury and for the ensuing reduction in spinal cord neuronal GRK2.
Many neurotransmitters involved in pain perception transmit signals via G protein-coupled receptors (GPCRs). GPCR kinase 2 (GRK2) regulates agonist-induced desensitization and signaling of multiple GPCRs and interacts with downstream molecules with consequences for signaling. In general, low GRK2 levels are associated with increased responses to agonist stimulation of GPCRs. ⋯ Moreover, spinal cord GRK2 expression was not decreased in IL-1R(-/-) mice after L5 SNT. These data show that IL-1 beta signaling is not only required for the development of mechanical allodynia, but also to reduce neuronal GRK2 expression. These results suggest a functional relation between the L5 SNT-induced IL-1 beta-mediated decrease in GRK2 and development of mechanical allodynia.