Pain
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Comparative Study
Increased bias to report heat or pain following emotional priming of pain-related fear.
Emotional and attentional factors have been identified to play a significant role in modulating pain perception with negative emotions increasing pain sensitivity. Recent studies suggest that fearful images may activate the attentional components of fear driven behaviours and facilitate an attentional bias or sensitivity toward noxious stimuli. The current investigation examines whether priming of pain-related fear will affect performance by increasing sensitivity to punctuate heat stimuli. ⋯ The results indicated a significant facilitation of heat and pain perception at varying temperatures following emotional priming. In particular, there was an increase in the bias toward reporting a heat stimulus following emotional priming. The findings emphasise the efficacy of the visual dot probe task as a method of priming and provide a possible method for probing hypervigilance in chronic pain patients.
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Comparative Study
Role of spinal serotonin 5-HT2A receptor in 2',3'-dideoxycytidine-induced neuropathic pain in the rat and the mouse.
Several lines of evidence suggest that descending serotoninergic facilitatory pathways are involved in neuropathic pain. These pathways may involve 5-HT2A receptors known to play a role in spinal and peripheral sensitization. The implication of this receptor in neuropathy was investigated in a model of peripheral neuropathy induced by 2',3'-dideoxycytidine, a nucleoside analogue with reverse transcriptase inhibitory properties used in HIV/AIDS therapy. ⋯ Four days after 2',3'-dideoxycytidine administration, rats had developed thermal allodynia as well as mechanical hyperalgesia and allodynia, which dose-dependently decreased after epidural injection of MDL 11,939, a 5-HT2A receptor antagonist. Moreover, 5-HT2A receptor knock-out mice did not develop 2',3'-dideoxycytidine-induced neuropathy whereas their control littermates displayed a neuropathy comparable to that observed in rats. Our data show that 2',3'-dideoxycytidine-induced neuropathy is associated with alterations of nociceptive and non-nociceptive peripheral cells and that the 5-HT2A receptor is involved in the peripheral sensitization of nociceptors as well as in a wide central sensitization of dorsal horn neurons.
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Comparative Study
Psychosocial risk markers for new onset irritable bowel syndrome--results of a large prospective population-based study.
Irritable bowel syndrome (IBS) affects up to 22% of the general population. Its aetiology remains unclear. Previously reported cross-sectional associations with psychological distress and depression are not fully understood. ⋯ After adjustment for age, gender and baseline abdominal pain status, high levels of illness behaviour (odds ratio (OR)=5.2; 95% confidence interval (95% CI) 2.5-11.0), anxiety (OR=2.0; 95% CI 0.98-4.1), sleep problems (OR=1.6; 95% CI 0.8-3.2), and somatic symptoms (OR=1.6; 95% CI 0.8-2.9) were found to be independent predictors of IBS onset. This study has demonstrated that psychosocial factors indicative of the process of somatisation are independent risk markers for the development of IBS in a group of subjects previously free of IBS. Similar relationships are observed in other "functional" disorders, further supporting the hypothesis that they have similar aetiologies.
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Comparative Study
C-fiber spontaneous discharge evoked by chronic inflammation is suppressed by a long-term infusion of lidocaine yielding nanogram per milliliter plasma levels.
Nociceptors innervating inflamed tissue acquire an abnormal spontaneous discharge that is believed to be at least part of the reason for the persistent spontaneous pain, allodynia, and hyperalgesia that accompany inflammation. Recent studies suggest that patients with chronic inflammatory pain may obtain an analgesic effect with transdermal application of lidocaine that yields very low plasma levels (130-225 ng/ml). The aim of this study was to investigate whether a 7-day exposure to such low plasma levels of lidocaine had an effect on inflammation-evoked spontaneous discharge in the rat. ⋯ Lidocaine infusion had no effect on the incidence of spontaneous discharge in muscle or cutaneous A-fibers. Lidocaine infusion reduced mechano-hyperalgesia but had no effect on mechano-allodynia or heat-hyperalgesia. We conclude that the analgesic effects seen clinically with transdermal lidocaine administration yielding low plasma levels may be due to a systemic drug action on spontaneously active C-fibers.
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Neuropathic pain consequent to peripheral injury is associated with local inflammation and overexpression of nitric oxide synthases (NOS) and inflammatory cytokines in locally recruited macrophages, Schwann and glial cells. We investigated the time course and localization of nitric oxide synthases (NOS) and cytokines in the central (spinal cord and thalamus) and peripheral nervous system (nerve and dorsal root ganglia), in a mouse model of mononeuropathy induced by sciatic nerve chronic constriction injury. ATP is recognized as an endogenous pain mediator. ⋯ PPADS (25mg/kg) completely reversed nociceptive hypersensitivity and simultaneously reduced the increased NO/NOS system and IL-1beta in both peripheral (injured sciatic nerve and L4-L6 ipsilateral dorsal root ganglia) and central steps of nervous system (L4-L6 spinal cord and thalamus) involved in pain signalling. IL-6 was overexpressed only in the peripheral nervous system and PPADS prolonged administration reduced it in sciatic nerve. In conclusion, we hypothesize that NO/NOS and IL-1beta have a pronociceptive role in this neuropathy model, and that purinergic antagonism reduces pain hypersensitivity by inhibiting their overactivity.