Pain
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Tibia fracture in rats initiates a cascade of nociceptive, vascular, and bone changes resembling complex regional pain syndrome type I (CRPS I). Previous studies suggest that the pathogenesis of these changes is attributable to an exaggerated regional inflammatory response to injury. We postulated that the pro-inflammatory cytokine tumor necrosis factor alpha (TNF) might mediate the development of CRPS-like changes after fracture. ⋯ After fracture the rats developed hindpaw mechanical allodynia and unweighting, which were reversed by sTNF-R1 treatment. Consistent with the behavioral data, spinal Fos increased after fracture and this effect was inhibited by sTNF-R1 treatment. Collectively, these data suggest that facilitated TNF signaling in the hindlimb is an important mediator of chronic regional nociceptive sensitization after fracture, but does not contribute to the hindlimb warmth, edema, and bone loss observed in this CRPS I model.
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Trying to control pain is a common human goal. But little is know about what happens when one loses control over pain. This paper reports an experiment with 74 healthy volunteers, half of whom were given control over a pain stimulus and subsequently lost control, and half of whom never had control over the pain. ⋯ These findings are discussed within the context of a dual process model of coping with uncontrollable adverse events [Brandtstädter J, Renner G. Tenacious goal pursuit and flexible goal adjustment: explication and age-related analysis of assimilative and accommodative strategies of coping. Psychol Aging 1990;5:58-67] and possible mechanisms for perseverance with ineffective solutions.
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Painful hypersensitivity to norepinephrine (NE) has been reported in various chronic pain conditions that exhibit sympathetically-maintained pain (SMP), particularly CRPS-I and II. We investigated the parallels between the nociceptive and vascular sensitivity to NE in rats with chronic post-ischemia pain (CPIP), an animal model of CRPS-I induced by hind paw ischemia-reperfusion injury. Intradermal injections of NE to the affected hind paw induced dose-dependent nociceptive behaviours in CPIP rats, but not sham animals. ⋯ These results suggest CPIP rats display abnormal nociceptive responses to adrenergic and non-adrenergic vasoconstrictive agents. Furthermore, the nociceptive responses to NE in CPIP rats are paralleled by enhanced vasoconstrictive responses to NE, and are relieved by alpha-adrenergic antagonists or a vasodilator. We conclude that persistent tissue ischemia and hypersensitivity to sympathetic vasoconstriction are important mechanisms for pain in CPIP rats, and that either reducing vasoconstriction or enhancing vasodilatation may be effective methods of relieving the pain of CRPS-I.
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Attenuation of the lower limb nociceptive flexion reflex (NFR) during the cardiac cycle has been attributed to inhibition of sensorimotor function by arterial baroreceptor activation. It has been proposed that cardiopulmonary baroreceptors might have similar inhibitory effects. ⋯ Nociceptive responding and pain ratings did not differ between postures suggesting no cardiopulmonary effects. This phasic modulation of the upper limb withdrawal response provides further support for arterial baroreceptor-mediated inhibition of nociceptive transmission.