European journal of pain : EJP
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Little is known about the factors that predict the transition of acute, time limited pain to chronic pathological pain following postero-lateral thoracotomy. The aim of the present prospective, longitudinal study was to determine the extent to which (1) pre-operative pain intensity, pain disability, and post-traumatic stress symptoms (PTSS) predict post-thoracotomy pain disability 6 and 12 months later; and (2) if these variables, assessed at 6 months, predict 12 month pain disability. Fifty-four patients scheduled to undergo postero-lateral thoracotomy for intrathoracic malignancies were recruited before surgery and followed prospectively for one year. ⋯ This suggests that pain may serve as a traumatic stressor which causes increased emotional numbing. The results also support recent suggestions that avoidance and emotional numbing constitute separate PTSS clusters. Further research is required to determine the source(s) of emotional numbing after postero-lateral thoracotomy and effective interventions.
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Diabetes mellitus is the leading cause of peripheral neuropathy worldwide. Despite this high level of incidence, underlying mechanisms of the development and maintenance of neuropathic pain are still poorly understood. Evidence supports a prominent role of glial cells in neuropathic pain states. ⋯ Astrocytic activation in this model appears to be limited and is unaffected by Gabapentin treatment. Consequently, spinal microglial activation is a key mechanism underlying diabetic neuropathy. Furthermore, we suggest that Gabapentin may exert its anti-allodynic actions partially through alterations of microglial cell function.
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Dorsal horn neuron (DHN) sensitization can be induced and maintained by nociceptor activation. In previous studies, only a small increase in ongoing DHN activity was present immediately after plantar incision; yet, powerful activation of nociceptors was prominent 1 day after incision. In the present study, rats underwent plantar incision or sham surgery as control. ⋯ This study demonstrates that 1 day after incision, DHN sensitization manifests in markedly increased spontaneous activities, enhanced responses to mechanical stimuli and expanded receptive fields (RFs). Separate groups of neurons appear to transmit spontaneous activity and enhanced responses to mechanical stimuli. Inhibition of spontaneous activity by blockade of afferent input indicates that the prolonged spinal hyperactivity remains largely dependent on the ongoing primary afferent activity.
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Osteoarthritis (OA) is associated with chronic debilitating joint pain. Pain is the result of an emotional and sensory experience and preclinical models of OA can thus be useful to better understand the underlying mechanisms of the disease and test new therapeutic options. We induced unilateral knee OA in Sprague-Dawley rats using monosodium iodoacetate (MIA), a glycolysis inhibitor and assessed the effects of acute and chronic morphine and gabapentin using a battery of quantitative behavioural outcome measures of pain and disability. ⋯ These measures were significantly reduced after both acute (13.3% of sham response, p<0.01, von Frey 6g) and chronic (38.3%, p<0.05) morphine whilst only chronic gabapentin (37.0%, p<0.05) had an effect. We show the reliability of the model in terms of mechanical hypersensitivity and demonstrate cooling hypersensitivity and ambulatory-evoked pain. In terms of translational research, the effects of morphine and gabapentin validate the model and suggest trials of these therapeutic approaches in OA patients.
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Temporomandibular disorders represent one of the major challenges in dentistry therapeutics. This study was undertaken to evaluate the time course of carrageenan-induced inflammation in the rat temporomandibular joint (TMJ) and to investigate the role of tachykinin NK(1) receptors. Inflammation was induced by a single intra-articular (i.art.) injection of carrageenan into the left TMJ (control group received sterile saline). ⋯ Treatment with SR140333 substantially inhibited the increase in plasma extravasation and leukocyte influx at 4 and 24h, as well as the production of TNFalpha and IL-1beta into the joint cavity, but failed to affect changes in head-withdrawal threshold. The results obtained from the present TMJ-arthritis model provide, for the first time, information regarding the time course of this experimental inflammatory process. In addition, our data show that peripheral NK(1) receptors mediate the production of both TNFalpha and IL-1beta in the TMJ as well as some of the inflammatory signs, such as plasma extravasation and leukocyte influx, but not the nociceptive component.