Pain
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Incidence rate estimates of neuropathic pain are scanty and mostly address single types whereas the scope of the disease is wide. We aimed to calculate the incidence rates of neuropathic pain conditions in the Dutch general population and to assess treatment strategies in primary care. The study population included persons registered for at least one year in the Integrated Primary Care Information (IPCI) database between 1996 and 2003. ⋯ Anticonvulsants and tricyclic antidepressants were only used by 4.8 and 4.7% of cases. Neuropathic pain is a rather frequent condition with an annual incidence of almost 1% of the general population and affecting women and middle-aged persons more often. The treatment mostly consisted of regular analgesics suggesting that pharmacological treatment of neuropathic pain is suboptimal.
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Randomized controlled trials and meta-analyses provide evidence for the efficacy of cognitive-behaviourally informed treatment (CBT) programmes for chronic pain. The current study aims to provide practice-based evidence for the effectiveness of CBT in routine clinical settings. Over a 10-year period 1013 pain patients were accepted into a 4 week in-patient pain management programme. ⋯ There was also evidence that a small percentage of patients (1-2%) reliably deteriorated during the period of treatment. The limitations in the inferences that can be drawn from this study and of the methodology are discussed. A case is made for the application of benchmarking methods using data from RCTs in order to more fully evaluate practice and to generate better quality practice based evidence.
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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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Pain is common in adult life, and the extent to which pain interferes with daily activities rises with age. Little is known about the social factors associated with disabling pain. The objective was to determine the individual and neighbourhood social factors that predict pain that interferes with daily activities. ⋯ Whilst the onset of pain which disrupts daily life is influenced mainly by the characteristics of the pain and by the psychological factors, there are links with the social factors, particularly individual measures of perceived income adequacy. The onset of disabling pain is also influenced by the place where one lives. Policies to prevent disabling pain need to consider the contribution of neighbourhood deprivation and income inequalities to the extent of the problem.
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Peripheral nerve injury causes neuropathic pain including mechanical allodynia and thermal hyperalgesia due to central and peripheral sensitization. Spontaneous ectopic discharges derived from dorsal root ganglion (DRG) neurons and from the sites of injury are a key factor in the initiation of this sensitization. Numerous studies have focused primarily on DRG neurons; however, the injured axons themselves likely play an equally important role. ⋯ The function of these accumulated channels was verified by local application of ZD7288, a specific HCN blocker, which significantly suppressed the ectopic discharges from injured nerve fibers with no effect on impulse conduction. Moreover, mechanical allodynia, but not thermal hyperalgesia, was relieved significantly by ZD7288. These results suggest that axonal HCN channel accumulation plays an important role in ectopic discharges from injured spinal nerves and contributes to the development of mechanical allodynia in neuropathic pain rats.