Pain
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When opioid therapy is initiated for a new pain condition, it may be unknown whether the pain will persist beyond the time of tissue healing. The aim of this study was to determine the prevalence of prescription patterns indicating persistent and/or problematic opioid use in a cohort of opioid-naive patients starting therapy with weak opioids. Data were drawn from the nationwide Norwegian Prescription Database. ⋯ Of these subjects, 686 patients were dispensed more than 365 DDDs of opioids in 2008 and are probably persistent users. There were 191 subjects who met our criteria for probable problematic opioid use. In a cohort of new opioid users who started treatment with weak opioids, only 0.3% and 0.08% developed prescription patterns indicating persistent opioid use and problematic opioid use, respectively.
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The present study examined existing communal and operant accounts of children's pain behavior by looking at the impact of parental presence and parental attention upon children's pain expression as a function of child pain catastrophizing. Participants were 38 school children and 1 of their parents. Children completed a cold pressor pain task (CPT) twice, first when told that no one was observing (alone condition) and subsequently when told that they were being observed by their parent (parent-present condition). ⋯ Specifically, low-catastrophizing children expressed more pain in the presence of their parent, whereas high-catastrophizing children showed equally pronounced pain expression when alone or in the presence of a parent. Furthermore, children's catastrophizing moderated the impact of parental attention upon facial displays and self-reports of pain; higher levels of parental nonpain talk were associated with increased facial expression and self-reports of pain among high-catastrophizing children; for low-catastrophizing children, facial and self-report of pain was independent of parental attention to pain. The findings are discussed in terms of possible mechanisms that may drive and maintain pain expression in high-catastrophizing children, as well as potential limitations of traditional theories in explaining pediatric pain expression.
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This study examined processes that contribute to the changing painfulness of a repeatedly presented thermal (heat) stimulus. The 3-second pulses were presented to the side of the hand at a rate of 4/min, too slow to engage wind-up. Over the course of 32 trials, pain intensity (measured by verbal report on a 0-100 scale) first declined and then (in most cases) rose again, indicating adaptation and sensitization, respectively. ⋯ Adaptation and sensitization were comparable in participants with fibromyalgia, temporomandibular disorders, and in healthy controls, indicating that these processes occur before the perceptual amplification that characterizes fibromyalgia and temporomandibular disorders. The ability of vibration to reduce pain has previously been shown to involve segmental inhibition; the finding in the present study that vibratory gating of pain is significantly (inversely) related to the rate of sensitization suggests that the latter also reflects segmental processes. Several lines of evidence thus point to the conclusion that adaptation and sensitization occur at early stages of sensory information processing.
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This systematic investigation of the neurocognitive correlates of complex regional pain syndrome (CRPS) in a single case also reports agnosia for object orientation in the context of persistent CRPS. We report a patient (JW) with severe long-standing CRPS who had no difficulty identifying and naming line drawings of objects presented in 1 of 4 cardinal orientations. In contrast, he was extremely poor at reorienting these objects into the correct upright orientation and in judging whether an object was upright or not. ⋯ The neuroanatomical correlates are discussed. The patient had no structural brain lesion, raising the possibility that nonstructural reorganisation of cortical networks may be responsible for his deficits. Other patients with CRPS may have related neurocognitive defects.