The Clinical journal of pain
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Research on the pathophysiology of chronic pain has begun to challenge the traditional diagnostic and treatment paradigms for the patient with neuropathic pain. The heterogeneous nature of neuropathic pain indicates that more than one anatomic lesion is most likely responsible for the clinical presentation of a particular syndrome. Numerous pharmacologic agents that have shown improved efficacy in the treatment of neuropathic pain have been developed over the past decade. For the practicing clinician, an important concern is whether the current paradigm for classification of neuropathic pain syndromes is comprehensive enough to address this rapidly expanding body of knowledge.
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Randomized Controlled Trial Clinical Trial
Flumazenil potentiation of postoperative morphine analgesia.
The goal of this study was to test the effect of concomitant administration of flumazenil (FL) and morphine (MO) on immediate postoperative analgesia and the MO requirement to control pain in human beings. ⋯ Flumazenil afforded lower MO consumption during the immediate postoperative period. Cognitive, hemodynamic, and respiratory functions were better after MO plus FL than after MO alone.
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The goal of this study was to assess physician consultation and use of medication in Dutch children and adolescents (0-18 years old) having chronic pain in relation to sociodemographic factors and pain characteristics. ⋯ Chronic pain is a common complaint in children and adolescents, frequently resulting in consultation of a physician and medication use. Regarding physician consultation, children and adolescents with a lower educational level seem to be a group at risk.
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Although pain is always intense and unpleasant, the capacity to experience this sensation is, under normal circumstances, fundamental to the preservation of bodily integrity. Clinically, however, after injury to peripheral tissue or directly to the nervous system, spontaneous and evoked pain manifest that serve no physiologic function, are crippling to patients, and are difficult to treat. ⋯ This spinal neuronal plasticity is shown to be a key contributor to pathologic pain hypersensitivity. The potential for the molecular mechanisms responsible for the spinal plasticity in revealing new targets for future treatment is also discussed.