Der Schmerz
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Chest pain is a symptom commonly reported by persons in the general population and represents a differential diagnostic challenge. ⋯ There is a need for controlled studies on the symptomatic treatment of pain in irritable esophagus, non-cardiac chest pain, postmastectomy and poststernotomy syndromes.
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Abdominal and thoracic surgical procedures can result in significant acute postoperative pain. Present evidence shows that postoperative pain management remains inadequate especially after "minor" surgical procedures. Various therapeutic options including regional anesthesia techniques and systemic pharmacotherapy are available for effective treatment of postoperative pain. ⋯ Special focus is given to the controversial debate about the indication for epidural analgesia, as well as various alternative therapeutic options, including transversus abdominis plane (TAP) block, paravertebral block (PVB), wound infiltration with local anesthetics, and intravenous lidocaine. In additional, indications and contraindications of nonopioid analgesics after abdominal and thoracic surgery are discussed and recommendations based on scientific evidence and individual risk and benefit analysis are made. All therapeutic options discussed are eligible for clinical use and may contribute to improve postoperative pain outcome after abdominal and thoracic surgical procedures.
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Complex regional pain syndrome (CRPS) may develop following fractures, limb trauma, or lesions of the peripheral or central nervous system. The clinical picture consists of a triad of symptoms including autonomic, sensory, and motor dysfunction. Diagnosis is based on clinical signs and symptoms according to the Budapest criteria. ⋯ Distinct methods of physical therapy and pharmacological strategies are the mainstay of therapy. Pharmacotherapy is based on individual symptoms and includes steroids, free radical scavengers, treatment of neuropathic pain, and agents interfering with bone metabolism. In some cases invasive methods may be considered.
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It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. ⋯ Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?