Der Schmerz
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Multimodal pain management is a comprehensive treatment of complex chronic pain syndromes. In addition to medical therapy various other specialized therapeutic interventions based on the biopsychosocial model of pain origin and chronic pain development, are added. During the last few years treatment centers for chronic pain have been established throughout Germany. ⋯ In daily practice there is, however, still a lack of clarity and of consistency about the components that multimodal pain management should contain. This is the reason for the ad hoc commission on multimodal interdisciplinary pain management of the German Pain Society to propose the following position paper that has been worked out in a multilevel and interdisciplinary consensus process. The paper describes the mandatory treatment measures in the four core disciplines of multimodal pain management, pain medicine, psychotherapy, exercise therapy including physiotherapy and assistant medical professions including nurses.
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A 34-year-old woman presented with a complex pain disorder and a previous diagnosis of the rare Gitelman syndrome but with a negative genetic test. The patient was admitted to a routine ward for treatment of the pain but was transferred to the intensive care unit after suffering severe hypokalemia and a narcoleptic attack. ⋯ With consent the patient's belongings were inspected and many diuretics and laxatives were found. The patient admitted to uncontrolled self-medication so that the diagnosis of Gitelman syndrome also appeared to be an artificial disorder.
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The neuropeptide calcitonin gene-related peptide (CGRP) is known to play a major role in the pathogenesis of pain syndromes, in particular migraine pain; however, its implication in inflammatory processes is not well known. The CGRP receptor antagonist BIBN4096BS was shown to reduce migraine pain and trigeminal neuronal activity. An analgesic action of this compound can also be found in rats with induced acute inflammation by injection of complete Freund's adjuvant (CFA) in one hindpaw. ⋯ In vivo electrophysiological studies performed in rats injected with CFA using recordings of wide dynamic range neurons in deep dorsal horn layers of the lumbar spinal cord, confirmed a reduction of neuronal activity after systemic drug administration. The same considerable amount of reduction occurred after topical administration onto the paw with resulting systemic plasma concentrations in the low nanomolar range. Spinal administration of BIBN4096BS did not modify the neuronal activity in the CFA model which suggests that peripheral blockade of CGRP receptors by BIBN4096BS significantly alleviates inflammatory pain.