Der Schmerz
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The European Association for Palliative Care (EAPC) considers sedation to be an important and necessary therapy option in the care of selected palliative care patients with otherwise refractory distress. Prudent application of this approach requires due caution and good clinical practice. ⋯ Procedural guidelines are helpful to educate medical providers, set standards for best practice, promote optimal care and convey the important message to staff, patients and families that palliative sedation is an accepted, ethical practice when used in appropriate situations. EAPC aims to facilitate the development of such guidelines by presenting a 10-point framework that is based on the pre-existing guidelines and literature and extensive peer review.
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Biofeedback is a direct feedback of a physiological function. The aim of biofeedback is to change the physiological function into a required direction. To manage this, the physiological function has to be fed back visually or acoustically and it has to be perceived consciously. ⋯ Biofeedback has proved to be successful in non-medical treatment of pain. According to more recent meta-analyses biofeedback reveals high evidence in the treatment of migraine or tension-type headache. In these headaches biofeedback procedures are considered highly effective.
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In 2009, the German version of ICD-10 (ICD-10 GM version 2009) introduced the diagnosis of "chronic pain disorder with somatic and psychological factors", because current ICD-10 diagnoses did not address the biopsychosocial character of chronic pain adequately. For most patients, a dichotomous classification into psychologically versus biomedically caused pain is inappropriate and does not reflect current knowledge on pain. The new code F45.41 addresses the relevance of psychological factors for chronic pain persistence and chronic pain treatment, even in those conditions with a clear biomedical cause at the beginning. ⋯ The distinction of this new diagnosis from other pain-associated diagnoses and recommendations for the coding of comorbid conditions are presented. The differentiation of everyday pain symptoms from pain disorders is outlined. Finally, contextual factors of the classification process, as well as problems in integrating this new diagnosis into diagnosis-related group (DRG) systems of financial reimbursement are discussed.
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Neuropathic pain syndromes are characterised by the occurrence of spontaneous ongoing and stimulus-induced pain. Stimulus-induced pain (hyperalgesia and allodynia) may result from sensitisation processes in the peripheral (primary hyperalgesia) or central (secondary hyperalgesia) nervous system. The underlying pathophysiological mechanisms at the nociceptor itself and at spinal synapses have become better understood. ⋯ These mechanisms include reorganisation of cortical somatotopic maps in sensory or motor areas (highly relevant for phantom limb pain and CRPS), increased activity in primary nociceptive areas, recruitment of new cortical areas usually not activated by nociceptive stimuli and aberrant activity in brain areas normally involved in descending inhibitory pain networks. Moreover, there is evidence from PET studies for changes of excitatory and inhibitory transmitter systems. Finally, advanced methods of structural brain imaging (voxel-based morphometry, VBM) show significant structural changes suggesting that chronic pain syndromes may be associated with neurodegeneration.
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In order to transform a nociceptive stimulus into a painful perception, a highly specialized chain of structural and functional elements is necessary. This system comprises nociceptors in the periphery with specific molecular properties for differential coding of noxious submodalities, ascending and descending tracts that can control the input into the dorsal horn of the spinal cord as well as supraspinal processing that regulates the integration of nociceptive information with other sensory modalities and autonomic function. In this article, structures involved in nociceptive signal processing starting from the periphery up to spinal and cerebral structures are discussed in the order of their spatio-temporal activation sequence - as far as these are known. ⋯ Different input to the dorsal horn of the spinal cord by different nerve fiber populations to superficial and deep layers is explained, ascending tracts as well as descending systems capable of either facilitating or inhibiting the upstream flow of nociceptive information, together with their known transmitters. Finally, thalamic relay nuclei for sensory and nociceptive signals, as well as subcortical and cortical projection targets are discussed. To complete the current view of the nociceptive system, information from molecular biology and anatomic tracing studies as well as data from functional electrophysiologic cell recordings in animals and imaging studies in humans are assembled.