Der Schmerz
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Disregarding pain resulting from vitamin deficiency, an analgesic effect seems to be exerted only by vitamin B1 (thiamine), vitamin B6 (pyridoxines), and vitamin B12 (cobalamine), particularly when the three are given in combination. The analgesic effect is attributed to an increased availability and/or effectiveness of noradrenaline and 5-hydroxytryptamine acting as inhibitory transmitters in the nociceptive system. In animal experiments, high doses of these vitamins administered alone or in combination inhibited nociceptive behavior and depressed the nociceptive activity evoked in single neurons of the dorsal horn of the spinal cord and in the thalamus. ⋯ The use of high doses of vitamin B6 may be limited by a neurotoxic effect. The effectiveness of B vitamins in depressing chronic pain has not been established. It would be interesting to know if the B vitamins are of use as adjuvants in the treatment of tumor pain.
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The WHO analgesic ladder, including the use of strong opioid analgesics for the treatment of cancer pain, is widely accepted. However, the use of opioids for the treatment of non-cancer pain is still controversial. This study investigates doctors' medical knowledge about basic aspects of pain management. Additionally, we determined whether the deficiencies in the treatment of patients suffering from pain are based on the rigorous national narcotic control system in Germany. ⋯ Therapy with strong opioids is accepted practice, but significant deficits of legal and technical knowledge uphold the undertreatment of patients suffering from cancer and non-cancer pain. Patients with a legitimate need for pain relief by strong opioids are the unintended victims of tight narcotic regulations and deficits in medical education. An ease of regulatory conditions is mandatory to reduce the reluctance for prescribing opioids. On the other hand intensified continuous medical education is mandatory to reduce the undertreatment of patients with severe pain conditions.
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In recent years most industrialized nations have been confronted with a dramatic increase in cases dealing with back pain which, because of the associated costs, has put a strain on health care systems. Because of the tremendous costs caused by patients with chronic illnesses, there is a common interest in identifying determinants responsible for the pain becoming chronic. According to the fear-avoidance model, chronic back pain is the cause of specific patient beliefs according to their perception and appraisal of back pain and their assumptions about the connection between pain and work activities. These fear-avoidance beliefs are assumed as the main cognitive factors of adapting to chronic invalidism. In this study a German version of a self-reporting instrument that assesses fear-avoidance beliefs (FABQ, Waddell et al. 1993) is presented. ⋯ The results suggest that primary target points for further investigation include an analysis of the patients' beliefs about their pain, with special emphasis on fear-avoidance beliefs. It is also necessary to analyze the behavioral assumptions of the fear-avoidance model in an experimental design. Furthermore, our results concerning the psychometric properties of the questionnaire should be proved in a far larger sample of back pain patients.
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This paper reviews instruments in German language for the psychological assessment and classification of pain. Usually chronic pain syndromes are classified within the International Classification of Diseases (ICD). Instead of the psychiatric chapter of the ICD, it is possible to use the Diagnostic and Statistical Manual of Mental Disorders (DSM). ⋯ The MASK-P part of the diagnosis is composed of graduation on these levels. Differential axis of the pain syndromes are described phenomenologically and specifically. MASK provides the possibility of establishing an integrative, interdisciplinary diagnosis.
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Several pathophysiological mechanisms may be responsible for initiation and maintenance of chronic postherpetic pain. (1) Peripheral nociceptive fibers can develop abnormal sensitization. Secondary to this, central nociceptive "second-order" neurons in the spinal cord dorsal horn can also be sensitized, i.e. they become hyperexcitable and start responding to non-noxious stimuli. (2) Degeneration of nociceptive neurons may trigger anatomical sprouting of low-threshold mechanosensitive terminals to form connections with central nociceptive neurons and may subsequently induce functional synaptic reorganization in the dorsal horn. According to these mechanisms theoretical possibilities of therapeutical interventions to prevent postherpetic neuralgia are (1) adequate analgesia in the acute phase (analgesics, antidepressants, sympathetic blocks) and (2) prevention of C-fiber degeneration by reducing the inflammatory reaction (antiviral drugs, corticosteroids, neurotrophins). ⋯ Although there is no clear evidence in favor of a prevention of postherpetic neuralgia for any of the interventions, it is definitely reasonable to perform the best analgesia possible during the acute phase of herpes zoster.