Der Schmerz
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Neuropathic pain syndromes may be treated by intervention at the sympathetic nervous system. The pain in these syndromes is therefore called sympathetically maintained pain (SMP). Typical disorders with a SMP component are complex regional pain syndromes (reflex sympathetic dystrophy and causalgia), traumatic neuralgias and herpes zoster. ⋯ Open questions are how the efferent sympathetic nervous system is capable of influencing pain sensation and which mechanisms underly the autonomic dysregulation often observed in these syndromes.(1) Somatic afferents that project through the sympathetic trunk do not exist. Therefore, a pure sympathetic block does not block afferent information arising from the affected extremity. What alternatives are possible? Under pathophysiological conditions a functional interaction of efferent sympathetic fibers and afferent nociceptive fibers could be demonstrated in patients and animal studies. The intensity of this coupling varies considerably between individual patients and is not necessary for the diagnosis of the disorder. (2) Sympathetically maintained pain and signs of autonomic dysfunction are independent clinical and pathophysiological phenomena without any causal relation. However, it is possible to treat both the SMP and the autonomic dysfunction with sympathetic blocks.
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Hydromorphone is a micro receptor agonist opioid. According to WHO recommendations, hydromorphone is to be classified in step III of pain therapy. An oral formulation with a prolonged duration of action of 12 hours has been evaluated only recently. The controlled release capsule is especially suited for the regular twice a day administration in cases of severe and persistent pain. The oral formulation of hydromorphone increases the number of opioid analgesics available for pain therapy in step III. Hydromorphone is recommended when morphine fails to produce sufficient pain relief (despite increase of doses) or causes intolerable side effects (despite treatment of symptoms). In principle, no differences in efficacy of morphine and hydromorphone are to be expected. However, clinical experience shows that changing one opioid analgesic to another one can improve the treatment of patients so that hydromorphone may replace another opioid analgesic to which a patient fails to respond well or develops side effects. The dose of hydromorphone equivalent to 2 times 30 mg controlled release morphine is about 2 times 4 mg. The values for the absorption, bioavailability and maximum plasma concentration after the administration of controlled release hydromorphone every 12 hours -of three times the dose- are equivalent to those of an immediate release tablet given every 4 hours. In several open label and controlled studies, hydromorphone proved to be of good efficacy in the treatment of acute and persistent pain, especially in patients with severe cancer pain. With regard to the incidence of side effects, no significant differences between morphine and hydromorphone could be established. In general, the side effects of hydromorphone are typical for opioid analgesics. ⋯ In conclusion, controlled release hydromorphone seems to be well suited for the control of severe chronic pain when given twice daily.
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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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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.