Articles: acute-pain.
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Aim of the present prospective longitudinal study was the statistical foundation and thus further replication of recent findings of Hasenbring [13], who postulated a significant importance of specific, within the psychological pain research long neglected pain coping strategies as risk factors concerning pain chronification: appeals to "stick it out" on the cognitive level and endurance strategies on the behavioural level. ⋯ These results corroborate the finding that this subgroup of chronic low back pain patients might indeed carry a bad prognosis and call for further research into this area, especially with regard to rehabilitation potential and facilities of reintegration into working life.
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Central pain mechanisms are deeply embodied in the psychophysical problem of pain. They are located in the brain and spinal cord and are becoming increasingly recognised as playing a major role in the generation and maintenance of pain and disability associated with neuromusculoskeletal problems. Central mechanisms participate in all pain states, acute and chronic. ⋯ In reality, as key players in the healing process, central mechanisms are profoundly affected by manual therapy even when it is directed at a peripheral problem. Treatment of peripheral mechanisms can be performed through central techniques because both peripheral and central mechanisms are always part of the same clinical problem. Consequently, manual therapy must change its mindset from a peripheral standpoint and integrate central mechanisms into clinical practice as a means of improving therapeutic efficacy and to prevent the descent of acute pain into chronic.
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Anaesthetists who manage acute and chronic pain need to be familiar with current research and practice guidelines in these areas. New local anaesthetics and new routes of administration for opioids and adjuvants may further improve our management of acute pain. ⋯ The limitations of nerve blocks are acknowledged and guidelines for managing chronic pain and opioids are available. Anaesthetists must recognize psychological difficulties as a significant perpetuating factor in chronic pain.
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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.