Annals of medicine
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Basic scientific evidence suggests that an analgesic intervention made before surgery will produce a better outcome than the same intervention made after surgery. The evidence from randomized controlled trials (RCTs) which tested this hypothesis in patients is reviewed. Four studies with paracetamol or NSAIDs did not show any pre-emptive effect. ⋯ The opioid studies which did show a pre-emptive effect had other technical weaknesses. One way to combat lack of power would be to combine data (meta-analysis). This is very difficult in this field because of the outcome measures which investigators are using.
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Recent research has demonstrated the increasing importance of the spinal cord in processing and modulating nociceptive input. Different groups of drugs, each acting by a unique mechanism, have been shown to block nociceptive afferent transmission. None of the currently available spinally administered local anesthetics, opioids or non-opioids produce analgesia without side effects. ⋯ Preliminary results suggest that the neuropeptide octreotide has potent analgesic effects. 'Balanced spinal analgesia' using a combination of low doses of drugs, with separate but synergistic mechanisms of analgesia, may produce the best results. The optimal drug combinations and dosages remain to be determined. It is essential that animal neurotoxicity studies followed by controlled clinical trials are performed before widespread spinal administration of new drugs.
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This paper describes the responses of peripheral and central visceral nociceptive systems to acute injury and discusses these observations in relation to the concept of 'pre-emptive analgesia'. Visceral nociceptors are known to respond to injury but are also known to become sensitized to non-noxious stimuli during the inflammatory process that follows intense noxious stimulation. ⋯ Therefore it is proposed that the concept of 'pre-emptive analgesia', as such, has no neurophysiological basis. Any analgesic procedure aimed at reducing postoperative pain must not only prevent the arrival in the CNS of the initial afferent barrage evoked in nociceptive endings but also reduce or eliminate the persistent discharges of sensitized nociceptors during the inflammatory repair process that are critically important for the maintenance of the central pain state.
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Many studies in several species, including humans, have identified a subset of primary afferent nerve fibres that are activated by potential or actual tissue-damaging stimuli. Discharge patterns of these nociceptive afferents faithfully reproduce some aspects of the applied stimuli (e.g. shape of the stimulus-response function) but not others (e.g. time-course of a sustained stimulus). ⋯ Therefore, the painfulness of a stimulus cannot be deduced from nociceptor discharges alone; central processing needs to be taken into account, particularly central summation. In addition to the immediate responses of nociceptive afferents to external stimulation, acute pain mechanisms also comprise the short-term plasticity of the nociceptive system as a consequence of prolonged noxious stimulation.
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Vulvodynia is a complex multifactorial and multidisciplinary clinical syndrome of unexplained vulvar pain, sexual dysfunction, and psychological disability. Because of the absence of abnormal physical findings among such patients, vulvodynia was long thought to be solely a psychosomatic syndrome. The incidence or prevalence of vulvodynia has not been well studied. ⋯ The most common subtypes are vulvar vestibulitis syndrome, cyclic vulvovaginitis and dysesthetic vulvodynia. Simple practice guidelines can be developed to facilitate the evaluation and management of such patients. Systematic epidemiological, etiological and therapeutic studies of vulvodynia are urgently needed.