Articles: neuralgia.
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Clinical Trial Controlled Clinical Trial
Topical EMLA pre-treatment fails to decrease the pain induced by 1% topical capsaicin.
Topical capsaicin has been reported to be beneficial for the treatment of neurogenic pain. However, due to the burning pain associated with topical capsaicin, many patients discontinue treatment before therapeutic benefits are obtained. This study assessed the efficacy of EMLA (eutectic mixture of 2.5% prilocaine and 2.5% lidocaine) to block pain induced by the topical application of 1% capsaicin. ⋯ The 6 h treatment with high dose topical capsaicin (1%) produced significant desensitization to heat stimuli that was not affected by EMLA treatment. EMLA fails to produce a long lasting attenuation of the pain induced by topical application of 1% capsaicin. These results argue against the use of EMLA to block pain to topical capsaicin during the treatment of neurogenic pain.
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The purpose of this review is to identify important issues and to review the data that underlie the controversial effectiveness of opioids in relieving neuropathic pain. This controversy seems related to the use of multiple definitions of neuropathic pain together with its distinct mechanisms in both experimental animal models and human neuropathic pain syndromes, methodological shortcomings in available randomized controlled clinical trials, different methods of pain assessment, the inappropriate use of terms like efficacy and responsiveness, differential responses in spontaneous versus evoked pains, interindividual differences to specific opioids and opioid doses, and duration of follow-up. ⋯ Active placebo's mimicking side-effects should be included in the double-blind design, and control of unmasking should be performed. Individual titration of the opioid dose and active management of side-effects in long-term follow-up studies need to measure both pain relief and quality of life.
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In the this study we have investigated the threshold plasma concentration of lidocaine for reversal of mechanical 'allodynia' in a neuropathic pain model in the rat, defined the concentration-dependent limits of that reversal and compared the acute reversal during intravenous drug infusion with the persistent relief of allodynia assayed 48 h later. Actions of i.v. lidocaine on ipsilateral and contralateral legs were also assessed. Forty rats were sorted into five groups (n = 7-10) and underwent spinal root (L5-6) ligation to produce allodynia, as quantified by a lower force of von Frey hairs at the plantar hindpaw required to elicit paw withdrawal (PWT, paw withdrawal threshold). ⋯ Contralateral allodynia, despite its acute reversal during infusion to 2.1 microg/ml and higher, was not persistently relieved after infusion of lidocaine to any concentration. Repeated infusions to subthreshold levels (<2 microg/ml) did not provide persisting relief of allodynia on either side, and infusions of saline were impotent. These findings show that experimental allodynia results from multiple factors, only some of which are sensitive to lidocaine treatment, and that prolonged reversal of allodynia is limited in extent and likely influenced by pre-existing factors.
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Ugeskrift for laeger · Mar 1999
Case Reports[Diagnosis and treatment of postoperative nerve damage. Chronic neuropathic pain].
Neuropathic pain is caused by lesions in the peripheral and/or central nervous system. Patients with pain due to nerve damage after operations are often misinterpreted and met with suspicion of malingering. Neuropathic pain typically presents with a characteristic set of sensory disorders independent of the cause. ⋯ Instead, antidepressants and anticonvulsants may be tried. The pain condition is unknown to most physicians. This may result in mistreated patients having undergone several unnecessary and ineffective investigations and treatments.
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Chronic constriction injury (CCI) of the sciatic nerve results in persistent mechanical hyperalgesia together with Fos protein expression in the lumbar spinal cord. We have examined the relationship between mechanical hyperalgesia and Fos expression within the lumbar spinal cord on days 14, 35 and 55 after either CCI or sham operation. To determine the role of NMDA receptor mechanisms in the maintenance of hyperalgesia and Fos expression, the NMDA antagonist MK-801 (0.3 mg kg-1 s.c.) was administered daily on days 28 to 34 after operation. ⋯ Fos expression in sham group animals was not inhibited by MK-801 treatment at day 35. These results indicate that Fos expression is maintained by differing mechanisms following nerve injury or sham operation. The functional consequences of Fos expression following nerve injury and sham operation are discussed.