Articles: neuralgia.
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Comparative Study Clinical Trial Controlled Clinical Trial
Topical acetylsalicylic acid versus lidocaine for postherpetic neuralgia: results of a double-blind comparative clinical trial.
A double-blind comparative clinical trial was performed with topical aspirin versus lidocaine for the treatment of 40 patients with postherpetic neuralgia. The percentage improvement following topical aspirin application was 72.2 +/- 19.9 S. ⋯ D. These results suggest that the effect of topical treatment with aspirin is as good as that with lidocaine, since there was no significant difference (P = 0.778) between the two drugs in respect of pain reduction and accordingly the topical application of acetylsalicylic acid can be equally recommended.
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Acta Neurol. Scand., Suppl.c · Jan 1999
ReviewGabapentin: a new tool in the treatment of neuropathic pain.
Human neuropathic pain remains a prevalent and pervasive problem in our society. Pharmacologically there is also no single, uniformly well-tolerated drug that is reliably helpful. ⋯ Gabapentin proved to be a significantly better analgesic than placebo, was well tolerated in the elderly population, and had a significant positive impact on several subjective and objective outcome measures. A discussion of the standard treatments and the studies supporting this new tool is the purpose of this review.
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Case Reports
Responses to median and tibial nerve stimulation in patients with chronic neuropathic pain.
Somatosensory evoked magnetic fields and electrical potentials were measured in eight patients with unilateral neuropathic pain. After median nerve stimulation on the painful side, the amplitudes of the evoked responses were enhanced 2 to 3 times at a latency of about 100 ms compared to the responses of the contralateral, unaffected side. After posterior tibial nerve stimulation an enhancement was found at latencies around 110 ms and 150 ms. ⋯ Three (of the eight) patients underwent spinal cord stimulation (SCS) for their pain. The enhancement of the evoked responses to stimulation of the painful side decreased after spinal cord stimulation. After a long period of spinal cord stimulation only (e.g., a year) during which the patient reported to be pain free, these "abnormal" responses were no longer observed.
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This article reviews the peripheral and central mechanisms of neuropathic pain. The main mechanisms involved in neuropathic pain are: (1) ectopic activities, (2) ephapses, (3) sensitization of nociceptors. Central morphological alterations could also be involved: (1) medullar neuronal reorganization, (2) hyperexcitability of central nervous system nociceptive neurones. The relative resistance of these neuropathic pains to opioid drugs could be related to a decrease in the number of opioid receptors to an amino acid mediator related spinal neurons hyperexitability and to an increase in non opioid peptides such as cholecystokinin.
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We investigated the effects of OT-7100, a novel analgesic compound (5-n-butyl-7-(3,4,5-trimethoxybenzoylamino)pyrazolo[1,5-a]pyrimidi ne), on prostaglandin E2 biosynthesis in vitro, acute hyperalgesia induced by yeast and substance P in rats and hyperalgesia in rats with a chronic constriction injury to the sciatic nerve (Bennett model), which is a model for peripheral neuropathic pain. OT-7100 did not inhibit prostaglandin E2 biosynthesis at 10(-8)-10(-4) M. Single oral doses of 3 and 10 mg/kg OT-7100 were effective on the hyperalgesia induced by yeast. ⋯ Indomethacin had no effect in this model. While amitriptyline (10 and 30 mg/kg) and clonazepam (3 and 10 mg/kg) significantly normalized the nociceptive threshold in the injured paw, they also increased the nociceptive threshold in the uninjured paw. These results suggest that OT-7100 is a new type of analgesic with the effect of normalizing the nociceptive threshold in peripheral neuropathic hyperalgesia.