Articles: neuralgia.
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The idea of using Ketamine to treat chronic pain is mainly based on the central antinoceptive effect of the substance acting as a noncompetitive antagonist at the NMDA-receptor. In the present meta analysis over a period from 1/1981 up to 6/1996 twelve publications (1994-1996), which have dealt the use of Ketamine for patients with chronic pain, are evaluated and discussed. The entire positive evaluation of the drug is based on the results of the studies under consideration. ⋯ Here, the therapy had to break off in two cases. In nine cases the side effects could be suppressed by Droperidol. For the future, research with more study power is necessary to establish Ketamine in the therapy of chronic pain.
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Neuropathic pain or persistent dysesthesias may be initiated by mechanical, chemical, or ischemic damage to peripheral sensory nerves. In animal models of neuropathic pain, transection or constrictive injury to peripheral nerves produces ectopic discharges originating at both injury sites and related dorsal root ganglia (DRG), and, consequently, hyperexcitability in associated dorsal horn (DH) neurons of the spinal cord. Since ectopic discharges are inhibited by agents that block voltage-sensitive Na+ channels, it has been postulated that accumulation of Na+ channels in the membrane at nerve injury sites may contribute to, or be responsible for, the development of ectopic neuronal activity (ENA). ⋯ Inhibition of ENA in neuromas and DRG did not recover within 10 min after 100 or 300 microg/kg TTX. By comparison, the ED50 value for the initial decrease of HR was 17.9 (15.0-21.5) microg/kg, and partial recovery occurred within approximately 3 min. These data support the hypothesis that Na+ channel accumulation contributes to the generation of ectopic discharges in neuromas and DRG, and suggest that TTX-sensitive Na+ channels located at the nerve injury site and DRG play an important role in the genesis of neuropathic pain.
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Case Reports Randomized Controlled Trial Clinical Trial
Relief of glossopharyngeal neuralgia by ketamine-induced N-methyl-aspartate receptor blockade.
We examined whether ketamine, which is a noncompetitive blocker of N-methyl-D-aspartate (NMDA) receptors, had the ability to relieve glossopharyngeal neuralgia. A tentative hypothesis is that glossopharyngeal neuralgia involves hyperactivity in the central nociceptive neurons and that the development of this hyperactivity is dependent on activation of NMDA receptors. ⋯ This case report shows that ketamine-induced NMDA receptor blockade significantly relieved glossopharyngeal neuralgia in this patient. Therefore, NMDA receptors may play a significant role in the pathogenesis of the pain syndrome described.
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Comparative Study Clinical Trial Controlled Clinical Trial
Neuropathic pain and prolonged regional inflammation as two distinct symptomatological components in complex regional pain syndrome with patchy osteoporosis--a pilot study.
To reappraise symptomatology of complex regional pain syndrome (CRPS), we investigated the clinical symptoms of seven patients with CRPS who showed associated patchy osteoporosis. The incidence of moderate to severe spontaneous pain, burning pain, mechanical allodynia was higher in patients with significant nerve injury than in those without. Periarticular tenderness adjacent to osteoporotic bones, abnormalities of blood flow, edema and impairment of motor function were seen in both groups of patients. Our clinical observations of patients with CRPS associated with patchy osteoporosis suggest that CRPS may have the following two distinct components: (1) neuropathic pain that includes severe spontaneous pain or severe persistent mechanical allodynia and (2) prolonged regional inflammation, the early phase of which could be indicated by positive inflammatory symptoms of pain (tenderness), heat, redness, swelling and loss of function and their alleviation with corticosteroids.
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Scand J Urol Nephrol · Aug 1997
Case ReportsEntrapment neuropathy of the internal pudendal nerve. Report of two cases.
Entrapment neuropathy of the internal pudendal nerve in the Alcock canal is a rare entity and literature on the subject is lacking. The pathogenesis of this disease is probably related to repeated microtraumatisms of the perineal region acting on the Alcock canal or dysmetabolic diseases favouring compression of the pudendal nerve inside the Alcock canal. In this article two new cases which have come to our attention are described and literature on the topic, with special regard to diagnosis and treatment, is reviewed.