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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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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Wallerian degeneration is required for both neuropathic pain and sympathetic sprouting into the DRG.
Chronic loose constriction of the sciatic nerve produces mechanoallodynia and thermal hyperalgesia in rats and mice, and the behaviour develops during the time in which the nerve distal to the ligature site is undergoing Wallerian degeneration. There is a sympathetic component to the pain generated by this and other rodent models of neuropathic pain, yet the site at which this sympathetic-sensory coupling remains unknown. It has been shown that following sciatic nerve transection or spinal nerve lesion, sympathetic axons invade the dorsal root ganglion (DRG) where they sometimes form pericellular baskets around mostly large diameter DRG neurons--a possible anatomical substrate for sympathetically maintained pain (SMP). ⋯ We found that both indices of neuropathic pain were significantly attenuated in Wld mice compared to wild-type mice, with the wild-type mice increasing in sensitivity to both thermal and mechanical stimulation in the first week post-operative (PO), while Wld mice showed marked hypoalgesia following CCI. Histological examination of the DRG showed that sympathetic sprouting into the DRG was also markedly delayed in Wld mice compared to wild-type mice: 1 week following injury, sympathetic fibres had invaded the ipsilateral DRG of wild-type mice, while sprouting in ipsilateral DRG of Wld mice was only slightly increased at 3 weeks PO. These results show that Wallerian degeneration is tightly linked to the development of both pain and sympathetic sprouting following CCI, and we speculate on the possible role of NGF as a mediator of both phenomena.
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Randomized Controlled Trial Clinical Trial
Phase III placebo-controlled trial of capsaicin cream in the management of surgical neuropathic pain in cancer patients.
A minority of cancer survivors develops long-term postsurgical neuropathic pain. Based on evidence that capsaicin, the pungent ingredient in hot chili peppers, might be useful for treating neuropathic pain, we developed the present clinical trial. ⋯ A topical capsaicin cream decreases postsurgical neuropathic pain and, despite some toxicities, is preferred by patients over a placebo by a three-to-one margin among those expressing a preference.