Articles: neuralgia.
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Journal of neurosurgery · Feb 1998
Follow-up results of using microvascular decompression for treatment of glossopharyngeal neuralgia.
Glossopharyngeal neuralgia (GPN) is an uncommon disorder that is characterized by a severe lancinating pain commonly induced by swallowing. There has been some debate among various authors as to which surgical procedure should be adopted to treat cases of GPN: microvascular decompression (MVD) or partial rhizotomy. The latter necessitates the partial destruction of normal neural structures. ⋯ Pain was relieved in all cases. Two patients complained of persistent mild hoarseness, causing the inability to speak loudly, and two patients complained of occasional coughing episodes that occurred for a couple of years after the surgery. No other complications were reported and no recurrence of pain was noted during the follow-up period. This procedure provided satisfactory results by preserving important perforating arteries in this area and by repositioning offending arteries in a safer and surer fashion, thus reducing complications and recurrence of GPN.
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Neuroscience letters · Jan 1998
Tactile allodynia, but not thermal hyperalgesia, of the hindlimbs is blocked by spinal transection in rats with nerve injury.
Spinal nerve ligation produces signs of neuropathic pain in rats. Different neuronal pathways may underlie the abnormal sensory responses to thermal and tactile stimuli. Here, the possibility that local circuitry in the spinal cord and/or spinal-supraspinal loops might be involved in tactile allodynia and thermal hyperalgesia of the hindpaws was investigated by transecting the spinal cord of sham-operated or L5/L6 nerve ligated rats. ⋯ Tail-withdrawal responses to tactile probing were very robust after spinal transection in both groups, demonstrating loss of descending inhibition. These observations suggest that thermal hyperalgesia of the paw seen after nerve injury involves both spinal and supraspinal circuits, while tactile allodynia depends on a supraspinal loop. This difference may reflect afferent inputs associated with different fiber types.
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Antagonists of NMDA glutamate receptors have been shown to alleviate neuropathic pain in rats and humans. However, NMDA antagonists can cause significant side effects ranging from behavioral disturbances to injury of neurons in the posterior cingulate/retrosplenial (PC/RS) cortex. We have found that alpha-2 adrenergic agonists prevent the PC/RS neurotoxic side effects of NMDA antagonists. ⋯ In separate experiments on normal unoperated rats, we found that clonidine (0.05 mg/kg s.c.) counteracted the hyperactivity induced by MK-801 (0.05 mg/kg s.c.) and returned activity levels to a normal range. These findings signify that clonidine, which does not specifically relieve neuropathic pain, can potentiate the neuropathic pain-relieving action of MK-801, while also protecting against neurotoxicity and hyperactivity side effects of MK-801. The potentiation is of a sufficient magnitude that it permits cutting the MK-801 dose requirement in half, thereby achieving prolonged neuropathic pain relief while doubling the margin of safety against any type of side effect that might be mediated by blockade of NMDA receptors.