Articles: neuralgia.
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Randomized Controlled Trial Comparative Study Clinical Trial
Relief of post-herpetic neuralgia with the N-methyl-D-aspartic acid receptor antagonist ketamine: a double-blind, cross-over comparison with morphine and placebo.
Pain and sensory thresholds were examined before and after intravenous administration of ketamine (0.15 mg/kg), morphine (0.075 mg/kg) or saline in 8 patients with post-herpetic neuralgia. A randomized, double-blind, cross-over study design was used. Post-herpetic neuralgia was associated with impaired sensory function, as shown by reduced tactile and warm sensation in the affected compared with the contralateral non-affected skin area. ⋯ Side effects were observed in all the 8 patients after injection of ketamine and in 6 patients after injection of morphine. The present results support the hypothesis that the N-methyl-D-aspartic acid (NMDA) receptors are involved in the control of post-herpetic neuralgia including allodynia and wind-up-like pain. The NMDA receptors also may play a role in the modulation of thermal perception.
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To demonstrate the possibilities of the use of oral ketamine in the treatment of postherpetic neuralgia. ⋯ Oral ketamine may provide an alternative in the treatment of postherpetic neuralgia. The possible mechanism of action by its N-methyl-D-aspartate (NMDA) blocking properties is discussed.
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In the paper the possibilities of therapeutic use of capsaicin are presented. This drug seems to be very effective in neuralgia after zoster, and less effective in painful diabetic neuropathy. Attempts are also undertaken at its use in cluster headache, trigeminal neuralgia and arthralgia. Confirmation of the effectiveness of the discussed drug in these pain syndromes requires further studies.
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Herpes zoster neuralgia and post-zoster neuralgia (PZN) are common disabling pain syndromes. While pain from acute herpes zoster is self-limited in most cases, as pain may disappear without treatment, post-zoster neuralgia is difficult to manage. Pathological findings in acute herpes zoster include infiltration of ganglia, demyelinization and loss of axons; yet the pathogenesis of pain remains largely unknown. ⋯ The same is true for specific zoster hyperimmunoglobulins and non-specific immunoglobulins; however, there are no definite results. In the future, controlled, double-blind studies on the effect of therapeutic measures in preventing postzosteric neuralgia need to be conducted. So far, the positive effect of sympathetic blocks in preventing the late pain complications of herpes zoster can only be suggested and recommended based on subjective experience.
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Herpes zoster is an infection caused by reactivation of dormant varicella-zoster virus. The acute course of herpes zoster is generally benign; however, some patients will experience postherpetic neuralgia characterized by severe, relentless, and at times disabling pain that is often refractory to treatment. While herpes zoster responds to acyclovir, cost-benefit considerations limit the drug's usefulness to only a select group. Postherpetic neuralgia requires a holistic approach, including pharmacologic therapy using several different classes of drugs.