Abstract

Anticonvulsants (antineuropathies) for neuropathic pain syndromes. (University of Wisconsin Hospital and Clinics, Madison, WI) Clin J Pain 2000;16:S67–72.This review concentrated on randomized clinical trials of anticonvulsants for neuropathic pain syndromes. The discussion included the use of phenytoin, benzodiazepines, valproic acid, lamotrigine, and gabapentin (GBP). GBP has a favorable side effects profile, and based on the results of these studies, it should be considered a first‐line treatment for neuropathic pain. GBP mechanisms of action are still not thoroughly defined, but GBP is effective in relieving indexes of allodynia and hyperalgesia in animal models. It still remains to be seen whether GBP is as effective in other painful disorders. One small clinical trial with lamotrigine demonstrated improved pain control in trigeminal neuralgia. Evidence in support of the efficacy of anticonvulsant drugs in the treatment of neuropathic pain continues to evolve, and benefits have been clearly demonstrated in the case of GBP and carbamazepine. More advances in our understanding of the mechanisms underlying neuropathic pain syndromes should further our opportunities to establish the role of anticonvulsants in the treatment of neuropathic pain. Comment by Enrique Reig, MD.The clinical efficacy of anticonvulsants is clearly established after years of use in patients with chronic neuropathic pain. However, there are few controlled studies to support their clinical efficacy. Not all anticonvulsant drugs have the same mode of action, which explains why their relief of the different symptoms of neuropathic pain (allodynia, hyperalgesia, burning pain, etc.) is varied. Gabapentine is a first‐choice drug for relieving allodynia and hyperalgesia, but it is usually less effective for decreasing paresthesia and dysaesthesia.This article does not refer to clonazepam (a benzodiazepine acting on GABA, which is useful in stabbing pain) or topiramate. The latter is an antiepileptic drug with a good profile for the treatment of neuropathic pain. It has a triple action mechanism: Na+ channel blockade, increased GABA transmission, and antagonism of the kainate‐glutamate/AMPA.

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