Anticonvulsants (antineuropathics) for neuropathic pain syndromes

Our knowledge about the pathogenesis of neuropathic pain has grown signific antly during last two decades. Basic research with animal models of neuropa thic pain and human clinical trials with neuropathic pain have accumulated solid evidence that a number of pathophysiologic and biochemical changes ta ke place in the nervous system at a peripheral or central level as a result of the insult or disease. Many similarities between the pathophysiologic p henomena observed in some epilepsy models and neuropathic pain models justi fy the rationale for the use of anticonvulsant drugs in the symptomatic man agement of neuropathic pain disorders. Carbamazepine (CBZ) was the first re presentative from this class of drugs to be studied in clinical trials. It has been used for the treatment of neuropathic pain syndromes, in particula r, trigeminal neuralgia (TN), for the longest time of any of the drugs in t his class. Results from clinical trials support the use of CBZ in the treat ment of TN, painful diabetic neuropathy, and postherpetic neuralgia. The us e of CBZ was not studied for complex regional pain syndrome, phantom limb p ain, and other neuropathic conditions, however. Phenytoin was the first ant iconvulsant to be used as an antinociceptive agent, but based on clinical t rials, there is no evidence for its efficacy in relieving neuropathic pain. Newer anticonvulsants have marked a new era in the treatment of neuropathi c pain, with clinical trials of higher quality standards. Gabapentin (GBP) has most clearly demonstrated an analgesic effect for the treatment of neur opathic pain, specifically for the treatment of painful diabetic neuropathy and postherpetic neuralgia. Gabapentin has a favorable side effects profil e, and based on the results of these studies, it should be considered a fir st-line treatment for neuropathic pain. Gabapentin 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 w hether GBP is as effective in other painful disorders. One small clinical t rial with lamotrigine demonstrated improved pain control in TN. Evidence in support of the efficacy of anticonvulsant drugs in the treatment of neurop athic pain continues to evolve, and benefits have been clearly demonstrated in the case of GBP and CBZ. More advances in our understanding of the mech anisms underlying neuropathic pain syndromes should further our opportuniti es to establish the role of anticonvulsants in the treatment of neuropathic pain.