Lamotrigine in the Prevention of Migraine With Aura

A Narrative Review

Dan Buch, MD; Hugues Chabriat, MD, PhD

Disclosures

Headache. 2019;59(8):1187-1197. 

In This Article

Discussion

Although the use of LTG to prevent MA seems to be based on a solid rational at experimental level, results obtained from previous randomized trials of LTG in migraine prevention appear mainly disappointing. However, the negative results of these trials were raised from samples of limited size that have comprised a small number of MA patients. A careful analysis suggests that these studies were most likely underpowered to reach any firm conclusion, particularly in MA patients. In the first randomized trial performed by Steiner et al,[85] 77 patients with migraine were included, initially comprising 31 patients with MA. Only 53 individuals completed the study and the number of patients with MA used for analysis was not described. The second randomized trial performed by Gupta et al[86] comprised 47 patients and from them, only 19 had MA. Although the results were considered negative, on the primary objective of 50% responder rate, the results were found positive on the monthly migraine reduction.

In contrast, a positive effect of LTG was repeatedly reported in multiple small pilot and open studies or in specific disorders that can lead to repeated MA attacks. The burden of aura manifestations in some groups of migraineurs because of their high frequency or prolonged duration or specific underlying disorder may justify highly effective and well-tolerated treatments. In this context, LTG appears as a molecule with a high potential, especially for the preventive treatment of MA attacks. Based on previous reports, a target dose of 100 mg could be proposed for a future trial of LTG to prevent MA. To expect a 80% chance of detecting an increase of responders from 22% (given the pooled proportion of responders to orally administrated placebo in meta-analysis[101]) in the placebo group to 44% (considered a meaningful and plausible objective[101]) in the experimental group, inclusion of 136 patient would be necessary.

In conclusion, data from the literature suggest that LTG presents with a highly promising profile for treating particularly patients suffering from MA attacks. Since alterations of cortex excitability and the occurrence of CSD remains very uncertain in individuals who suffered attacks of migraine without aura, previous studies were obviously not designed and enough powered for detecting a potential benefit of LTG in MA. Since LTG is well tolerated and has a low-risk profile, we advocate that this treatment should be specifically evaluated in MA patients, particularly in subjects with frequent attacks or with disabling and repeated aura manifestations.

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