Lamotrigine in the Prevention of Migraine With Aura

A Narrative Review

Dan Buch, MD; Hugues Chabriat, MD, PhD


Headache. 2019;59(8):1187-1197. 

In This Article

MA Is Associated With Increased Neuronal Excitability and CSD

One third of migraineurs present with transient focal neurological symptoms before or during their headache, collectively termed "aura."[1] The International Headache Society [IHS] defines typical migraine aura as a "recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5–20 minutes and last for less than 60 minutes.[1] More than 14 different subtypes of MA have been depicted in the most recent International Classification of Headache Disorders (IHCD-3rd Edition [beta version]). By frequency, visual, sensory, aphasic symptoms are the most common manifestations reported during MA attacks. Other atypical neurological symptoms have been observed such as blindness, hemiplegia, prosopagnosia, Alice in Wonderland syndrome, and transient confusion or even coma.[2,3] Besides, vestibular migraine is also quite common.[4] In some patients, aura symptoms can become debilitating when they are disabling, recurrent, or long-lasting. Recently, aura symptoms lasting more than 1 hour have been reported in at least 1 out of 4 patients.[5] There is also accumulating evidence suggesting that MA patients present with neuronal hyperexcitability. At cortical level, an increased interictal excitability has been repeatedly observed in patients with visual aura[6,7] that is further amplified in patients with multiple aura symptoms.[8] Hyperexcitability has been also reported at the neuromuscular junction level in migraineurs.[9] This is detected in cases of migraine with isolated visual aura and seems further increased in patients having migraine with prolonged[10] or complex auras.[8,11] Accumulating evidence suggests that CSD, a wave of depolarization that propagates slowly across the brain surface is the main physiological substrate of MA.[12] Aura symptoms develop slowly and across neurovascular boundaries as repeatedly observed during experimental CSD.[13] CSD can also trigger the trigeminovascular system which presumably leads to dilation and inflammation of meningeal vessels during migraine headache.[14] Whether CSD is involved in all MA subtypes remains, however, undetermined.[15] Conversely, the involvement of CSD in MO appears much more disputed.[16–18]