In reply
I am grateful to Dr Schürks for his comments, which provide an opportunity to further elaborate on the commonalities between migraine and epilepsy. Current theories of migraine recognize that activation and sensitization of the trigeminovascular system are responsible for the throbbing pain in a migraine attack.1 However, in migraine with aura and perhaps also migraine without aura, cortical phenomena are believed to underlie episodic activation of the trigeminovascular system. The pivotal role of cortical mechanisms is an aspect of the pathophysiology of migraine shared with epilepsy. Nevertheless, new information has challenged the current dogma that presupposes neural events always precede trigeminovascular system activation.2,3 There is emerging recognition that vascular phenomena could in some circumstances be the primary trigger in a migraine attack, although in migraine with aura (and presumably also migraine without aura) neural mechanisms must necessarily come into play.