Moreover, the hypothesis that migraine aura may represent a preictal state fur­ther unies these observations. According to this view, the neurovascular coupling mechanisms that underlie the migraine aura—beginning with an initial wave of hyperexcitability and followed by massive ionic shifts across neuronal mem­branes—can facilitate seizure onset in a cortex already predisposed to epilepsy. Essentially, when the rapid changes induced by a migraine aura occur in a brain susceptible to synchronized discharges, they may pave the way for a seizure [8, 9]. Thus, both hypotheses converge on the idea that a hyperexcitable cortex is central to the pathogenesis of these conditions. Depending on individual susceptibility and the dynamics of the underlying neurovascular processes, this hyperexcitability may manifest as either a migraine with aura, an epileptic seizure, or even a scenario where the migraine aura itself triggers the seizure.

An alternative hypothesis proposes that aura-triggered seizures represent a form of reex epilepsy, in which activation of a task-specic neural network induces excessive neuronal synchronization, ultimately leading to a seizure. However, this explanation appears less effective in accounting for the observed phenomena [8].

phonophobia, facial ushing, and nausea. These attacks occurred approximately two to four times per month and were disruptive enough to interfere with her daily activities signicantly. In response to her worsening symptoms, prophylactic treat­ment with unarizine was started, leading to a notable improvement in her condi­tion. Given the strong family history of migraines, a genetic diagnostic evaluation was performed by a Next Generation System (NGS) panel to explore potential inherited causes. However, the genetic investigation revealed no pathogenic variants among the genes examined. Despite the improvement with unarizine, at the age of 10, the patient experienced 2 distinct episodes where her typical aura was followed in less than 20min by a sudden loss of consciousness, with a tonic–clonic seizure, which resolved spontaneously. A similar episode occurred during a subsequent febrile illness the following year. In light of these seizure episodes, further neuro­logical evaluation was pursued. An interictal electroencephalography (EEG) revealed the presence of sharp waves, in particular in the centrotemporal regions, while a brain MRI returned normal ndings.

2. The occurrence of an epileptic seizure within 1h of the headache onset.

rion B below.

B. Occurring in a patient with 1.2 Migraine with aura, and during or within 1h

after an attack of migraine with aura.

C. Not better accounted for by another ICHD-3 diagnosis.

As observed, migraine aura-triggered seizure is a diagnosis of exclusion, mean­ing that other potential conditions must be ruled out rst. Therefore, it is essential to

exclude confounding factors such as visual phenomena of epileptic origin (e.g., occipital lobe epilepsy), syncope, and psychogenic non-epileptic seizures (PNES) [10]. Additionally, for this diagnosis, the association between epileptic seizures and migraine without aura remains unclear.

In particular, to differentiate visual aura from visual epileptic phenomena, it is necessary to know their features, as described in Table4.1.

Step 3: Additional diagnostic evaluations for the differential diagnosis.

– Score ≥5 points: probably migraine visual aura. – Score ≤5 points: improbable migraine visual aura.