The Relationship Between Headache and Epilepsy is Complicated

Editorial - The crossover between headache and epilepsy - Expert Rev. Neurother. 13(3), 231–233 (2013)
“The relationship between headache and epilepsy is complicated and although the  nature of this association is not yet fully clear, several plausible explanations have been proposed.”
The relationship between headache and epilepsy is complicated and although the nature of this association is not yet fully clear, several plausible explanations have been proposed. To achieve a definitive international consensus on the crossover between headache and epilepsy, during the last 100 years, many authors have devoted countless efforts to reach an agreement on the ­ multiple aspects of this intriguing topic [1] . 

The clinically based hypothesis that headache and epilepsy are related dates back to the 19th century, when Sir William Richard Gowers’ famous book, published in 1907, first suggested that “migraine is in the borderland of epilepsy” [1] , sharing several pathophysiological mechanisms related above all – “we can say today in the light of modern knowledge” – to neuro­ transmitter and ion channel dysfunctions. If we compare the current knowledge with those of Gowers’ times, the etiopathogenesis of headache and of epilepsy are nowadays, in the most important aspects, well known. However, in his own time, during an epoch before EEG, Gowers stated that “…in extremely rare instances one affection may develop while the other goes on,” suggesting a possible partial overlap between them. More than 100 years later, in the era of digital EEG recordings, we can firmly report that sometimes “headache itself can even be epilepsy,” and, in certain cases (probably largely underestimated), “the headache can represent the only ictal epileptic phenomenon” [1,2] . 

There are insufficient etiophysiopathological studies of the pediatric population for tension-type headache and other primary headache (cluster headache and other trigeminal autonomic cephalalgias), which are so rare or even exceptional in pediatric age; so, here we can discuss only data related to the physiopathology of migraine. In this respect, it has been shown that hyperexcitation occurs in epilepsy, while in migraine a brief hyperexcitation period (depolarization) is followed by a long hypoexcitation period (spreading depression), followed again by hyperexcitation as a rebound phenomenon. Moreover, a disexcitability (hyper- and hypo-excitation in the same migrainous patient at different points in time) condition has even been ­demonstrated [1] .

“Cortical spreading depression seems to be the connecting point between migraine and epilepsy…” Cortical spreading depression (CSD) seems to be the connecting point between migraine and epilepsy [3,4] , even in patients suffering from migraine without aura, whereas the presence of CSD in silent cortical areas has been hypothesized as a possible underlying mechanism. CSD is characterized by a slowly propagating wave (2–6 mm/min) of sustained strong neuronal depolarization that generates transient intense spike activity as it progresses into the brain tissue, followed by neural suppression that may last for minutes. The depolarization phase is associated with an increase in regional cerebral blood flow, whereas the phase of reduced neural activity is ­associated with a ­ reduction in blood flow [5] .

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