May migraine post-patent foramen ovale closure sustain the microembolic genesis of cortical spread depression?

Background: Cortical spreading depression has been suggested to be the main substrate for migraine, but its pathobiology is not completely understood. Recently, the microembolic hypothesis as a promoting factor of cortical spreading depression has been demonstrated in an animal model. Our study is aimed to present a series of patients in whom early migraine attacks immediately after closure procedure predicted migraine with aura resolution on the long term, suggesting a role for microembolization in migraine genesis.

Methods: Our study consisted of 42 patients with migraine (36 female, mean age 35±6.7 years, mean Migraine Disability Assessment Score 29.9±9) and previous stroke who underwent transcatheter PFO closure during the last 2 years at the Rovigo General Hospital using different devices selected on the basis of specific anatomies. Procedural, technical, and clinical variables have been recorded and analyzed searching for potential relationships among postprocedural migraine, migraine improvement, and microembolization.

Results: Sixteen patients (38%) experienced a migraine attack of mean duration 3.5±2.4 h immediately (<60 min) after closure procedure. These patients more frequently had a severe migraine with aura and a permanent shunt on transcranial Doppler. There were no differences in terms of procedure time, occlusion time, and type of device used. After a mean follow-up of 32.2±10.6 months, only patients with postprocedural migraine attacks reported resolution of aura and a significant improvement in migraine symptoms.

Conclusions: Our series seem to indirectly confirm in vivo the experimental animal data of microembolization-driven cortical spreading depression. It also confers the recent hypothesis about air microbubble-induced cerebral deoxygenation linking the micromebolic hypothesis with cortical spreading depression.