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Objective: To investigate whether intravenously infused provokes migraine aura and migraine headache in migraine patients with aura. Background: Migraine with aura has been associated with endothelial dysfunction and increased stroke risk. The initiating mechanism of migraine aura symptoms is not known. Experimental provocation of migraine headache using vasoactive peptides has provided tremendous advances in the understanding of migraine pathophysiology but substances that can induce migraine aura have not been identified. Endothelin‐1 (ET‐1), an endogenous, potent vasoconstrictor peptide released from the vascular endothelium, has been proposed to trigger migraine aura. This hypothesis is based on reports of increased plasma ET‐1 levels early during the migraine attacks and the observation that ET‐1 applied to the cortical surface potently induces the cortical spreading depolarization, the underlying electrophysiological phenomenon of migraine aura, in animals. Further, endothelial damage due to, for example, carotid puncture and vascular pathology is known to trigger aura episodes. Methods: We investigated whether intravascular ET‐1 would provoke migraine aura in patients. Using a two‐way crossover, randomized, placebo‐controlled, double‐blind design, we infused high‐dose (8 ng/kg/minutes for 20 minutes) intravenous ET‐1 in patients with migraine with typical aura. The primary end‐point was the difference in incidence of migraine aura between ET‐1 and placebo. Experiments were carried out at a public tertiary headache center (Danish Headache Center, Rigshospitalet Glostrup, Denmark). Results: Fourteen patients received intravenous ET‐1. No patients reported migraine aura symptoms or migraine headache during or up to 24 hours following the ET‐1 infusion. Four patients reported mild to moderate headache only on the ET‐1 day, 3 patients reported moderate headache on the placebo day, and 1 patient reported mild headache on both days. No serious adverse events occurred during or after infusion. Conclusions: Provocation of migraine aura by procedures or conditions involving vascular irritation is unlikely to be mediated by ET‐1. [ABSTRACT FROM AUTHOR]

Background: We investigated the prevalence of post-procedural headache in patients who have undergone thrombectomy for ischemic stroke, and correlated history of migraine with risk of peri-procedural complications. A total of 314 patients underwent thrombectomy at the Danish National Hospital from January 2012 to December 2014. Eligible subjects were phone-interviewed using a purpose-developed semi-structured questionnaire according to the International Classification of Headache Disorders 3, beta version criteria. Findings: Among 96 eligible subjects, there was a significant decrease in migraine ( p = 0.022) within the first 3 months after EVT compared to 1 year before treatment, which was further evident at interview time (on average 1.6 years after EVT, p = 0.013). A minority of patients experienced headaches for the first time within 3 months of their EVT (migraine 2, TTH 9), which persisted at interview time for subjects with migraine. Out of 12 subjects with peri-procedural complications, 2 had a history of migraine with aura. Conclusion: Thrombectomy leads to a significant decrease in previously known migraine, and new onset of headache in a small subset of patients. A history of migraine does not appear to predispose to peri-procedural complications. [ABSTRACT FROM AUTHOR]