An association between migraine and ischemic events, especially ischemic stroke, has been debated for many years. Whether migraine is a risk factor for ischemic events or ischemia triggers migraine, or both, is still unclear. This thesis explores different relationships between migraine and ischemia: the effect of anticoagulants on migraine, the possible relationship between cardiac right-to-left shunts (RLS) and migraine, and antimigraine drug use in relation to ischemic complications and cardiovascular disease. The positive effect of anticoagulants on migraine has been described in case reports and observational studies. It remains unclear whether this concerns only a select group of migraineurs with certain common characteristics. We investigated the presence of thromboembolic risk factors and the effect of low-intensity acenocoumarol therapy on migraine attacks in four migraineurs with a self-reported reduction of attack frequency during previous use of anticoagulants. All patients had one or more thromboembolic risk factors. Two patients experienced a clear improvement of migraine during low-intensity acenocoumarol therapy. In a randomized, open, crossover study in twelve migraine patients we showed that low-intensity acenocoumarol treatment has no prophylactic effect on migraine. Several studies have shown that the prevalence of a cardiac RLS in patients with migraine with aura (MA+) (both risk factors for ischemic stroke [IS] in the young) is significantly higher than in patients without migraine. In a systematic review we showed a clear association between RLS and migraine, especially MA+. Data about the prevalence of RLS in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) with and without migraine, are controversial. In our transesophageal echocardiography study in seventeen CADASIL patients, the overall prevalence of cardiac RLS was comparable with the prevalence of RLS found in the general population. The prevalence of RLS was higher, though not statistically significant, in CADASIL patients with MA+ than in CADASIL patients without migraine, confirming previous small studies. Given the small sample sizes and the striking results in another small prevalence study, the possible relationship between RLS and MA+ in CADASIL patients should be further evaluated. Due to their vasoconstrictive properties triptans and ergotamine have been associated with complications as myocardial infarction and ischemic stroke in case reports. In our retrospective nested case-control study, triptan use and even overuse was not associated with an increased risk of ischemic complications. Overuse of ergotamine turned out to be a risk factor for ischemic complications. Patients overusing ergotamine and concomitantly using cardiovascular drugs were at highest risk. It is presently unclear to what extent triptans and ergotamine are prescribed to patients with a cardiovascular risk profile. Our retrospective observational study showed that during the past 17 years the percentage of migraine patients with known cardiovascular risk factors to whom ergotamine or triptans were prescribed remained low and constant. To unravel the intriguing link between migraine and ischemia, future trials should incorporate brain imaging, hemostatic abnormalities, and biomarkers for ischemic vascular events. Hopefully this will lead to the identification of subgroups in the migraine phenotype and helps to direct treatment to those who are most likely to respond
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