Official websites use. Share sensitive information only on official, secure websites. Corresponding author: M. Previous studies suggested that migraine is a risk factor for brain lesions, but methodological issues hampered drawing definite conclusions. We summarize our previously published results. We observed a higher lifetime prevalence of frequent syncope and orthostatic insufficiency in migraineurs; future research needs to clarify whether autonomic nervous system dysfunction could explain part of the increased risk of WMLs in female migraineurs.
Higher risks in those with higher attack frequency or longer disease duration were found consistent with a causal relationship between migraine and lesions. This summary of our population-based data illustrates that migraine is associated with a significantly increased risk of brain lesions. Longitudinal studies are needed to assess whether these lesions are progressive and have relevant long-term functional correlates. Migraine has been considered for decades as an episodic disorder without long-term consequences to the brain.
However, over the past 30 years several studies have been carried out looking at and delivering arguments for a possible association between migraine and brain changes. For this association, three lines of evidence can be recognized. Migrainous infarction has been estimated to occur with a low incidence 1. A meta-analysis summarized the evidence and calculated a pooled relative risk of 2.
Third, a number of clinic-based MRI studies found an increased prevalence of cerebral white matter hyperintense lesions WMLs in migraine patients; a meta-analysis calculated a pooled increased risk of 3.
However, in non-migraine patients, it has been shown that both clinical and subclinical brain lesions can lead to negative sequellae, affecting both physical and cognitive function. Therefore, it is of primary importance to investigate whether migraine is an independent risk factor for subclinical white matter lesions and infarcts. In addition, we collected data from neurologic physical examination and cognitive tests, to correlate these data with lesion load.
