Page 48 - Migraine, the heart and the brain

Chapter 2
posterior circulation territory infarct like lesions among women. In addition, the number of migraines, frequency of migraines, migraine severity, type of migraine, and migraine therapy were not associated with lesion progression. Increase in deep white matter hyperintensity volume was not signi cantly associated with poorer cognitive performance at follow-up.
This study has several strengths, including the longitudinal study design, length of follow-up, the relatively well characterized cohort, use of standardized International Headache Society criteria-based diagnosis of migraine by headache experts, and sensitive and reproducible methods of MRI reading. The sensitive MRI techniques used allowed for a more detailed analysis of the brain, in particular the cerebellum. Approximately one-third of the original baseline population could not be reinvestigated. This may have introduced selection bias. However, there were no differences in baseline MRI parameters between participants and nonparticipants and there was no imbalance between the proportions and demographic and clinical characteristics of nonparticipating individuals with migraine and controls. Because of differences between the semiquantitative baseline reading of deep white matter hyperintensities and the current quantitative volume measurements that were not available for the nonresponders, additional imputation analyses to support the sensitivity of the current results could not be performed. An additional study limitation is that con dence intervals are wide (Table 3).
The number of migraine attacks, frequency of migraines, migraine severity, type of migraine headaches, and migraine therapy were not associated with lesion progression. In contrast, our baseline data showed that more frequent migraine headaches were associated with a higher prevalence of MRI ndings.4
However, our ndings at baseline regarding frequency-related difference in MRI ndings was most pronounced among those in the migraine group who were 50 years or younger and less so in older patients. Thus, with increasing age of the study population, when attacks generally diminish,1 other migraine disease-related conditions leading to white matter hyperintensities are possibly increasing, complicating the detection of migraine attack-related associations. A similar, age-dependent mechanism is also seen for the risk of stroke in participants with migraine, which is increased in young patients only.14,21 At older age, other risk factors such as hypertension may obscure or overcome any potential role of migraine. In the present case, we hypothesize there are at least 2 different types of vascular mechanisms that may cause structural brain changes in migraine: one, which is primarily related to attacks and mainly present at younger age, and another, which is probably ongoing as part of having the disease migraine. The observation of migrainous stroke, with stroke occurring during a migraine attack,
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