Page 167 - Migraine, the heart and the brain

During the follow up of our cohort, new posterior circulation silent infarcts were found in migraineurs, irrespective of gender or migraine type, in 5% compared to 0% of controls. This again was not associated with persistent migraine activity, nor with migraine frequency or life time migraine attack load. (Chapter II)
One of the questions that remained after CAMERA-I was: “What is the actual pathological substrate of the so called infarct like lesions, which are found more in the cerebellum of migraine patients”? 8 A recent human combined ex vivo MRI and histopathological study on 40 cerebellar specimens demonstrated that deep cavities in the cerebellum with “infarct-like” appearance on MRI, similar as those identi ed in our migraine study MRI scans, were indeed true infarcts. The observation of migrainous stroke occurring during a migraine attack would also support the hypothesis of ischemia.9 Silent infarcts in the cerebellum by de nition have not caused any noticeable clinical symptoms, however these silent infarcts were associated with an increased risk of clinical stroke in a non-migraine study.10 A recent meta-analysis4 of 19 studies showed that silent infarcts were not more common in migraine wit aura than controls (p=0.52). After this meta-analysis the population based Northern Manhattan Study (NOMAS) was published, which was partly inline with our ndings, that migraine was associated with silent brain infarction, however location was not predominantly in the cerebellum which was not consistent with our study.11 The underlying mechanism of the relation we found between silent cerebellar infarcts and migraine (both with and without aura) remains unclear.
Hypotheses raised are essentially the same as for the relation between white
matter lesions and migraine. We found that migraineurs with silent cerebellar
infarcts had a less favorable cardiovascular risk pro le compared to the migraineurs
without these infarcts, but the numbers behind this observation are small, thus
results must be interpreted carefully. Both hypertension and hypercholesterolemia
were overrepresented in the silent infarct group. An underlying (genetic) factor
influencing, and causing, both migraine and infarcts may be possible. It also has been 9 shown that migraineurs have endothelial dysfunction12 and increased aortic stiffness.
13 Recently it was also shown that high sensitivity C-reactive Protein (hs-CRP) and brinogen (both biomarkers of hypercoagulability and inflammation) were elevated in persons with migraine compared to controls.(personal communication) These are all systemic ndings increasing the cardiovascular risk.
Summary and general discussion
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