Cephalalgia

Migraine, in particular with aura, has been associated with an increased risk for ischemic stroke and coronary heart disease. The underlying mechanism is unknown. In a cross-sectional case control study we investigated whether an enhanced risk of atherosclerosis in migraineurs explains this increased cardiovascular risk.

Subjects were participants from the population-based Erasmus Rucphen Family study. Atherosclerosis was assessed in 360 migraineurs (209 without aura and 151 with aura) and 617 subjects without migraine or severe headache. Atherosclerosis was quantified by intima media thickness, pulse wave velocity and ankle-brachial index.

Migraineurs, especially with aura, were found more likely to smoke, have diabetes or a modestly decreased HDL-cholesterol. No differences were found for the atherosclerosis parameters.

In this large population-based study, migraineurs have no increased risk of atherosclerosis. Therefore, enhanced atherosclerosis is an unlikely explanation for the increased cardiovascular risk seen in migraineurs.

Migraine has been considered a vascular risk factor especially in young women. Factors predisposing to endothelial damage in migraine are still being debated. The insufficiency of circulating endothelial precursor circulating cells (EPCs) suggested a link between migraine and cardiovascular risk. This research aimed to study a subtype of EPCs, those expressing e-selectin, to assess endothelial activation and, therefore, endothelial dysfunction in migraine.

Consecutive headache patients (n = 99) and 35 adjusted controls were recruited. Total EPCs, defined as CD34+/KDR+ cells, and EPC colony-forming units (CFUs) were assayed. We identified as “early” EPCs those CD62E– EPCs, and “late” EPCs, CD62E+, a surrogate marker for endothelial damage. Plasmatic calcitonin-gene related protein (CGRP) and vascular-endothelial growth factor (VEGF) were analyzed.

We did not find differences in the total number of CFUs among clinical groups. Means of total CD34+/KDR+ and “early” EPCs were not significant among clinical groups. Nevertheless, the mean of “late” EPCs was lower (log₁₀-transformed mean = 1.715; SD = 0.393) in the control group than in the migraine patients (log₁₀-transformed mean = 2.167; SD = 0.685), even after adjustment by VEGF plasma level and other confounding factors. Linear regression analyses disclosed significant predictors for “late” EPCs for controls vs migraine (β = 0.452 SE ± 0.13; p = 0.001). We did not observe differences between migraine with or without aura.

We observed higher number of activated EPCs in migraine patients than in controls. CD62E+ EPCs might be considered a marker for vascular damage in migraine patients.

Using functional magnetic resonance imaging (fMRI), we aimed to explore the habituation behaviour to trigemino-nociceptive as well as olfactory stimuli in migraine patients. We exclusively focussed on intrasessional behavioural rating patterns and the related blood oxygen level dependent (BOLD) signal changes.

We observed that groups significantly differ in the time course of pain intensity ratings during the stimulation session: whereas interictal migraineurs sensitized (increasing pain ratings), control subjects habituated (decreasing pain ratings). Pain ratings of ictal patients remained unchanged. This behaviour is accompanied by a similar time course of neuronal activity in the bilateral anterior insula, in the middle cingulate cortex and in the thalamus. In these areas, the brain activity increased in migraineurs but decreased in the control group during the session. In contrast to these findings, the rating patterns for the olfactory stimuli (rose odour) did not differ between patients and controls and a gradual decrease of perceived stimulus intensity was found in all three groups. This stimulus specific response may occur because the olfactory system is the only sensory system not passing the thalamus.

Our data suggest that impaired habituation in functional brain systems in migraine is fundamental only to specific modalities including the trigemino-nociceptive, but, at least, excluding the olfactory system. Our findings further suggest that there is no single neuronal modulator responsible for the altered rating pattern in migraineurs.

Data on the prevalence and characteristics of chronic migraine (CM) and chronic daily headache (CDH) in the Asia-Pacific region are limited.

We performed a systematic review on this topic, searching for studies published from 1996 to 2012 that reported the prevalence (population-based studies) or frequency (clinic studies) of CM or CDH. We calculated 95% confidence intervals for the prevalence in population studies. Results were qualitatively described.

Seven population studies and 19 hospital clinic studies from Asia were included. The CDH prevalence in population studies was 1.0–3.9% (median 2.9%). Only two studies from Taiwan reported the population prevalence of CM (1.0% and 1.7%). In addition, we derived a prevalence of 0.6% from a Malaysian study. Eleven clinic studies reported a CM frequency of 4.7–82% (median 52%) as a subset of CDH; classification of medication overuse varied. CM was associated with substantial disability.

The prevalence of CM and CDH in Asia appears lower than the global average, but applying the above prevalence estimates to the Asia-Pacific population would suggest that CM alone affects between 23 and 65 million individuals in the region.