Cephalalgia : an international journal of headache
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Randomized Controlled Trial
Prostaglandin I2 (epoprostenol) triggers migraine-like attacks in migraineurs.
Prostacyclin [prostaglandin I(2) (PGI(2))] activates and sensitizes meningeal sensory afferents. In healthy subjects PGI(2) triggers headache in healthy subjects. However, the migraine-eliciting effect of PGI(2) has not been systematically studied in patients with migraine. ⋯ There was a significant V(MCA) decrease (P = 0.015) and superficial temporal artery diameter increase (P < 0.001) on PGI(2) compared with placebo. In conclusion, PGI(2) may trigger a migraine-like attack in migraine sufferers. We suggest sensitization of perivascular nociceptors and arterial dilation as the mode of action of PGI(2)-induced headache and migraine-like attacks.
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The aim was to assess the relative frequency of migraine and the headache characteristics of complex regional pain syndrome (CRPS) sufferers. CRPS and migraine are chronic, often disabling pain syndromes. Recent studies suggest that headache is associated with the development of CRPS. ⋯ Migraine may be a risk factor for CRPS and the presence of migraine may be associated with a more severe form of CRPS. Specifically: (i) migraine occurs in a greater percentage of CRPS sufferers than expected in the general population; (ii) the onset of CRPS is reported earlier in those with migraine than in those without; and (iii) CRPS symptoms are present in more extremities in those CRPS sufferers with migraine compared with those without. In addition, as we also found that the presence of aura is reported in a higher percentage of those CRPS sufferers with migraine than reported in migraineurs in the general population, further evaluation of the cardiovascular risk profile of CRPS sufferers is warranted.
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Previous studies have suggested that migraine is a risk factor for brain lesions, but methodological issues hampered drawing definite conclusions. Therefore, we initiated the magnetic resonance imaging (MRI) ‘CAMERA’ (Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis) study. We summarize our previously published results. ⋯ 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.
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In the present study we used high-density EEG brain mapping to investigate spatio-temporal aspects of brain activity in response to experimentally induced muscle pain in 17 patients with migraine without aura and 15 healthy controls. Painful electrical stimuli were applied to the trapezius muscle and somatosensory-evoked potentials were recorded with 128-channel EEG with and without concurrent induced tonic neck/shoulder muscle pain. ⋯ In patients, but not in controls, the dipole changed position from baseline to the tonic muscle pain condition (z = 29 mm vs. z = -13 mm, P < 0.001) and from baseline to the post-tonic muscle pain condition (z = 29 mm vs. z = -9 mm, P < 0.001). This may be the first evidence that the supraspinal processing of muscle pain is abnormal in patients with migraine without aura.
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Population-based epidemiological studies about the prevalence of chronic migraine using the 2004 International Headache Society (IHS) classification definition are rare. We analysed the data of the Deutsche Migräne und Kopfschmerz Gesellschaft headache study, which included 7417 adults in three regions of Germany, with respect to their headache. Additionally, body mass index, alcohol consumption and smoking behaviour were recorded. ⋯ The skewed distribution of the numbers of attacks per patient supports the recommendation to differentiate between episodic migraine with low and high attack frequency, as is done in the classification of tension-type headache. It further suggests that migraine with high attack frequency might be biologically different. The higher prevalence of smokers and of patients with a body mass index ≥ 30 in chronic migraine or MOH supports the idea of a frontal dysfunction in these patients.