Cephalalgia : an international journal of headache
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We studied the association of chronic headache and chronic rhinosinusitis in 30,000 persons aged 30-44 years from the general population. They received a mailed questionnaire. Those with possible chronic headache were interviewed by neurological residents. ⋯ Compared with the general population, persons with chronic rhinosinusitis have an at least ninefold increased risk of having chronic headache. A 3-year follow-up showed that HACRS symptoms were significantly improved after treatment with nasal surgery, nasal corticosteroids, discontinuation of overused headache medications and discontinuation of nasal decongestants or unspecified reasons. Chronic rhinosinusitis is significantly associated with chronic headache, and HACRS is likely to be a distinct type of headache.
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Nummular headache (NH) is characterized by focal pain fixed within a small round or elliptical area of the head surface. Sensory dysfunction is apparently restricted to the symptomatic area, but a thorough analysis of cranial pain sensitivity has not been performed. Pressure pain sensitivity maps were constructed for 21 patients with NH and 21 matched healthy controls. ⋯ In both groups an anterior to posterior gradient was found on each side, with no significant differences of PPT measurements between sides or groups. In patients with NH, only the symptomatic area showed a local decrease of PPT (significant in comparison with the non-symptomatic symmetrical point, P < 0.001). These findings further support that NH is a non-generalized disorder with a peripheral source.
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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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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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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.