The journal of headache and pain
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Comparative Study
Methylprednisolone blocks interleukin 1 beta induced calcitonin gene related peptide release in trigeminal ganglia cells.
Methylprednisolone (MPD) is a rapid acting highly effective cluster headache preventive and also suppresses the recurrence of migraine attacks. Previously, we could demonstrate that elevated CGRP plasma levels in a cluster headache bout are normalized after a course of high dose corticosteroids. Here we assess whether MPD suppresses interleukin-1β (IL-1β)- and prostaglandin E2 (PGE2)-induced CGRP release in a cell culture model of trigeminal ganglia cells, which could account for the preventive effect in migraine and cluster headache. Metoprolol(MTP), a migraine preventive with a slow onset of action, was used for comparison. ⋯ MPD but not MTP suppresses cytokine (IL-1β)-induced CGRP release from trigeminal ganglia cells. We propose that blockade of cytokine mediated trigeminal activation may represent a potential mechanism of action that mediates the preventive effect of MTP on cluster headache and recurrent migraine attacks.
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The exact pathophysiology of cluster headache is unclear. We examined the influence of interneurons on the trigemino-facial reflex arch and the effect of oxygen, by using the nociception specific blink reflex parameters. ⋯ The nociception specific blink reflex seems not a suitable instrument for exploring the pathophysiology of cluster headache.
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Cluster headache is classified as a primary headache by definition not caused by an underlying pathology. However, symptomatic cases of otherwise typical cluster headache have been reported. ⋯ Neuroimaging should be considered in all patients with CCH, especially those with an atypical presentation or evolution. Response to acute treatment does not exclude a secondary form of cluster headache. There may be shared pathophysiological mechanisms of primary and secondary cluster headache.
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Urotensin-II (U-II) is a peptide recognized by its potent vasoconstrictor activity in many vascular events, however the role of urotensin-II in migraine has not been considered yet. The molecular mechanisms and genetics of migraine have not been fully clarified yet, but it is well-known that vascular changes considerably contribute in pathophysiology of migraine and also its complications. The aim of this study was to analyze the plasma U-II levels along with genotype distributions and allele frequencies for UTS2 Thr21Met and Ser89Asn polymorphisms among the patients with migraine without aura (MWoA). ⋯ Our study suggests that U-II may play a role in migraine pathogenesis; also Thr21Met polymorphism was associated with the risk of migraine disease. Further studies are needed for considering the role of U-II in migraine pathophysiology and for deciding if UTS2 gene may be a novel candidate gene in migraine cases.
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The trigeminal nociceptive system plays a pivotal role in the pathophysiology of migraines. The present study investigated whether there are differences between patients with episodic migraine (EM) and patients with chronic migraine (CM) in trigeminal pain processing at the brainstem and cortical levels using the nociceptive blink reflex (nBR) and pain-related evoked potentials (PREP). ⋯ In the present study, the facilitation in the trigeminal nociceptive pathway of the EM group suggests the occurrence of migraine-specific hyperexcitability. Additionally, the suppression of R2 at the brainstem level in the CM group may relate to impaired or dysfunctional descending pain modulation. These findings suggest that there are adaptive or maladaptive responses due to the chronification of migraine attacks.