Montelukast in the Prophylaxis of Migraine: A Potential Role for Leukotriene Modifiers

Sheftell, Fred D.; Rapoport, Alan M.; Weeks, Randall E.; Walker, B.; Gammerman, I.; Baskin, Steven M.

doi:10.1046/j.1526-4610.2000.00022.x

Cited by 59 publications

(37 citation statements)

References 18 publications

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“…LTC 4 , however, does not affect the mechanosensitivity of airway afferents (Riccio et al, 1996). In our current study, we found that LTC 4 did not affect meningeal nociceptors even when applied at the highest dose and for up to 1 h. Although there is evidence to suggest that leukotriene receptor modifiers, such as montelukast, which blocks signal transduction through the leukotriene receptor CysLT1 (Funk, 2005), can serve as prophylactic migraine drugs (Sheftell et al, 2000), our results suggest that if LTC 4 or its metabolites play a role in migraine precipitation, their action may not be mediated by promoting the activation or sensitization of meningeal nociceptors.…”

Section: Discussioncontrasting

confidence: 53%

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

Zhang¹,

Strassman²,

Burstein³

et al. 2007

J Pharmacol Exp Ther

150

125

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Intracranial headaches such as migraine are thought to result from activation of sensory trigeminal pain neurons that supply intracranial blood vessels and the meninges, also known as meningeal nociceptors. Although the mechanism underlying the triggering of such activation is not completely understood, our previous work indicates that the local activation of the inflammatory dural mast cells can provoke a persistent sensitization of meningeal nociceptors. Given the potential importance of mast cells to the pain of migraine it is important to understand which mast cell-derived mediators interact with meningeal nociceptors to promote their activation and sensitization. In the present study, we have used in vivo electrophysiological single-unit recording of meningeal nociceptors in the trigeminal ganglion of anesthetized rats to examine the effect of a number of mast cell mediators on the activity level and mechanosensitivity of meningeal nociceptors. We have found that that serotonin (5-HT), prostaglandin I 2 (PGI 2 ), and to a lesser extent histamine can promote a robust sensitization and activation of meningeal nociceptors, whereas the inflammatory eicosanoids PGD 2 and leukotriene C 4 are largely ineffective. We propose that dural mast cells could promote headache by releasing 5-HT, PGI 2 , and histamine.

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Section: Discussioncontrasting

confidence: 53%

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

Zhang¹,

Strassman²,

Burstein³

et al. 2007

J Pharmacol Exp Ther

150

125

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“…These studies have shown the following: 1) that plasma histamine levels are elevated during migraine attacks in a subpopulation of migraineurs [20]; 2) the ability of histamine infusion to promote a migraine-like headache in most patients [21]; and 3) that antihistaminergic drugs can serve as potent prophylactic agents in migraine [22][23][24]. Recent studies also have implicated other proinfl ammatory MC-derived molecules in migraine pathophysiology, including leukotrienes [25], tumor necrosis factor (TNF)-α, interleukin (IL)-6 [6], and endothelin-1 [26]. Finally, a role for MC in migraine has been suggested based on epidemiological studies showing a signifi cantly higher prevalence of migraine in patients affl icted with other MC-related disorders such as asthma, eczema, rhinitis, and interstitial cystitis [27].…”

Section: Evidence For Mast Cell Involvement In Migrainementioning

confidence: 99%

Migraine pain, meningeal inflammation, and mast cells

Levy

2009

Current Science Inc

169

138

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Migraine pain has been attributed to an episode of local sterile meningeal inflammation and the subsequent activation of trigeminal primary afferent nociceptive neurons that supply the intracranial meninges and their related large blood vessels. However, the origin of this inflammatory insult and the endogenous factors that contribute to the activation of meningeal nociceptors remain largely speculative. A particular class of inflammatory cells residing within the intracranial milieu, known as meningeal mast cells, was suggested to play a role in migraine pathophysiology more than five decades ago, but until recently the exact nature of their involvement remained largely unexplored. This review examines the evidence linking meningeal mast cells to migraine and highlights current experimental data implicating these immune cells as potent modulators of meningeal nociceptors' activity and the genesis of migraine pain.

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“…While the role of mast cells in pathogenesis of asthma is well established, there is growing evidence that mast cells contribute to migraine genesis as well by secretion of vasoactive, pro-inflammatory, and neurosensitizing mediators following trigeminal activation [95]. However after encouraging open label trials montelukast [91], an agent blocking the action of leukotriene D4, which is released from mast cells and mediates inflammation, failed to prove efficacy in migraine prophylaxis [16].…”

Section: Migraine Asthma and Allergiesmentioning

confidence: 99%

Migraine-associated risks and comorbidity

2008

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This review reports important co-morbid conditions of migraine and resulting consequences for the choice of acute and preventive treatments of migraine. Comorbidity in this context means the occurrence of two diseases in an individual beyond chance. The basis of comorbidity can be genetic and/or based on common environmental factors. In some cases, the temporal relationship is unclear and one disease can cause another disease. In order to prove a real comorbidity, large-scale and well-performed epidemiological studies are required.

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Montelukast in the Prophylaxis of Migraine: A Potential Role for Leukotriene Modifiers

Cited by 59 publications

References 18 publications

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

Migraine pain, meningeal inflammation, and mast cells

Migraine-associated risks and comorbidity

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