Sumatriptan: A Receptor-Targeted Treatment for Migraine

Moskowitz, M. A.

doi:10.1146/annurev.med.44.1.145

Cited by 23 publications

(33 citation statements)

References 26 publications

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“…Proinflammatory mediators have been cited widely as playing a role in the pathophysiology of migraine both centrally and peripherally. 1–3 Nonsteroidal anti‐inflammatory agents and acetylsalicylic acid have been used both abortively and preventively in its treatment. 1 In addition, triptans inhibit neurogenic inflammation as a part of their mechanism of action.…”

Section: Lt Antagonist Pharmacokinetic Profilesmentioning

confidence: 99%

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

et al. 2000

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Section: Lt Antagonist Pharmacokinetic Profilesmentioning

confidence: 99%

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

et al. 2000

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“…Both sumatriptan and dihydroergotamine block this neurogenic extravasation of plasma but do not affect extravasation of plasma mediated by substance P or neurokinin A, suggesting that the vascular action of sumatriptan as a selective carotid vasoconstrictor is not necessary for its antiinflammatory effect 20. However, there is no clear clinical evidence to support the theory of a sterile inflammation in migraine.…”

Section: Mechanism Of Actionmentioning

confidence: 94%

“…Moskowitz has suggested that the pain of migraine is due to a sterile inflammation in the aura mater mediated by the release of calcitonin gene related peptide described above 20. Both sumatriptan and dihydroergotamine block this neurogenic extravasation of plasma but do not affect extravasation of plasma mediated by substance P or neurokinin A, suggesting that the vascular action of sumatriptan as a selective carotid vasoconstrictor is not necessary for its antiinflammatory effect 20.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Fortnightly Review: Diagnosis and management of migraine

Goadsby

Olesen

1996

BMJ

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Summary points Before a primary headache such as migraine is diagnosed, secondary headaches should be considered and eliminated on clinical grounds or by appropriate investigations Migraine is primarily diagnosed by eliciting a history of episodic headache with characteristic associated features. The use of diagnostic headache diaries and simple calendars is strongly encouraged Optimum treatment of migraine requires explaining the problem to the patient and identifying and avoiding precipitating factors Treatment may be non-pharmacological or pharmacological. Drugs may be for treating acute attacks, which is required by nearly all patients, or prophylaxis, which is used by patients with frequent severe attacks Treatment for an acute attack should result in mild or no headache by two hours after drug ingestion, while prophylactic treatment should result in a 50% reduction in the frequency of attacks Characterisation of the 5-hydroxytryptamine receptor of the 5-HT1 class has provided better treatments for acute attack and impetus for studying mechanism of migraine

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“…In addition, antagonists at the neurokinin‐1 receptor attenuate plasma protein leakage. While neurokinin‐1 receptor antagonists failed in clinical trials to abort migraine attacks (May & Goadsby, 2001) the agonists at the 5‐HT 1B/D receptor are powerful antimigraine drugs (Moskowitz & Cutrer, 1993).…”

Section: Neurovascular Models For Pharmacological Developmentmentioning

confidence: 99%

“…The triptans are thought to inhibit the abnormal activation of peripheral nociceptors. The triptans are potent inhibitors of experimental neurogenic inflammation and PPE (Moskowitz & Cutrer, 1993), presumably by inhibiting the activation of nociceptors and preventing the peripheral release of vasoactive peptides, including substance P and CGRP. Also consistent with a peripheral action for triptans, venous CGRP is elevated in the external jugular vein, both after stimulation of the trigeminal ganglion (Goadsby et al ., 1988) and during a migraine attack (Goadsby et al ., 1990), and treatment with sumatriptan reduces CGRP levels as the migraine subsides (Goadsby & Edvinsson, 1993).…”

Section: New Approaches To Studying the Trigeminovascular Systemmentioning

confidence: 99%

Animal models of migraine: looking at the component parts of a complex disorder

Bergerot

Holland

Akerman

et al. 2006

Eur J of Neuroscience

113

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Animal models of human disease have been extremely helpful both in advancing the understanding of brain disorders and in developing new therapeutic approaches. Models for studying headache mechanisms, particularly those directed at migraine, have been developed and exploited efficiently in the last decade, leading to better understanding of the potential mechanisms of the disorder and of the action for antimigraine treatments. Model systems employed have focused on the pain-producing cranial structures, the large vessels and dura mater, in order to provide reproducible physiological measures that could be subject to pharmacological exploration. A wide range of methods using both in vivo and in vitro approaches are now employed; these range from manipulation of the mouse genome in order to produce animals with human disease-producing mutations, through sensitive immunohistochemical methods to vascular, neurovascular and electrophysiological studies. No one model system in experimental animals can explain all the features of migraine; however, the systems available have begun to offer ways to dissect migraine's component parts to allow a better understanding of the problem and the development of new treatment strategies.

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Sumatriptan: A Receptor-Targeted Treatment for Migraine

Cited by 23 publications

References 26 publications

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

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

Fortnightly Review: Diagnosis and management of migraine

Animal models of migraine: looking at the component parts of a complex disorder

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