Migraine — Current Understanding and Treatment

Goadsby, Peter J.; Lipton, Richard B.; Ferrari, Michel D.

doi:10.1056/nejmra010917

Cited by 1,707 publications

(1,353 citation statements)

References 126 publications

(109 reference statements)

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“…Thus, BIBN4096BS could produce, at a postjunctional level (by CGRP receptor blockade), effects similar to those that triptans cause by reducing CGRP release, and that result in inhibition of CGRP receptor signalling. Indeed, triptans inhibit trigeminal CGRP release in animal experimental models [55,63], and clinical data show that sumatriptan normalised the elevated CGRP levels with alleviation of migraine [55] and cluster headache attack [65]. These findings have suggested that BIBN4096BS could be developed as an effective antimigraine drug.…”

Section: Cgrp Antagonists In Migrainementioning

confidence: 98%

“…However, it is possible that genetic abnormalities initiate the alteration of the response threshold to migraine-specific triggers in the brain [55]. Studies using positron emission tomography have shown increased blood flow (an index of neuronal activity) during spontaneous migraine attacks in the cerebral hemispheres (cingulate, auditory and visual suppression areas) and suggest that the process driving the migraine attack and the area susceptible to the migraine triggers may be located in the brain stem [56].…”

Section: Migraine and Neurogenic Inflammationmentioning

confidence: 99%

“…There is also evidence in experimental animals that the migraine aura, rather than from an ischaemic phenomenon, derives from an initial neuronal dysfunction and is probably the clinical manifestation of a cortical spreading depression [58,59]. A reflex painful vasodilatation of the cranial blood vessels follows the cerebral oligaemia, and probably derives from activation of the trigeminal perivascular innervation [55,57].…”

Section: Migraine and Neurogenic Inflammationmentioning

confidence: 99%

“…Ergotamine and triptans have been proposed to abort migraine attacks by diverse mechanisms, including constriction of dilated cranial blood vessels and carotid arteriovenous anastomoses [68], reduction of CGRP release from perivascular trigeminal nerve endings, and inhibition of nociceptive transmission on peripheral and central endings of trigeminal sensory nerves [55]. Similarly to rodents, human trigeminal ganglia/sensory nerves express abundant 5-HT1B/1D receptors [69], thus strengthening the evidence in favour of the presynaptic inhibitory effects of triptans [62].…”

Section: Action Of Drugs Effective On Neurogenic Vasodilatationmentioning

confidence: 99%

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CGRP and migraine: neurogenic inflammation revisited

Geppetti

Capone²,

Trevisani

et al. 2005

J Headache Pain

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The term 'neurogenic inflammation' refers to a series of proinflammatory responses produced by the stimulation of peripheral terminals of a subset of primary sensory neurons and the subsequent release of the neuropeptides, calcitonin gene-related peptide (CGRP) and the tachykinins, substance P (SP) and neurokinin A (NKA) [1]. The neurons that produce inflammation comprise a heterogeneous cell population with A-delta and C fibres, defined as polymodal nociceptors because they sense thermal, chemical and high-threshold mechanical stimuli. These neurons express on their plasma membrane a large panel of excitatory and inhibitory receptors and channels, and some of these signalling proteins have been successfully used as targets for analgesic or anti-inflammatory drugs. Among the channels expressed on peptidergic primary sensory neurons, transient receptor potential vanilloid-1 (TRPV1) [2], activated by the xenobiotic capsaicin, the pungent ingredient of plants of the genus Capsicum, is of paramount importance. Capsaicin produces burning pain by stimulating TRPV1 and by releasing sensory neuropeptides causes neurogenic inflammation. However, high concentrations/doses of capsaicin have the ability, after an initial excitatory phase, to desensitise the sensory nerve terminals, thus reducing the transmission of sensory/pain signals and abolishing neurogenic inflammation [3, 4]. This specific feature of capsaicin has greatly contributed to define the role of this subset of sensory nerves in pathophysiological models of human diseases and has been Pierangelo Geppetti Jay Guido Capone Marcello Trevisani Paola Nicoletti Giovanni Zagli Maria Rosalia Tola Abstract For more than a century neurogenic inflammation has been proposed to have a role in various human diseases. The present review will cover the conceptual steps of the itinerary that has led to the conclusion that neurogenic inflammation is important in migraine. Of particular relevance for the object of this article is the observation that tachykinindependent neurogenic inflammatory responses are evident in rodents, but much less pronounced or absent in other mammal species, including man, whereas neurogenic vasodilatation, most likely mediated by CGRP, occurs in most mammalian species and also in man. Recent evidence that a CGRP receptor antagonist was effective in the treatment of migraine attack supports the hypothesis that neurogenic vasodilatation is a major underlying mechanism of migraine.

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Section: Cgrp Antagonists In Migrainementioning

confidence: 98%

Section: Migraine and Neurogenic Inflammationmentioning

confidence: 99%

Section: Migraine and Neurogenic Inflammationmentioning

confidence: 99%

Section: Action Of Drugs Effective On Neurogenic Vasodilatationmentioning

confidence: 99%

See 2 more Smart Citations

CGRP and migraine: neurogenic inflammation revisited

Geppetti

Capone²,

Trevisani

et al. 2005

J Headache Pain

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“…4 The development of triptans, serotonin 5-HT 1B/1D receptor agonists, 5 was a substantial advance in acute migraine therapy, although only one third of patients are headache-free 2 hours after treatment. 6 Moreover, there are important contraindications to their use in the setting of cardiovascular and cerebrovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Headache

Goadsby

2010

Neurotherapeutics

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Migraine and Risk of Cardiovascular Disease in Men

Kurth

Gaziano²,

Cook³

et al. 2007

Arch Intern Med

213

223

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Background: The vascular component of the migrainespecific physiologic profile and the observed adverse cardiovascular risk profile in migraineurs suggest an association between migraine and cardiovascular disease (CVD). In women, migraine has been associated with increased risk of CVD, including coronary events. Compatible data in men are lacking. Methods: Prospective cohort study of 20 084 men aged 40 to 84 years participating in the Physicians' Health Study. In yearly questionnaires, men were asked for information on migraine, risk factors, and the occurrence of study end points. We classified men as having migraine if they indicated migraine during the first 5 years, after which time follow-up began. Information on aura was not available. All the men were free of CVD at the start of followup. During a mean of 15.7 years, we followed up participants for the occurrence of a first major CVD event (nonfatal ischemic stroke, nonfatal myocardial infarction, or death from ischemic CVD). We also evaluated the individual end points, coronary revascularization, and angina. Results: A total of 1449 men (7.2%) reported migraine, and during follow-up, 2236 major CVD events occurred. Compared with nonmigraineurs, men who reported migraine had multivariable-adjusted hazard ratios (95% confidence intervals) of 1.24 (1.06-1.46; P =.008) for major CVD, 1.12 (0.84-1.50; P =.43) for ischemic stroke, 1.42 (1.15-1.77; PϽ.001) for myocardial infarction, 1.05 (0.89-1.24; P =.54) for coronary revascularization, 1.15 (0.99-1.33; P=.068) for angina, and 1.07 (0.80-1.43; P=.65) for ischemic cardiovascular death. Conclusion: In this large prospective cohort of apparently healthy men, migraine was associated with increased risk of major CVD, which was driven by increased risk of myocardial infarction.

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Migraine — Current Understanding and Treatment

Cited by 1,707 publications

References 126 publications

CGRP and migraine: neurogenic inflammation revisited

CGRP and migraine: neurogenic inflammation revisited

Headache

Migraine and Risk of Cardiovascular Disease in Men

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