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Click here for Vydura®▼ (rimegepant) Prescribing Information for Great Britain and Northern Ireland.
Adverse event reporting information can be found at the bottom of the page.
Once thought of as a vascular disease, caused by vasodilation, it is now established that migraine is a neurological disorder, although the vasculature may impact the mechanisms involved.1,2 Activation of nociceptive neurons originating in the trigeminal ganglion and innervating dural blood vessels results in vasodilation within the meninges, neurogenic inflammation and central sensititisation. These effects can cause headache and are associated with other symptoms, including aura.1,3
Research has shown that several anatomic regions within the brain and specific molecular pathways are likely responsible for the different symptoms experienced across different phases of migraine.1
Prodrome:
symptoms occurring up to 72 hours before the headache phase1
Aura:
visual or other sensory symptoms usually preceding the headache phase1
Headache phase:
often severe, unilateral, pulsating pain1
The following classes of drugs specifically target pathophysiological pathways involved in migraine.3,7,8
Click to reveal mechanism of action
Triptans are serotonin analogues, and bind selectively to 5-HT1 receptors.3
| PROPOSED CENTRAL MECHANISM4 | PERIPHERAL MECHANISM4 | |
|---|---|---|
| Disruption of the afferent return of nociceptive signals to the trigeminal nucleus Decreased transmission of pain signal |
Binding to the 5-HT1B receptor results in vasoconstriction Reduced pain due to cranial vasodilation |
Binding to the 5-HT1D receptor blocks release of vasoactive peptides Reduced neuroinflammation |
Due to the vasoactive effects of triptans, they are contraindicated in patients with cardiovascular or cerebrovascular disease and uncontrolled hypertension.3
Reference: 3. Ong J J Y, De Felice M. Neurotherapeutics 2018;15:274-290
Calcitonin gene-related peptide (CGRP) is a strong vasodilator, and has a role in cranial nociception, especially when released from trigeminal ganglion neurons. Raised plasma levels of CGRP are associated with headache in migraine.8
The mechanism of action of anti-CGRP or anti-CGRP receptor mAbs has not yet been fully elucidated. mAbs cannot typically cross the blood-brain-barrier, so action is likely to be at a peripheral site, such as CGRP receptors in the brainstem.5,8
It is thought that by binding to CGRP or the receptor, and thus blocking activation, the mAbs prevent CGRP-induced trigeminal nociceptive transmission.8
Clinical trials indicate a reduction in headache frequency and in acute medication use with anti-CGRP mAbs versus placebo.8
Clinical trials indicate a reduction in headache frequency and in acute medication use with anti-CGRP mAbs versus placebo.8
Reference: 8. Pellesi L et al. Clin Pharmacol Drug Dev 2017;6:534-547
mAbs have been
designed to target the
CGRP-CGRP receptor
interaction.8
CGRP: calcitonin gene-related peptide; mAb: monoclonal antibody
Adverse events should be reported. Reporting forms and information can be found at www.mhra.gov.uk/yellowcard or search
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Adverse events should also be reported to Pfizer Medical Information on 01304 616161
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