Triptans, CGRP-targeted drugs and migraine preventives
The trigeminovascular basis of migraine drugs, 5-HT1B/1D and 5-HT1F agonists, gepants and CGRP monoclonal antibodies, how preventives such as topiramate, propranolol and botulinum toxin work, key interactions and worked NNTs.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Migraine pain arises from trigeminovascular activation: trigeminal afferents around meningeal vessels release CGRP, substance P and PACAP, causing vasodilation, neurogenic inflammation and sensitisation of second-order neurons in the trigeminocervical complex.
- Acute drugs act on this pathway: triptans (5-HT1B/1D), gepants (CGRP receptor antagonists) and ditans (5-HT1F).
- Preventives either target CGRP (monoclonal antibodies, gepants, botulinum toxin) or reduce cortical and brainstem excitability (topiramate, valproate, beta-blockers, amitriptyline, candesartan).
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Sources
- Therapeutic Guidelines: Neurology (Migraine)AU/NZTherapeutic Guidelines Ltd, 2026
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- Australian and New Zealand Headache Society: CGRP pathway treatments and migraine management resourcesAU/NZAustralian and New Zealand Headache Society, 2024
- Rimegepant: Public Summary Document, March 2024 PBAC meetingAU/NZPharmaceutical Benefits Advisory Committee, 2024
- The American Headache Society consensus statement: update on integrating new migraine treatments into clinical practiceHeadache (Ailani J et al., 2021;61:1021-39), 2021
- Sumatriptan (oral route of administration) for acute migraine attacks in adultsCochrane Database of Systematic Reviews (Derry CJ et al., 2012), 2012
- Last updated
- 14 November 2026
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