Beta-blockers (e.g., propranolol, metoprolol)
- Rationale: Reduce sympathetic nervous system activity, which may play a role in migraine pathogenesis.
- Antidepressants (e.g., amitriptyline, venlafaxine)
- Rationale: Tricyclic antidepressants (TCAs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) modulate pain pathways.
- Antiepileptics (e.g., topiramate, valproate)
- Rationale: Stabilize neuronal excitability, reducing cortical spreading depression.
- CGRP antagonists (e.g., erenumab, fremanezumab)
- Rationale: Block calcitonin gene-related peptide (CGRP), a key player in migraine pathophysiology.
- OnabotulinumtoxinA (Botox)
- Rationale: Inhibits neurotransmitter release at the neuromuscular junction, reducing pain transmission.
- Calcium channel blockers (e.g., verapamil)
- Rationale: Modulate vascular tone and neuronal excitability.
- NSAIDs (e.g., naproxen, ibuprofen)
- Rationale: Reduce inflammation, which may contribute to migraine.
- Dietary supplements (e.g., riboflavin, magnesium, coenzyme Q10)
- Rationale: May improve mitochondrial function and reduce oxidative stress.
Guidelines:
- AHA/ASA (2021) recommend beta-blockers, TCAs, and antiepileptics as first-line options.
- EHF (2020) suggests CGRP antagonists for patients with frequent or severe migraines.