Give a tight mechanistic explainer that **closes the loop from receptor → pathway → less pain** for both **acute** and **preventive** migraine options. Keep it plain-language, no tables.
**First, the shared pain pathway (brief):** trigeminovascular activation → CGRP release → meningeal vasodilation + sterile neurogenic inflammation → peripheral/central sensitization → pain perception.
**Acute mechanism → relief (map binding site → cellular → network effects):**
• **Triptans** (5-HT1B/1D agonists)
• **Lasmiditan** (5-HT1F agonist)
• **Gepants** (CGRP-receptor antagonists)
• **Riboflavin / Vitamin B2** (include here as a mechanistic contrast even though preventive)
For each: say if it **causes vasoconstriction (Y/N)** and why that matters; connect to **time-to-relief** and **route** choices (oral/ODT/nasal/SC) in nausea/vomiting or severe attacks; give **one key safety/contra**; and note **MOH tendency/neutrality** if relevant.
**Acute “bundle” / clinic-ED migraine cocktail (briefly, mechanism-linked):**
Explain how combining a **dopamine-antagonist antiemetic** (e.g., prochlorperazine/metoclopramide) + **NSAID** (e.g., ketorolac) + **IV fluids ± magnesium** can act on different nodes of the pathway (nausea centers, inflammatory mediators, CGRP-linked vasodilation/sensitization, dehydration). Note typical **synergy**, common **adverse effects** (e.g., akathisia) and the rationale for **diphenhydramine co-use** to mitigate it. *(If details extend beyond the session content, label them as general clinical practice.)*
**Preventive mechanism → fewer attacks (map class → core MOA → how sensitization/cortical hyperexcitability is reduced):**
• **Beta-blockers** (metoprolol, propranolol, atenolol)
• **ARB** candesartan
• **Anti-seizure**: topiramate, valproate
• **Antidepressants**: amitriptyline, nortriptyline, venlafaxine
• **CGRP monoclonal antibodies**: erenumab, fremanezumab, galcanezumab; **eptinezumab** IV
• **Preventive gepants**: rimegepant (qod), atogepant (daily)
• **OnabotulinumtoxinA** (q12 weeks), **nerve blocks/devices** (mechanism sketch)
• **Riboflavin/Vitamin B2**: tie mitochondrial electron transport support → improved neuronal energy homeostasis → less cortical hyperexcitability → fewer attacks.
**Close with 3–5 rules-of-thumb** that tie mechanism to **who benefits & when to choose** (e.g., vascular disease → avoid vasoconstrictors; prominent nausea → non-oral routes/antiemetic-forward; high attack frequency → prevention threshold and which class to try first vs CGRP-targeted options).
Keep it concise (≈12–18 bullets total) and make every step explain *how the mechanism yields less pain or fewer attacks*.