Migraine

Build the medication list first - Ask specifically about triptans, ergots, beta blockers, valproate or divalproex, topiramate, amitriptyline, and CGRP monoclonal antibodies such as erenumab. Each changes something about your plan, and patients don't volunteer "migraine pills" as medications.

Triptans and serotonergic drugs - All triptans are 5-HT1B/1D agonists. Sumatriptan is metabolized by monoamine oxidase, so pairing it with other serotonergic agents raises serotonin syndrome risk. 5-HT1B receptors also sit on coronary arteries, so triptans cause coronary vasoconstriction and are avoided in known cardiovascular disease; sumatriptan is not given IV because of vasospasm. Watch for the "triptan sensations" — paresthesia, flushing, neck pain, chest tightness — and don't reflexively call chest tightness ischemia without an ECG.

Ergots - Ergotamine and dihydroergotamine are potent 5-HT1B/1D agonists that also inhibit norepinephrine uptake and stimulate alpha receptors, so their vasoconstriction is prolonged and extremity blood flow drops. Layering sympathomimetics on top exaggerates it. Ergotamine is cleared by CYP3A4 and should not be combined with CYP3A4 inhibitors; it is also avoided in peripheral vascular disease, coronary artery disease, stroke, uncontrolled hypertension, renal or hepatic impairment, sepsis, and pregnancy.

Beta blockers - Propranolol is the most common first-line preventive, 40 up to 320 mg daily. Expect bradycardia, blunted chronotropic response, fatigue, and cold extremities, and know it can cause bronchospasm — it's avoided in severe asthma, peripheral vascular disease, severe bradycardia, and heart block. Propranolol also raises rizatriptan concentrations, capping rizatriptan at 5 mg in those patients.

Anticonvulsant and antidepressant preventives - Valproate and divalproex cause hyperammonemia and tremor and are avoided in severe liver disease, so check LFTs and think ammonia if a patient is unexpectedly slow to wake. Topiramate precipitates kidney stones, acute myopia, and angle-closure glaucoma. Amitriptyline is dosed 25 to 150 mg daily and brings its own anticholinergic load.

Hemiplegic and basilar migraine - Triptans are not used in patients whose aura includes motor weakness or brainstem symptoms. Ask what the aura actually looks like rather than accepting "migraine with aura."

Gastric stasis and PONV - Nausea and vomiting are part of the attack, and migraine-induced gastric stasis is the reason oral abortives fail. A patient arriving mid-attack has a stomach that hasn't emptied — plan accordingly and give multi-agent PONV prophylaxis.

Triggers - About 76% of patients can name their own triggers. Ask what theirs are and avoid what the schedule allows you to avoid.

A new headache is not their headache - Postoperative headache in a migraineur isn't automatically migraine. The SNOOP red flags and any new neurologic symptom point toward imaging rather than another dose of the usual abortive.

Migraine is a genetically influenced neurovascular disorder of recurrent moderate-to-severe, usually unilateral headache with nausea and light and sound sensitivity. It affects about 12% of the population — 17% of women and 6% of men yearly — and 75% of cases occur without aura.

The old vascular theory (vasodilation causes the headache, vasoconstriction the aura) is dead. The current model is cortical spreading depression: a self-propagating wave of neuronal and glial depolarization that produces the aura, activates trigeminal afferents, and alters blood-brain barrier permeability. Trigeminovascular activation releases substance P, CGRP, and neurokinin A around pial vessels, producing neurogenic inflammation in the pain-sensitive meninges and, over time, central sensitization that converts episodic migraine to chronic. Attacks unfold in four phases — prodrome, aura, headache, postdrome — over hours to days, and gastric stasis during an attack is why oral abortives often fail.