Migraine

Migraine is a primary headache disorder — the headache itself is the disease, not a symptom of something else — causing recurrent attacks of moderate-to-severe, often unilateral, pulsating head pain lasting 4-72 hours if untreated, typically accompanied by nausea and/or vomiting and sensitivity to light and sound.^[1] About a quarter to a third of people with migraine experience a fully reversible neurologic aura — usually visual — before or alongside the headache. Migraine is classified as episodic (fewer than 15 headache days a month) or chronic (15 or more headache days a month, with features of migraine on at least 8 of those days, for more than 3 months).^[2] Diagnosis is clinical, based on the ICHD-3 criteria and a normal neurologic examination — routine neuroimaging is not indicated in a patient who meets migraine criteria and has no red flags for a secondary headache disorder.^[3]

The 4 phases of an attack

• Prodrome — hours to 1-2 days before the headache: mood change, fatigue, food cravings, neck stiffness, yawning. Recognizing it is the single most useful skill for treating an attack early.
• Aura — present in roughly a quarter to a third of patients; most often visual (zigzag lines, scintillating scotoma, expanding blind spot).
• Headache — the attack itself, as defined above.
• Postdrome — the "migraine hangover": fatigue, difficulty concentrating, mood change, sometimes lasting a day or more after the headache resolves.

Menstrual migraine

Attacks occurring on day −2 to +3 of menses in at least 2 of 3 cycles, related to the perimenstrual estrogen drop — relevant to both acute-treatment timing and preventive strategy (see Special Populations).

• Family history of migraine — the single strongest risk factor; migraine has a substantial genetic component.
• Female sex — migraine is roughly 3 times more common in women than men, largely hormonally mediated.
• Age — onset is most common before age 40, with peak prevalence between 25 and 55.
• Hormonal fluctuation — the perimenstrual estrogen drop, pregnancy, perimenopause, and combined hormonal contraceptive/hormone therapy use can all influence attack frequency.
• Obesity.
• Frequent use of acute headache medication itself — a key modifiable risk factor for progression from episodic to chronic migraine (medication overuse headache).
• Comorbid depression, anxiety, and other chronic pain conditions — migraine and mood disorders have a bidirectional relationship.
• Individual attack triggers — commonly stress (including post-stress "let-down"), disrupted or insufficient sleep, skipped meals or fasting, dehydration, alcohol, specific foods, weather/barometric pressure change, and strong sensory stimuli (bright or flickering light, strong odours). Triggers are highly individual; a headache diary is more useful than a generic avoidance list.

History

• Characterize attack frequency, duration, and quality against the ICHD-3 criteria above, and distinguish headache days from migraine days per month — this distinction drives both the chronic-migraine definition and the preventive-therapy threshold decision.
• Ask specifically and quantitatively about acute medication use frequency (days per month, by class) at every assessment — this is the single most important, most commonly missed history item, since it identifies evolving medication overuse headache before it derails treatment.
• Screen for red flags (above), prior neuroimaging, prior preventive trials and why they were stopped, and menstrual-cycle relationship in patients who menstruate.
• A headache diary or tracking app (e.g., the Canadian Migraine Tracker app) meaningfully improves the quality of this history over recall alone.^[4]

Examination

A normal general and neurologic examination is expected in migraine and should be documented; any abnormal finding is itself a red flag requiring further workup rather than a migraine diagnosis by default.

Investigations

No laboratory testing or neuroimaging is routinely required to diagnose migraine in a patient who meets ICHD-3 criteria, has a normal examination, and has no red flags — the yield of imaging in this population is very low, and incidental findings can generate unnecessary anxiety and further testing.^[3]

Episodic vs. chronic migraine

Chronic migraine is defined as 15 or more headache days a month, with features of migraine (or response to migraine-specific treatment) on at least 8 of those days, for more than 3 months. This distinction matters directly for treatment: chronic migraine is the specific indication for onabotulinumtoxinA and receives its own graded recommendations in the updated CHS prevention guideline.^[2]

• Rapid, complete, and consistent relief of individual attacks, with minimal recurrence, using the fewest doses needed.
• Restore normal function during an attack rather than merely blunting pain.
• Keep acute-medication use below the frequency that risks medication overuse headache.
• For patients who qualify, reduce attack frequency, severity, and duration through preventive therapy, and reduce migraine-related disability and lost function.
• Identify and treat comorbid depression, anxiety, and sleep disruption, which both worsen migraine burden and are worsened by it.

• Regular sleep, regular meals (avoid skipping meals/prolonged fasting), and adequate hydration — inconsistency in these basics is one of the most common, most modifiable attack triggers.
• Regular aerobic exercise has independent preventive benefit.
• Identify individual triggers with a headache diary rather than broad, anxiety-generating avoidance of common but non-universal triggers (foods, weather, etc.) — over-restriction has not been shown to help and can itself add disability.
• Stress management, relaxation training, cognitive behavioural therapy, and biofeedback are well-supported behavioural treatments and should be considered alongside — not instead of — pharmacotherapy.^[3]
• Neuromodulation devices — external trigeminal nerve stimulation (Cefaly) and non-invasive vagus nerve stimulation (gammaCore) — are available in Canada as an adjunct; they are safe and effective but generally not covered by insurance.^[4]
• For patients with typical migraine, a normal exam, and no red flags who are anxious about a serious underlying cause, clear explanation of the diagnosis and reassurance is often more helpful than ordering imaging "just in case."^[3]

Pregnancy

Breastfeeding

Acetaminophen, ibuprofen, and sumatriptan (minimal transfer into breast milk) are considered compatible with breastfeeding. Propranolol and amitriptyline are also generally compatible with monitoring. Topiramate is present in breast milk in measurable amounts — use with infant monitoring. Avoid opioids and ergotamine/dihydroergotamine.

Migraine with aura and hormonal contraception

Combined hormonal contraceptives (estrogen-containing) meaningfully increase ischemic stroke risk in patients with migraine with aura and should generally be avoided in this group in favour of progestin-only or non-hormonal contraception — this applies regardless of age or smoking status.

Menstrual migraine

For predictable perimenstrual attacks, options include standard acute treatment, short-term "mini-prophylaxis" with a longer-acting triptan (frovatriptan or naratriptan) started a few days before the expected attack window and continued through it, or continuous/extended-cycle hormonal contraception to reduce estrogen withdrawal — the latter two are best arranged with specialist input.

Hemiplegic and brainstem-aura migraine

Avoid triptans and dihydroergotamine given their vasoconstrictive mechanism; favour NSAIDs, antiemetics, and gepants for acute treatment instead.

• Track headache days, migraine days, and acute-medication treatment days per month with a diary or tracking app at every follow-up — this single habit catches both inadequate control and emerging medication overuse before either becomes entrenched.^[4]
• For a new or adjusted oral preventive, reassess at the target or maximally tolerated dose after 8-12 weeks before judging efficacy — a common and avoidable error is abandoning a preventive too early.
• The standard responder benchmark for preventive therapy is a 50% or greater reduction in monthly headache or migraine days.^[6]
• For a CGRP monoclonal antibody, assess response after 3 monthly doses (or after the first quarterly dose for agents dosed every 3 months); if inadequate, consider switching within the class, to onabotulinumtoxinA (chronic migraine), or addressing an unrecognized medication-overuse pattern before concluding the class has failed.
• Periodically reassess ongoing need for preventive therapy — a supervised taper trial is reasonable after a sustained period of good control, commonly 6-12 months, individualized to the patient.
• Screen for comorbid depression, anxiety, and sleep disruption at follow-up given their bidirectional relationship with migraine burden.

1. Reconfirm the diagnosis — reassess for red flags and secondary causes, especially if the headache pattern has genuinely changed rather than simply persisted.
2. Confirm the acute agent was taken early in the attack, at an adequate dose, and by a route appropriate to the attack (switch to a nasal spray, subcutaneous injection, or orally-dissolving tablet if nausea/vomiting is limiting oral absorption).
3. Screen for and address medication overuse headache before judging any acute or preventive agent to have failed — an overused acute medication blunts response to everything, including preventive therapy, and often needs to be tapered/withdrawn first.
4. Before abandoning the triptan class, try a second triptan — response is agent-specific, not fully predictable from class, and a meaningful proportion of patients who fail one triptan respond to another.
5. If a full acute-medication class fails or is contraindicated, move to a mechanistically different option (NSAID failure → triptan; triptan failure/contraindication → gepant).
6. For preventive therapy, confirm an adequate trial (target/tolerated dose sustained 8-12 weeks) was actually completed before switching; if a genuine adequate trial has failed, move to a different first-line oral class or escalate to a CGRP monoclonal antibody, or to onabotulinumtoxinA specifically for chronic migraine.
7. Refer to a headache specialist or neurology for refractory migraine (failure of multiple preventive classes), suspected hemiplegic or brainstem-aura migraine, status migrainosus (a debilitating attack lasting beyond 72 hours), or genuine diagnostic uncertainty.

• Ordering routine neuroimaging in a patient who meets migraine criteria, has a normal examination, and has no red flags.^[3]
• Prescribing opioids or butalbital-containing combination analgesics as first-line acute therapy — NSAIDs and triptans are first-line, and opioids raise both dependence and chronification risk.^[3]
• Not asking specifically about acute-medication treatment days per month — the single most commonly missed history item, and the one that catches evolving medication overuse headache.
• Declaring a triptan a "failure" after a single unsuccessful attack, or after taking it too late in the attack, rather than confirming an adequate trial (typically 2-3 attacks, taken early).
• Not offering a second triptan after the first one fails — response is agent-specific.
• Using a triptan or dihydroergotamine in a patient with hemiplegic migraine, brainstem-aura migraine, or a significant cardiovascular contraindication.
• Continuing topiramate in a patient who could become pregnant without an explicit teratogenicity and contraceptive-reliability discussion — topiramate can reduce combined hormonal contraceptive efficacy at higher doses.
• Prescribing combined (estrogen-containing) hormonal contraception to a patient with migraine with aura.
• Declaring a preventive agent a "failure" before completing an adequate trial — target or maximally tolerated dose sustained for 8-12 weeks.
• Escalating straight to a CGRP monoclonal antibody or onabotulinumtoxinA without first identifying and addressing medication overuse headache, since an overused acute agent blunts the response to any preventive.
• Focusing on drug selection while neglecting the non-pharmacologic foundations — sleep regularity, regular meals, hydration, and stress management.

How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment and pregnancy status. Select any drug name to open its complete Pharmasist Drug Database page.

Simple analgesics and NSAIDs (acute, mild-moderate attacks)

1st-line acute options. Cap use at under 15 treatment days/month to avoid medication overuse headache.

Triptans (acute, moderate-severe attacks)

Monthly cap of 10 dosing days. For all triptans except eletriptan, 2 doses are allowed in 24 hours (Canadian labelling limits eletriptan to 1 dose/24h, though many experts allow 2); the second dose can be taken 2 hours after the first for almotriptan, eletriptan, rizatriptan, sumatriptan, and zolmitriptan, and 4 hours after the first for frovatriptan and naratriptan.

Gepants (acute, triptan-contraindicated or triptan-non-responsive)

Monthly cap of 16 dosing days. Not vasoconstrictive — cardiovascular disease is not a contraindication and cardiovascular risk factors are not a precaution.

Ergotamine derivatives

Second-line, generally specialist-initiated given administration complexity and lower tolerability than triptans/gepants.

Antiemetics (adjunct for nausea/vomiting)

Preventive therapy — first-line oral agents

Titrate slowly; give an adequate trial (target/tolerated dose sustained 8-12 weeks) before judging failure.

Preventive therapy — CGRP-targeted and chronic-migraine-specific options

Strong recommendation across episodic and chronic migraine. Canadian drug plans typically require documented failure of 2 or more conventional oral preventives first.

Evidence note: Drug inventory, dosing, monthly caps, and comments reflect standard Canadian practice, cross-checked against the Canadian Headache Society acute^[5] and preventive^[2] guidelines and the Migraine Canada 2025 Adult Acute Dosing Guide^[4].