Primary Headaches — Migraine vs Cluster vs Tension-Type, with Drug of Choice

Written & medically reviewed by the Kinase Medical Team · Last reviewed

Quick Answer

Primary headaches have no underlying lesion. Migraine is unilateral, pulsating, lasts 4 to 72 hours with nausea and photophobia; triptans are first-line abortive drugs. Cluster headache is excruciating, orbital, lasts 15 to 180 minutes with autonomic features; treat with 100% oxygen or subcutaneous sumatriptan, prevent with verapamil. Tension-type headache is bilateral and band-like.

What are primary headaches and how do the three types differ?

A primary headache is a headache disorder in its own right, not a symptom of another disease. The three exam-relevant types are migraine, cluster headache (a trigeminal autonomic cephalalgia) and tension-type headache (TTH). TTH is the most common primary headache; migraine is the second most common and a leading cause of disability. The International Classification of Headache Disorders, 3rd edition (ICHD-3) defines each.

Headache - Overview (types, signs and symptoms, treatment)Hand-drawn overview of headache types: migraine, cluster and tension-type, with features and treatment.Video: Armando Hasudungan · 10:32 · Watch on YouTube · Loads from YouTube (privacy-enhanced mode) only when you press play.
Migraine vs cluster vs tension-type headache
FeatureMigraineCluster headacheTension-type headache
SideOften unilateralStrictly unilateral, orbital / supraorbital / temporalBilateral
QualityPulsating / throbbingExcruciating, non-fluctuating, explosiveDull, pressing, band-like tightness
IntensityModerate to severeVery severe (10/10)Mild to moderate
Duration4–72 hours15–180 minutes30 minutes to 7 days
BehaviourPrefers to lie still in a dark roomRestless, paces or rocksCan continue routine activity
AssociatedNausea, vomiting, photophobia, phonophobia; aura in someIpsilateral lacrimation, red eye, nasal congestion, ptosis / miosisNausea absent or very mild
Aggravated by routine activityYesNo (patient is restless)No
SexMore in womenMen about three times more than women—
Three schematic head drawings: tension headache shaded across the forehead band, migraine shaded over one side of the head, and cluster headache shaded around one eye.
Typical pain distribution: tension-type headache as a band across the forehead, migraine over one side of the head, cluster headache behind and around one eye.Image: Jairo Hernandez et al, CC BY 4.0

What are the diagnostic criteria and types of migraine?

Migraine is a genetically influenced neurological disorder of recurrent, moderate-to-severe, usually unilateral headaches with nausea and sensitivity to light and sound. It affects roughly 12% of the population (up to 17% of women and 6% of men), peaks between ages 35 and 39 and ranks among the leading causes of disability. Migraine without aura is the commonest type, accounting for 75% of cases.

ICHD-3 criteria for migraine without aura
CriterionRequirement
AAt least 5 attacks
BHeadache lasts 4–72 hours (untreated or unsuccessfully treated)
CAt least 2 of: unilateral, pulsating, moderate-to-severe, aggravated by (or causing avoidance of) routine activity
DDuring headache at least 1 of: nausea/vomiting, or photophobia and phonophobia
ENot better explained by another ICHD-3 diagnosis
  • Migraine with aura: at least 2 attacks with fully reversible aura (visual, sensory, speech, motor, brainstem or retinal). The aura develops gradually over 5 minutes or more, each symptom lasts 5–60 minutes, and the headache follows within 60 minutes. About 25% of patients have aura; visual aura is commonest.
  • Chronic migraine: headache on 15 or more days per month for more than 3 months, with migraine features on at least 8 days per month.
  • Hemiplegic migraine: aura with motor weakness. Familial types are channelopathies: FHM1 — CACNA1A (calcium channel, chromosome 19), FHM2 — ATP1A2 (Na+/K+ ATPase, chromosome 1), FHM3 — SCN1A (sodium channel).
  • Migraine with brainstem aura (formerly basilar migraine) and retinal migraine (monocular visual loss) are the other aura variants.
  • Complications: status migrainosus (attack over 72 hours), persistent aura without infarction (over 1 week) and migrainous infarction.

What is the pathophysiology of migraine?

The older vascular theory (vasodilation causes headache, vasoconstriction causes aura) is no longer considered viable. Current understanding is neuronal: cortical spreading depression of Leão, a propagating wave of neuronal and glial depolarisation, is thought to cause the aura and to activate trigeminal afferents, producing inflammation in the pain-sensitive meninges and the headache.

  • Trigeminovascular system: activation releases substance P, calcitonin gene-related peptide (CGRP) and neurokinin A, causing neurogenic inflammation and sensitisation.
  • CGRP is a potent vasodilator of cerebral and dural vessels and mediates pain transmission from trigeminal vessels. This is why CGRP-targeted drugs now exist (see below).
  • Serotonin is involved; PACAP levels rise during attacks.
  • Triggers: stress, hormonal change (menstruation), skipped meals, weather change, sleep disturbance, bright light, alcohol (particularly wine). About 76% of patients report triggers.
Migraine - physiology, pathology, clinical manifestations, diagnosis, treatmentMigraine physiology, clinical features, diagnosis and treatment.Video: Osmosis from Elsevier · 10:38 · Watch on YouTube · Loads from YouTube (privacy-enhanced mode) only when you press play.

How is migraine treated — abortive and preventive drugs?

Acute (abortive) treatment of migraine
OptionDetails
NSAIDs (ibuprofen, naproxen, diclofenac, aspirin) or paracetamolMild-to-moderate attacks without vomiting
Triptans (sumatriptan, zolmitriptan, eletriptan, rizatriptan, almotriptan)First-line for moderate-to-severe attacks, especially with allodynia. 5-HT1B/1D agonists. Sumatriptan 6 mg subcutaneous; limit to under 10 days per month
Antiemetics (metoclopramide, prochlorperazine, chlorpromazine)Adjunct for nausea; diphenhydramine to prevent dystonia with metoclopramide
CGRP receptor antagonists (gepants) — rimegepant, ubrogepantFor triptan non-responders or those with coronary disease
Ergots (ergotamine, dihydroergotamine)Parenteral rescue and bridge for status migrainosus; ischaemic complications
  • Preventive drugs: propranolol or metoprolol (beta-blockers), amitriptyline or venlafaxine, topiramate or valproate, flunarizine or verapamil, CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab).
  • OnabotulinumtoxinA for chronic migraine (headache on 15 or more days per month lasting 4 or more hours a day).
  • Indications for prevention: frequent or disabling attacks, failure or contraindication of acute drugs, risk of medication overuse, menstrual migraine, hemiplegic migraine, brainstem aura.

What is cluster headache and how is it treated?

Cluster headache is the commonest of the trigeminal autonomic cephalalgias (TACs), affecting about 0.1% of people; onset is typically around 30 years and men are about three times more often affected. Smoking is strongly associated. It is regarded as one of the most severe headaches, with 10/10 unilateral orbital or supraorbital pain.

  • ICHD-3: at least 5 attacks of severe unilateral orbital, supraorbital or temporal pain lasting 15–180 minutes, with at least one ipsilateral autonomic sign (conjunctival injection or lacrimation, nasal congestion or rhinorrhoea, eyelid oedema, forehead sweating, miosis or ptosis) or restlessness, at a frequency from one every other day to eight per day.
  • Autonomic signs: lacrimation/red eye in about 90%, nasal congestion in 84%.
  • Circadian pattern: attacks often at the same time, typically at night; the hypothalamus is implicated (PET activation of inferior hypothalamic grey matter).
  • Episodic (bouts of 7 days to 1 year separated by remission of 3 months or more) vs chronic (no remission, or remission under 3 months, for at least 1 year).
  • Triggers: alcohol, nitroglycerin, heat, stress.
Treatment of cluster headache
AimDrugNote
Acute100% oxygen by maskLevel A recommendation; unique to cluster headache; at least 66% respond within about 10 minutes
AcuteSubcutaneous sumatriptan, or zolmitriptan nasal sprayOral triptans are too slow
Prevention (first-line)Verapamil (starting 240 mg once daily)Monitor ECG
Transitional bridgeOral prednisone short course; suboccipital blockadeFor short, infrequent cluster periods or while waiting for verapamil to act
OthersLithium, valproate, melatonin; hypothalamic deep brain stimulation for refractory cases—

What is tension-type headache, and what is medication overuse headache?

Tension-type headache is the commonest primary headache. ICHD-3 requires at least 10 episodes; each lasts 30 minutes to 7 days, is bilateral, pressing or tightening (non-pulsating), of mild-to-moderate intensity and not aggravated by routine physical activity. Nausea, vomiting, photophobia and phonophobia are typically absent or very mild. It is classified as infrequent episodic, frequent episodic or chronic. Acute treatment is with ibuprofen 400 mg or paracetamol 1000 mg; for chronic TTH the best-studied preventive is amitriptyline.

Medication overuse headache (MOH), formerly rebound headache, is a secondary chronic headache occurring on 15 or more days per month for 3 or more months in a patient using acute treatment too often: simple analgesics or NSAIDs on 15 or more days per month, or triptans, ergots, opioids or combination analgesics on 10 or more days per month. Treatment is education and withdrawal of the overused drug; symptoms may worsen early and withdrawal effects last up to about 10 days.

How are headaches asked in NEET PG and INI-CET?

  • Drug of choice: abortive migraine → triptan; cluster headache attack → 100% oxygen; cluster prophylaxis → verapamil; paroxysmal hemicrania → indomethacin.
  • Duration clues: 4–72 hours migraine; 15–180 minutes cluster; 2–30 minutes paroxysmal hemicrania; seconds SUNCT.
  • Behaviour clue: restless and pacing = cluster; lies still in a dark room = migraine.
  • Genetics: familial hemiplegic migraine → CACNA1A, ATP1A2, SCN1A.
  • Contraindication: triptans in coronary artery disease and hemiplegic migraine.

Frequently asked questions

What is the drug of choice for an acute migraine attack?
Triptans are first-line abortive drugs for moderate-to-severe migraine, especially with allodynia. Sumatriptan can be given as 6 mg subcutaneously, nasally or orally. NSAIDs suit mild-to-moderate attacks. Triptans should be used on fewer than 10 days a month and are contraindicated in coronary disease, stroke, uncontrolled hypertension and hemiplegic migraine.
What is the best treatment for an acute cluster headache attack?
High-flow 100% oxygen by mask is the classic first-line treatment with a level A recommendation; at least two-thirds of patients respond, usually within about 10 minutes, and it has no significant risks. Subcutaneous sumatriptan or zolmitriptan nasal spray is the other level A option. Oral triptans act too slowly.
Which drug prevents cluster headache?
Verapamil is the most widely used preventive, started at about 240 mg once daily, with ECG monitoring because of cardiac effects. Short courses of oral corticosteroids or a suboccipital steroid block act quickly as a bridge. Other options include lithium, valproate and melatonin, and hypothalamic stimulation for refractory disease.
What are the ICHD-3 criteria for migraine without aura?
At least five attacks lasting 4 to 72 hours, with at least two of unilateral location, pulsating quality, moderate-to-severe intensity and aggravation by routine activity. During the headache there must be nausea or vomiting, or both photophobia and phonophobia. The headache must not be better explained by another diagnosis.
How do you distinguish cluster headache from migraine?
Cluster headache is brief, 15 to 180 minutes, strictly unilateral around the eye, with ipsilateral tearing, red eye or nasal congestion, and the patient is restless. Migraine lasts 4 to 72 hours, is pulsating, and brings nausea and light sensitivity; the patient prefers to lie still in a dark room.
What is the pathophysiology of the migraine aura?
The aura is attributed to cortical spreading depression of Leão, a slowly propagating wave of neuronal and glial depolarisation. It also activates trigeminal afferents, releasing CGRP, substance P and neurokinin A, which cause neurogenic inflammation and headache. The older vascular theory of vasoconstriction causing aura is no longer considered viable.
What is medication overuse headache?
It is a secondary chronic headache occurring on 15 or more days a month for at least three months in someone overusing acute treatment: simple analgesics or NSAIDs on 15 or more days, or triptans, ergots, opioids or combination analgesics on 10 or more days a month. It improves when the overused drug is withdrawn.
Which genes cause familial hemiplegic migraine?
Familial hemiplegic migraine is a channelopathy. Type 1 is caused by CACNA1A mutations in the voltage-gated calcium channel on chromosome 19, type 2 by ATP1A2 mutations in the sodium-potassium ATPase on chromosome 1, and type 3 by SCN1A mutations in the voltage-gated sodium channel. The aura includes motor weakness.

Sources

  1. StatPearls — Migraine Headache (NCBI Bookshelf)
  2. StatPearls — Cluster Headache (NCBI Bookshelf)
  3. StatPearls — Muscle Contraction Tension Headache (NCBI Bookshelf)
  4. StatPearls — Medication Overuse Headache (NCBI Bookshelf)
  5. StatPearls — Triptans (NCBI Bookshelf)

For exam preparation and education only — not a substitute for clinical judgement or local guidelines. How we write and review these pages: editorial policy.

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