Primary headache disorders

• Primary headache disorders are headaches that are not caused by another condition: the common ones are migraine, tension-type headache and the trigeminal autonomic cephalalgias, of which cluster headache is the most important.
• Migraine is a recurrent unilateral (or bilateral) pulsating headache lasting 4 to 72 hours, with nausea or sensitivity to light and sound; in migraine with aura the headache is preceded or accompanied by fully reversible focal neurological symptoms. ^[1]
• Tension-type headache is a bilateral pressing pain of mild to moderate intensity that is not aggravated by routine activity and has no associated features; cluster headache is a severe one-sided pain around the eye lasting 15 to 180 minutes with ipsilateral tearing, red eye, nasal symptoms and restlessness. ^[1]
• Diagnosis is clinical, made from the pattern in a headache history and a normal examination; the red flags in NICE CG150 tell you when to investigate for secondary causes.
• Acute attacks are treated with NSAIDs and/or triptans for migraine, simple analgesics for tension-type headache, and 100% oxygen or subcutaneous or nasal triptans for cluster headache; prevention is offered when attacks are frequent, and medication overuse is prevented by limiting acute drug use.^[1]

By the end of this page you should be able to:

1. Classify a headache into migraine, tension-type headache or cluster headache using the clinical features in the ICHD-3 and NICE CG150 criteria.
2. Recognise the aura of migraine, distinguish it from a transient ischaemic attack (TIA) and know which aura symptoms are atypical and need investigation.
3. Explain the current understanding of migraine pathophysiology, including the trigeminovascular system and calcitonin gene-related peptide (CGRP).
4. Choose acute and preventive treatment for each primary headache, name the usual drug classes and doses, and state the step at which CGRP-targeted therapies are used.
5. Recognise and manage medication-overuse headache, including withdrawal, and adjust management in pregnancy, childhood and older adults.
6. Outline the investigations that are needed, the indications for brain imaging, and the red flags that point to secondary headache.

The international standard is the International Classification of Headache Disorders, 3rd edition (ICHD-3, 2018), produced by the International Headache Society. The primary headaches are divided into four groups: migraine; tension-type headache; the trigeminal autonomic cephalalgias (TACs); and other primary headache disorders. The TACs share unilateral headache with ipsilateral cranial autonomic symptoms; cluster headache (3.1 in ICHD-3) is by far the most common and the most severe, and the other TACs (paroxysmal hemicrania, SUNCT and SUNA, hemicrania continua) are mentioned here only so that they are not confused with cluster headache.

A headache diagnosis is made on the clinical pattern. The ICHD-3 criteria require a minimum number of attacks (five for migraine without aura and for cluster headache) so that a single atypical attack is not labelled prematurely. If a patient does not meet all criteria, the diagnosis is "probable" and the diary is repeated.^[2]

Headache disorders are among the most common conditions worldwide. The 2023 Global Burden of Disease headache analysis estimated that about 2.9 billion people worldwide are affected by a headache disorder, giving a global age-standardised prevalence of 35% and a disability burden (years lived with disability, YLD) of 542 per 100,000 population. Although tension-type headache is nearly twice as prevalent as migraine, migraine accounts for roughly 90% of the YLDs attributed to headache disorders. The same analysis placed migraine eighth among all conditions for age-standardised YLD, at 487 per 100,000 population, and the disability burden was about twice as high in females as in males. The 2021 Global Burden of Disease nervous system analysis estimated that about 1.16 billion people worldwide are affected by migraine.^[3]

Migraine is about three times more common in women than in men, and the peak incidence is in early adult life (the third and fourth decades), falling after midlife. Prevalence rates in routine records are often lower than these survey-based figures, which is usually attributed to underdiagnosis rather than to genuinely lower prevalence. Tension-type headache is even more common: its lifetime prevalence ranges from 30% to 78% in different community studies, so it is the commonest primary headache of all and a frequent cause of mild everyday headache. Cluster headache is much rarer, with onset usually between 20 and 40 years, and affects men about three times as often as women. About 10 to 15% of people with cluster headache have the chronic form, with no remission period longer than a month.^{[2] [3]}

No modifiable environmental cause has been identified for migraine, tension-type headache or cluster headache. The risk factors that matter clinically are those that push episodic headache towards chronic headache or medication overuse:

• female sex and the reproductive years for migraine, with a strong perimenstrual pattern in many women;
• family history of migraine, consistent with polygenic inheritance;
• obesity, caffeine overuse or withdrawal, irregular sleep, and psychological comorbidity (anxiety and depression in particular) for progression to chronic migraine and medication overuse;
• head and neck trauma and whiplash for secondary or worsened headache;
• heavy alcohol use as a trigger during a cluster period (cluster attacks can be provoked by alcohol within minutes);
• medication overuse itself, which converts episodic into chronic headache.

Tension-type headache is associated with pericranial muscle tenderness and with stress; the increased pericranial tenderness seen on examination is, in ICHD-3, the basis for marking pain as "associated with pericranial tenderness". Cluster headache may be familial in a small minority (autosomal dominant inheritance is described in about 5% of cases) and is more common in smokers.^[2]

Migraine is understood as a neurobiological disorder, not a vascular one, although vessels are involved secondarily. Current models put migraine in four linked phases.

1. Brainstem and hypothalamic activation. Functional imaging shows activation in the hypothalamus, periaqueductal grey and trigeminal nucleus caudalis before and during an attack. This explains the prodromal symptoms (yawning, food craving, neck stiffness) that can precede the headache by hours.
2. Cortical spreading depression. In migraine with aura, a slow wave of depressed neuronal activity spreads across the cortex and produces the aura symptoms; this is then followed by the headache. In migraine without aura, cortical spreading depression is not thought to occur.
3. Trigeminovascular activation and CGRP. Activation of the trigeminal nerve releases neuropeptides, of which calcitonin gene-related peptide (CGRP) is the key. CGRP is a potent vasodilator and a modulator of nociceptive transmission, and its levels rise during an attack and fall with successful treatment. CGRP receptor antagonists (the gepants) and anti-CGRP monoclonal antibodies target this step.
4. Central sensitisation. Repeated nociceptive input leads to sensitisation of trigeminal second-order neurons and of the thalamus, producing cutaneous allodynia (pain from normal touch) and the progression to chronic migraine in some people.

Serotonin (5-HT) is also central. Triptans are 5-HT1B/1D receptor agonists: they constrict dilated cranial vessels and inhibit the release of CGRP from trigeminal endings. 5-HT1F agonists (the ditans, represented by lasmiditan) act on neural non-vasoconstrictive pathways. Gepants act by competitive antagonism at the CGRP receptor.^[2]

Tension-type headache, particularly the frequent and chronic forms, is thought to involve increased pericranial myofascial nociception and central sensitisation of pain pathways, with the peripheral muscles being the main source in the infrequent form and central mechanisms dominating in chronic tension-type headache.

Cluster headache is a disorder of the trigemino-autonomic reflex and of the posterior hypothalamus (ipsilateral posterior hypothalamic grey matter is activated during attacks), which explains the circadian rhythmicity of the attacks (they often wake people from sleep at the same time each night), the short duration, the autonomic symptoms and the response to oxygen and to hypothalamic-targeted treatment.

Migraine without aura (ICHD-3 1.1). At least five attacks of headache lasting 4 to 72 hours (2 to 72 hours in children) that have at least two of: unilateral location; pulsating quality; moderate or severe intensity; worsening with or causing avoidance of routine physical activity. During the headache there is nausea and/or vomiting, or both photophobia and phonophobia. The pain builds over about 15 to 30 minutes, is often frontotemporal, and many patients lie down in a dark room. Attacks can be triggered by sleep loss, stress or its relief, menstruation, certain foods and the menopause transition. Migraine with and without aura can coexist in the same patient.^[1][2]

Migraine with aura (ICHD-3 1.2). A migraine aura consists of fully reversible neurological symptoms that develop gradually (either alone or in succession) over at least 5 minutes, and last 5 to 60 minutes. The aura usually precedes the headache (sometimes only by a few minutes, sometimes longer), but it can occur with no headache at all ("acephalgic" migraine). The typical aura is visual: flickering or shimmering lights, scotoma or zigzag lines (fortification spectra). Sensory aura (numbness or pins and needles spreading over minutes) and dysphasic speech disturbance are also recognised. Rarer subtypes include migraine with brainstem aura, hemiplegic migraine (with motor weakness) and retinal migraine (monocular visual loss). Atypical auras such as motor weakness, double vision, visual symptoms in one eye only, poor balance or a fall in consciousness need further investigation, because they may mimic a transient ischaemic attack and are not typical of migraine aura. The same warning features are listed in NICE CG150.^[1][2]

Examination. The neurological examination is normal in a primary headache, and a general examination (blood pressure, temperature, neck, fundi) looks for secondary causes. In tension-type headache the key physical finding is increased pericranial tenderness on palpation of the frontal, temporal, masseter, pterygoid, sternocleidomastoid, splenius and trapezius muscles, which is interictally present and worse during attacks. In migraine the examination is normal between attacks. In cluster headache the patient is characteristically restless and may pace during an attack (rather than lie still), with ipsilateral autonomic signs. A "red flags" assessment is carried out at presentation. Any positive neurological or systemic finding converts the case to a secondary headache until proven otherwise.

The main task is to distinguish the primary headaches from each other and from secondary causes (subarachnoid haemorrhage, giant cell arteritis, acute glaucoma, meningitis, intracranial mass). The following table compares the three common primary headaches directly.

A summary of the ICHD-3 criteria used at the bedside is given below.

• Migraine without aura: at least 5 attacks lasting 4 to 72 hours, at least 2 of: unilateral; pulsating; moderate or severe; aggravated by routine activity; and at least 1 of: nausea and/or vomiting, or photophobia and phonophobia. In children and adolescents attacks may last 2 to 72 hours. ^[2]
• Migraine with aura: fully reversible aura symptoms developing over at least 5 minutes and lasting 5 to 60 minutes, followed (or, less often, accompanied) by a migraine headache; typical aura with headache and typical aura without headache are both recognised.
• Chronic migraine: headache on 15 or more days per month, of which at least 8 have migrainous features, for more than 3 months. ^[1]
• Episodic migraine: fewer than 15 headache days per month. ^[1]
• Menstrual-related migraine: migraine occurring predominantly between 2 days before and 3 days after the start of menstruation in at least 2 out of 3 menstrual cycles. ^[1]
• Tension-type headache: episodes lasting from 30 minutes to continuous, with at least 2 of: bilateral; pressing or tightening quality; mild or moderate intensity; not aggravated by routine activity; no nausea or vomiting; and at most a single one of light sensitivity (photophobia) or sound sensitivity (phonophobia). Frequency subtypes as in the table above. ^[1]
• Cluster headache: at least 5 attacks of severe or very severe unilateral orbital, supraorbital or temporal pain lasting 15 to 180 minutes, occurring between once every other day and 8 times a day, with ipsilateral autonomic features or restlessness or agitation. ^[1]
• Medication-overuse headache: headache on 15 or more days per month as a consequence of regular overuse for more than 3 months, with the drug-specific thresholds described below. ^[1]
• Chronic cluster headache: bouts occurring without a pain-free period of at least a month in a 12-month period, which affects about 10 to 15% of patients with cluster headache.^[2]

The diagnosis of a primary headache is clinical. Investigations are done to exclude secondary causes or to manage frequent or refractory disease, not for reassurance. NICE CG150 lists the features that should trigger further investigation or referral: a new headache with any of: worsening with fever; sudden onset reaching maximum intensity within 5 minutes (thunderclap); new neurological deficit; new cognitive dysfunction; change in personality; impaired level of consciousness; recent head trauma (within 3 months); headache triggered by cough, Valsalva or sneeze; headache triggered by exercise; orthostatic headache; symptoms of giant cell (temporal) arteritis; symptoms or signs of acute narrow-angle glaucoma; a substantial change in the characteristics of the headache. New-onset headache in people who are immunocompromised, who are under 20 years old with a history of malignancy, who have a malignancy known to metastasise to the brain, or with unexplained vomiting also needs investigation or referral. ^[1]

The aim is to treat early, while the pain is mild, and to restore function. The NICE CG150 guideline (last updated 03 June 2025) recommends offering combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol, for the acute treatment of migraine, taking into account the person's preference, comorbidities and risk of adverse events. For people who prefer to take a single drug, consider monotherapy with an oral triptan, an NSAID, aspirin 900 mg or paracetamol. For young people aged 12 to 17 years a nasal triptan is considered in preference to an oral one. Ergots and opioids should not be offered for acute migraine treatment. An anti-emetic (for example metoclopramide or prochlorperazine) is considered in addition even when nausea is absent, particularly when oral preparations are ineffective or not tolerated, with non-oral routes used in that situation.^[1]

Triptans are migraine-specific 5-HT1B/1D agonists. They are contraindicated in symptomatic cardiovascular disease, including coronary artery disease, history of stroke or transient ischaemic attack, peripheral vascular disease and uncontrolled hypertension, because of vasoconstriction; in one US epidemiological study about 13% of people with episodic migraine had at least one such contraindication. Many triptans also require caution in other cardiovascular risk factors. Common adverse effects (paraesthesia, flushing, chest tightness) are usually mild and brief. When prescribing a triptan, NICE recommends starting with the one with the lowest acquisition cost and, if that is consistently ineffective, trying one or more alternatives, because response is partly individual; the American Headache Society consensus statement recommends trying at least two oral triptans before switching to a different drug class.^[1][5]

Gepants (small-molecule CGRP receptor antagonists) are an alternative when triptans are contraindicated, poorly tolerated or ineffective. Available agents include ubrogepant (50 mg or 100 mg), rimegepant (75 mg, taken orally or as an orally dissolving tablet) and intranasal zavegepant (10 mg). They lack cardiovascular contraindications and, unlike triptans, are not associated with medication-overuse headache, and one agent (ubrogepant) has shown efficacy when taken in the prodromal phase. Disadvantages are cost and interactions: ubrogepant and rimegepant should be avoided with strong CYP3A4 inhibitors, and all gepants are contraindicated after acute stroke for a period and in small-vessel cerebrovascular disease, with caution in people aged 65 or over with prior stroke or hypertension.^[5]

For acute menstrual-related migraine that does not respond adequately to standard acute treatment, NICE CG150 considers frovatriptan 2.5 mg twice a day or zolmitriptan 2.5 mg two or three times a day on the days the migraine is expected. A large systematic review and consensus from the European Headache Federation (EHF, 2026) found sumatriptan the most effective first-line acute treatment for menstrual migraine, with lasmiditan as a further option, and confirmed frovatriptan 2.5 mg twice daily as the most effective short-term preventive for menstrual migraine, with naratriptan, zolmitriptan and naproxen also showing benefit.^[1][4]

Prevention is considered when migraines occur on 4 or more days a month, when attacks are prolonged or very disabling, or when acute treatments fail or are poorly tolerated. NICE CG150 first-line preventive options are propranolol, topiramate or amitriptyline, after a discussion of benefits, risks and suitability, with specific safety notes for people with depression (caution with propranolol) and for the safe prescribing of antidepressants. Gabapentin should not be offered. If propranolol, topiramate and amitriptyline do not work or are not tolerated, a course of up to 10 sessions of acupuncture over 5 to 8 weeks may be considered. Riboflavin 400 mg once daily may help in some people. Combined hormonal contraceptives should not be routinely offered for contraception to women and girls who have migraine with aura.^[1]

For chronic migraine (15 or more headache days a month, at least 8 migrainous, for more than 3 months), NICE endorses onabotulinumtoxinA (Botox) only when at least three preventive medicines have failed or are not tolerated, with a review of response. CGRP-targeted therapies (the monoclonal antibodies erenumab, fremanezumab, galcanezumab and eptinezumab given by subcutaneous or intravenous injection, and the oral gepant atogepant) are recommended as options only when at least three preventive medicines have not worked or are not tolerated, in adults with at least 4 migraine days a month. NICE specifies erenumab at the 140 mg dose for this indication. The EHF 2026 consensus provides specific preventive doses used in trials: galcanezumab 120 mg subcutaneously monthly and erenumab 70 mg subcutaneously monthly were effective at achieving at least a 50% reduction in monthly migraine days; long-term prevention for menstrual migraine includes topiramate (50 to 200 mg a day) and anti-CGRP monoclonal antibodies. Topiramate should not be used for migraine prophylaxis in pregnancy or in women of childbearing potential unless the conditions of the pregnancy prevention programme (including highly effective contraception) are met.^[1][4]

Prophylaxis is reviewed 3 to 6 months after it is started. CGRP-targeted treatments are stopped after 12 weeks if migraine frequency has not fallen by at least 50% in episodic migraine or by at least 30% in chronic migraine. Botulinum toxin type A is stopped if headache days do not fall by at least 30% after two treatment cycles, or if the condition becomes episodic migraine for 3 consecutive months.^[1]

Acute treatment is high-flow oxygen and/or a subcutaneous or nasal triptan. NICE CG150 specifies 100% oxygen at a flow rate of at least 12 litres per minute through a non-rebreathing mask with a reservoir bag, with home and ambulatory oxygen arranged. Paracetamol, NSAIDs, opioids, ergots and oral triptans should not be offered for acute cluster headache. Prophylaxis during a bout is with verapamil, with electrocardiogram monitoring; NICE advises seeking specialist advice if verapamil is unfamiliar, or if cluster headache does not respond. Specialist advice is also sought for treatment needed during pregnancy. The gepants review notes a role for galcanezumab 120 mg monthly in episodic cluster headache, though this should be directed by a specialist.^[1][5]

For acute attacks NICE considers aspirin, paracetamol or an NSAID, taking into account preference, comorbidities and adverse-event risk; preparations containing aspirin are not offered to people under 16 because of Reye's syndrome, and opioids are not offered. For chronic tension-type headache, prophylaxis is a course of up to 10 sessions of acupuncture over 5 to 8 weeks.^[1]

Medication-overuse headache is secondary headache caused by overuse of acute treatment and it resolves only when the overused drug is withdrawn. It should be suspected when an established headache worsens while a drug is taken on 10 or more days per month for 3 months (triptans, opioids, ergots or combination analgesics) or on 15 or more days per month for 3 months (paracetamol, aspirin or an NSAID). NICE advises explaining that treatment is by withdrawal, stopping all overused acute headache medications abruptly for at least 1 month, warning that headache and withdrawal symptoms worsen initially before improving, and providing close follow-up and support. Prophylaxis for the underlying primary headache disorder is considered in addition. Inpatient withdrawal is not routine, but is considered for people using strong opioids, with relevant comorbidities, or after repeated failed withdrawals. The diagnosis and management are reviewed 4 to 8 weeks after withdrawal starts. Gepants appear not to cause medication-overuse headache and may reduce opioid or butalbital use in those already overusing.^[1][5]

• Status migrainosus: an unusually prolonged and debilitating migraine attack.
• Migrainous infarction: a cerebral ischaemic event occurring during an attack, in the appropriate vascular territory.
• Persistent aura without infarction: aura symptoms lasting more than a week without infarction on imaging.
• Migraine aura-triggered seizure.
• Medication-overuse headache, converting episodic to chronic daily headache.
• Progression from episodic to chronic migraine (chronic migraine: 15 or more headache days a month, at least 8 migrainous, for more than 3 months). In one longitudinal cohort, crude one-year rates of progression to chronic migraine were similar in women and men, although adjusted hazard ratios were higher in men at 6 to 12 months.^[4]
• Vascular complications: migraine with aura is associated with an increased risk of ischaemic stroke in large population-based studies, more so in smokers, in women taking combined hormonal contraception and in the presence of patent foramen ovale. Combined hormonal contraceptives are not routinely offered to women and girls with migraine with aura for this reason. An adjusted odds ratio of 1.67 for cerebrovascular disease was reported among patients with migraine in one large population-based study.^[1][3]
• In cluster headache, severe co-morbid depression and occasional suicidal ideation are well described and warrant direct enquiry.
• Tension-type headache rarely has complications, but chronic daily headache and functional impairment are common.

Migraine is a lifelong tendency with periods of remission and relapse. Attacks often remit in pregnancy and may improve after the menopause, but can be replaced by (or accompanied by) medication-overuse headache in older adults. The best prognostic factors are early effective acute treatment, appropriate prophylaxis when indicated and avoidance of medication overuse. Cluster headache often remits for months or years between bouts, and about 10 to 15% of patients develop chronic cluster headache without remissions. Tension-type headache is usually benign and episodic; the chronic form is more troublesome and is associated with comorbid anxiety and depression.^[2]

The most effective "prevention" of progression is the management of triggers and limits on acute drugs. Practical points that apply to all primary headaches:

• Identify and limit trigger factors (sleep irregularity, missed meals, dehydration, alcohol in cluster headache, perimenstrual factors).
• Use a headache diary for at least 8 weeks to confirm the diagnosis and to measure response.
• Keep acute medication use below the overuse thresholds and review it at every visit.
• Screen for depression, anxiety and sleep disturbance, because they worsen all three headaches.
• Red flags (listed in the investigations section) are the trigger for imaging and referral; routine brain imaging solely for reassurance is not recommended.^[1]
• Peri-menstrual and pregnancy advice (frovatriptan short-term for menstrual migraine; paracetamol, with triptans or NSAIDs used cautiously, in pregnancy) is part of prevention.^[1][4]

Children and adolescents. Migraine in children is more often bilateral and frontotemporal and may last 2 to 72 hours; attacks shorter than 2 hours are not typical and call for caution. Photophobia and phonophobia may be inferred from behaviour rather than reported. Episodic syndromes such as abdominal migraine, cyclical vomiting and benign paroxysmal vertigo are migraine equivalents. For acute treatment, paracetamol or an NSAID is used first, with a nasal triptan preferred to an oral one in 12- to 17-year-olds (an off-label use except for nasal sumatriptan). Prophylaxis follows the same principles as adults, with topiramate and amitriptyline used off-label in younger people and the pregnancy-prevention programme for topiramate.^[1]

Pregnancy. Paracetamol is offered for acute migraine in pregnancy. A triptan or an NSAID may be considered after discussing the need for treatment and the risks of each in pregnancy; triptans are considered to be largely safe on available data, though there is a small signal of postpartum haemorrhage with second-trimester use, and NSAIDs carry the usual late-pregnancy cautions. Prophylaxis in pregnancy needs specialist advice; greater occipital nerve blocks and onabotulinumtoxinA have reassuring pregnancy data, while anti-CGRP agents are avoided because pregnancy safety data are limited. Cluster headache in pregnancy needs specialist assessment, and verapamil is used with specialist advice.^[1][4]

Breastfeeding. Sumatriptan and other triptans transfer into breast milk in very small amounts (relative infant doses under 10% for all studied triptans) and are considered compatible with breastfeeding; a single dose of rimegepant also has very low transfer. Acetaminophen, NSAIDs, caffeine, beta-blockers and tricyclic antidepressants are generally regarded as safe, and onabotulinumtoxinA and greater occipital nerve blocks can be used.^[4]

Older adults. New headache after age 50 usually needs investigation for secondary causes such as giant cell arteritis. Triptans are generally avoided or used with care where there is cardiovascular disease; gepants should be used cautiously in people 65 or over with prior stroke or hypertension. Prevalence and severity of migraine decline after the fifth decade.^[3][5]

• Diagnosis is clinical; a careful 8-week headache diary is the single most useful test and costs nothing.
• Simple NSAIDs, aspirin, paracetamol and caffeine are effective acute treatments and are widely available.
• High-flow oxygen for cluster headache can be provided from an oxygen cylinder with a high-flow mask; a subcutaneous triptan is the alternative when oxygen is unavailable.
• Amitriptyline and propranolol are inexpensive prophylactics; topiramate and CGRP therapies are usually too costly or unavailable.
• When stroke and other secondary causes cannot be excluded clinically, any imaging available locally should be prioritised; in their absence, vascular risk factors and the features of giant cell arteritis should be managed on clinical grounds.

• Primary headaches (migraine, tension-type headache, cluster headache and other TACs) are diagnosed clinically from the ICHD-3 criteria; secondary causes are excluded by the history and examination, with imaging only when red flags are present.
• Migraine: recurrent 4 to 72 hour pulsating headache with nausea or sensitivity to light and sound; aura is a fully reversible focal neurological symptom developing over at least 5 minutes and lasting 5 to 60 minutes.
• Tension-type headache: bilateral pressing pain, mild to moderate, not aggravated by routine activity, with no nausea and at most one of photophobia or phonophobia; chronic when present on 15 or more days a month for more than 3 months.
• Cluster headache: severe one-sided orbital pain lasting 15 to 180 minutes, one every other day to eight times a day, with ipsilateral autonomic features or restlessness; 10 to 15% is chronic.
• Medication overuse: triptans, opioids, ergots or combination analgesics on 10 or more days a month, or simple analgesics or NSAIDs on 15 or more days a month for 3 months.
• Acute: combination of triptan plus NSAID or paracetamol for migraine; simple analgesics for tension-type headache; 100% oxygen at at least 12 L/min or subcutaneous or nasal triptan for cluster; no opioids or ergots for migraine or tension-type headache.^[1]
• Prophylaxis: propranolol, topiramate or amitriptyline first line; CGRP-targeted drugs and botulinum toxin for chronic or refractory migraine after at least three preventives fail; verapamil for a cluster bout.^[1]
• Combined hormonal contraceptives should not routinely be offered to women and girls with migraine with aura; triptans are contraindicated in symptomatic cardiovascular disease.^[1][5]
• Medication-overuse headache is treated by abrupt withdrawal of all overused acute drugs for at least 1 month, with close follow-up.^[1]
• Migraine accounts for about 90% of the disability burden of headache disorders worldwide, despite tension-type headache being nearly twice as common.^[3]

• Ischaemic stroke and transient ischaemic attack
• Giant cell (temporal) arteritis
• Subarachnoid haemorrhage
• Epilepsy and headache
• Contraception
• Pregnancy and medicines
• Acute pain management
• Mental health and somatic disorders