Headache

Meet the patient

A 24-year-old man is woken at 2 am by a headache that climbed from nothing to the worst pain of his life inside a minute — "like someone kicked the back of my head". He vomited once and felt his neck stiffen. He has never had a headache like this.[11]

The question that decides his next hour is the question that decides every headache: is this primary or secondary? A thunderclap peaking within one minute is subarachnoid haemorrhage until proven otherwise — CT now, then LP for xanthochromia. Name the killers first; the benign pattern can wait.[7]

The brain cannot feel pain — where headache actually comes from

Headache never comes from the brain. The parenchyma is pain-insensitive; pain arises from the dura, the large intracranial arteries and venous sinuses, the scalp, skull periosteum, cervical muscles, eyes, sinuses and teeth.[2][5]

The innervation splits the head into two maps the examiner wants verbatim: trigeminal V1 carries the anterior two-thirds (forehead to vertex), and upper cervical roots C2/C3 carry the posterior third (occiput and neck) — which is why headache and neck pain share pathways and why meningeal irritation feels like neck stiffness.[1]

The clinical art of headache is therefore not naming a primary syndrome (the pattern usually declares itself) but excluding a secondary cause. The disciplined sequence: screen every patient with SNNOOP10, investigate if any flag is positive, then classify the primary headache by ICHD-3 if the screen is clean.[4]

Primary vs secondary — run SNNOOP10 on every headache

Every headache gets the same first question, and it is not "migraine or tension?" — it is "is a killer hiding in here?" The SNNOOP10 screen (Dodick) is the highest-yield bedside tool you own; any positive answer mandates investigation for a secondary cause.[4]

The topic mantra, repeat it on every round: Primary vs secondary first — run SNNOOP10 on every headache. Thunderclap is SAH, new-over-50 is GCA, fever with neck stiffness is meningitis — exclude the killers before you name the benign pattern.[4]

Classification — the ICHD-3 master split

The International Classification of Headache Disorders, 3rd edition (ICHD-3) is the framework examiners quote. It sorts every headache into three buckets.[3]

Category 1 — primary: the headache is the disease — migraine (without aura 75 to 80 percent, with aura 20 to 25 percent; chronic migraine 15 or more days a month for over 3 months, at least 8 with migraine features), tension-type, the trigeminal autonomic cephalalgias (cluster, paroxysmal hemicrania, SUNCT/SUNA — united by unilateral trigeminal pain plus ipsilateral autonomic features), and the other primaries (stabbing, cough, exercise, sexual-activity, thunderclap, hypnic, new daily persistent).[1]

Category 2 — secondary: attributable to an underlying disorder. Remember them as "VENOM" — Vascular, Infectious, Neoplasm, Other (IIH, low CSF pressure), Medication/Metabolic — subarachnoid haemorrhage, meningitis, brain tumour, idiopathic intracranial hypertension, spontaneous intracranial hypotension, giant-cell arteritis, angle-closure glaucoma, hypertensive crisis, cerebral venous sinus thrombosis, RCVS, carbon monoxide, trauma.[1]

Category 3 — painful cranial neuropathies and facial pains: trigeminal neuralgia, glossopharyngeal neuralgia, occipital neuralgia, persistent idiopathic facial pain.[1]

The three-way primary face-off — one question separates them

Three primaries, one discriminating question: does routine movement make it worse? That single answer splits migraine from the other two more reliably than any scan.[3]

One-line discriminator: aggravation by routine movement — migraine yes, cluster and tension-type no. Pair it with behaviour — migraine lies still, cluster paces, tension-type carries on — and you have the diagnosis at the bedside.[1][3]

How common, who gets it

Headache is one of the commonest of all human symptoms, and migraine is the single largest contributor to years lived with disability in the under-50s worldwide. Lifetime prevalence of any headache approaches 96 percent.[1][2]

The risk-factor portrait sharpens each type: migraine chases female sex, family history, hormonal flux, obesity, stress and let-down, skipped meals and sleep disturbance; tension-type tracks stress, anxiety, depression, poor posture and TMJ dysfunction; cluster tracks male sex and smoking (over 70 percent are smokers), with alcohol triggering attacks only during a bout; medication-overuse headache almost always grows out of a pre-existing migraine or tension-type once opioids or combination analgesics creep in.[1]

For secondary headache, the risk-factor shortcut is the patient in front of you: over 50 (GCA, mass), immunocompromised (opportunistic infection, lymphoma), pregnancy or peripartum (pre-eclampsia, CVST, pituitary apoplexy, RCVS), recent trauma (subdural), anticoagulated (haemorrhage), cancer (metastasis).[1]

Pathophysiology — three mechanisms, one molecule

The three primaries have distinct mechanisms, and the molecular detail drives the drug choice — which is why this is an examination favourite.[1]

Migraine — cortical spreading depression plus the trigeminovascular system

Migraine is a sensory-processing disorder of the brain, not simply a vascular event. Three mechanisms converge.[5][1]

First, cortical spreading depression of Leao — a self-propagating wave of neuronal and glial depolarisation sweeping the cortex at 2 to 6 mm/min, followed by a depolarisation block. This is the neural substrate of the aura (the scintillating scotoma marching across the visual field at the same speed), and it fires the trigeminovascular system by releasing potassium, glutamate, nitric oxide and CGRP at the meningeal surface.[1]

Second, trigeminovascular activation — V1 fibres on the meningeal vessels release CGRP and substance P, causing vasodilation, mast-cell degranulation and plasma-protein extravasation (neurogenic inflammation), which sensitises the trigeminal nucleus caudalis. This is the pain of migraine, and it is exactly where the drugs act: triptans (5-HT1B/1D agonists) vasoconstrict via 5-HT1B, block neuropeptide release via 5-HT1D, and inhibit the trigeminal nucleus caudalis.[5]

Third, central sensitisation and brainstem modulation — PET lights up the dorsolateral pons and dorsal midbrain (the "migraine generator"), and allodynia (combing hair hurts) marks sensitisation of third-order thalamic neurons. Allodynia predicts a poor triptan response — treat early, before sensitisation sets in.[1]

CGRP — the molecule that unifies the new drug class

Calcitonin gene-related peptide is the central molecular mediator of migraine. CGRP levels rise during an attack, intravenous CGRP triggers migraine in sufferers, and the entire modern drug class targets this one pathway: gepants (ubrogepant, rimegepant, zavegepant — small-molecule CGRP receptor antagonists) and the monoclonal antibodies against CGRP or its receptor (erenumab, fremanezumab, galcanezumab, eptinezumab).[9]

The oestrogen-fluctuation hypothesis explains the female predominance, the menstrual-migraine pattern, and the improvement with pregnancy and after menopause — perimenstrual oestrogen withdrawal is a powerful trigger.[1]

Tension-type — muscle plus reduced descending inhibition

Tension-type is driven by peripheral nociception from sustained pericranial and cervical muscle contraction, compounded by central sensitisation of the trigeminal nucleus caudalis and reduced descending inhibition. That last point is why tricyclics (amitriptyline) work — they restore serotonergic and noradrenergic inhibition.[10]

Cluster — a hypothalamic circadian disorder

Cluster is a neurovascular disorder of the hypothalamus. PET during attacks shows activation of the ipsilateral posterior hypothalamus (May, Lancet 1998) — the region governing circadian and circannual rhythm — which is why attacks strike with clockwork regularity, often at the same hour each night, and bouts cluster in spring and autumn.[8]

Hypothalamic discharge drives trigeminovascular and parasympathetic outflow through the sphenopalatine ganglion, producing ipsilateral periorbital pain (CGRP release) plus ipsilateral lacrimation, nasal congestion, conjunctival injection and a partial Horner. It is also why verapamil and, in refractory cases, deep-brain stimulation of the posterior hypothalamus work.[1]

Secondary — mechanism by cause

Each secondary headache hurts through its own anatomy: SAH irritates the pain-sensitive basal meninges; meningitis inflames them; a mass lesion traction on dura and vessels as it expands (pain worse with raised pressure — early morning, worse on bending or coughing); IIH raises CSF pressure without a mass; giant-cell arteritis granulomatously inflames the cranial arteries; angle-closure glaucoma stretches the ciliary nerves; hypertensive crisis breaks through autoregulation with vasogenic oedema.[1]

Clinical presentation — the ICHD-3 criteria reproduced verbatim

Migraine — learn the criteria, then learn the patient

Migraine without aura (ICHD-3 1.1): at least five attacks, each lasting 4 to 72 hours untreated, with at least two of unilateral, pulsating, moderate-to-severe, or aggravated by routine activity, and at least one of nausea or vomiting, or photophobia and phonophobia — not better accounted for by another ICHD-3 diagnosis.[3]

Migraine with aura (1.2): at least two attacks with a fully reversible aura (visual, sensory, language, motor, brainstem) lasting 5 to 60 minutes, at least one symptom spreading gradually over 5 minutes, and headache beginning with or within 60 minutes of the aura.[3]

Visual aura is commonest — the scintillating scotoma, a jagged expanding fortification zigzag that marches across the visual field over 20 to 30 minutes. Sensory and dysphasic aura follow; motor aura defines hemiplegic migraine (familial — CACNA1A, ATP1A2, SCN1A).[1]

Know the phases: prodrome (hours to days before — yawning, mood change, cravings, neck stiffness), aura (one-third), headache (4 to 72 h), postdrome (up to 48 h of fatigue and the "migraine hangover"). At the bedside the patient lies still in a dark quiet room, photophobic and nauseated, and is reliably worsened by movement — the feature that separates migraine from tension-type.[1]

Tension-type — the criteria

Tension-type (infrequent 2.1, frequent 2.2, chronic 2.3): at least 10 attacks of 30 minutes to 7 days, with at least two of bilateral, pressing or tightening (non-pulsating), mild or moderate, and not aggravated by routine activity; no nausea; and no more than one of photophobia or phonophobia. Chronic means 15 or more days a month for over 3 months.[3]

The patient describes a "tight band around the head" or a "weight pressing on top", bilateral, gradual, often linked to stress or screen work, with pericranial tenderness — and carries on with the day, the opposite of migraine.[1]

Cluster — the criteria

Cluster headache (3.1.1): at least five attacks of severe or very severe unilateral orbital, supraorbital or temporal pain lasting 15 to 180 minutes untreated, with at least one ipsilateral feature — conjunctival injection or lacrimation, nasal congestion or rhinorrhoea, eyelid oedema, forehead or facial sweating, miosis or ptosis (partial Horner), or restlessness and agitation.[3][8]

Frequency runs from one every other day to eight a day, in bouts. Episodic cluster (80 percent): bouts of 7 days to 1 year with at least 1 month remission. Chronic cluster (20 percent): over a year without remission, or remission under a month.[1]

The circadian regularity is pathognomonic — attacks wake the patient at the same hour each night (often around 2 am) and bouts cluster in spring and autumn. Alcohol and nitroglycerin trigger attacks during a bout but not in remission. The pain is a boring, drilling "hot poker in the eye", severe enough that patients bang their heads or contemplate suicide.[1]

The other primaries — and the indomethacin trio

Beyond the big three, three short-lasting primaries repay knowing:[3]

• Paroxysmal hemicrania (a TAC) — unilateral, 2 to 30 min attacks, five or more a day, with autonomic features — absolutely responsive to indomethacin.
• Hemicrania continua — strictly unilateral continuous headache with exacerbations — absolutely responsive to indomethacin.
• Hypnic headache — always wakes the patient from sleep, age over 50, 15 min to 4 h — the "alarm-clock headache", responsive to lithium or caffeine at bedtime.[1]

Everyone forgets: paroxysmal hemicrania and hemicrania continua are absolutely indomethacin-responsive — the response is the diagnostic test. A unilateral daily headache that melts on indomethacin 25 to 50 mg TDS is one of these until proven otherwise.[3]

SUNCT/SUNA (very brief, high-frequency, touch-triggered), primary thunderclap headache (peak within 1 minute; a diagnosis of exclusion after SAH is excluded), and new daily persistent headache (daily from onset; the patient remembers the exact first day, often after a viral illness) round out the list.[1]

Secondary — presentation by cause

Humour is off here; these are the killers.[4]

• Subarachnoid haemorrhage — thunderclap, maximum intensity within 1 minute ("worst headache of my life"), often occipital, with brief loss of consciousness, meningism and photophobia; a sentinel headache may precede rupture.
• Meningitis — subacute onset with fever, neck stiffness, photophobia and altered mental status, ± a meningococcal rash; Kernig and Brudzinski signs.
• Brain tumour — progressive, worse in the morning, worse on bending, coughing or Valsalva, with focal neurology or papilloedema.
• Giant-cell arteritis — age over 50, new temporal headache, jaw claudication (most specific feature), scalp tenderness, visual symptoms, polymyalgia rheumatica, and systemic upset.
• Idiopathic intracranial hypertension — young overweight woman, daily headache, pulsatile tinnitus, transient visual obscurations, papilloedema, VI palsy, worse on bending.
• Cerebral venous sinus thrombosis — subacute headache with seizures, focal deficit or a delirium, in pregnancy, on the OCP, or prothrombotic.
• Acute angle-closure glaucoma — painful red eye, reduced vision, haloes, a mid-dilated fixed pupil, nausea — an ophthalmic emergency.
• Carbon monoxide poisoning — headache and nausea in several household members, winter, faulty heater.[1]

Differential diagnosis — the discriminating questions

A complete differential hinges on a handful of discriminating questions, asked in order.[2][4]

Key discriminating questions: Sudden (thunderclap)? → SAH. Fever/neck stiffness? → meningitis. Worse upright? → low-pressure headache. Worse lying/coughing/morning? → raised ICP / mass. Jaw claudication, age over 50? → GCA. Red eye + haloes? → angle-closure glaucoma. Brief electric shocks on face? → trigeminal neuralgia. [1]

Clinical and bedside assessment

Every headache patient needs vital signs (blood pressure in both arms), a general examination (rash, temporal artery, sinus and dental tenderness) and a full neurological examination including fundoscopy, meningeal signs and a mental-status screen.[1]

The named bedside manoeuvres earn marks:[1]

• Kernig sign — supine, hip flexed 90 degrees, knee extension resisted by hamstring pain (meningeal irritation).
• Brudzinski sign — passive neck flexion triggers involuntary hip and knee flexion (meningeal irritation).
• Temporal artery palpation — in suspected GCA a tender, thickened, pulseless or nodular artery supports the diagnosis; its absence does not exclude it.
• Fundoscopy — papilloedema (blurred disc margins, loss of venous pulsation) signals raised intracranial pressure; do it on every red-flag patient.
• Partial Horner (ptosis, miosis) persisting between cluster attacks is a key clue.
• Intraocular pressure where glaucoma is suspected.[1]

Investigations — driven entirely by red flags

Primary headache is a clinical diagnosis: no scan, no LP, no bloods when SNNOOP10 is negative and the pattern is typical. Investigation is driven by red flags, and only by red flags.[4][7]

Neuroimaging — when and what:[1]

• Non-contrast CT head — first-line emergency imaging for any thunderclap or red-flag headache; near 100 percent sensitivity for acute SAH within the first 6 hours on a modern multidetector scanner, falling thereafter.
• CT angiography — to find the aneurysm if SAH is confirmed; also for RCVS, arterial dissection and CVST.
• MRI brain with contrast — for subacute or progressive headache, mass lesion, CVST (MRV), posterior fossa and Chiari lesions, and to clarify equivocal CT.[1]

Lumbar puncture — the indications and the one rule you must not break:[1]

• Suspected SAH with negative CT — LP is mandatory; xanthochromia (bilirubin in the CSF supernatant) appears at 12 hours and persists up to 2 weeks. Always measure opening pressure.
• Suspected meningitis or encephalitis — cell count, protein, glucose, Gram stain, culture and viral PCR (HSV).
• Suspected IIH — opening pressure over 25 cmH2O with normal CSF, after a normal CT or MRI to exclude a mass.
• Suspected spontaneous intracranial hypotension — low opening pressure, often failing to flow.[1]

The classic trap: never LP before imaging if papilloedema or focal neurology is present — the risk is tonsillar herniation. Image first, always.[1]

Blood tests by context:[1]

• ESR and CRP — mandatory in any new headache over 50; GCA classically has ESR over 50 mm/h (often 80 to 100), and about 4 percent of biopsy-proven GCA have a normal ESR — a raised CRP lifts sensitivity over 95 percent.
• FBC, coagulation, urea and electrolytes, LFT, glucose — baseline, especially before LP or in pregnancy.
• Beta-hCG — in any woman of reproductive age with new headache.
• Carboxyhaemoglobin — for carbon monoxide poisoning.[1]

Two named tools, reproduced verbatim:[1]

• Ottawa Subarachnoid Haemorrhage Rule (Perry) — investigate (CT, ± LP) if any is present: age 40 or older; neck pain or stiffness; witnessed loss of consciousness; onset during exertion; thunderclap (instantly peaking) headache; limited neck flexion on examination. Sensitivity is about 100 percent for SAH (it is a rule-out, not a rule-in).[7]
• Temporal artery biopsy — the gold standard for GCA, showing granulomatous arteritis with multinucleated giant cells and disruption of the internal elastic lamina. GCA has skip lesions, so a negative biopsy does not exclude it — take a long segment (at least 1 cm), ideally within 2 weeks of starting steroids, and do NOT delay steroids for biopsy.[4]

Migraine Disability Assessment (MIDAS) quantifies headache-related disability over 3 months to guide prophylaxis: 0 to 5 little or none, 6 to 10 mild, 11 to 20 moderate, 21 or more severe — prophylaxis strongly indicated.[1]

Management — the killers first (humour off)

[1]

Resuscitation in headache is resuscitation of the secondary causes. Get these right and the rest is refinement.[7][11]

Subarachnoid haemorrhage — thunderclap is SAH until proven otherwise

ABCDE first; secure the airway if GCS drops. Immediate non-contrast CT head — if positive, CTA to localise the aneurysm and urgent neurosurgical or endovascular referral (clipping or coiling). If CT is negative but suspicion remains, LP for xanthochromia — performed between 12 hours and 2 weeks after the ictus, xanthochromia was present in every proven SAH, and a normal CT plus absent xanthochromia on spectrophotometry excludes a ruptured aneurysm.[11][22]

Control blood pressure while the aneurysm is unsecured — blood-pressure control before aneurysm treatment is an accepted means of preventing re-bleeding, and patients with lower maximal systolic pressure before repair had better functional outcome at 3 months — and give nimodipine 60 mg orally every 4 hours for 21 days: in the British aneurysm nimodipine trial it reduced cerebral infarction by 34 percent and death or severe disability by 40 percent.[13][12]

Bacterial meningitis — never delay antibiotics for the LP

Do not delay antibiotics for LP or imaging. Give empirical IV antibiotics within 1 hour: ceftriaxone 2 g IV 12-hourly (add vancomycin if pneumococcal resistance; add ampicillin if listeria risk — age over 50 or immunocompromised), and aciclovir 10 mg/kg IV 8-hourly if herpes simplex encephalitis is possible. Dexamethasone 10 mg IV 6-hourly before or with the first dose in suspected pneumococcal meningitis. Blood cultures first if obtainable immediately.[1]

Giant-cell arteritis with visual symptoms — steroids now, biopsy later

Start high-dose corticosteroid immediately — do not wait for biopsy. Sight is at risk. The classic trap: never delay GCA steroids for biopsy — the fellow eye is at risk within days.[4]

Prednisolone 40 to 60 mg daily for uncomplicated GCA; IV methylprednisolone 500 mg to 1 g daily for 3 days if there is visual loss or amaurosis (to protect the fellow eye), then high-dose oral. Arrange temporal artery biopsy within 2 weeks, and add low-dose aspirin unless contraindicated.[1]

Hypertensive emergency

Controlled IV antihypertensive (e.g. labetalol infusion), targeting a 10 to 20 percent mean arterial pressure reduction in the first hour.[1]

Management — migraine, the acute ladder

Treat early — before allodynia and central sensitisation develop, because sensitisation halves triptan efficacy. Choose by severity and prior response.[1][5]

Step 1 — mild to moderate: simple oral analgesia — an NSAID (ibuprofen, naproxen, aspirin, diclofenac) or acetaminophen (paracetamol), all with Level A/B evidence in the AHS assessment, with an antiemetic (metoclopramide or prochlorperazine — probably effective, Level B) that treats the nausea of migraine.[15]

Step 2 — moderate to severe, or failure of Step 1:[1]

• Triptans (selective 5-HT1B/1D agonists): at marketed doses all oral triptans are effective and well tolerated. Sumatriptan 100 mg PO — 59 percent 2-hour headache response, 29 percent 2-hour pain-free. Rizatriptan 10 mg has better efficacy and consistency; almotriptan 12.5 mg similar 2-hour efficacy with better tolerability and consistency; zolmitriptan 2.5 to 5 mg, eletriptan 40 mg and rizatriptan 5 mg perform very similarly to sumatriptan 100 mg; naratriptan 2.5 mg and eletriptan 20 mg trade lower efficacy for better tolerability. Sumatriptan comes in oral, nasal-spray, subcutaneous and rectal formulations and zolmitriptan in oral and nasal — all Level A (AHS evidence assessment).[14][15]
• Triptan plus NSAID — the sumatriptan/naproxen combination is an effective Level A option (AHS evidence assessment).[15]
• Newer acute drugs — the CGRP receptor antagonists (gepants) ubrogepant and rimegepant, and lasmiditan, a selective 5-HT1F agonist: usable where triptans are contraindicated. Celecoxib oral solution and remote electrical neuromodulation were also newly introduced (AHS Consensus 2021).[9][16]

The classic trap: never prescribe a triptan in unrecognised cardiovascular disease — the meta-analysis of 53 triptan trials is explicit that all triptans are contraindicated in the presence of cardiovascular disease.[14]

Step 3 — status migrainosus (over 72 hours): IV metoclopramide 10 mg or prochlorperazine 10 mg IV (often dramatic as monotherapy), IV fluids, ketorolac 30 mg IV, dihydroergotamine 0.5 to 1 mg (avoid with recent triptan), valproate 300 to 1000 mg, magnesium 1 to 2 g IV (especially with aura). A short steroid course may shorten status.[1]

Management — migraine prophylaxis

Start prophylaxis at 4 or more headache days a month, or with disability despite acute therapy, acute-therapy failure or contraindication, hemiplegic or basilar migraine, or patient preference. Aim for a 50 percent reduction; review at 3 and 6 months; trial 2 to 3 agents before declaring failure.[1][9]

[1]

CGRP-pathway monoclonal antibodies — injectable, few interactions, no monitoring: erenumab (anti-CGRP-receptor) 70 mg SC monthly (up to 140 mg); fremanezumab (anti-CGRP) 225 mg monthly or 675 mg quarterly; galcanezumab 240 mg loading then 120 mg monthly; eptinezumab 100 to 300 mg IV every 3 months.[1]

OnabotulinumtoxinA — 155 units in 31 head and neck sites every 12 weeks — is licensed for chronic migraine (15 or more days a month) ONLY, not episodic. Add nutraceuticals with evidence — magnesium 400 to 600 mg, riboflavin 400 mg, coenzyme Q10 100 to 300 mg daily — and the non-drug backbone of regular sleep, meals, hydration and trigger avoidance.[1]

Management — tension-type

Acute: ibuprofen 400 mg or paracetamol 1 g; avoid opioids and combination analgesics (overuse risk). Prophylaxis for frequent or chronic tension-type is amitriptyline 10 to 75 mg nocte first-line — and the Holroyd JAMA trial showed TCA plus stress management beats either alone, so prescribe the behaviour alongside the tablet.[10]

Management — cluster

Acute attacks must be aborted within minutes — oral drugs are too slow.[8][9]

• High-flow inhaled oxygen, 100 percent at 12 L/min by face mask for 15 minutes at attack onset — in the randomised crossover trial, 78 percent of attacks were pain-free at 15 minutes versus 20 percent on high-flow air, with no important adverse events.[17]
• Subcutaneous sumatriptan 6 mg and 100 percent oxygen (flow of at least 7 L/min over 15 minutes) are the first-choice acute drugs (EFNS guideline); the AHS guideline gives subcutaneous sumatriptan, zolmitriptan nasal spray and high-flow oxygen Level A recommendations for acute treatment. Oral drugs act too slowly for attacks that last minutes.[18][19]

Transitional (short-term) prevention to bridge while verapamil builds: oral prednisone 100 mg daily for 5 days, then tapering 20 mg every 3 days, in parallel with verapamil up-titration — the multicentre randomised trial found prednisone reduced attacks in the first week (mean 7.1 vs 9.5 with placebo). Alternatively, suboccipital steroid injections (three injections 48 to 72 hours apart) rapidly reduce attack frequency in patients with more than two attacks per day.[20][21]

Prophylaxis during a bout: verapamil at a daily dose of at least 240 mg (maximum dose limited by efficacy or tolerability) is first-choice prophylaxis — in trials it was started at 40 mg three times daily and increased to 120 mg three times daily. Lithium and topiramate are recommended alternative preventives (EFNS), and the AHS guideline gives suboccipital steroid injections its only Level A recommendation for cluster prophylaxis.[18][19][20]

Management — medication-overuse headache

Definition (ICHD-3): headache on 15 or more days a month for over 3 months in a patient with a pre-existing headache disorder, caused by regular overuse — ergotamine, triptans, opioids or combination analgesics on 10 or more days a month for over 3 months, or simple analgesics on 15 or more days a month for over 3 months.[6]

Always ask about analgesic intake — medication-overuse headache has a 1-year prevalence of 1 to 2 percent in the general population, is commoner in women, and travels with comorbid depression, anxiety and other chronic pain. Treatment has three components: education and counselling to reduce the intake of acute medication, withdrawal (discontinuation) of the overused drug in those who need it, and preventive drug therapy, which some patients require from the outset.[6]

Specific subtypes and scenarios

• Menstrual migraine — attacks 2 days before to 3 days after menses, usually without aura and often refractory. Acute: a triptan (frovatriptan, naratriptan — long half-life). Perimenstrual prophylaxis: frovatriptan 2.5 mg BD or naproxen 500 mg BD for the window.
• Vestibular migraine — recurrent episodic vertigo with migraine features; the commonest cause of spontaneous recurrent vertigo. Treat as migraine.
• Hemiplegic migraine — motor aura lasting hours; familial (FHM, autosomal dominant — CACNA1A, ATP1A2, SCN1A). Avoid triptans and ergots.
• Basilar migraine (now "migraine with brainstem aura") — brainstem aura (dysarthria, vertigo, tinnitus, diplopia, ataxia, bilateral paraesthesia), no motor weakness.
• Chronic migraine — 15 or more days a month for over 3 months, at least 8 with migraine features; onabotulinumtoxinA or a CGRP-mAb.
• Paroxysmal hemicrania and hemicrania continua — absolutely responsive to indomethacin 25 to 50 mg TDS (the diagnostic test).
• Hypnic headache — bedtime lithium 300 to 600 mg or caffeine (a strong coffee before bed); also indomethacin.
• Idiopathic intracranial hypertension — weight loss (most effective long-term), acetazolamide 1 to 4 g/day, topiramate; surgery (optic nerve sheath fenestration or a VP or LP shunt) if vision is threatened.
• Spontaneous intracranial hypotension — orthostatic headache; conservative (bed rest, hydration, caffeine), epidural blood patch if persistent.[1][2][3]

Complications and pitfalls

Medication-overuse headache is the commonest iatrogenic complication — fail to recognise it and you guarantee chronicity. Chronic migraine evolves from episodic under the weight of acute-medication overuse, obesity, depression and sleep apnoea; status migrainosus brings dehydration and, rarely, migraine infarction.[6]

The sight-and-life pitfalls are the ones that end careers: delaying GCA steroids for biopsy (the fellow eye goes blind within days); missing the SAH sentinel bleed (sent home as migraine, re-bleed days 4 to 14 carries high mortality); a triptan in unrecognised coronary disease; misreading angle-closure glaucoma as migraine (red eye, fixed pupil); LP before imaging with papilloedema (herniation); and missing carbon monoxide in winter.[1][4]

Prognosis and disposition

Primary headaches are chronic relapsing conditions; with correct diagnosis, trigger management, acute therapy and prophylaxis when needed, most achieve meaningful control. Migraine often improves after menopause and with age, cluster may remit permanently in a minority, and MOH is reversible once the drug is withdrawn.[1]

Most primary headache patients go home with safety-netting. Admit for status migrainosus needing IV therapy, intractable vomiting or dehydration, suicidal cluster pain, or any suspected secondary cause needing inpatient workup (SAH, meningitis, RCVS, severe GCA, IIH with threatened vision). Secondary prognosis is that of the cause — SAH case fatality up to 50 percent, bacterial meningitis mortality 10 to 30 percent, GCA excellent with steroids, IIH vision-threatening if papilloedema is uncontrolled.[1]

Special populations

• Pregnancy and breastfeeding — migraine often improves (especially second and third trimesters) but may worsen postpartum. Safe acute therapy: paracetamol, metoclopramide, propranolol. Avoid NSAIDs in the third trimester (ductus arteriosus, oligohydramnios); avoid triptans (limited data). Avoid topiramate and valproate (teratogenic). New headache in pregnancy or postpartum: think pre-eclampsia, CVST, pituitary apoplexy, RCVS, PRES — image.
• Over 50 — any new headache is GCA until ESR and CRP exclude it; mass lesion and giant-cell arteritis dominate. Hypnic headache is a disease of the elderly. Avoid NSAIDs where renal, cardiac, ulcer or anticoagulation status makes them hazardous; triptans are more often contraindicated.
• Children — migraine is often bilateral, shorter (1 to 72 h), with vomiting and abdominal pain. Acute: ibuprofen 10 mg/kg, paracetamol 15 mg/kg; age-licensed triptans. Prophylaxis: propranolol, topiramate, amitriptyline, cyproheptadine. Always image a child whose headache wakes them from sleep, is progressive, or comes with vomiting on waking, focal neurology or papilloedema.
• Women of childbearing age — avoid valproate (Pregnancy Prevention Programme) and counsel on topiramate; prefer propranolol, amitriptyline, a CGRP-mAb.
• Anticoagulated — any new or thunderclap headache is intracranial haemorrhage until proven otherwise; image immediately and reverse anticoagulation if confirmed.
• Immunocompromised — lower the threshold to image and LP; consider toxoplasmosis, cryptococcus, lymphoma, PML.[1]

Evidence, guidelines and regional differences

ICHD-3 (2018) is the diagnostic framework reproduced throughout this page. NICE (UK) emphasises SNNOOP-style red-flag assessment, triptans first-line for migraine, avoidance of opioids and codeine, prophylaxis review at 6 months, and CGRP-pathway drugs via specialist commissioning. AAN/AHS endorse propranolol, timolol, topiramate, valproate, onabotulinumtoxinA (chronic) and the CGRP monoclonal antibodies. EHF supports the same acute ladder and CGRP-mAb plus botulinum toxin for chronic migraine.[1][9]

The landmark papers behind these recommendations:[5][6][8][10]

• Goadsby, NEJM 2002 (PMID 11807151) — the review of migraine pathophysiology (cortical spreading depression, trigeminovascular, CGRP) and treatment.
• May et al., Lancet 1998 (PMID 9690407) — PET demonstration of hypothalamic activation in cluster, establishing its hypothalamic origin.
• Diener et al., Lancet Neurology 2019 (PMID 31174999) — the definitive review of medication-overuse headache.
• Perry et al., JAMA 2013 (PMID 24065011) — derivation of the Ottawa Subarachnoid Haemorrhage Rule, sensitivity near 100 percent.
• Holroyd et al., JAMA 2001 (PMID 11325322) — RCT showing amitriptyline plus stress management is the best therapy for chronic tension-type headache.[1]

[1] [1]

Exam pearls

• Brain parenchyma is insensitive to pain — pain from dura, vessels, sinuses, scalp, cervical roots, cranial nerves V, VII, IX, X; V1 anterior two-thirds, C2/C3 posterior third.
• Migraine = unilateral throbbing, 4 to 72 h, photo and phonophobia, nausea, aggravated by movement, lies still.
• Migraine aura = fully reversible, spreads over 5 min, lasts under 60 min, headache within 60 min; scintillating scotoma commonest.
• Triptans are 5-HT1B/1D agonists; at marketed doses all oral triptans are effective and well tolerated (sumatriptan 100 mg: 59 percent 2-hour response) — contraindicated in the presence of cardiovascular disease.[14]
• Migraine prophylaxis (4 or more days a month): propranolol, topiramate, amitriptyline, valproate, flunarizine, candesartan, CGRP-mAb; onabotulinumtoxinA for chronic migraine only.
• Tension-type: bilateral band, no nausea, not aggravated by movement; prophylaxis amitriptyline.
• Cluster: strictly unilateral periorbital, ipsilateral autonomic features and Horner, bouts, paces, nocturnal; acute 100 percent oxygen (12 L/min for 15 min) or SC sumatriptan 6 mg; prophylaxis verapamil at least 240 mg/day.[17][18]
• Thunderclap = SAH — CT then LP for xanthochromia (between 12 hours and 2 weeks); nimodipine 60 mg PO 4-hourly for 21 days reduces cerebral infarction and poor outcome.[22][12]
• GCA: age over 50, jaw claudication (most specific), tender temporal artery, ESR over 50 — start prednisolone 40 to 60 mg at once; fellow eye at risk.
• MOH: overuse of acute medication driving chronic headache — education and counselling, withdrawal of the overused drug, plus preventive therapy.[6]
• Paroxysmal hemicrania and hemicrania continua are absolutely indomethacin-responsive — the diagnostic test.
• IIH: young obese woman, papilloedema, opening pressure over 25 cmH2O with normal CSF — weight loss plus acetazolamide.
• CGRP is the central molecular mediator of migraine — gepants and monoclonal antibodies target it.[1]

Exam application bank (NEET-PG / INICET)

One-line answer

Headache (cephalalgia) is pain arising from the pain-sensitive structures of the head (dura, vessels, sinuses, scalp, cervical roots, cranial nerves V, VII, IX, X) but NOT the brain parenchyma itself (it is insensate). The single most important clinical step is to separate primary from secondary headache using the SNNOOP10 red-flag screen: a secondary headache has an underlying cause (haemorrhage, infection, mass, giant-cell arteritis, raised pressure) and may be life-threatening. The three primary headaches are migraine (unilateral throbbing, 4 to 72 h, photophobia, phonophobia, nausea, aura in one-third), tension-type (bilateral pressing band, no nausea, not aggravated by routine), and cluster (unilateral periorbital excruciating 15 to 180 min attacks in bouts, ipsilateral autonomic features and Horner syndrome). A thunderclap headache (peak intensity within 1 minute) is subarachnoid h

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Headache.

The mantra

[4]

The mantra: Primary vs secondary first — run SNNOOP10 on every headache. Thunderclap is SAH, new-over-50 is GCA, fever with neck stiffness is meningitis — exclude the killers before you name the benign pattern.[1][4][7][11]

Ward-round test — four stems, thirty seconds each

Stem 1 — the 24-year-old thunderclap (answer)

A 24-year-old man, woken at 2 am by a headache peaking within one minute, with neck stiffness and one vomit. CT is negative. What next, and when? Model: A thunderclap peaking within one minute is SAH until proven otherwise — the Ottawa rule was derived in patients whose headache reached maximal intensity within 1 hour and is highly sensitive. A negative CT does not end the workup — perform LP looking for xanthochromia: xanthochromia was present in every proven SAH when lumbar puncture was done between 12 hours and 2 weeks after the ictus, so a normal CT plus absent xanthochromia on spectrophotometry excludes a ruptured aneurysm. If xanthochromia is present, CTA to localise the aneurysm and urgent neurosurgical referral; start nimodipine 60 mg PO every 4 hours for 21 days, which reduced cerebral infarction by about a third and poor outcome by 40 percent in the British aneurysm nimodipine trial.[7][22][12]

Stem 2 — the man who paces at night (answer)

A 38-year-old smoker has 45-minute attacks of excruciating left periorbital pain, every night at 2 am for three weeks, with a watering left eye and a drooping left eyelid. He cannot sit still. What is it, and what do you give now? Model: This is cluster headache — strictly unilateral periorbital pain with ipsilateral autonomic features and partial Horner, occurring in bouts, with the hallmark restlessness (he paces — the opposite of migraine). Acute now: 100 percent oxygen at 12 L/min by face mask for 15 minutes (78 percent pain-free at 15 minutes versus 20 percent on air in the randomised trial) or subcutaneous sumatriptan 6 mg — with 100 percent oxygen these are the first-choice acute drugs. Then start prophylaxis with verapamil at a daily dose of at least 240 mg.[17][18]

Stem 3 — the 68-year-old with a tender temple (answer)

A 68-year-old woman has a new temporal headache for a week, jaw tiredness on chewing, and this morning a curtain coming down over her right eye. ESR is 92. What is the single most important action in the next hour? Model: This is giant-cell arteritis with visual symptoms — the one diagnosis where you treat first and biopsy later. Start prednisolone 40 to 60 mg immediately; because sight is threatened, give IV methylprednisolone 500 mg to 1 g daily for 3 days to protect the fellow eye. Arrange temporal artery biopsy within 2 weeks and add low-dose aspirin. Never delay steroids for biopsy — skip lesions mean a negative biopsy does not exclude GCA, and the fellow eye is at risk within days.[4]

Stem 4 — the daily headache that will not stop (answer)

A 42-year-old with long-standing migraine now has headache 20 days a month. She takes a combination analgesic containing codeine six days a week. What happened, and what is the treatment? Model: This is medication-overuse headache — regular or frequent use of analgesics and acute antimigraine drugs has increased her headache frequency and driven the transition from episodic migraine to chronic daily headache (1-year prevalence in the general population 1 to 2 percent). Always ask about analgesic intake. Treatment has three components: education and counselling to reduce the intake of acute medication, withdrawal (discontinuation of the overused combination analgesic), and preventive drug therapy, which some patients need from the outset.[6]

References

1. [1]Eigenbrodt AK, Ashina H, Khan S, et al. Diagnosis and management of migraine in ten steps Nat Rev Neurol, 2021.PMID 34145431
2. [2]Rizzoli P, Mullally WJ. Headache Am J Med, 2018.PMID 28939471
3. [3]Headache Classification Committee of the International Headache Society (IHS). Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition Cephalalgia, 2018.PMID 29368949
4. [4]Dodick DW. Diagnosing Secondary and Primary Headache Disorders Continuum (Minneap Minn), 2021.PMID 34048392
5. [5]Goadsby PJ, Lipton RB, Ferrari MD. Migraine--current understanding and treatment N Engl J Med, 2002.PMID 11807151
6. [6]Diener HC, Dodick D, Evers S, et al. Pathophysiology, prevention, and treatment of medication overuse headache Lancet Neurol, 2019.PMID 31174999
7. [7]Perry JJ, Stiell IG, Sutherland MR, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache JAMA, 2013.PMID 24065011
8. [8]May A, Bahra A, Büchel C, et al. Hypothalamic activation in cluster headache attacks Lancet, 1998.PMID 9690407
9. [9]Ogunlaja OI, Goadsby PJ Headache: Treatment update eNeurologicalSci, 2022.PMID 36636337
10. [10]Holroyd KA, O'Donnell FJ, Stensland M, et al. Management of chronic tension-type headache with tricyclic antidepressant medication, stress management therapy, and their combination: a randomized controlled trial JAMA, 2001.PMID 11325322
11. [11]Ducros A, Bousser MG. Thunderclap headache BMJ, 2013.PMID 23303883
12. [12]Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial BMJ, 1989.PMID 2496789
13. [13]Eagles ME, Veilleux C, Riva-Cambrin J, Macdonald RL. Blood Pressure Targets After Aneurysmal Subarachnoid Hemorrhage: Is Lower Better? Neurosurgery, 2025.PMID 40488458
14. [14]Ferrari MD, Goadsby PJ, Roon KI, Lipton RB. Triptans (serotonin, 5-HT1B/1D agonists) in migraine: detailed results and methods of a meta-analysis of 53 trials Cephalalgia, 2002.PMID 12383060
15. [15]Marmura MJ, Silberstein SD, Schwedt TJ. The acute treatment of migraine in adults: the american headache society evidence assessment of migraine pharmacotherapies Headache, 2015.PMID 25600718
16. [16]Ailani J, Burch RC, Robbins MS; Board of Directors of the American Headache Society. The American Headache Society Consensus Statement: Update on integrating new migraine treatments into clinical practice Headache, 2021.PMID 34160823
17. [17]Cohen AS, Burns B, Goadsby PJ. High-flow oxygen for treatment of cluster headache: a randomized trial JAMA, 2009.PMID 19996400
18. [18]May A, Leone M, Afra J, et al. EFNS guidelines on the treatment of cluster headache and other trigeminal-autonomic cephalalgias Eur J Neurol, 2006.PMID 16987158
19. [19]Robbins MS, Starling AJ, Pringsheim TM, Becker WJ, Schwedt TJ. Treatment of Cluster Headache: The American Headache Society Evidence-Based Guidelines Headache, 2016.PMID 27432623
20. [20]Obermann M, Nägel S, Ose C, et al. Safety and efficacy of prednisone versus placebo in short-term prevention of episodic cluster headache: a multicentre, double-blind, randomised controlled trial Lancet Neurol, 2021.PMID 33245858
21. [21]Leroux E, Valade D, Taifas I, et al. Suboccipital steroid injections for transitional treatment of patients with more than two cluster headache attacks per day: a randomised, double-blind, placebo-controlled trial Lancet Neurol, 2011.PMID 21903477
22. [22]Vermeulen M, Hasan D, Blijenberg BG, Hijdra A, van Gijn J. Xanthochromia after subarachnoid haemorrhage needs no revisitation J Neurol Neurosurg Psychiatry, 1989.PMID 2769274