Headache Disorders

Headache is one of the commonest neurological complaints and a guaranteed NEET PG topic because it tests pattern recognition: the examiner gives you a vignette and expects you to slot it into migraine, tension-type, cluster, or a sinister secondary cause. The whole subject pivots on two skills — classifying primary headaches by their stereotyped phenotype, and spotting the red flags that mandate neuroimaging.

Classification: primary vs secondary

The International Classification of Headache Disorders (ICHD-3) divides headache into:

• Primary headaches — the headache is the disease; no underlying structural lesion. The big three are migraine, tension-type headache (TTH), and trigeminal autonomic cephalalgias (TACs, chiefly cluster).
• Secondary headaches — symptomatic of an underlying disorder: raised intracranial pressure (ICP), subarachnoid haemorrhage (SAH), meningitis, giant cell arteritis, venous sinus thrombosis, idiopathic intracranial hypertension (IIH), medication-overuse headache, etc.
• Painful cranial neuropathies — e.g. trigeminal neuralgia.

High-yield: Tension-type headache is the most common primary headache overall in the general population, while migraine is the most common headache for which patients consult a doctor / present to clinics. Don't confuse "most common" with "most consulted."

The big three primary headaches — comparison

Feature	Migraine	Tension-type	Cluster
Sex predilection	Female (3:1)	Female slight	Male (3:1)
Site	Unilateral (60%)	Bilateral, band-like	Unilateral, orbital/temporal
Quality	Throbbing/pulsating	Dull, pressing, tightening	Boring, stabbing, excruciating
Severity	Moderate–severe	Mild–moderate	Very severe ("suicide headache")
Duration	4–72 h (untreated)	30 min – 7 days	15–180 min per attack
Periodicity	Episodic, often menstrual	Stress-related	Circadian, clusters over weeks
Aggravated by	Routine activity, light, sound	Not by activity	Restless, paces about
Associated	Nausea, photo/phonophobia, aura	Usually none	Ipsilateral autonomic features
Behaviour	Lies still in dark room	Continues activity	Agitated, restless

High-yield: Behaviour during an attack is a discriminator — the migraineur lies still in a dark, quiet room, whereas the cluster patient is restless and paces/rocks. A vignette stressing restlessness points to cluster.

Migraine

Pathophysiology

The modern view abandons the old purely "vascular" theory. Migraine is a primary neuronal/neurovascular disorder:

• Cortical spreading depression (CSD) — a wave of neuronal depolarisation followed by suppression spreading across the cortex at ~3 mm/min — is the substrate of the aura (e.g. the slowly marching scintillating scotoma).
• Activation of the trigeminovascular system releases calcitonin gene-related peptide (CGRP), substance P and neurokinin A → neurogenic inflammation and dural vessel dilatation → pain.
• Serotonin (5-HT) dysregulation underlies therapy: triptans are 5-HT1B/1D agonists.

High-yield: CGRP is the key migraine mediator — basis of the newest drugs (gepants like rimegepant/ubrogepant; monoclonal antibodies erenumab, fremanezumab, galcanezumab for prophylaxis).

Clinical phases and features

Migraine has up to four phases: prodrome → aura → headache → postdrome.

• Without aura (common migraine, ~75%): recurrent attacks, unilateral throbbing, nausea, photophobia/phonophobia.
• With aura (classic migraine, ~25%): fully reversible focal neurological symptoms preceding/accompanying headache. The classic aura is visual — a scintillating scotoma or fortification spectra (teichopsia) — a zig-zag expanding edge. Aura develops over ≥5 min and lasts 5–60 min.

High-yield: A scintillating scotoma (expanding zig-zag with shimmering edge) is the hallmark visual aura. It is fully reversible — a prolonged or fixed deficit demands you reconsider a structural lesion or TIA.

Diagnostic criteria (ICHD-3, migraine without aura)

≥5 attacks, each lasting 4–72 h, with ≥2 of (unilateral, pulsating, moderate/severe, aggravated by routine activity) AND ≥1 of (nausea/vomiting OR photophobia + phonophobia).

Mnemonic — POUND for migraine likelihood: Pulsatile, lasts One day (4–72 h), Unilateral, Nausea, Disabling. ≥4 of 5 → high probability of migraine.

Management of migraine

Stepwise acute approach: Identify trigger/avoid → simple analgesic (paracetamol/NSAID) + antiemetic → triptan if inadequate → consider gepant/ditan → prophylaxis if frequent.

• Acute (abortive): NSAIDs/paracetamol for mild; triptans (sumatriptan) are the drug of choice for moderate–severe attacks. Add metoclopramide/domperidone for nausea and to aid absorption. Newer: lasmiditan (ditan, 5-HT1F agonist) and gepants.
• Prophylaxis (indicated if ≥4 headache days/month or disabling): propranolol (first-line; also topiramate, amitriptyline, flunarizine, valproate, candesartan). Botulinum toxin and anti-CGRP mAbs for chronic migraine.

Drug class	Example	Key caution
Triptan	Sumatriptan	Contra in IHD, uncontrolled HTN, hemiplegic/basilar migraine; avoid with ergots/MAOI
Ergot	Ergotamine	Vasospasm, ergotism; largely superseded
Beta-blocker (prophylaxis)	Propranolol	Avoid in asthma
Anticonvulsant (prophylaxis)	Topiramate	Weight loss, paraesthesia, stones; teratogenic
Anti-CGRP mAb	Erenumab	Prophylaxis of chronic migraine

High-yield: Sumatriptan (a triptan, 5-HT1B/1D agonist) is the abortive drug of choice for acute migraine; propranolol is the classic first-line prophylactic. Triptans are contraindicated in ischaemic heart disease and in hemiplegic/basilar-type migraine.

Tension-type headache (TTH)

The commonest primary headache. Features:

• Bilateral, pressing/tightening (non-pulsatile), band-like ("hatband") quality.
• Mild–moderate, not aggravated by routine physical activity.
• No nausea/vomiting; at most one of photophobia or phonophobia.
• Often associated with pericranial muscle tenderness, stress, poor posture.

Classified as infrequent episodic (<1 day/month), frequent episodic (1–14 days/month), and chronic (≥15 days/month for >3 months).

Management: simple analgesics (paracetamol, NSAIDs) for acute attacks; amitriptyline is the prophylactic drug of choice for chronic/frequent TTH. Address stress, posture, and avoid analgesic overuse (risk of medication-overuse headache).

High-yield: TTH = bilateral, band-like, non-throbbing, no nausea, not worsened by activity. Prophylaxis of choice = amitriptyline.

Cluster headache (a trigeminal autonomic cephalalgia)

The most severe of the primaries.

• Strictly unilateral, orbital/supraorbital/temporal, excruciating, boring/stabbing.
• Attacks last 15–180 minutes, occur up to 8 times/day, often at the same time each day (alarm-clock headache) and frequently wake the patient ~90 min after sleep onset (REM-linked).
• Bouts ("clusters") last weeks–months with remissions; alcohol is a potent trigger during a bout.
• Ipsilateral cranial autonomic features: lacrimation, conjunctival injection, rhinorrhoea/nasal congestion, ptosis, miosis (partial Horner syndrome), eyelid oedema, facial sweating.
• Patient is restless and agitated.

Management:

• Acute: 100% oxygen (12–15 L/min via non-rebreather mask) — the classic abortive; subcutaneous sumatriptan (fastest triptan route) is the drug of choice for aborting an attack.
• Transitional/prophylaxis: Verapamil is the prophylactic drug of choice; short courses of steroids (prednisolone) or greater occipital nerve block to break a bout; lithium for chronic cluster.

High-yield: Cluster headache acute therapy = high-flow 100% oxygen and/or subcutaneous sumatriptan; prophylaxis = verapamil. Autonomic features are ipsilateral, and a partial Horner's (ptosis + miosis) may persist.

TAC differentiation (one classic trap)

TAC	Attack duration	Frequency	Distinguishing point
Cluster	15–180 min	1–8/day	Restless; oxygen-responsive
Paroxysmal hemicrania	2–30 min	>5/day	Absolute response to indometacin
SUNCT	1–600 sec	many	Very short, conjunctival injection + tearing

High-yield: Paroxysmal hemicrania is defined by its complete response to indometacin — a favourite single-best-answer.

Trigeminal neuralgia (for differential)

Brief (seconds), electric-shock-like, lancinating pain in V2/V3 distribution, triggered by touch/chewing/cold; often due to vascular loop compression (superior cerebellar artery); in the young/bilateral think multiple sclerosis. Carbamazepine is the drug of choice; microvascular decompression for refractory cases.

Secondary headache & RED FLAGS

The exam's favourite secondary scenarios:

• Subarachnoid haemorrhage: sudden "thunderclap" headache, "worst headache of my life," maximal within seconds, neck stiffness. → Non-contrast CT head first; if normal and suspicion high, do LP looking for xanthochromia.
• Raised ICP / space-occupying lesion: headache worse on waking / lying down, aggravated by coughing, bending, Valsalva, with morning vomiting (often projectile) and papilloedema; may have focal deficit/seizure.
• Meningitis/encephalitis: fever, neck stiffness, photophobia, rash.
• Giant cell (temporal) arteritis: age >50, new headache, scalp tenderness, jaw claudication, raised ESR/CRP; risk of blindness → start high-dose steroids immediately, then temporal artery biopsy.
• Idiopathic intracranial hypertension (IIH): obese young woman, headache + visual obscurations + papilloedema; CT/MRI normal, raised opening pressure on LP.
• Cerebral venous sinus thrombosis: headache + seizures/focal signs, prothrombotic state, pregnancy/OCP.
• Medication-overuse headache: analgesic/triptan use ≥10–15 days/month.

Mnemonic for red flags — SNNOOP10 / simplified "SSNOOP": Systemic symptoms (fever, weight loss), Secondary risk (cancer, HIV, immunosuppression), Neurological deficit, Onset sudden (thunderclap), Older (>50, new headache), Pattern change/positional/precipitated by Valsalva, Papilloedema, Pregnancy.

High-yield: A sudden thunderclap "worst-ever" headache = SAH until proven otherwise → non-contrast CT first, LP for xanthochromia if CT negative. Headache worse in the morning / on bending / with vomiting + papilloedema = raised ICP.

When to image / investigate

Approach to a headache vignette:

1. Is there a red flag? → urgent neuroimaging.
2. Sudden/thunderclap → NCCT head → LP (xanthochromia).
3. Suspected mass/raised ICP → MRI/CT; avoid LP before imaging if focal signs/papilloedema (risk of coning).
4. ?GCA in elderly → ESR/CRP + temporal artery biopsy, start steroids first.
5. No red flag + classic phenotype → clinical diagnosis, no imaging needed.

High-yield: Investigation of choice for suspected SAH = non-contrast CT (highest sensitivity within 6 h); if negative → lumbar puncture for xanthochromia (peaks at 12 h). In suspected raised ICP with papilloedema, do NOT do LP before imaging.

Complications

• Migraine: status migrainosus (>72 h), migrainous infarction (rare; aura + stroke), chronic migraine, medication-overuse headache. Migraine with aura is an independent stroke risk factor, especially with smoking + combined OCPs.
• Cluster: depression/suicidality from severity; verapamil can cause bradycardia/heart block (monitor ECG).
• Raised ICP: visual loss, herniation/coning.
• GCA: irreversible blindness (anterior ischaemic optic neuropathy).

High-yield: Migraine with aura + smoking + combined oral contraceptive pill markedly raises ischaemic stroke risk — combined OCPs are contraindicated in migraine with aura.

Key differentials at a glance

• Throbbing unilateral + photophobia + nausea → migraine.
• Bilateral band-like, no nausea → TTH.
• Severe unilateral orbital + autonomic + restless → cluster.
• Worst-ever sudden → SAH.
• Morning headache + papilloedema + projectile vomiting → raised ICP.
• Elderly + jaw claudication + raised ESR → GCA.
• Obese young woman + papilloedema, normal scan → IIH.
• Lightning facial pain on touch → trigeminal neuralgia.

Recently asked / exam angle

• Drug of choice questions are perennial: acute migraine → sumatriptan; migraine prophylaxis → propranolol; cluster acute → oxygen / SC sumatriptan; cluster prophylaxis → verapamil; trigeminal neuralgia → carbamazepine; TTH prophylaxis → amitriptyline; paroxysmal hemicrania → indometacin.
• The CGRP story (mediator + new gepants/mAbs) is increasingly tested.
• Aura identification: scintillating scotoma / fortification spectra; aura is fully reversible and develops over minutes (distinguishes from TIA's abrupt onset).
• Red-flag → investigation matches: thunderclap → NCCT then LP; papilloedema → image before LP.
• Behaviour clue: restless = cluster, still in dark room = migraine.
• Contraindications: triptans in IHD and hemiplegic/basilar migraine; OCP in migraine with aura.
• CSD as the basis of aura; trigeminovascular activation for pain.
• IIH classic demographic and management (acetazolamide, weight loss, CSF shunt/optic nerve fenestration for vision threat).

Rapid revision

1. TTH = most common primary headache; migraine = most common to consult for.
2. Migraine = unilateral, throbbing, 4–72 h, photo/phonophobia, nausea; lies still in the dark.
3. Scintillating scotoma / fortification spectra = classic visual aura; fully reversible over 5–60 min.
4. CSD causes aura; CGRP is the key pain mediator.
5. Acute migraine DOC = sumatriptan; prophylaxis DOC = propranolol (≥4 headache days/month → prophylax).
6. Triptans contraindicated in IHD and in hemiplegic/basilar migraine.
7. Cluster = unilateral orbital, 15–180 min, circadian, ipsilateral autonomic features (partial Horner's), restless.
8. Cluster acute = 100% O₂ / SC sumatriptan; prophylaxis = verapamil.
9. Paroxysmal hemicrania = absolute response to indometacin; trigeminal neuralgia → carbamazepine.
10. Thunderclap headache → SAH → NCCT first, then LP for xanthochromia.
11. Raised ICP = morning headache, worse on Valsalva/lying, projectile vomiting, papilloedema; image before LP.
12. GCA (>50, jaw claudication, high ESR) → immediate steroids then biopsy; migraine with aura + OCP + smoking → high stroke risk.