Headache: migraine, tension-type and cluster headache

Overview

Headache is one of the most common reasons people see a doctor. Most headaches are primary (the headache is the disease): migraine, tension-type and cluster headache. A small number are secondary to something serious, such as meningitis, subarachnoid haemorrhage, raised intracranial pressure or giant cell arteritis.

The diagnosis of primary headache rests on the history. Examination and scans are normal; their job is to exclude a secondary cause. PGET questions focus on telling the three primary headaches apart and on choosing acute and preventive drugs.

Why the head hurts

• The brain tissue itself has almost no pain receptors.
• Pain arises from meninges, large intracranial vessels and venous sinuses, scalp, muscles, sinuses, eyes and teeth.
• Pain signals travel in the trigeminal (V) and glossopharyngeal (IX) nerves and the upper cervical roots. That is why posterior fossa pain can refer to the neck and occiput.

Primary versus secondary headache

Red flags (think secondary headache)

Migraine

Who gets it

• The commonest cause of recurrent episodic headache: it affects 15–20% of women but only 5–10% of men.
• Usually starts around puberty; onset is before 40 in most. Family history is common.

Mechanism (only what explains the exam facts)

• Migraine is now thought to be mainly neural, not primarily vascular.
• Cortical spreading depression: a slow wave of neuronal depolarisation, then silence, that crawls forward from the occipital cortex. This explains the aura and why it moves across the visual field.
• The headache comes from activation of the trigeminovascular system (trigeminal fibres around dural and large intracranial vessels). These fibres release CGRP (calcitonin gene-related peptide), substance P and other peptides, which inflame and dilate meningeal vessels.
• Sensitised trigeminal pathways make normal stimuli (light, noise, movement, touching the scalp) painful.

Triggers

Too much or too little sleep; stress (and the "let-down" after it); skipped meals; alcohol; bright light and loud noise; falling oestrogen (menstrual migraine just before a period, the combined pill, the menopause). Specific foods are much less often to blame than patients think.

Clinical features: migraine without aura (common migraine)

Diagnostic pattern:

• Recurrent attacks lasting 4–72 hours (untreated).
• Two or more of: one-sided pain; throbbing; moderate or severe; worse with movement or routine activity.
• One or more of: nausea or vomiting; photophobia and phonophobia.
• Normal examination and no other cause.

The patient wants to lie still in a dark, quiet room; sleep helps. The scalp may be tender (allodynia). A washed-out feeling follows.

Migraine with aura (classical migraine)

• About 25% of people with migraine have an aura in some attacks.
• The aura builds up over 5–20 minutes, lasts under 60 minutes, and is followed by headache.
• Visual aura is the commonest: shimmering, zigzag lines (teichopsia, fortification spectra), broken-glass images, a moving scotoma, sometimes hemianopia.
• Tingling that spreads up a limb, speech disturbance and, rarely, weakness may follow the visual symptoms.

Variants

• Hemiplegic migraine: rare, often autosomal dominant; hemiparesis with headache, recovering within 24 hours.
• Brainstem (basilar-type) aura: vertigo, double vision, perioral tingling, unsteadiness, rarely reduced consciousness.
• Vestibular migraine: episodes of vertigo lasting hours linked to migraine.
• Chronic migraine: headache on 15 or more days a month for over 3 months; often driven by medication overuse.

Treatment of migraine

General measures

Explain the condition, keep a headache diary, identify and avoid triggers, keep regular sleep and meals, and limit painkiller days.

Acute (abortive) treatment: step by step

Avoid opioids (codeine, tramadol): they work poorly and readily cause medication overuse headache.

Triptans

• Mechanism: agonists at 5-HT1B receptors on cranial vessels (vasoconstriction) and 5-HT1D receptors on trigeminal nerve endings (block CGRP release and pain transmission).
• Side-effects: tingling, warmth, chest tightness, drowsiness.
• Contraindications: ischaemic heart disease, previous MI or stroke, peripheral vascular disease, uncontrolled hypertension, coronary vasospasm (Prinzmetal angina), hemiplegic or brainstem aura.
• Do not take with ergotamine. Care with SSRIs and SNRIs (serotonin syndrome).

Ergotamine and the ergot derivatives

Ergotamine is the old specific anti-migraine drug, now largely replaced by triptans.

• Action: partial agonist at 5-HT receptors and α-adrenergic receptors (also dopamine). Causes strong, long-lasting and cumulative vasoconstriction.
• Use: only for the acute attack, best taken in the prodrome or very early; it works poorly if delayed. It has no value for prevention and is not an analgesic for other pain.
• Forms: tablets, sublingual, suppository; often combined with caffeine (1 mg ergotamine with 100 mg caffeine) to improve absorption.
• Dose limit: no more than 6 mg per attack and 10 mg per week.
• Dihydroergotamine (injection or nasal) is used for severe, intractable migraine and during in-hospital withdrawal in medication overuse headache.
• Side-effects: nausea, vomiting, diarrhoea (the commonest), muscle cramps; with overdose ergotism: prolonged vasospasm, cold painful limbs, gangrene, bowel ischaemia.
• Contraindications: coronary artery disease, peripheral vascular disease (including Raynaud), uncontrolled hypertension, pregnancy (uterine stimulant), severe liver or kidney disease, combination with triptans or strong CYP3A4 inhibitors (ritonavir, clarithromycin, azole antifungals), which raise levels and cause ergotism.
• Methysergide (an ergot once used for prevention) was withdrawn because long-term use caused retroperitoneal, pleural and heart valve fibrosis.

Preventive (prophylactic) treatment

When: attacks are frequent (more than 1–2 a month) and disabling, acute drugs fail or are overused, or there are prolonged or hemiplegic auras.

How: start low, increase slowly, and judge the effect after an adequate course. A course of 3–6 months typically halves attack frequency, and the benefit often persists after stopping. Prevention fails if analgesic overuse continues.

Migraine in pregnancy and with the pill

• Migraine often improves in pregnancy (steady oestrogen) and returns after delivery.
• Use paracetamol; sumatriptan may be used if needed. Avoid ergotamine and avoid topiramate and valproate.
• For prevention in pregnancy, low-dose propranolol or amitriptyline may be used.

Medication overuse headache

• Taking analgesics or triptans on 10 or more days a month (especially codeine or combination painkillers) can convert episodic headache into chronic daily headache (15 or more days a month for 3 months).
• Treatment: explain, withdraw the overused drug (expect a temporary rebound), and start a preventive.

Tension-type headache

• The commonest headache overall, but usually mild, so many never consult.
• Bilateral, pressing or tightening "band round the head", pressure behind the eyes; mild to moderate.
• No nausea or vomiting, not worsened by routine activity; at most one of photophobia or phonophobia.
• Often linked with stress, poor sleep, depression and anxiety.
• Examination is normal (pericranial muscles may be tender).

Management:

• Acute: simple analgesics (paracetamol, aspirin, NSAID), limited to avoid overuse.
• Non-drug: reassurance, stress management, relaxation, physiotherapy, massage.
• Frequent or chronic: amitriptyline is the preventive of choice.

Cluster headache

Cluster headache is one of the trigeminal autonomic cephalalgias: one-sided pain in the ophthalmic division of V with same-side autonomic features.

Features

• Uncommon (about 1 in 1000); mainly men aged 20–40; smokers and drinkers over-represented.
• Excruciating, boring pain around or behind one eye (temple), always the same side in a bout.
• Same-side: tearing, red eye, blocked or running nostril, eyelid swelling, ptosis and miosis (partial Horner syndrome), facial sweating.
• Attacks last 30–90 minutes, up to several a day, often waking the patient at the same time each night.
• Bouts (clusters) last 1–2 months, then remission for months or a year, often recurring at the same time of year.
• The patient is restless, paces or rocks, unlike the still migraine patient.
• Alcohol triggers attacks during a bout.
• Functional imaging shows hypothalamic activation (explains the clock-like timing).

Management

Other primary headaches (short attacks)

Comparing the three main headaches

Two mimics to remember: trigeminal neuralgia (seconds-long electric-shock pain in V2 or V3 triggered by touch or chewing; carbamazepine) and giant cell arteritis (over 50, jaw claudication, high ESR; start steroids at once to protect vision).

Quick revision

• Migraine: 4–72 h, one-sided, throbbing, nausea, photophobia; aura in about a quarter (visual zigzags).
• Acute migraine: aspirin/NSAID/paracetamol + metoclopramide, then triptan; SC sumatriptan if vomiting.
• Triptans: 5-HT1B/1D agonists; avoid in coronary, cerebrovascular and peripheral vascular disease.
• Ergotamine: abortive only; give early; max 6 mg per attack, 10 mg per week; avoid in vascular disease and pregnancy; ergotism and gangrene.
• Prevention when more than 1–2 disabling attacks a month: propranolol, topiramate, amitriptyline first; valproate, candesartan, pizotifen, flunarizine next; botulinum toxin for chronic migraine.
• Tension-type: bilateral band, no vomiting; analgesics, amitriptyline for prevention.
• Cluster: men, 30–90 min, nightly, ipsilateral autonomic signs, restless; SC sumatriptan + oxygen; verapamil.
• Paroxysmal hemicrania: indometacin. Painkillers on 10 or more days a month cause medication overuse headache.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; Katzung's Basic and Clinical Pharmacology).

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