20.1 — Headache and Migraine

Migraine affects around 1 in 7 people worldwide. It is the second leading cause of years lived with disability globally, and until 2018 there was no drug developed specifically to prevent it — every preventive in use had been borrowed from another condition.

That changed, and migraine treatment has improved more in the last few years than in the preceding fifty.

The kinds of headache

Primary — the headache is the disease. Migraine, tension-type, cluster. Around 90 percent of headaches.

Secondary — a symptom of something else. And the task is identifying the small proportion that are.

The red flags

These are worth knowing, because they are what separate an ordinary headache from an urgent one.

Thunderclap — maximum intensity within seconds. Subarachnoid haemorrhage until proven otherwise (Chapter 11.10).

And the suddenness matters more than the severity. A headache that takes minutes to build is far less likely.

Fever with neck stiffness and photophobia — meningitis.

Worse on lying flat, or worse in the morning, with vomiting — raised intracranial pressure.

Worse on coughing, straining or bending.

New focal neurological signs, or a seizure.

New headache over 50 — and jaw claudication, scalp tenderness or visual symptoms in that age group means giant cell arteritis (Chapter 21.5). Steroids the same day, before biopsy, because the alternative is irreversible blindness.

Progressive worsening over weeks.

New headache in someone immunosuppressed or with cancer.

Head injury.

And headache with a red painful eye, blurred vision, halos and vomiting — acute angle-closure glaucoma (Chapter 11.11), which is frequently mistaken for migraine.

Everything else is almost always primary.

Migraine

Not just a bad headache. A neurological disorder involving the trigeminal nerve system and the brainstem, with a genetic component — around 50 to 60 percent heritability.

Two to three times commoner in women, and the difference appears at puberty.

The phases, and knowing them is useful because treatment differs by phase.

Prodrome — hours to days before. Mood change, food cravings, yawning, neck stiffness, frequent urination. Around 70 percent experience it, and recognising your own prodrome allows earlier treatment.

Aura — in around 25 to 30 percent. Usually visual: a zigzag line expanding across the field, or a blind spot with shimmering edges, building over 5 to 20 minutes and lasting under an hour. Also sensory — tingling spreading up an arm to the face — and speech disturbance.

The mechanism is cortical spreading depression — a wave of neuronal activity followed by suppression, moving across the cortex at about 3 millimetres a minute, which matches the speed at which the visual disturbance expands.

And a first-ever aura, particularly over 50, is investigated, because it can mimic a TIA.

Headache — typically one-sided, throbbing, moderate to severe, worse with movement, with nausea and sensitivity to light and sound. Lasting 4 to 72 hours.

And "worse with movement" is one of the more useful discriminators from tension headache, where movement makes no difference.

Postdrome — the "migraine hangover", lasting a day or more, with fatigue and difficulty concentrating.

Triggers, and an honest note about them.

Common ones: stress — and frequently the let-down after stress rather than the stress itself, which is why weekend migraines are so common; sleep changes in either direction; missed meals; dehydration; hormonal changes; alcohol, particularly red wine; bright or flickering light; and weather changes.

And the food trigger literature is weaker than commonly believed. Chocolate craving is frequently part of the prodrome rather than a trigger — the person eats chocolate because the migraine has already started, and then blames the chocolate.

Elimination diets are usually unrewarding, and a headache diary identifying genuine personal patterns is more useful than a generic list.

Treating an attack

Take it early. Treatment taken during the prodrome or at the first sign of pain is substantially more effective, because gastric emptying slows during an attack and absorption falls.

Simple analgesia — aspirin 900 mg or ibuprofen, ideally with an antiemetic, which both treats the nausea and improves absorption.

Triptans — serotonin agonists, the first migraine-specific drugs. Effective in around 60 percent. Available as tablets, nasal sprays, wafers and injections — the non-oral forms matter when vomiting.

Contraindicated in coronary and cerebrovascular disease, because they constrict vessels.

Gepants — the newer CGRP receptor antagonists. Effective, no vasoconstriction, so usable where triptans are not, and — importantly — they do not appear to cause medication overuse headache.

Ditans — another new class acting on a different serotonin receptor.

Anti-nausea drugs.

And rest in a dark quiet room, which is not merely comfort — sensory stimulation genuinely worsens the attack.

Medication overuse headache

And this deserves its own section because it is common, causes years of suffering, and is entirely reversible.

Taking acute painkillers too often — more than 10 to 15 days a month depending on the drug — converts episodic headache into chronic daily headache.

Opioids and combination analgesics are the worst offenders; simple analgesics the least.

The trap is obvious once stated: the headache gets worse, so more painkillers are taken, which makes it worse.

Treatment is withdrawal of the offending drug, which produces a temporary worsening over 1 to 2 weeks and then substantial improvement in most people.

Anyone with headache on more than half the days of the month should be asked how often they take painkillers, and it is a question that transforms a proportion of "intractable" headaches.

Prevention

Considered when attacks occur on 4 or more days a month, or are disabling.

The borrowed drugs, all developed for something else and found to work: propranolol; topiramate; amitriptyline; candesartan; and sodium valproate — which is avoided in women of childbearing potential (Chapter 4.6).

And the new ones, which are the reason this chapter is optimistic.

CGRP monoclonal antibodies — erenumab, fremanezumab, galcanezumab, eptinezumab. Given monthly or quarterly by injection.

The first drugs designed specifically to prevent migraine, based on the discovery that CGRP — a neuropeptide — is released during attacks and causes pain.

They reduce migraine days by around 50 percent in about half of patients, including many who had failed multiple previous preventives, and they are well tolerated, which is the largest practical difference from the older drugs.

Botulinum toxin — for chronic migraine, 15 or more headache days a month (Chapter 6.2).

Neuromodulation devices — external nerve stimulators, with modest evidence and no drug side effects.

And non-drug measures with real evidence: regular sleep, regular meals, hydration, aerobic exercise, and stress management. Riboflavin, magnesium and coenzyme Q10 have modest supporting evidence and are reasonable to try.

Tension-type headache

The commonest headache of all — most people experience it.

Bilateral, pressing or tightening, mild to moderate, not worsened by movement, without nausea.

The old idea that it is caused by muscle tension is not well supported — the mechanism appears to involve altered central pain processing.

Treatment: simple analgesia used sparingly, stress management, exercise, and amitriptyline for the chronic form.

Cluster headache

Rare, and among the most severe pains in medicine — sometimes called suicide headache.

Strictly one-sided, around the eye, excruciating, lasting 15 minutes to 3 hours, occurring one to eight times a day, in bouts lasting weeks to months.

With autonomic features on the same side: watering eye, red eye, drooping eyelid, blocked or running nostril (Chapter 11.9).

And a distinctive behavioural feature: unlike migraine, where people lie still, cluster patients are agitated and pace.

Strikingly regular in timing — frequently waking people at the same hour each night, which points to a hypothalamic mechanism.

Commoner in men, and strongly associated with smoking.

Treatment:

High-flow oxygen — 100 percent at 12 to 15 litres a minute through a non-rebreathing mask. Aborts an attack in around 70 percent within 15 minutes, and it is remarkably effective and remarkably under-provided.

Subcutaneous sumatriptan — fastest acting.

Prevention: verapamil, at doses higher than cardiac use, with ECG monitoring.

And it is frequently misdiagnosed as sinusitis or dental problems for years, which is worth knowing because the treatment is so effective once the diagnosis is made.

Other headaches worth knowing

Trigeminal neuralgia — brief electric-shock stabs triggered by light touch (Chapter 11.7). Responds to carbamazepine, not to painkillers, which is diagnostic in itself.

Idiopathic intracranial hypertension — raised pressure without a mass. Typically in young women with obesity, with headache, visual disturbance and a swollen optic disc. Sight-threatening, and weight loss is a genuinely effective treatment alongside acetazolamide.

Cervicogenic headache — from the neck.

Post-lumbar-puncture headache — worse on sitting up, relieved by lying flat (Chapter 11.10).

And hypnic headache — waking an older person at the same time each night, and responding to caffeine before bed, which is unexpected.

The practical summary

Most headaches are benign and treatable.

Know the red flags — thunderclap, fever with neck stiffness, new focal signs, new headache over 50, and progressive worsening.

Treat attacks early and adequately.

Count how many days a month you take painkillers, because overuse headache is common and reversible.

And if you have four or more migraine days a month, prevention is available and it is now genuinely good — which is a sentence that could not have been written a decade ago.

What the next page fixes

Chapter 20.2 covers epilepsy — what a seizure actually is, what to do when someone has one, and why the majority of people with epilepsy become seizure-free on treatment.