Headache and Migraine

Headache is one of the most common reasons a human being seeks medical help, and yet it is one of the hardest complaints to take well. The overwhelming majority of headaches are benign primary disorders — the brain tissue itself has no pain receptors, so a headache is almost never "a tumour" — but a small, dangerous minority are the first sign of a subarachnoid haemorrhage, meningitis, or raised intracranial pressure. The whole clinical art lies in confidently reassuring the many while never missing the few. This page teaches you to think like a neurologist at the bedside: separate primary from secondary headache, understand what actually happens in the migraine brain, recognise the red flags that demand imaging, and manage attacks and prevent them.

Learning Objectives

• Distinguish primary headaches (migraine, tension-type, cluster) from secondary headaches, and list the major causes of each.
• Explain migraine pathophysiology: cortical spreading depression, trigeminovascular activation, and CGRP.
• Recognise headache red flags using the SNNOOP10 framework and choose appropriate investigations.
• Apply the diagnostic criteria for migraine with and without aura.
• Select acute (abortive) and preventive treatment, including modern CGRP-targeted therapies.
• Avoid the common trap of medication-overuse headache.

Quick Answer

Headaches are classified as primary (the headache is the disease — migraine, tension-type, cluster) or secondary (a symptom of something else — bleed, infection, tumour, temporal arteritis, medication overuse). Most are primary and benign. Migraine is a recurrent disorder of episodic brain dysfunction: waves of cortical spreading depression produce the aura, and activation of the trigeminovascular system with release of the peptide CGRP produces the throbbing, disabling pain. Diagnosis is clinical, using pattern recognition and screening for red flags (thunderclap onset, fever, focal deficit, papilloedema, new headache over age 50, immunosuppression). Acute treatment uses NSAIDs, triptans, or gepants; prevention uses beta-blockers, topiramate, amitriptyline, or CGRP monoclonal antibodies. The single most important management error to avoid is medication-overuse headache.

Where It Came From

Headache is older than medicine itself. Neolithic skulls from as early as 7000 BCE show trephination — holes deliberately bored through living bone — and many healed, meaning patients survived. Some were almost certainly done to release the "spirits" or pressure thought to cause chronic head pain. The Ebers Papyrus (~1550 BCE) describes headache remedies, and by the 2nd century CE the Greek physician Aretaeus of Cappadocia gave the first clear clinical description of migraine, coining the term heterocrania — "half-head pain" — capturing the characteristic one-sided quality. Galen later Latinised it to hemicrania, from which "migraine" descends through Old French.

For most of history migraine was blamed on the humours or the stomach. The turning point came in the 17th century when Thomas Willis — the Oxford physician who mapped the circle of Willis — proposed that migraine arose from dilation of blood vessels in the head. This vascular theory dominated for three centuries: aura was blamed on vasoconstriction starving the cortex of blood, and the throbbing headache on rebound vasodilation. It fitted the pulsating pain and the effect of ergot (a vasoconstrictor) beautifully, and it was wrong in its essentials.

The neuronal theory grew out of two lines of evidence. In 1941 the neuropsychologist Karl Lashley timed his own visual aura and calculated that the disturbance spread across his visual cortex at about 3 mm per minute. Independently, the physiologist Aristides Leão described in 1944 a wave of intense neuronal firing followed by suppression sweeping across the cortex of experimental animals — cortical spreading depression (CSD), moving at exactly the speed Lashley had inferred. The two observations were only later joined. The modern synthesis, led by figures such as Michael Moskowitz (trigeminovascular system, 1980s) and the discovery that CGRP rises during attacks, reframed migraine as a primary brain disorder in which vascular changes are downstream, not causal. This history is worth carrying: it explains why old drugs target vessels while new ones (gepants, anti-CGRP antibodies) target a neuropeptide.

Primary versus Secondary Headache

The first fork in every headache assessment is: is this headache a disease in itself, or a symptom of another process?

Primary headaches account for roughly 90% of presentations. There is no underlying structural cause; the pain-processing system is itself dysfunctional. The three big ones:

• Tension-type headache — the most common of all. Bilateral, pressing or "band-like", mild to moderate, not aggravated by routine activity, no significant nausea. Patients describe a tight cap or vice.
• Migraine — usually unilateral, throbbing, moderate to severe, worsened by movement, with nausea and photophobia/phonophobia. Attacks last 4–72 hours. May be with or without aura.
• Cluster headache — the "suicide headache". Strictly unilateral, excruciating pain around the eye, lasting 15–180 minutes, striking in clusters over weeks, with dramatic autonomic features on the same side: tearing eye, runny/blocked nostril, ptosis, and a restless, agitated patient (contrast the migraineur who lies still in the dark). More common in men.

Secondary headaches are the symptom of an identifiable cause. The dangerous list to hold in mind: subarachnoid haemorrhage (thunderclap), meningitis/encephalitis (fever, neck stiffness), raised intracranial pressure/tumour (worse on waking, on coughing or lying flat, with papilloedema), giant cell (temporal) arteritis (age over 50, scalp tenderness, jaw claudication, raised ESR — a neuro-ophthalmic emergency because it blinds), cerebral venous sinus thrombosis, carbon monoxide poisoning, and medication-overuse headache.

A worked example

A 34-year-old woman reports recurrent right-sided throbbing headaches over ten years, lasting a day, with nausea and a need to lie in the dark; before some attacks she sees a shimmering zig-zag that spreads and clears over 20 minutes. Examination is normal. This is textbook migraine with aura — a primary headache. No imaging is needed. Contrast: a 62-year-old man with a new daily headache, tender temporal arteries, and blurred vision in one eye. This is secondary — giant cell arteritis until proven otherwise: start high-dose steroids immediately, check ESR/CRP, and arrange temporal artery biopsy. The clinical stories could not be more different, and the difference is everything.

Migraine Pathophysiology

Migraine is best understood as a state of a hyperexcitable brain that episodically loses its ability to regulate sensory input. Genetics load the gun (twin studies show high heritability; rare familial hemiplegic migraine is caused by ion-channel genes such as CACNA1A), and triggers pull it — sleep disruption, missed meals, hormonal shifts, stress let-down, red wine, dehydration.

The aura: cortical spreading depression. In about a third of migraineurs, attacks begin with a slow wave of intense neuronal and glial depolarisation that propagates across the cortex at ~3 mm/min, followed by a longer-lasting suppression of activity. Because it usually starts in the occipital (visual) cortex, the patient experiences a growing scintillating scotoma — a shimmering, expanding blind spot with a jagged bright edge — over 5–60 minutes. CSD also transiently changes local blood flow (oligaemia), which is why the old vascular theory seemed to fit. Crucially, CSD is thought to be the trigger that activates the pain machinery.

The pain: trigeminovascular activation. The only pain-sensitive structures in the head are the meninges and their blood vessels, innervated by the trigeminal nerve (mainly the ophthalmic division, V1). CSD activates these trigeminal afferents. They release vasoactive neuropeptides — above all calcitonin gene-related peptide (CGRP) — causing sterile neurogenic inflammation, vasodilation, and mast-cell activation around the meningeal vessels. Signals travel to the trigeminal nucleus caudalis in the brainstem and up to the thalamus and cortex, producing the throbbing pain. Convergence of these fibres with upper cervical inputs explains why migraine pain radiates to the neck.

Sensitisation explains the rest of the syndrome. Peripheral sensitisation makes the throb worse with each pulse of the artery and with movement. Central sensitisation (in the trigeminal nucleus) produces cutaneous allodynia — the scalp, or even brushing hair, becomes painful — and is a clinical clue that a triptan given late will fail. The nausea, photophobia, and phonophobia reflect involvement of the hypothalamus and brainstem, which is also why premonitory symptoms (yawning, food cravings, mood change) can precede the headache by a day.

Why this matters for drugs. Triptans (5-HT1B/1D agonists) both constrict vessels and, more importantly, block neuropeptide release from trigeminal endings. Gepants (small-molecule CGRP-receptor antagonists) and anti-CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab) target the CGRP pathway directly — the clearest proof that CGRP is central, not incidental.

Red Flags and Investigation

Most headaches need no imaging. The skill is knowing when they do. A widely used memory aid is SNNOOP10:

• S — Systemic symptoms (fever, weight loss) or Secondary risk (cancer, HIV/immunosuppression)
• N — Neurological deficit or altered consciousness
• N — Onset that is sudden/thunderclap (peak in less than one minute — think subarachnoid haemorrhage)
• O — Onset after age 50 (think giant cell arteritis, tumour)
• O — Pattern change or progressive headache
• P10 — Papilloedema; Positional headache; Precipitated by Valsalva (cough, exertion, sex); Pregnancy/puerperium; Painful eye with autonomic features; Post-traumatic onset; Painkiller (analgesic) overuse; and a Prior different headache.

A thunderclap headache — maximal within a minute, "the worst headache of my life" — is a subarachnoid haemorrhage until excluded: urgent non-contrast CT head, and if that is normal but the story is convincing, a lumbar puncture at 12 hours looking for xanthochromia. Fever plus neck stiffness means suspected meningitis — do not delay antibiotics for imaging. Papilloedema, morning headaches, and headache worse on lying flat point to raised intracranial pressure and warrant MRI. Reassuringly, a normal neurological examination in a patient with a long, stable history of typical migraine is a powerful negative finding.

Real-World Applications

• Primary care triage. The GP who knows the red flags reassures the anxious student with classic migraine (no scan) while fast-tracking the older patient with jaw claudication to same-day steroids and bloods — preventing blindness.
• Emergency medicine. "Worst headache ever" triggers a CT-then-LP pathway; getting this reflex right saves lives from re-bleeding aneurysms.
• Occupational and everyday life. Migraine is a leading cause of years lived with disability worldwide and of lost workdays. Trigger diaries, sleep regularity, hydration, and regular meals are genuinely effective self-management. Advising a shift worker to protect sleep is real medicine.
• Women's health. Migraine with aura combined with the combined oral contraceptive pill and smoking raises stroke risk — a specific, examinable prescribing caution.

Common Mistakes

1. "A throbbing headache means high blood pressure." Wrong: routine hypertension rarely causes headache; only a hypertensive emergency (very high pressures with end-organ signs) does. Attributing every headache to blood pressure both over-treats the mild and misses migraine. Correction: treat the headache on its own clinical merits.
2. Giving a triptan too late. Triptans work best taken early, at the first sign of pain, before central sensitisation and allodynia set in. Once the scalp is allodynic, they often fail. Correction: treat early and adequately dose; add an antiemetic to aid absorption.
3. Missing medication-overuse headache. A patient using acute painkillers (including triptans, codeine, or simple analgesics) on 10–15+ days a month develops a daily rebound headache that looks like "worsening migraine". Escalating the painkiller makes it worse. Correction: recognise the pattern and withdraw the overused drug while starting a preventive.
4. Scanning stable typical migraine "to be safe". Imaging a classic long-standing migraine with a normal exam yields nothing but incidental findings, cost, and anxiety. Correction: reserve imaging for red flags or a change in pattern.

Comparison and Connections

Feature	Migraine	Tension-type	Cluster
Site	Usually one-sided	Bilateral, band-like	Strictly one-sided, around eye
Quality	Throbbing/pulsating	Pressing, tightening	Boring, excruciating
Duration	4–72 hours	30 min to days	15–180 min, in bouts
Behaviour	Lies still, dark room	Continues activity	Restless, paces, agitated
Associated	Nausea, photophobia, aura	Few or none	Ipsilateral tearing, nasal congestion, ptosis
Sex ratio	More women	Slight female excess	More men

Aura versus TIA/stroke. Migraine aura spreads and marches over minutes (a growing zig-zag), is usually positive (bright, shimmering) then negative, and resolves fully; a TIA is sudden and typically negative (loss of function). This distinction matters most in first-ever aura over age 40. Migraine versus subarachnoid haemorrhage: migraine builds over minutes to an hour; SAH peaks in seconds to a minute.

Practice Questions

Recall

Q: Name the three main primary headache disorders. A: Migraine, tension-type headache, and cluster headache.

Understanding

Q: Explain how cortical spreading depression relates to the migraine aura and to the pain. A: CSD is a wave of neuronal/glial depolarisation followed by suppression, spreading across the cortex at ~3 mm/min. Starting in visual cortex it produces the marching scintillating scotoma of aura. CSD then activates trigeminal meningeal afferents, which release CGRP and cause the neurogenic inflammation and vasodilation underlying the pain — linking the two phases.

Application

Q: A 28-year-old woman with migraine with aura asks to start the combined oral contraceptive pill. What is your concern? A: Migraine with aura plus the combined (oestrogen-containing) pill increases ischaemic stroke risk, especially with smoking. Combined hormonal contraception is generally contraindicated; offer a progestogen-only or non-hormonal method instead.

Analysis

Q: A 55-year-old presents with a new, constant right-temporal headache, scalp tenderness when combing hair, and transient loss of vision in the right eye. ESR is 88. What is the diagnosis and immediate action, and why can you not wait for the biopsy? A: Giant cell (temporal) arteritis. Start high-dose corticosteroids immediately — before temporal artery biopsy — because the untreated disease can cause irreversible bilateral blindness within days from anterior ischaemic optic neuropathy. Biopsy findings persist for a week or more after steroids begin, so treatment must not be delayed.

FAQ

Is my migraine a sign of a brain tumour? Almost never. Tumour headaches are typically new, progressive, worse on waking or coughing, and accompanied by other signs (papilloedema, focal deficit, seizures). A long, stable pattern of typical migraine with a normal examination is reassuring.

Why does light and sound make it so much worse? Migraine involves hyperexcitability and sensitisation of brainstem and thalamic pathways that process sensory input, so normal light and sound are amplified into pain. This is why a dark, quiet room genuinely helps.

What is the difference between a "sinus headache" and a migraine? Most self-diagnosed "sinus headaches" are actually migraines — migraine causes facial pressure and nasal congestion through autonomic activation. True sinusitis usually has fever, purulent discharge, and follows a cold. If over-the-counter decongestants keep "not quite working", suspect migraine.

Can I take painkillers every time I get a headache? Not routinely. Using acute painkillers (including triptans and codeine) on more than about 10–15 days a month can cause medication-overuse (rebound) headache, creating a daily headache that only worsens with more medication. If you need acute treatment that often, you need a preventive instead.

Do migraines ever go away? They often change over a lifetime. Many people find attacks become less frequent with age, and migraine frequently improves after menopause in women. Good preventive treatment and trigger management can substantially reduce the burden meanwhile.

Quick Revision

• Primary headache = the disease itself (migraine, tension-type, cluster); secondary = symptom of another cause.
• Brain tissue has no pain receptors; headache pain comes from meninges, vessels, and the trigeminal nerve.
• Migraine: unilateral, throbbing, 4–72 h, nausea + photophobia; patient lies still. Cluster: peri-orbital, autonomic, restless.
• Aura = cortical spreading depression (~3 mm/min); pain = trigeminovascular activation with CGRP release.
• Red flags: SNNOOP10 — thunderclap, fever, focal deficit, papilloedema, onset over 50, Valsalva-triggered, immunosuppression.
• Thunderclap headache = SAH until excluded (CT then LP at 12 h for xanthochromia).
• New headache + scalp tenderness + age over 50 = giant cell arteritis: steroids now, then biopsy.
• Acute: NSAIDs, triptans (take early), gepants + antiemetic. Prevent: beta-blocker, topiramate, amitriptyline, anti-CGRP antibodies.
• Migraine with aura + combined pill + smoking raises stroke risk.
• Biggest management error: medication-overuse headache — withdraw the overused drug, start a preventive.

Related Topics

Prerequisites

• Neurology overview
• Cranial nerve anatomy, especially the trigeminal nerve — see Anatomy

Related Topics

• Pharmacology — triptans, NSAIDs, and CGRP-targeted drugs
• Stroke and TIA (for distinguishing aura from ischaemia)
• Emergency assessment of the acute severe headache — see Emergency Medicine

Next Topics

• Stroke and cerebrovascular disease
• Epilepsy and seizures
• Raised intracranial pressure and idiopathic intracranial hypertension