Primary Headache Disorders: Diagnosis and Management

Introduction

Headache is one of the commonest presenting complaints in medicine, and the overwhelming majority are primary headache disorders - conditions in which the headache itself is the disease, rather than a symptom of some other structural or systemic problem.¹ The three major primary headache disorders are migraine, tension-type headache and cluster headache, distinguished chiefly by pattern, associated features and duration.

The central task in any headache presentation, examined relentlessly in finals, is not memorising diagnostic criteria in isolation but first asking whether this is a primary headache at all, or whether red flag features point to a secondary headache - subarachnoid haemorrhage, giant cell arteritis, raised intracranial pressure, meningitis, or venous sinus thrombosis, among others, which are covered in their own articles.

Migraine alone affects around 1 in 7 people and is a leading cause of disability worldwide, so getting acute and preventive management right has a real impact on quality of life, not just exam marks.

A practical framework helps when a patient presents with headache. First, ask whether this is a new headache or a longstanding pattern - new headaches, particularly in the over-50s or the immunosuppressed, carry a far higher yield of secondary pathology. Second, establish the tempo: thunderclap onset points to subarachnoid haemorrhage, a progressive daily headache to raised intracranial pressure, and a stable episodic pattern over years to a primary disorder. Third, look for the red flag features listed later in this article. Only once these are addressed is it safe to classify the headache as primary.

It is worth keeping the base rates in mind. The overwhelming majority of headaches presenting in primary care are primary disorders, and tension-type headache is the commonest of all, though migraine accounts for most of those severe enough to prompt consultation. Secondary causes are uncommon, but their prevalence rises sharply in specific groups - new headache over 50, immunosuppression, pregnancy, known malignancy - which is exactly why the red flag screen is applied selectively rather than investigating everyone.

Migraine

Pathophysiology

Migraine is now understood as a primary neurological disorder of sensory processing, involving activation of the trigeminovascular system and release of neuropeptides (notably calcitonin gene-related peptide, CGRP) that cause neurogenic inflammation and vasodilatation of meningeal vessels. It is not simply a vascular headache, despite the historical name.

Clinical features

Migraine attacks classically progress through phases, though not everyone experiences all of them: a premonitory phase (hours to a day before, with mood change, yawning, food cravings), an aura in around a third of patients, the headache phase, and a postdrome (fatigue, mood change lasting up to a day).

• Headache: unilateral (though can be bilateral), throbbing/pulsating, moderate-to-severe, aggravated by routine physical activity, lasting 4-72 hours untreated
• Associated features: nausea and/or vomiting, photophobia and phonophobia - patients often want to lie in a dark, quiet room
• Aura (when present): fully reversible visual, sensory or speech symptoms developing gradually over 5-60 minutes before or during the headache. Visual aura is commonest - zigzag lines (fortification spectra), scintillating scotoma, or spreading visual loss
• Hemiplegic migraine: aura includes motor weakness - an important mimic of stroke or TIA in a younger patient, sometimes with a family history (familial hemiplegic migraine)

Triggers

• Hormonal change - menstruation is a particularly common and important trigger
• Sleep disturbance, both deprivation and excess
• Stress, and the let-down after stress ('weekend migraine')
• Dietary triggers - alcohol (especially red wine), caffeine withdrawal, chocolate, cheese (though evidence for many specific foods is weaker than commonly believed)
• Dehydration and missed meals
• Bright or flickering lights

Management - acute attack

• A triptan (for example sumatriptan) combined with an NSAID or paracetamol, taken as early as possible in the attack³
• An antiemetic (for example metoclopramide or prochlorperazine), which also helps gastric stasis-related poor absorption of oral analgesia
• Non-oral routes (nasal or subcutaneous triptan, buccal/rectal antiemetic) if vomiting prevents oral treatment

Management - prevention

Preventive treatment is considered when attacks are frequent (generally more than 1 a week or significantly disabling), or when acute treatment is poorly tolerated or overused.

Riboflavin (vitamin B2) and magnesium have some evidence as adjuncts. Menstrual migraine can be managed with peri-menstrual prophylaxis (for example, a short course of a triptan or NSAID around the expected time).

Two practical prescribing points cause frequent difficulty. The first is timing: triptans work best taken at the onset of headache rather than during the aura, and a patient who habitually waits to see whether the attack will be severe often loses the window of best response. The second is gastric stasis, which occurs early in migraine and impairs absorption of oral drugs - which is why an antiemetic such as metoclopramide is given not only for nausea but to promote absorption of the analgesia, and why non-oral routes are preferred when vomiting occurs.

Preventive treatment also needs realistic framing. It is offered as a trial at an adequate dose for at least 8-12 weeks before being judged ineffective, and success is defined as roughly halving attack frequency rather than abolishing attacks. Patients who expect immediate or complete resolution frequently abandon an effective drug too early, so this expectation should be set explicitly at the point of prescribing.

Tension-type headache

Tension-type headache is the commonest primary headache disorder, though it is under-represented in clinic attendances because it is usually mild and self-managed.

• Bilateral, pressing or tightening ('band-like') quality
• Mild-to-moderate intensity - does not typically stop normal activity
• Not aggravated by routine physical activity (a key distinction from migraine)
• No, or only mild, associated nausea, photophobia or phonophobia (at most one of these, unlike migraine)
• Often related to stress, poor posture, or muscular tension in the scalp and neck

Management is with simple analgesia (paracetamol, NSAIDs) for episodic attacks, and addressing contributing factors - stress, sleep, posture. For frequent or chronic tension-type headache, amitriptyline is the preventive agent of choice. Analgesia should be limited to avoid medication overuse headache.

Cluster headache

Cluster headache is much rarer than migraine or tension-type headache but is important to recognise because the pain is among the most severe known to medicine, and the treatment is entirely different.

• Severe, unilateral, periorbital or temporal pain, often described as boring or piercing
• Attacks last 15 minutes to 3 hours, occurring in clusters - typically once or more daily for weeks, followed by remission periods of months to years
• Prominent ipsilateral autonomic features: lacrimation, conjunctival injection, rhinorrhoea or nasal congestion, ptosis and miosis (partial Horner syndrome), eyelid oedema
• Patients are characteristically restless and agitated during an attack, pacing or rocking - in contrast to migraine, where patients want to lie still
• More common in men, and often associated with smoking
• Attacks frequently occur at night, waking the patient at the same time

Management

• Acute attack: high-flow 100% oxygen via a non-rebreathe mask for 15-20 minutes, plus a subcutaneous or nasal triptan
• Prevention during a cluster period: verapamil is first-line; a short course of a glucocorticoid can bridge the period until verapamil takes effect
• Referral to neurology for ongoing management and consideration of other preventive options if verapamil is insufficient
• ECG monitoring is needed at higher doses of verapamil because of the risk of cardiac conduction effects

Differential diagnosis and red flags

Before applying primary headache criteria, screen every headache presentation for features suggesting a secondary cause.⁴

• Giant cell arteritis - new headache over 50, scalp tenderness, jaw claudication, visual disturbance; urgent ESR/CRP and steroids while arranging temporal artery biopsy
• Medication overuse headache - chronic daily headache in someone taking acute analgesics or triptans on 10 or more days a month (or simple analgesics on 15 or more) - covered further below
• Idiopathic intracranial hypertension - headache with papilloedema, typically in a woman of childbearing age with obesity
• Trigeminal autonomic cephalalgias other than cluster (paroxysmal hemicrania, SUNCT) - shorter, more frequent attacks, responsive to indometacin in paroxysmal hemicrania
• Trigeminal neuralgia - brief, electric shock-like pain in a trigeminal distribution, covered in its own article
• Sinusitis - facial pain and pressure with nasal symptoms

Medication overuse headache

Medication overuse headache is a chronic daily or near-daily headache that develops in someone with a pre-existing primary headache disorder who regularly uses acute headache medication - triptans, opioids or combination analgesics on 10 or more days per month, or simple analgesics (paracetamol, NSAIDs) on 15 or more days per month, for at least 3 months.²

Withdrawal is best approached with a clear plan agreed in advance. Patients should be warned that headache typically worsens for one to two weeks before improving, given a defined stop date, offered a bridging strategy where appropriate, and reviewed at around four to eight weeks - by which point the true underlying headache pattern becomes visible and effective prophylaxis can be started.

Prognosis

Migraine and tension-type headache both typically follow a relapsing-remitting course over years, often improving with age and, in women, after the menopause. Effective acute and preventive treatment substantially reduces disability and time lost to attacks. Cluster headache follows a cyclical pattern of active periods and remission that can persist for decades, though some patients develop a chronic form without remission. Recognising and correcting medication overuse is essential, since it perpetuates chronic headache and blunts the response to preventive treatment until addressed.

A headache diary is one of the most useful and underused tools in this area. Recording attack frequency, duration, severity, likely triggers and - critically - the number of days on which acute medication is taken serves three purposes at once: it establishes the diagnosis where the pattern is unclear, it identifies medication overuse before it becomes entrenched, and it provides the objective baseline against which any preventive treatment is judged. Asking a patient to keep one for two to three months before starting prophylaxis is rarely wasted time.

Two groups deserve particular consideration. In women with migraine with aura, the combined oral contraceptive pill is contraindicated because of a further increase in ischaemic stroke risk, and this is a frequently examined and clinically important prescribing point. In pregnancy, most preventive agents are avoided - topiramate is teratogenic and valproate absolutely contraindicated - so management leans on paracetamol, non-pharmacological measures and, where prophylaxis is genuinely necessary, specialist advice.