Prevalence: 10%

Risk factors:

  • Female (3:1)
  • Family history


The pathogenesis of migraine is poorly understood. Acute episodes are thought to be caused by transient activation of trigeminal nerve afferents. The phenomenon of aura is thought to be caused by cortical spreading depression – synchronised activity which spread across the cortex.


Migraine is a headache disorder which presents with repeated, stereotyped attacks of headache which are often preceded and followed by characteristic transient neurological symptoms.

In acute migraine episodes, there is often a characteristic sequence of phases which evolve and desist over roughly 24 hours:

  • Prodrome:
    • Fatigue
    • Low/high mood
    • Irritability
  • Aura (positive or negative symptoms):
    • Visual: e.g. zigzags (‘fortification spectra’)
    • Auditory: e.g. tinnitus
    • Somatosensory: e.g. pain
    • Vestibular aura
    • Motor aura: in familial hemiplegic migraine
  • Headache
    • Features:
      • Dull
      • Unilateral
      • Throbbing
    • Associated with:
      • Nausea
      • Vomiting
      • Photophobia
      • Phonophobia
      • Osmophobia
      • Allodynia
    • Relieved by: lying still in a dark, quiet room
  • Post-drome
    • Fatigue
    • Low/high mood

Triggers of acute migraine headache:

  • Stress
  • Sleep disturbance (too much or too little)
  • Fasting
  • Menstrual cycle stage
  • Weather changes
  • Alcohol


Migraine can be classified as follows:

  • Episodic migraine
    • With aura
      • Typical aura
        • Visual
        • Auditory
        • Somatosensory
      • Atypical aura
        • Motor
        • Brainstem
        • Retinal
        • Vestibular
      • Without aura
    • Chronic migraine


Diagnosis of migraine is clinical and based on the ICHD-3 diagnostic criteria. Core features of migraine include:

  • Episodes last 4 – 72 without treatment
  • Features of the headache itself:
    • Unilateral
    • Pulsatile
    • Moderate-severe pain
    • Worse on exertion
  • Associated symptoms during an attack
    • Nausea / vomiting
    • Photophobia & phonophobia
  • With or without aura

Further investigation is only required if there is suspicion for an alternative diagnosis. Dangerous causes of headache to exclude are:

  • Raised intracranial pressure
  • Meningitis
  • Space-occupying lesion
  • Giant cell arteritis
  • Vascular: Subarachnoid haemorrhage, arterial dissection, venous thrombosis

Atypical forms of migraine aura or prominent aura without headache should also raise suspicion for another cause of transient neurological symptoms, of which the most important are:

  • Transient ischaemic attack (TIA)
  • Seizure
  • Metabolic: hypoglycaemia, hyponatraemia, hypercalcaemia
  • Syncope

The differential diagnosis also includes psychiatric disorders (i.e. panic disorder), other primary headache disorders, and a wide variety of other neurological conditions which may mimic migraine aura.


The management of migraine involves treatment of acute episodes and, in selected patients, prophylaxis of further episodes.

Management of acute attacks

  • Mild-moderate: simple analgesia (NSAIDs, paraceteamol) +/- anti-emetic
  • Moderate-severe: triptan +/- simple analgesia +/- anti-emetic

NSAIDS & Paracetamol

Non-steroidal anti-inflammatory drugs such as ibuprofen, naproxen, and diclofenac are non-selective COX inhibitors which are helpful in terminating acute migraine attacks. Paracetamol is also highly effective and can be used as monotherapy or in combination with an NSAID.


  • Aspirin: 900mg
  • Ibuprofen 400mg
  • Naproxen: 750 – 1250mg
  • Paracetamol: 1g


Triptans are a class of 5-HT1B/D agonists which are effective in the acute treatment of migraine. Their mechanism of action is not fully understood. They promote vasoconsction and modulate pain perception.

Commonly-used triptans include almotriptan, eletriptan, rizatriptan, and sumatriptan, zolmitriptan, and naratriptan.

Triptans are available as oral, nasal (zolmitriptan), and subcutaneous (sumatriptan) forms. Non-oral forms are particularly useful if the patient is feeling sick or vomiting. In addition, acute migraine is often accompanied by gastroparesis, which delays absorption of oral drugs.

There is no hard-and-fast guidance on which triptan to use. If the patient is unable to swallow a non-oral preparation should be used. A previous good response to a particular triptan predicts future good responses.

Triptan therapy should be started at the onset of the headache.

Given their vasoconstrictor effects, triptans are not used in situations where acute reductions in cerebral or cardiac blood flow may lead to significant tissue hypoxia, i.e. coronary or cerebrovascular disease.

Contra-indications to triptans:

  • Hemiplegic migraine
  • Basilar migraine
  • Ischaemic stroke
  • Ischaemic heart disease
  • Coronary vasospasm
  • Severe uncontrolled hypertension
  • Pregnancy

There are also specific cautions for individual triptans.

Adverse effects include nausea, dizziness, sleepiness, dry mouth, and ‘triptan sensations’ – a hot sensation, limb and chest tightness, tingling, and flushing. These effects are usually self-limiting.

Migraine prophylaxis

Lifestyle measures are an essential component of migraine prophylaxis. All people with migraine should be encouraged to keep a headache diary to identify lifestyle triggers and patterns in their headaches. Common triggers include diet, sleep, stress, and stage in the menstrual cycle.

Many people with migraine benefit from prophylactic treatment, i.e. long-term drug therapy to reduce the frequency and severity of attacks. Recognised indications for prophylaxis include:

  • Regarding the attacks
    • Frequent
    • Severe
  • Regarding acute treatment
    • Serious adverse reaction to acute treatment
    • Contra-indication to acute treatment
  • At-risk of medication overuse headache
  • Regarding the type of migraine
    • Menstrual migraine
    • Basilar migraine
    • Hemiplegic migraine
    • Migraine with prolonged aura

Various classes of drug used as migraine prophylaxis:

  • Beta-blockers
  • Antidepressants
  • Anticonvulsants

The aims of preventative treatment are:

  • To reduce the frequency and severity of attacks
  • To reduce acute relief medication use

The general principles of drug prophylaxis are:

  • Start low, go slow: up-titrate doses slowly
  • Trials of at least 6 – 8 weeks at maximum dose should be given before a treatment is considered to have failed
  • Treatment should be tailored to the individual’s risk-benefit profile


Propranolol (80-240mg/day) is the recommended first-line beta blocker in migraine. Alternatives are timolol, atenolol, nadolol, and metoprolol. Beta-blockers should be avoided in people with:

  • Asthma
  • Diabetes
  • Bradycardia
  • Peripheral vascular disease
  • Raynaud’s phenomenon
  • Depression

They may be ideal in people with anxiety disorders.


There is evidence for the use of topiramate (50 – 200mg/day), valproate (800 – 1500mg/day), and gabapentin (1200 – 2400mg/day) in migraine. Topiramate and valproate are contra-indicated in pregancy as they are teratogenic. They should therefore be avoided, where possible, in women of childbearing age. Other contra-indications to topiramate use include renal stones and angle-closure glaucoma. Valproate is contra-indicated in obesity and liver disease.


Amitryptilline (25 – 150mg/day) is the recommended first-line antidepressant in migraine. Alternatives include venlafaxine and nortryptilline.

Other therapies

Several other therapies are available for people who continue to have severe or recurrent attacks despite optimisation of lifestyle factors, abstinence from acute relief medications, and the use of maximum dose prophylactic agents.

These include pizotifen, methylsergide, flunarizine, botulinum toxin, and nerve blocks.