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Independents' Day

May 2008: Tailor treatment to the patient with migraine

How is migraine diagnosed?

When should patients with migraine be referred?

What evidence-based treatments are available?

How is migraine diagnosed?

When should patients with migraine be referred?

What evidence-based treatments are available?

Migraine is a common, disabling primary headache disorder. it affects 15% of the UK population (7.6% of men and 19.1% of women) and is especially prevalent in patients <50 years. It contributes to 25 million lost work or schooldays every year.1

Migraine is a chronic disease with episodic manifestations. The natural history tends to follow a waxing and waning course, with patients experiencing phases of infrequent attacks and/or chronic headaches interspersed with attack-free remissions.2

Migraine can be classified into two major subtypes, with and without aura, occurring in 20-30% and 70-80% of cases, respectively.

Other clinically important variants include chronic migraine, basilar and hemiplegic migraine, migraine in pregnancy and menstrual migraine.


Migraine is a neurovascular disorder that occurs in genetically susceptible individuals. The primary event is neural.

Aura is thought to be generated by a wave of neural depolarisation and hyperpolarisation.

There is activation of brainstem pathways in established migraine attacks. Vascular changes are thought to be secondary to neural activation and a response to pain.3,4

The initial trigger for this ‘migraine cascade' is probably a combination of genetic factors and external triggers such as psychosocial stress, alcohol, menstruation, dehydration and missing meals.5 Individual causative genes have been identified in some types of familial hemiplegic migraine.

Phases of migraine

41190516As many as two-thirds of patients with migraine have a prodromal phase, which can consist of varied neurological and general symptoms (see table 1,left).6

This may be followed by headache with or without aura. The headache phase may be accompanied by non-headache symptoms including confusion, fatigue, difficulty finding the right words and autonomic disturbance. Postdromal symptoms may include fatigue, drowsiness and scalp tenderness.

Migraine without aura

A reliable diagnosis of headache disorders relies almost entirely on thorough history taking.

The International Headache Society diagnostic criteria for migraine without aura (see table 2, attached)7 may be used to differentiate between the main primary headaches – migraine, tension headache and trigeminal autonomic cephalalgias (cluster headache, paroxysmal hemicrania and SUNCT [short lasting unilateral neuralgiform headache with conjunctival injection and tearing]/ SUNA [short lasting unilateral neuralgiform headache with cranial autonomic features]). Table 3, attached, shows how these primary headache disorders may be distinguished clinically.

Tension-type headache is often overdiagnosed and mistaken for milder forms of migraine. Tension headache is never severe and features characteristic of migraine are entirely absent.

Trigeminal autonomic cephalalgias are strictly unilateral headaches with typical periodicity and marked autonomic symptoms, such as conjunctival injection and congestion; lacrimation; rhinorrhoea; facial/periorbital swelling; and flushing. One in four patients with migraine may also experience mild unilateral autonomic symptoms during their attacks.8

Typical features of migraine may also occur with other primary or secondary headache disorders, ie headache caused by underlying pathology such as a tumour or subarachnoid haemorrhage.

Migraine with aura

Aura is a fully reversible focal neurological syndrome, which develops over five minutes and lasts for 5-60 minutes.7 It is typically followed, or accompanied, by headache. Rarely, aura may continue to cause focal disturbance for hours, days, or longer (persistent aura or aura status). Generally, it is advisable to avoid triptans and/or oestrogen-containing oral contraceptives in those who have experienced bouts of prolonged aura beyond one hour in duration because of the theoretical risk of stroke.

Aura may be: visual, including positive and negative features (flickering lights, fortification spectra with zig-zag disturbance, shimmering, scotoma); sensory (‘spreading' pins and needles, numbness); dysphasic speech disturbance or combinations of all three. Symptoms tend to develop slowly, involving the whole or part of the face and limbs in succession. This is in contrast to vascular events such as transient ischaemic attack and stroke, where the neurological deficit is abrupt and maximum at onset.

Motor weakness, ie hemiparesis or monoparesis, can also occur as migraine aura. This is a more typical feature of hemiplegic migraines. Family history, appropriate investigations and the pattern of subsequent attacks will help clarify the diagnosis.

Rarer forms of aura may include an acute confusional state, amnesia and coma.

Prolonged or persistent aura requires specialist assessment. Aura may be followed by a non-migrainous headache or no headache at all. Migraine with and without aura may coexist.

Chronic migraine

Migraine can evolve from episodic headaches to a chronic pain syndrome. Chronic migraine is defined as a migraine headache occurring on 15 or more days per month for more than three months in the absence of medication overuse.7

History taking will often reveal a typical transition from acute to chronic migraine, characterised by:

• Increasingly frequent attacks (± more severe)
• Milder migrainous headaches between severe attacks
• Loss of response to acute attack medications, leading to an increasing use of strong medications.

Patients often seek medical advice when OTC drugs or drugs prescribed for acute attacks are no longer effective. Patients may complain that an acute drug no longer works, but continue to take it knowing that the headache will get even worse without it.

Caffeine-containing products may also be involved in the evolution from acute to chronic migraine.

Patients with chronic migraine commonly develop other symptoms. These include fatigue; neck pain (often in a ‘coathanger' distribution); back pain; muscle tenderness; dizziness; vertigo; sensory disturbance (including tingling, numbness); mood change (including irritability, depression and emotionalism); and insomnia.

Many of these patients may also have restless legs syndrome and/or periodic limb movements of sleep, which perpetuate migraine through poor quality sleep. Discontinuation of caffeine and acute attack medications will often be all that is required to get rid of these symptoms.

Many of the associated symptoms of chronic migraine can lead to frequent consultations and unnecessary investigations. Conditions such as fibromyalgia, chronic fatigue syndrome and myalgic encephalomyelitis should never be diagnosed without first taking a detailed headache history.

The risk factors for migraine progression are an increased baseline frequency of attacks; comorbidities such as obesity, depression and sleep apnoea; persistent triggers such as psychosocial stress; high caffeine intake; and medication overuse.2

Hemiplegic migraine and Basilar migraine

Hemiplegic migraine can be familial or sporadic, and prevalence is estimated to be 0.01%.9

The aura in hemiplegic migraine consists of unilateral reversible motor weakness, which can occur in combination with visual, sensory or speech symptoms.

Familial hemiplegic migraine is genetically heterogeneous.10 Diagnosis is based on a history of similar attacks in at least one first-degree or second-degree family member.7

In basilar migraine, the aura is a combination of brain stem features, including diplopia; dysarthria; vertigo; ataxia; decreased level of consciousness; or bilateral visual field or sensory symptoms.

Patients with these symptoms should be referred to a specialist.

Menstrual migraine

Menstrual migraine is a term used for attacks occurring exclusively from two days before to three days after menstruation. It is caused in part by oestrogen withdrawal following high oestrogen levels.

Menstruation is a well recognised trigger for most types of migraine and attacks will occur at other times of the cycle as well.

Management of migraine

An integral part of management is the assessment of disability. Validated scales such as the Migraine Disability Assessment (MIDAS) questionnaire are helpful for measuring the impact of migraine on the patient's life and selecting management options.

Patient education

A clear explanation of migraine as a neurovascular event, including its genetic basis, environmental trigger factors and natural history, will help the patient accept the diagnosis and establish realistic treatment goals. Patients should be encouraged to keep headache diaries.

Addressing trigger factors

Modifiable trigger factors include: sleep deprivation; missing meals; alcohol; dehydration; exercise; and specific odours and foods. Patients should be advised to avoid regular caffeine intake and use of pain medication, as these can cause rebound headache.

Acute treatment11-13

The goal of acute treatment is to relieve symptoms rapidly and consistently, enabling the patient to resume normal activities. Choice of drug therapy is dependent on the severity of attacks, drug efficacy, side-effects, comorbidities and patient preference.

It is important to start treatment very early in the headache phase, before scalp sensitivity (cutaneous allodynia) sets in and the attack becomes established.

Mild to moderate attacks

First-line treatments include simple analgesics, such as paracetamol, aspirin, NSAIDs and combination therapies. Soluble drugs are probably more useful.

If attacks are associated with nausea and vomiting, the addition of an antiemetic that does not delay gastric emptying (for example domperidone) is advised.

Severe attacks

Triptans are the gold standard of treatment in severe migraine.

As with all acute attack drugs, triptans should be used at the onset of a typical throbbing headache; they may be ineffective if used during the aura phase or once allodynia has occurred.

Naratriptan and frovatriptan have a slow onset of action compared with sumatriptan, but longer plasma half-lives. They may be suitable for patients with long-lasting attacks in whom headaches recur within a few hours of successful treatment.

It is important to tailor treatment to the patient. This may involve some experimentation and various routes of administration are available. Nasal spray, wafer and injectable formulations are useful when vomiting is a prominent feature of migraine.

Patients who fail to respond to one triptan often respond to a different one. Triptan response is not specific to migraine and should not be used as a marker of diagnosis.

Contraindications to triptan therapy include: untreated arterial hypertension; coronary heart disease; cerebrovascular disease; Raynaud's disease; pregnancy and lactation; age younger than 18 and older than 65 years; and severe liver or kidney failure.

Fleeting symptoms such as chest tightness and paresthesia may be experienced immediately after triptan use, especially with sumatriptan. The risk of developing serotonin syndrome (pyrexia, tachycardia, autonomic instability) with concomitant triptan and SSRI/ SNRI therapy is very remote.14

Attacks that continue unabated (status migrainosus) require parenteral treatment. In these patients, it is important to stop all acute attack drugs, provide antiemetic cover (for example oral or rectal domperidone) and give intravenous rehydration. Occasionally steroids will be helpful, but these are rarely needed.

Recent randomised controlled trials have shown that triptans and NSAIDs are similarly effective in the treatment of acute migraine. Fixed combination drugs, such as sumatriptan plus naproxen sodium, are more effective than either drug alone.15

Preventative medication

Prophylactic drug treatment should be considered when migraine severely impacts on the patient's daily life. It is also indicated if the patient suffers two to four attacks per month; has a poor response to acute treatment; a tendency to overuse analgesics and triptans; or chronic migraine.

In patients with frequent and/or chronic migraine, medication and caffeine overuse need to be eliminated before starting prophylactics.

Patients need to be warned that they are likely to develop worse headaches for about 7-9 days after cessation of medication. An antiemetic should be taken at the onset of an acute attack.

Preventative treatment should be initiated at the lowest effective dose and gradually increased. Drugs should be trialled for three to four months to see if they are effective (continued for 6-12 months if helpful). Comorbidities and drug interactions should also be taken into consideration.

If the medication is ineffective or the patient is intolerant, another class of prophylactic should be tried. The preventative drug should be given at a dose that is effective or a ‘maximum tolerated dose', preferably one that does not cause sedation or slowed cognition.

Beta blockers (propranolol, metoprolol) and anticonvulsants (such as valproate and topiramate) have the best evidence base. Amitriptyline is also effective. Pizotifen, methysergide, lithium and gabapentin have lower grades of evidence.

Migraine in pregnancy

Migraines in pregnancy may be treated with paracetamol and non-drug therapies such as relaxation and massage. The safety of high-dose NSAID treatment in pregnancy is not clear.

Metoprolol and magnesium can be used for prophylaxis, although beta blockers may cause intrauterine growth retardation. Tricyclics have not been shown to be harmful, although no drug is guaranteed to be safe.

Menstrual migraine

No treatment is currently licensed for the prevention of menstrual migraine.

Triptans are effective for acute treatment. Women who have regular periods and can reliably predict attacks can be treated with short-term preventive therapy during the perimenstrual period. Regular perimenstrual NSAIDs, triptans and oestrogen gel have been used.

Continuous combined oral contraceptive pill regimens have not been evaluated in clinical trials but have been effective in practice, especially when tricycled. However, they should not be used in women who have migraine with aura because of the increased risk of ischaemic stroke.16


When patients first present with migraine, GPs should take a careful history and conduct a directed physical examination to exclude causes of secondary headache. Red flags include: an acute onset of ‘worst ever' headache; severe headache brought on by exertion; symptoms of raised intracranial pressure; new onset of headache in patients older than 50 years; change in a stable headache pattern; systemic features, such as fever, weight loss and jaw claudication; neurological symptoms such as meningism, seizures and hemiparesis; and abnormal neurological signs on examination.

These patients should be referred for urgent investigations, including imaging.

Patients with a recurrent, typical history of migraine and normal physical examination rarely have abnormalities on brain imaging (approximately 1 in 1,000 scans may be abnormal).17

Specialist input should be sought for hemiplegic and basilar phenotypes; migraine with prolonged and/or atypical aura; difficulty differentiating between migraine and trigeminal autonomic cephalalgias; unresponsive chronic migraine; and abrupt change in migraine patterns, such as new daily persistent headache.


Migraine is a common, chronic disorder that can normally be managed well in primary care. Diagnosis is based on a thorough history and a normal physical examination. Migraine management requires a multifaceted approach. Recognition of migraine disability, patient education and early, structured treatment are key to effective therapy. Complicated migraine syndromes should be referred for specialist input.


Dr Anita Krishnan
specialist registrar in neurology

Dr Nicholas Silver
consultant neurologist, The Walton Centre
for Neurology & Neurosurgery, Liverpool

Migraine Key points Table 2: International headache society criteria for migraine without aura Table 3: Migraine and other primary headache disorders Tab1_migraine

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