By | May 14, 2012

Migraine is a primary headache. Diagnosis can be made from the history. However, investigation may be required to exclude headache of other aetiology.


There are vascular and neural hypotheses. The ophthalmic division of the trigeminal nerve supplies painful structures within the head. Stimulation of the trigeminal ganglion releases a peptide from trigeminal neurones which innervate the cranial circulation. This peptide is called calcitonin gene-related peptide (CGRP). It is a powerful vasodilator. It is thought CGRP also causes neurogenic inflammation. Experimental work has been limited because of the absence of an animal model on which hypotheses and drugs can be tested. Agonists for a subtype of 5 — hydroxytryptamine receptor known as 5HT1 agonists have been useful. The 5HT1 receptor has its own subpopulation of receptors, one of which, known as 5HT15, is involved in the mechanism of CGRP action.


Diagnostic criteria have been described by the Headache Classification Committee of the International Headache Society. Migraine is classified as migraine without aura and migraine with aura (classical migraine). The former is more common.

Diagnostic criteria for migraine without aura

1. At least five attacks fulfilling criteria 2-4.

2. Headache lasts 4-72 h, untreated or unsuccessfully treated.

3. Headache has at least two of the following characteristics:

• Unilateral location.

• Pulsating quality.

• Moderate or severe intensity (inhibits or prohibits daily activities).

• Aggravation by walking up/down stairs, or similar routine physical activity.

4. During headache at least one of the following:

• Nausea and/or vomiting.

• Photophobia and phonophobia.

History, examination and/or investigation must exclude another disorder which could account for the headache. If such a disorder is present, diagnosis of migraine requires that attacks do not occur for the first time in close temporal relation to that disorder.

Premonitory symptoms can occur before an attack of migraine without aura. They usually consist of hyper — or hypoactivity, depression, craving for particular foods or repetitive yawning.

Aura is a complex of neurological symptoms which can initiate or accompany an attack. Symptoms may be localized to the cerebral cortex or brain stem. Typical aura are visual disturbances, sensory symptoms, weakness or dysphasia. Migraine aura can be unaccompanied by headache.

Migraine can be triggered by factors such as stress, withdrawal from caffeine, dietary factors such as the ingestion of chocolate, cheese, wines and seafood, and hormonal changes due to the menstrual cycle or hormonal medication. Stress and hormonal factors are each identified triggers in 60% of migraine sufferers. Dietary factors have been implicated in approximately 20%. Frequently there is a family history of migraine.


Management is by prevention of attacks and intermittent treatment of attacks. The choice between prophylactic therapy and the sole use of abortive treatments depends on the frequency, severity and impact of acute attacks.


Drag therapy used for prevention aims to reduce the frequency of attacks by 50% and that attacks should be less severe when they do occur. The effect of the drag on the headache and its associated symptoms should be closely monitored. All drags have side-effects and their benefits need to be accurately compared to their disadvantages.

Explanation and reassurance reduce the incidence and severity of attacks. Patients should be educated to avoid triggers where possible. Systematic review has been undertaken of the following therapies.

CCB drugs are effective in the prophylaxis of migraine. Flunarizine, nimodipine, verapamil, nifedipine and diltiazem are all equally as effective. A reduction in migraine frequency of approximately 50% can be expected after 2 months of treatment with any of these drags. ‘Systemically active’ Ca2+ blockers cause predominantly vascular and gastrointestinal problems, whilst ‘cerebro-specific’ Ca2+ blockers cause behavioural and muscular side-effects.

Anticonvulsant drugs have been shown to be effective. This suggests a neural mechanism for migraine. They are thought to work via γ-amino butyric acid (GABA) enhancement of inhibitory pathways.

• β-Blockers (for example, propranolol 80-240 mg daily in divided doses) are thought to have some activity at 5HT subreceptors. Propranolol has been shown to induce a 43% reduction in migraine headache activity. When improvements were assessed using further outcomes they were found to be 20% greater. Propranolol 160 mg daily yielded a 44% reduction in migraine activity when daily headache recordings were used to assess outcome. With less conservative outcome measures there was a 65% reduction in migraine activity.

Relaxation and thermal biofeedback training have been shown to yield an initial reduction in migraine headache activity of 43% which was estimated to be 20% greater at further assessment.

Pizotifen is a 5HT antagonist that has been shown to confer a prophylactic benefit in patients who take sumatriptan for acute treatment of symptoms. Pizotifen does not alter the severity of migraine. Its proven effect therefore is one of reducing the use of sumatriptan. Its principal side-effect is weight gain.

Occlusal splinting devices have been shown to reduce the frequency and duration of migraine. A trial design used a ‘placebo’ intraoral device that covered the palatal mucosa but did not alter the mechanics of occlusion.

Treatment of attacks

Evidence from randomized controlled trials supports:

Sumatriptan. This is a 5HT15 agonist. Its major advantages are rapid onset and high efficacy. Given orally at a dose of 50 or 100 mg the attack is relieved in half to two thirds of patients. If the symptoms are not relieved a subsequent dose should not be taken. If symptoms are relieved but later recur a further dose can be taken, up to a maximum of 300 mg in 24 h. The subcutaneous injection of 6 mg relieves 88% of attacks. Headache settles in approximately 30 min. It should be used with caution in patients with a history of cardiovascular disease.

In addition reports of success with the following have been made:

Paracetamol with metodopramide.

• Nonsteroidal anti-inflammatory drugs (NSAIDs) can be effective. They are given with antiemetics to treat a relatively mild attack. They have the advantage of being available in parenteral and suppository forms should nausea occur and preclude the oral route.

Biofeedback techniques, hypnosis and acupuncture have also been used for the treatment of acute attacks. They are best used early.

Ergotamine is given as a dose of 2 mg initially, repeated with 1 mg to a maximum of 5 mg. It is a powerful vasoconstrictor and should not be given to those with peripheral, cerebral or coronary vascular disease, nor to the pregnant patient or the known drug abuser.

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