How Is Migraine Diagnosed?
Migraines are underdiagnosed31
The diagnosis of migraine without aura, according to the International Headache Society (IHS),1, 33
can be made according to the following criteria:
[table id=5 /]
For migraine with aura, only two attacks are required to justify the diagnosis.1, 33
What Are the Signs and Symptoms of Migraine?
The four phases of migraine are common but are not always present.33
About 60% of people who experience migraines report premonitory symptoms that occur hours to days before headache onset. Although the prodromal features vary, they tend to be consistent for a given individual and may include the following:
- Heightened sensitivity to light, sound, and odours
- Lethargy or uncontrollable yawning
- Food cravings
- Mental and mood changes (e.g. depression, anger, euphoria)
- Excessive thirst and increased urination
- Fluid retention
- Loss of appetite or inability to eat
- Constipation or diarrhoea
The migraine aura is a complex of neurologic symptoms that may precede or accompany the headache phase or may occur in isolation. It usually develops over 5-20 minutes and lasts less than 60 minutes. The aura can be visual, sensory, or motor or any combination of these. When an aura is not followed by a headache, it is called a migraine equivalent, silent migraine or acephalic migraine.33
Auras most commonly consist of visual symptoms, which may be negative or positive.
- Negative symptoms include negative scotomata or negative visual phenomena, such as:
- Homonymous hemianopic (visual loss on the left or right side)
- Quadrantic field defects (visual loss in a quadrant of the visual field)
- Central scotomas (visual loss in the centre of the visual field)
- Tunnel vision (the loss of peripheral vision)
- Altitudinal visual defects (visual loss in the upper or lower parts of the visual field)
- Complete blindness
- The most common positive visual phenomenon is the scintillating scotoma. This consists of an arc or band of absent vision with a shimmering or glittering zigzag border.
Paresthesias (commonly referred to as pins and needles), occurring in 40% of cases, are the next most common aura; they often present with tingling starting in the hand, migrating to the arm, and then jumping to involve the face, lips, and tongue. As with visual auras, positive symptoms typically are followed by negative symptoms (paresthesias may be followed by numbness).33
Motor symptoms occur in 18% of patients and usually are associated with sensory symptoms. Motor symptoms often are described as a sense of heaviness of the limbs before a headache but without any true weakness. Speech and language disturbances have been reported in 17-20% of patients. These disturbances are commonly associated with upper extremity heaviness or weakness.33
3. Pain phase
The typical migraine headache is unilateral, throbbing, with moderate to severe intensity aggravated by physical activity. The pain may be bilateral at the onset or start on one side and become generalised. The location of the headache usually alternates sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides and usually lasts between 4 to 72 hours in adults and 1 to 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several each week. The average migraine patient experiences one to three headaches a month. The head pain varies greatly in intensity.
4. Postdromal symptoms
Postdromal symptoms (symptoms experienced after the headache has subsided), may persist for 24 hours after the headache and can include the following:
- Tired, “washed out,” or irritable feelings
- More commonly refreshed or euphoric feelings
- Muscle weakness or muscle pain
- Loss of appetite or food cravings
A history of migraine triggers may be identified. Common triggers include:
- Hormonal changes (e.g. those resulting from menstruation, ovulation, oral contraceptives, or hormone replacement)
- Head trauma
- Lack of exercise 28
- Sleep changes
- Medications (e.g. nitroglycerin, histamine, reserpine, hydralazine, ranitidine, estrogen)
- Abrupt weather changes
- Skipping meals
- Certain foods and beverages (aged cheese, chocolate, red wine, beer, coffee, and many others)
- Food additives or preservatives (such as nitrates and monosodium glutamate)
Biofeedback, cognitive-behavioral therapy, and relaxation therapy are frequently effective against migraine headaches and may be used adjunctively with pharmacologic treatments.
Reduction of migraine triggers
Patients should avoid factors that precipitate a migraine attack (e.g. lack of sleep, fatigue, stress, certain foods, use of vasodilator medications). Patients should be encouraged to use a daily diary to document the headaches. Patients may need to discontinue any medications that exacerbate their headaches.
Occipital nerve stimulators
Occipital nerve stimulators may be helpful in patients whose headaches are refractory to other forms of treatment. In 2013, the FDA approved the Cerena Transcranial Magnetic Stimulator (Cerena TMS), the first device to relieve pain caused by migraine headache with aura for use in patients aged 18 years and older. Users hold the device with both hands to the back of the head and press a button to release a pulse of magnetic energy that stimulates the occipital cortex. The recommended daily usage of the device is not to exceed one treatment in 24 hours.34, 35
Based upon a previous randomised trial (the Disability in Strategies of Care, or DISC study), choosing a treatment strategy matched to the severity of headache-related disability proved superior to a step-care approach.
A step-care approach recommends all patients are initially treated with simple analgesics, and treatment escalates if necessary. The stratified approach produced a significantly faster relief
from headache symptoms, and reduced disability time
compared to the step-care approach.36
The use of abortive therapy alone in the acute management of migraine may be an appropriate option for patients who experience fewer than two migraines per month or who use abortive medications less than two days per week.
Analgesics used in migraine include paracetamol, NSAIDs, and narcotic analgesics (e.g. oxycodone and morphine). Drugs marketed especially for migraines, such as the mixture of paracetamol and caffeine, also may relieve mild to moderate migraine discomfort but are insufficient alone for extreme migraines. If taken excessively or for a long time, some of these medications can result in ulcers, gastrointestinal bleeding as well as rebound headaches.
Triptans and ergot alkaloids
The two categories of migraine-specific oral medications are triptans and ergot alkaloids.
The specific ergot alkaloids include:
- Ergotamine; and
- Dihydroergotamine (DHE).37
The specific triptans include38
The efficacy of the ergots and triptans is primarily based on their interaction at the serotonin (5-HT) receptors. Both classes of drugs constrict the pain-producing intracranial, extracerebral blood vessels in the meninges. For many individuals with migraine attacks, triptans are the drug of preference. They are efficient in relieving the pain, nausea, and sensitivity to light and sound, which
are associated with migraine headaches. With the exception of sumatriptan which is listed on Australia's Pharmaceutical Benefits Scheme (PBS) as both an oral tablet and nasal spray, the other triptans are only available as oral tablets. Sumatriptan transdermal patches have been proven effective for migraine, and one such product has received FDA approval but is not yet listed on the PBS.
Ergotamine and caffeine combination drugs (Cafergot), which is no longer available as a suppository, are generally less effective than triptans. They seemed most reliable in those whose pain lasts for over 48 hours or who had difficulty keeping oral medications down as a result of vomiting.
Anti-emetics (e.g. prochlorperazine, promethazine) are used to treat the nausea associated with acute migraine attacks.
Indications for preventive therapy include:
First line agents
- Two or more attacks per month that produce disability lasting three or more days;
- Failure of or contraindication to acute treatment;
- The use of abortive treatment more than twice a week;
- The presence of uncommon migraine conditions (e.g. hemiplegic migraine, migraine with prolonged aura).
The first-line agents with the greatest efficacy are β-blockers, tricyclic antidepressants (TCAs), and valproic acid.
The scientific and clinical evidence supports β-blockers as the drugs of choice for the prevention of migraines.40
The most commonly used agent is propranolol. Generally, if one agent fails, another in its class may be tried, and this change may prove to be effective. It is imperative that abrupt stoppage of therapy is avoided.41
β-Blockers are not effective in reducing aura.40
In general, response to these agents is gradual, and it may take at least a month to see benefits.42
Tricyclic antidepressants are another class of medication considered as first-line treatment in migraine prophylaxis. Even without the presence of depression, these agents are effective in preventing migraines, and the response is usually more rapid (within 4 weeks) than with β-blockers.42, 43,44
Combined use with β-blockers does not reduce the incidence of migraines.40
Although the entire class is considered useful in prophylaxis, tertiary amines, such as amitriptyline, are more effective than the secondary amines, such as nortriptyline. Amitriptyline is the first-line agent of choice among the tricyclic antidepressants.
Valproic acid is also a first-line agent in migraine prevention. It is traditionally used as an anticonvulsant for patients treat epilepsy. Other anticonvulsants either have no efficacy or have not proved effecacy at this time.
Second line agents
Calcium channel blockers:
Calcium channel blockers are effective second-line agents.40, 42
They are usually slower in onset than β-blockers, and an initial increase in headache frequency may occur on starting therapy. They are a viable alternative in patients who cannot tolerate β-blockers.
Nonsteroidal anti-inflammatory drugs (NSAIDs):
NSAIDs can be used daily or intermittently. When migraine triggers are identified or are predictable—such as menstruation— intermittent therapy may be used (using NSAIDs one week before menses and then throughout menstruation).45, 46, 47
Naproxen is the most commonly used NSAID for migraine prophylaxis.40, 42
Other NSAIDs that may be substituted for naproxen are mefenamic acid, ketoprofen, and aspirin.
Third line agents.
Two medications that have proved effective in prophylaxis but are reserved for severe or refractory cases are:
- methysergide; and
Both should be reserved for use only by specialists in headache treatment.40, 41
Because of its side-effects profile, numerous precautions, and contra-indications, methysergide has become a last-line drug. Longer than 6 months of continuous use can lead to fatal retropleural, retroperitoneal, or cardiac fibrosis, and drug holidays must be instituted when methysergide is used.
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- MIA - Migraine Impact in Australia– survey by Stollznow Research, via national online panel, conducted in April 2011 amongst 507 Australians with migraine aged 18-64. The MIA survey was developed as a partnership initiative between Headache Australia and MSD. The survey was funded by MSD.
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